Hepatobiliary: Focal hypoattenuation along the falciform ligament, typical regions for regional focal fat deposition. Portal and hepatic veins are patent. Focal nodularity along the nondependent gallbladder wall measuring 3 mm (404:32), probably correlating to polyp seen on ultrasound. No biliary dilation.
Pancreas: Punctate hypodensity in the uncinate process (4 1:28).
Spleen: Splenomegaly, measuring up to 14.7 cm in AP diameter.
Adrenals: The adrenal glands are unremarkable.
Genitourinary: Few subcentimeter too small to characterize hypodensities in the left kidney. Nonobstructive calculus in the lower pole measuring 3 mm. No hydronephrosis. The bladder is unremarkable.
Gastrointestinal: Partial imaged circumferential thickening of the distal esophageal wall. Small hiatal hernia. Normal bowel caliber. No perienteric inflammation. The appendix is normal.
Lymphatics: No enlarged or abnormal appearing lymph nodes.
Vascular: Abdominal aorta is normal in caliber. Tiny paraspinal and paraesophageal varices.
MSK/Body Wall: No concerning bony lesion identified.
Peritoneum/Other: No extraluminal gas. No extraluminal fluid. Impression IMPRESSION: 1. No acute abnormalities identified in the abdomen or pelvis. 2. Nonobstructive right lower pole calculus. 3. Splenomegaly. 4. Small hiatal hernia with mild circumferential thickening of the distal esophageal wall, possibly esophagitis. Correlate with endoscopy findings. 5. Punctate hypodensity in the pancreatic uncinate process. Reference recommendation below
The blood work looked decent Sodium 135 Protein 7.7 Albumin 4.5 Billrubin 1.1 AST 16 ALT 19 INR 1.1 GGT 33 Platelets 209 WBC 5.02 RBC 4.54
I'll see the GI on the 29th and hopefully get more tests and answers but for right now I feel like I was given a death sentence.

Transient Capillary Leak Syndrome is one element of Junction Dysfunction. The following text is taken from https://en.wikipedia.org/wiki/Capillary_leak_syndrome
Capillary leak syndrome, or vascular leak syndrome, is characterized by the escape of blood plasma through capillary walls, from the blood circulatory system to surrounding tissues, muscle compartments, organs or body cavities. It is a phenomenon most commonly witnessed in sepsis, and less frequently in autoimmune diseases, differentiation syndrome, engraftment syndrome, hemophagocytic lymphohistiocytosis, the ovarian hyperstimulation syndrome, viral hemorrhagic fevers, and snakebite and ricin poisoning.[1] Pharmaceuticals, including the chemotherapy medications gemcitabine and denileukin diftitox, as well as certain interleukins and monoclonal antibodies, can also cause capillary leaks.[1][2] These conditions and factors are sources of secondary capillary leak syndrome.
Systemic capillary leak syndrome (SCLS), also called Clarkson's disease, or primary capillary leak syndrome, is a rare, grave and episodic medical condition observed largely in otherwise healthy individuals mostly in middle age.[3] It is characterized by self-reversing episodes during which the endothelial cells which line the capillaries, usually of the extremities, separate for one to three days, causing a leakage of plasma mainly into the muscle compartments of the arms and legs. The abdomen, the central nervous system, and the organs (including the lungs) are typically spared, but the extravasation in the extremities is sufficiently massive to cause circulatory shock and compartment syndromes, with a dangerous hypotension (low blood pressure), hemoconcentration (thickening of the blood) and hypoalbuminemia (drop in albumin, a major protein) in the absence of other causes for such abnormalities.[3][4] SCLS is thus a limb- and life-threatening illness, because each episode has the potential to cause damage to limb muscles and nerves, as well as to vital organs due to limited perfusion.[3][4] It is often misdiagnosed as polycythemia, polycythemia vera, hyperviscosity syndrome, or sepsis.[3]
Symptoms
Most SCLS patients succumb to viral infections manifesting themselves by way of flu-like symptoms (like a runny nose), gastro-intestinal disorders (diarrhea or vomiting), or general weakness or pain in the limbs, but others get no particular or consistent warning signs ahead of their episodes. They subsequently develop thirst and lightheadedness and the following conditions measurable in a hospital emergency-room setting: [3][4][5]
hemoconcentration (elevated hematocrit and hemoglobin readings, with hematocrit levels >49% in men and >43% in women, not because of an absolute increase in them but because of the leak of plasma); very low blood pressure (profound arterial hypotension, with systolic blood pressure levels <90 mm Hg); albumin deficiency (hypoalbuminemia measuring <3.0 g/dL); partial or generalized edema, and cold extremities; a paraprotein in the blood (an MGUS in approximately 80% of cases).
Cause
Although the precise molecular cause of SCLS remains undetermined, scientific research in recent years, conducted mainly at a unit (NIAID) of the U.S. National Institutes of Health, has shed some light on its biological and chemical roots. The study of the peripheral microvasculature from patients’ biopsy specimens has not evidenced gross anomalies, disrupted angiogenesis, or inflammatory cells or other factors suggestive of a disorder prone to damage the blood vessels by inflammation.[4] The absence of structural abnormalities is thus consistent with the hypothesis of some kind of defective but curiously reversible cellular phenomenon in the capillaries.[6]
Studies suggest that the presence of various inflammatory factors during episodes of SCLS may explain the temporarily abnormal permeability of the endothelial cells lining the inner surface of the capillaries. These include transient spikes in monocyte- and macrophage-associated inflammatory mediators[4] and temporary increases in the proteins vascular endothelial growth factors (VEGF) and angiopoietin-2.[6] The impairment of endothelial cells in laboratory conditions provoked by serum taken from patients who were having episodes of SCLS is also suggestive of biochemical factors at work.[6][7]
There is no evidence that SCLS is hereditary, and the role of specific gene defects in patients with SCLS, which might program their endothelial cells for an overreaction to external stimuli such as viral infections, has not been established.[4] The significance, if any, of the paraprotein (MGUS) present in most patients with SCLS is unknown, other than it has been a precursor to multiple myeloma in a minority (7% in the largest reported cohort) of SCLS patients.[4][8]
Diagnosis
SCLS is often difficult to recognize and diagnose on initial presentation, and thus misdiagnoses are frequent. The characteristic triad of profound arterial hypotension, hemoconcentration (elevated hematocrit, leukocytosis, and thrombocytosis), and hypoalbuminemia in the absence of secondary causes of shock and infection, requires diagnosis in a monitored hospital setting during or after an acute episode. The fact that the condition is exceedingly rare – an estimated one per million inhabitants – and that several other diseases exhibit features akin to SCLS, including secondary capillary-leak syndrome or hypoproteinemia, militate against early identification.[3][8] Preserved consciousness, despite severe shock and hypotension, is an additional and most intriguing clinical manifestation often reported during episodes at hospital admission.[5]
Treatment
The natural history of SCLS episodes indicates they usually resolve spontaneously within 2-to-4 days, and that they consist of two distinct phases:[3][4][5]
The capillary leak phase
The initial stage is the capillary leak phase, lasting from 1 to 3 days, during which up to 70% of total plasma volume invades body cavities, especially in the extremities.[3][4] The most common clinical features are flu-like symptoms such as fatigue; runny nose; lightheadedness up to and including syncope (fainting); limb, abdominal or generalized pain; facial or other edema; dyspnea; and hypotension that results in circulatory shock and potentially in cardiopulmonary collapse and other organ distress or damage.[3][4][5] Acute kidney injury or failure is a common risk due to acute tubular necrosis consequent to hypovolemia and rhabdomyolysis.[3][4][5] The escape of fluid out of the capillaries has similar effects on the circulation as dehydration, slowing both the flow of oxygen delivered to tissues and organs as well as the output of urine, causing oliguria.
Urgent medical attention in this phase often features fluid resuscitation efforts, mainly the intravenous administration of saline solution plus hetastarch or albumin and colloids (to increase the remaining blood flow to vital organs like the kidneys), as well as glucocorticoids (steroids like methylprednisolone, to reduce or stop the capillary leak).[3] However, the impact of such fluid therapy is always transient and leads to increased extravascular fluid accumulation, engendering multiple complications especially compartment syndrome and thus limb-destructive rhabdomyolysis.
Consequently, fluid resuscitation should be minimized as much as possible in patients experiencing episodes of SCLS, and they should be closely monitored in a hospital intensive-care setting including for orthopedic complications requiring surgical decompression.[3][4][5] Recent clinical experience suggests that administration of immunoglobulins (IVIG) with minimal additional intravenous fluids, close to the start of an episode of SCLS, is a safe way to support patients during their leak phase and is associated with rapid clinical improvement.[9]
The recruitment phase
The second stage features the reabsorption of the initially extravasated fluid and albumin from the tissues, and it usually lasts 1 to 2 days. Intravascular fluid overload leads to polyuria and can cause flash pulmonary edema and cardiac arrest, with possibly fatal consequences.[3][4] Death from SCLS typically occurs during this recruitment phase because of pulmonary edema arising from excessive intravenous fluid administration during the earlier leak phase.[3][4] The severity of the problem depends on to the quantity of fluid supplied in the initial phase, the damage that may have been sustained by the kidneys, and the promptness with which diuretics are administered to help the patient discharge the accumulated fluids quickly.[3] A recent study of 59 acute episodes occurring in 37 hospitalized SCLS patients concluded that high-volume fluid therapy was independently associated with poorer clinical outcomes, and that the main complications of SCLS episodes were recovery-phase pulmonary edema (24%), cardiac arrhythmia (24%), compartment syndrome (20%), and acquired infections (19%).[5]
The prevention of episodes of SCLS has involved two approaches. The earliest was advocated by the Mayo Clinic, and it recommended treatment with high doses of beta agonists such as terbutaline, phosphodiesterase-inhibitor theophylline, and leukotriene-receptor antagonists montelukast sodium.[8][10]
The rationale for use of these drugs was their ability to increase intracellular cyclic AMP (adenosine monophosphate) levels, which might counteract inflammatory signaling pathways that induce endothelial permeability.[4] It was the standard of care until the early 2000s, but was sidelined afterwards because patients frequently experienced renewed episodes of SCLS, and because these drugs were poorly tolerated due to their unpleasant side effects.[4][11][12]
The second, more recent approach pioneered in France during the early 2000s involves monthly intravenous infusions of immunoglobulins (IVIG), with an initial dose of 1-2 gkg/month of body weight, which has proven very successful as per abundant case-report evidence from around the world.[4][11][12][13]
IVIG has long been used for the treatment of autoimmune and MGUS-associated syndromes, because of its potential immunomodulatory and anticytokine properties. The precise mechanism of action of IVIG in patients with SCLS is unknown, but it is likely that it neutralizes their proinflammatory cytokines that provoke endothelial dysfunction.[6][11][12][13]
A review of clinical experience with 69 mostly European SCLS patients found that preventive treatment with IVIG was the strongest factor associated with their survival, such that an IVIG therapy should be the first-line preventive agent for SCLS patients.[12] According to an NIH survey of patient experience, IVIG prophylaxis is associated with a dramatic reduction in the occurrence of SCLS episodes in most patients, with minimal side effects, so it may be considered as frontline therapy for those with a clear-cut diagnosis of SCLS and a history of recurrent episodes.[11]
A recent study involving 59 patients to evaluate the safety of IVIG tapering and withdrawal in French and Italian patients with SCLS concluded that the incidence of severe flares was not statistically different across the different dosages of IVIG, but that withdrawal was associated with increased mortality and higher rates of recurrence, such that lifelong treatment with IVIG is recommended for patients with SCLS.[14]
Prognosis
In mostly European experience with 69 patients during 1996–2016, the 5- and 10-year survival rates for SCLS patients were 78% and 69%, respectively, but the survivors received significantly more frequent preventive treatment with IVIG than did non-survivors. Five- and 10-year survival rates in patients treated with IVIG were 91% and 77%, respectively, compared to 47% and 37% in patients not treated with IVIG.[12] Moreover, better identification and management of this condition appears to be resulting in lower mortality and improving survival and quality-of-life results as of late.[4]
History
The syndrome was first described by a team of New York City physicians led by Dr. Bayard D. Clarkson in 1960,[15] after whom it was later informally named. Beyond numerous case reports published since then, three comprehensive reviews of clinical and research experience were published in 2017.[4][5][12]

The following Podcast summary was created with the Recall Browser extension

Introduction (00:00:00)

• Andrew Huberman introduces the Huberman Lab Podcast which delivers zero-cost science and science-based tools to the public.
• The host has a cooking burn on his face, but assures everyone that despite the mishap, both he and his dog, Costello, are fine.
• The episode is sponsored by Four Sigmatic, a company that produces a mushroom coffee that Huberman personally enjoys due to its taste and beneficial ingredients like lion's mane mushroom and Chaga mushroom.
• A promotion for Blinkist is also offered, emphasizing its utility in summarizing key concepts of books in a short format which can be read or listened to.
• Theragun, another sponsor mentioned, provides a percussive therapy device for muscle tension relief, with Huberman sharing his own positive experience.

Hormone Optimization (00:05:50)

• The podcast will focus on hormone optimization, specifically regarding estrogen and testosterone.
• Hormones are highlighted for their significant influence on mood, behavior, feelings of optimism or pessimism, and how our actions and thoughts can also affect hormones.
• The previous episode discussed sexual development from chromosomes to puberty, while this one will concentrate on post-pubertal processes with an integration of practical optimization tips for hormones.

Salutogenesis: A Powerful Way to Conceptualize Health (00:07:00)

• The concept of salutogenesis is introduced as an approach emphasizing behaviors that promote well-being beyond the baseline, as opposed to the pathogenic model which focusses on avoiding diseases.
• Salutogenesis involves a proactive mindset towards health-driven behaviors like exercise and proper nutrition—not solely for disease prevention but for enhancing quality of life.
• The mindset and understanding of salutogenic actions can amplify their physiological benefits, as evidenced by studies showing better health outcomes when individuals are cognizant of the positive impacts of their behavior.

Estrogen and Testosterone: Sources, Levels & Ratios (00:10:03)

• Estrogen and testosterone, along with their derivatives, are sex steroids present in everyone, with varying ratios influencing well-being, anxiety, reproduction, and sexual behavior.
• These hormones can be optimized through behaviors, dietary supplements, and medications.
• Estrogen and testosterone are majorly produced by ovaries and testes, respectively, but adrenals can also produce testosterone.
• Aromatases are enzymes that convert testosterone into estrogen and are made by body fat and the testes.
• There is a wide range of hormonal levels between individuals and within an individual's lifespan.
• Hormonal levels vary greatly; for example, estrogen increases during puberty in females and decreases after menopause, while testosterone fluctuates less predictably in males, sometimes remaining high even into advanced age.
• The release of steroid hormones like testosterone from the adrenals is activated by competition.

The Power of Competition, Plus: Anxiety, Persistence & Dopamine (00:15:46)

• Competition is closely linked to sex steroid hormones, which in turn affect competitive behavior.
• Testosterone reduces anxiety and promotes novelty-seeking and competitive interactions, while binding to the amygdala to change stress thresholds.
• Both males and females with high testosterone engage in more novelty-seeking behaviors and have heightened libidos.
• Competitive environments can raise testosterone levels, and winning can increase both dopamine and testosterone.
• Dopamine released in the brain stimulates the production of more testosterone.
• All individuals within a species are involved in competition for resources and mates.

Testosterone & Libido Pre-Ovulation (00:20:58)

• Testosterone increases in females lead to a rise in libido, especially pre-ovulation.
• This effect is consistent regardless of the individual's chromosomal or gonadal background.

Estrogen & Sexual Receptivity; Libido In Males (00:21:48)

• In females, estrogen increases promote receptivity to mating, while in males, both testosterone and estrogen are necessary for libido, with estrogen playing a crucial role.
• Balance between hormone levels is important for sexual function in both males and females; high testosterone does not guarantee high libido without sufficient estrogen.

How Sex Behavior Impacts Testosterone: Observing vs. Actual vs. Abstinence (00:23:10)

• Testosterone promotes sex-seeking behavior and can be increased by sex.
• During sex, testosterone increases significantly, especially if there's no ejaculation.
• Observing sexual activity, such as pornography, leads to modest testosterone increases.
• Actual sexual intercourse leads to a greater increase (approximately 70%) in testosterone.
• Abstinence or avoiding ejaculation can lead to an increase in testosterone levels by up to 400%.
• Ejaculation does not decrease testosterone but increases prolactin, influencing the refractory period.

Testosterone & Prolactin: Sex Seeking vs Pair Bonding (00:26:46)

• Testosterone and dopamine rise during sex-seeking and sexual activity.
• After sex, prolactin levels increase, which may facilitate pair bonding by promoting calmness and intimacy.

DHEA (dehydroepiandrosterone): Effects on Levels/Ratios (00:27:30)

• DHEA increases both testosterone and estrogen.
• The effect of DHEA on hormone levels depends on a person's starting hormone levels and aromatase activity.
• Aromatase activity can shift DHEA conversion towards estrogen rather than testosterone production.

Behaviors That Decrease Testosterone (& Cortisol): Parenting & Prolactin (00:28:45)

• Parenting, especially among expecting fathers, can lead to decreased testosterone, decreased cortisol, and increased estradiol.
• Increased prolactin due to parenthood influences these hormonal changes.
• Prolactin suppresses sex steroid hormones and promotes hormones associated with parenting behavior.

How Illness Impacts Testosterone & Estrogen: Cytokines, e.g., IL-6 (00:31:24)

• Illness, by increasing inflammatory cytokines such as IL-6, reduces the desire for sex and hormones like testosterone and estrogen.
• IL-6 inhibits the gonads and interferes with hormone receptors.
• Modulating IL-6 and increasing IL-10, an anti-inflammatory cytokine, can support sex steroid hormones.

How Exactly Do Behaviors Change Hormones? (00:33:20)

• Behaviors can significantly influence hormone levels, like testosterone and estradiol.
• The mechanisms through which behaviors impact hormones may include exposure to smells or potentially pheromones.

Pheromones: Miscarriage, Menstrual Cycles, Puberty Onset, & Mate Recognition (00:34:18)

• Pheromone effects are well-established in animals but controversial in humans.
• The Lee-Boot effect shows the impact of male presence on female ovulation cycles, but a human equivalent is not identified.
• The Bruce effect involves pregnant animals aborting when the father is replaced by a new male due to male pheromones activating certain hormonal systems.
• The Vandenbergh effect accelerates female puberty when exposed to a novel sexually competent male; mature females can delay puberty in juveniles.
• Pheromones modulate menstrual cycles in other females, as shown in studies like Stern and McClintock's experiment with sweat on pads, without necessarily causing synchronization.
• The role of the vomeronasal organ (VNO), which detects pheromones, is unclear in humans, with Jacobson's organ being a potential equivalent.
• A study demonstrated that women could identify their partner's t-shirt from many others, suggesting the presence of imperceptible pheromone cues.
• Pheromones might influence mate recognition and attachment, and perfume manufacturers exploit this concept.
• Animals exhibit the flehmen response to detect mating pheromones, reflecting a connection between smell and taste similar to what might occur in humans through perfumes containing pheromones.

Apnea: A Powerful Bi-Directional Influence On Estrogen & Testosterone (00:43:33)

• Apnea, involving under-breathing and CO2 buildup, is linked to poor estrogen and testosterone levels.
• Both advanced menopause symptoms and early-onset andropause are associated with apnea.
• Estrogen and testosterone may influence breathing patterns; their receptors are found in lung-innervating neurons.
• Directionality is unclear, but improving breathing, especially during sleep, can optimize hormones.
• Apnea primarily refers to cessation of breathing during sleep and can be mitigated with practices like the physiological sigh.

Mouth vs. Nose Breathing & Hormone Levels: Effects Via Sleep and Direct Effects (00:47:44)

• Nasal breathing is superior to mouth breathing for numerous health benefits.
• Benefits include improved facial cosmetic features, better gas exchange, and hormone optimization.
• Proper nasal breathing contributes to the effectiveness of deep sleep, supporting gonad function and thus hormone production.
• Reducing apnea through proper breathing enhances males’ testosterone and females’ estrogen to testosterone ratios.
• Hormone optimization from proper nasal breathing stems from enhanced sleep quality and reduced stress.

How Sleep Adjusts Cortisol/Testosterone and Cortisol/Estrogen Ratios (00:51:11)

• Adequate sleep can modulate cortisol, thereby affecting testosterone and estrogen levels.
• Cholesterol can convert to either testosterone or estrogen, but high cortisol diverts it towards cortisol production, lowering sex hormones.
• Nasal breathing during the day and in sleep is crucial for reducing apnea and regulating cortisol, testosterone, and estrogen.
• For severe sleep apnea, a CPAP machine may be needed, while others might benefit from mouth taping during sleep.
• During the day, nasal breathing can be improved by dilating nasal passages to encourage better breathing habits.

02:CO2 Ratios, Nasal Breathing During Exercise (00:53:49)

• Breathing through the nose, especially during cardiovascular exercise, improves over time as sinuses dilate.
• Nasal breathing has several benefits including reducing apnea, increasing lung capacity, reducing cortisol levels, and indirectly raising testosterone and estrogen.
• This practice is cost-free and positively affects hormonal balance, sleep quality, and cosmetic aspects.
• Exceptions to nasal breathing include swimming and certain sports where mouth-breathing is appropriate.

Light Viewing Patterns & Hormones: Dopamine, GnRH (00:56:30) & Spring Fever: Tyrosinase, Hair Color, Mating Frequency (00:57:44)

• Light viewing, especially within the first hour of waking, can significantly impact hormone levels and fertility.
• The relationship between light, dopamine, and hormones influences libido, healing, and overall well-being.
• Dopamine, which promotes sex steroid hormone release, is linked to color changes in seasonal breeding animals.
• Increased sunlight exposure to the eyes elevates mood in humans, correlating with higher levels of sex steroids and reproductive behaviors.
• A protocol for optimal hormone levels involves exposing the eyes to bright light (not through sunglasses) early in the day for 2-10 minutes and avoiding bright light at night.

Specificity of Hormone Effects (01:04:39)

• Proper breathing and light-viewing habits, supporting healthy sleep, can positively influence sex steroid hormone levels.
• Light viewing increases the right hormone ratios whether one has higher estrogen or testosterone.
• The practice ensures the optimization of hormone ratios according to a person's natural levels.

Temperature: Cold & Hot Gonads (01:06:03)

• Temperature, along with day length and sunlight, affects hormone levels, with testosterone and estrogen typically being lower in colder months.
• In sports and bodybuilding communities, cold exposure at the gonadal level is used to try and increase testosterone and libido.
• Studies suggest that the cold does not directly affect hormone levels; instead, cold exposure leads to a rebound in vasodilation, increasing blood flow into the gonads.
• The vascular system, controlled by neurons, plays a role in hormone delivery. Cold exposure may temporarily shut down these neurons controlling vasoconstriction.
• After cold exposure and subsequent rewarming, a rebound hyper-vasodilation possibly delivers higher levels of hormones to stimulate gonad activity.
• There is no clear evidence that cold and heat directly affect testosterone and estrogen production; they more likely modulate hormone levels through mechanisms like blood flow.
• Excessive heat can damage sperm health and fertility, potentially altering proteins crucial for sperm function, independent of its role in hormone production.

How To Exercise: Types, Effort Level, Sequencing (01:14:10)

• Weight training of heavy resistance, in the 1-8 rep range, significantly boosts testosterone for a day or up to 48 hours in males and females.
• Studies focused on neuroscience indicate neurological engagement during high-threshold motor unit recruitment for moving heavy loads, but not to failure, stimulates increased testosterone or receptor activity.
• High-intensity, weight training that does not reach muscle failure is scientifically backed to best increase testosterone.
• Specific exercises or movements have not been fully explored for their direct mechanisms on boosting testosterone.

Cardio/Endurance vs. Resistance Training (First or Last?) Yes, It Matters (01:21:42)

• Performing weight training first, followed by cardio or endurance workouts, in the same session is optimal for testosterone.
• On separate days, the sequence of cardio and weight training does not impact testosterone.
• High-intensity interval training boosts testosterone, whereas prolonged endurance activity beyond 75 minutes may lower it, likely due to cortisol increases.
• It is unclear if less intense activities like hiking for extended durations have the same testosterone-reducing effect as more intense endurance exercises.
• To manage cortisol, endurance exercises should ideally be kept under 75 minutes and not be too intense.
• Professional endurance athletes occasionally use exogenous testosterone to negate cortisol-induced reductions during prolonged exertion.

Estrogen & Menopause: Compounds That May Ameliorate/Reverse Symptoms (01:24:41)

• Menopause is characterized by a massive reduction in estrogen due to depleted ovary function.
• Common menopausal symptoms include hot flashes, mood swings, migraine headaches, and brain fog.
• Hormone therapy is used to supplement estrogen, with varying success and potential side effects.
• Concerns arise when supplementing estrogen with a family history of breast cancer, due to estrogen-dependent cancers.
• Non-estrogenic alternatives, such as black cohosh and Panax ginseng, show modest benefits in improving menopause symptoms.
• Pueraria mirifica has evidence suggesting it is comparable to estrogen therapy in reducing menopause symptoms.
• All hormone-related treatments should be approached with caution and discussed with a healthcare provider.

Nutrients That Optimize The Foundation For Hormones (01:33:18)

• Certain nutrients are key for promoting proper testosterone and estrogen production, including vitamin D, zinc, and magnesium.
• Deficiencies in these nutrients negatively impact the endocrine system, including sex-steroid hormone production.
• Dosage for nutrients should be individual-dependent and based on blood work results.
• Regular blood work can help monitor and adjust levels of androgens and other vital nutrients.

Opioids as Severe Hormone Disruptors (01:36:00)

• Opioids dramatically reduce levels of sex-steroid hormones in both men and women.
• Opioid usage disrupts receptors on gonadotropin-releasing hormone neurons in the hypothalamus, affecting the pituitary.
• Long-term or high-dosage opioid use leads to endocrine syndromes such as gynecomastia in men and ovary disruptions in women.
• The major effect of opioids on hormones is the suppression of GnRH production, which in turn lowers testosterone and estrogen release.

Testes, Antlers & Ovaries (01:37:23)

• Various substances claimed to affect androgens range from deer antler material to consumption of bull testes.
• The industry around testosterone is vast and has historical roots.
• Understanding of estrogen structure led to birth control pill development.
• Scientific support exists for some supplements that can adjust androgens like testosterone and DHT.

Creatine & Increasing DHT (Dihydrotestosterone) (01:38:50)

• Creatine is observed to increase DHT levels, influencing masculinization and potentially contributing to hair loss depending on individual susceptibility.
• The mechanism by which creatine affects DHT is unclear, but may involve increased 5-alpha reductase activity or enhanced susceptibility of testosterone to enzymatic reactions.

Free and Bound Testosterone: SHBG (Sex Hormone Binding Globulin), Tongat Ali (01:40:14)

• Testosterone in the blood exists in both free and bound forms, with most being bound to SHBG or albumin for transport.
• The role of binding globulins is transportational, not merely to reduce bioavailable testosterone.
• Supplements like tongkat ali are reported to promote fertility, increase free testosterone, and have subtle aphrodisiac effects.

Nettles, Prostate, Boron, & Blood Brain Barrier (01:43:23)

• Nettles may free up testosterone but could also affect the prostate and liver.
• Boron has some scientific support for increasing free testosterone.
• Albumin is important for allowing testosterone to reach the brain and influence behavior.

Hormone Related Cancers: Sometimes Reducing Estrogen and Testosterone Is Optimal (01:45:27)

• Modulating hormones can impact tissues that depend on those hormones, making tissues with rapid cell turnover, like breast and testicular tissue, susceptible to cancer.
• Anti-androgenic drugs are used to prevent testosterone from promoting tumor growth.
• An increase in androgens or estrogens is not universally beneficial; moderation is key, especially given the link to cancer in rapidly replicating tissues.

Ecdysteroids: Mimic Mammalian Hormones (01:47:43)

• Ecdysteroids like turkesterone from spinach have similarities with cholesterol, the precursor to testosterone, cortisol, and estrogen.
• Ecdysteroids are bioavailable, or their metabolites are, and can be effective in humans, having traditionally been thought limited to other species.
• A study suggests ecdysteroids significantly increase muscle mass and strength above placebos, prompting recommendations for their prohibition in sports.
• There is ongoing debate around hormone augmentation in sports, particularly testosterone following injuries, which legally enhances recovery and performance.
• Estrogens and testosterones modulate gene expression and the brain's response to effort and anxiety.
• Supplementation effects are generally more subtle compared to direct hormone injections.

Optimizing Brain Hormones: Chorionic Gonadotropin, Fadogia Agrestis (01:51:50)

• Hormones like luteinizing hormone (LH) from the pituitary promote the release of other hormones in the body; LH specifically aids in sperm/testosterone production and egg/estrogen production.
• Synthetic human chorionic gonadotropin (hCG) increases fertility in both genders by mimicking the effect of LH.
• hCG, at one time collected from the urine of pregnant women, is now synthetically available and used for fertility and sometimes athletic performance.
• The supplement Fadogia agrestis has been shown to increase LH, which in turn raises levels of testosterone and estrogen.
• The ratio of hormones can affect the increase for individuals with different chromosomal or gonadal backgrounds.
• The importance of blood work is emphasized for anyone considering hormone-modifying supplements due to potential negative feedback mechanisms.

Additional Compounds, Liver Toxicity, Overall Milieu (01:57:18)

• The list of compounds affecting estrogen and testosterone is extensive, but focus is on those with human studies.
• Bulbine natalensis increases testosterone in rat studies, but has concerns about liver toxicity and lacks robust human studies.
• Sponsored research may provide biased evidence for certain compounds compared to independent studies.
• Other supplements mentioned, such as magnesium, D3, and zinc, create a supportive milieu for normal hormone production rather than significantly increasing levels.
• Differentiating between supplements that offer general support and those that cause major hormonal changes is important for understanding individual effects.

https://doi.org/10.1080/10942912.2023.2275528

Effect of ketogenic diet and hypocaloric Mediterranean diet on metabolic and endocrine parameter in women suffering from Polycystic Ovary Syndrome

Abstract

PCOS is the most prevalent female endocrine disorder and is characterized by polycystic ovaries, hyperandrogenism, and protracted anovulation. In PCOS, obesity, low-grade chronic inflammation, and insulin resistance (IR) frequently coexist. The Mediterranean diet (MD) and Ketogenic diet act as an anti-inflammatory eating plan that is high in complex carbohydrates, fiber, and monounsaturated fat, whereas the Keto diet is high in fat content. PCOS is associated with obesity, low-grade chronic inflammation, insulin resistance, and hormonal imbalances. The aim of the present study was to measure the metabolic and endocrine effects of a ketogenic and hypocaloric Mediterranean diet in women with polycystic ovarian syndrome. For this purpose, 80 participants were divided into two groups. Group 1 was on the ketogenic diet and Group 2 was on the Mediterranean diet for 9 weeks. The result of the present study showed that significant weight was reduced among the keto group (−10.9 kg) as compared to the Mediterranean group (−5.1 kg). Total cholesterol and Low-Density Lipoprotein among the keto group was 181. 5 ± 22.2 and 85.3 ± 16.2 u/L whereas, in the Mediterranean group 190.3 ± 22.7 and 91.3 ± 15.9 u/L were observed. Blood glucose levels among the Keto and Mediterranean groups reduced significantly 83.47 ± 5.81 and 91.7 ± 5.8 (mg/dl). C-peptide, LH, and FSH also improved more significantly as compared to the Mediterranean group respectively. This study revealed that a ketogenic diet is superior to a hypocaloric Mediterranean diet for lowering Triglyceride, Cholesterol, LDL, blood glucose, insulin, C peptide, HOMA-IR, LH/FSH, Serum Albumin, Facilitating Hormone, and Sex hormone-binding globulin levels. Females having PCO may improve health with the ketogenic diet
------------------------------------------ Info ------------------------------------------
Open Access: True (not always correct)
Authors:

• Iqra Masood
• Sana Noreen
• Komal Raza
• Waseem Khalid
• Muhammad Abdul Rahim
• Khalid Abdelsamea Mohamedahmed

Additional links:

• https://www.tandfonline.com/doi/pdf/10.1080/10942912.2023.2275528?needAccess=true

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I am here to expose my theory, of what I consider could be one of the mechanisms behind the quinolone toxicity syndrome (my opinion, I am not a medical authority).
I suffered a severe reaction after only 2 applications of moxifloxacin eye drops, in total I applied 4 drops, two in each eye. I have read in this group people who also had a severe reaction with topical quinolones.
I was a healthy person and after those 4 drops, I was unable to walk for months to the point of almost rupturing my achilles and forearm tendons. I had to stop training and lost more than 20 kilos, I developed a plethora of neurological symptoms, tinnitus, vertigo, fasciculations, neuropathy, dysautonomia and a long list of other symptoms .... after what? only 4 drops!!!
In studies in healthy volunteers, a tear concentration of ofloxacin was observed of 5.7 - 31 micrograms/g for 40 minutes after the last dose on day 11. Peak serum concentrations of ofloxacin, after 10 days of topical dosing were approximately 1000 times lower than those reported after standard oral doses of ofloxacin.
Would a ridiculous dose of 4 drops be enough to account for global mitochondrial damage affecting all organ systems of the body? Could an immunological reaction be a possible explanation in which it would make sense that the amount of drug would not correlate with the severity of the reaction?
Before taking moxifloxacin, I was taking cholecalciferol (vitamin D), omeoprazole, NAC, topical minoxidil (for growing my bear ^^ ) daily and with the moxifloxacin treatment I was prescribed dexamethasone to reduce inflammation and naproxen. Guess what? Surprisingly enough, the only meds I can't tolerate under any circumstances because they cause severe tendon relapse, neurological symptoms and what appears to be a cascade of vascular inflammation with splinter hemorrhages in my hands, are the ones I take in conjunction with the moxifloxacin.
I have tried taking them one by one, even when I fully recovered for two years, and they all activate that inflammatory response within a few hours.
It is amazing, but what is even more amazing is that I can tolerate ibuprofen, prednisone, esomeprazole, pantoprazole and topical finasteride with no problem, they are all analogous brothers to the drugs that cause brutal relapses in my body and yet I can take them with no problem.
If there was prior damage at the cellular level one should expect a similar result with those sister drugs, some of which are even more toxic than the ones I discussed at the beginning.
I asked two guys from a whatsapp group in my city who had suffered an acute reaction to quinolones and they both had splinter hemorrhages in their nails, some very subtle, but they had started to notice them since taking the fluoroquinolone.
One told me that these hemorrhages were made much worse by taking a medicine that he had been taking since he was a child for an ADHD: atomoxetine and that he also associated the splinter hemorrhages with a general worsening of tendons and neurological symptoms. They changed his medication to viloxazine and all of his symptoms improved.
What am I trying to say with this? Can the reaction by quinolones be divided into two phases? An acute phase, where regardless of the amount ingested, quinolones would produce direct toxic damage to tendons and tissues of the nervous system and this in turn, in some people due to genetic or multifactorial factors, activates an aberrant immune response, an inflammatory cascade mediated by a type III (antibody-mediated) or type IV (cellular mediated) hypersensitivity reaction that, for unknown reasons, in many cases, cannot be abated with drug withdrawal, causing persistent damage at the microcirculation level, which could be an explanation for the multiple symptoms that most of us experience?
Referring to the flox report, although it is an old document, it comments on several things that I find interesting.
I quote what it says:
​

Blood has to travel all over the body in order to supply every cell of the body with nutrients and oxygen, and to remove the wastes from all the tissues. The blood has to be able to send its white blood cells into the surrounding tissue cells to clean it up and respond to injury.
These functions of blood require that it can exchange its materials with its surrounding tissues. Arteries and veins are not designed for exchange but merely for transport. It is in the tissue where the exchange has to take place. Therefore, the capillaries (microvessels), which lie in the cellular matrix between arteries and veins, must be the regions for exchange. The quinolone antibiotics alter the cellular matrix and also target the vasa vasorum and vasa nervorum, either changing the capillaries permeability (the microvessels are one cell thick and allow the exchange of substances through openings), or inducing the deposition of immunological complexes inside them, or causing a spasm-like narrowing of their ducts, or simply chemically damaging them. In any case, the result is the same: muscles, skin, nerves, heart, brain and other organs are deprived of adequate blood flow (ischemia), and owerwhelmed by toxic intermetiate compounds and they die or do not work properly.
For the sake of simplicity, in this report we call quinolone-vasculitis the degradation of the extracellular matrix plus an alteration of the microvessel walls with vascular damage or attending tissue injury.
What nobody knows and requires much more research are the factors that determine the duration of disease, the type of tissues involved and their damage, as well as how to target therapies at inflammation without interfering with healing. Apparently, part of the process explained earlier is conveyed through an immune response of the body.
Immune complexes with certain immuno-chemical characteristics activate a complementary cascade that induces neutrophil mediated damage to the vessel wall. The presence of granulocytes is usually associated with fibrinoid necrosis as would be expected on the basis of their release of toxic enzymes during inflammation. Necrosis in the vessel wall is a large contributor to scarring and the delayed sequelae present in some cases of vasculitis, such as the quinolone-induced vasculitis.
Accumulation of inflammatory cells in the vessel wall is the common feature of common vasculitis, although it is not well understood how tissue damage occurs. It is widely admitted that there is a threestage process:
1- initiation of the injury
2- recruitment of inflammatory cells and tissue damage
3- regulation of the immune response.
Quinolone vasculitis is a systemic vasculitide (so called because of its multi-organ nature). Inflammation and damage can be transient or more permanent. The alterations in coagulation and vasomotor tone result from local damage to the endothelium (inner part of the walls of the ducts of large caliber and is the only layer of the wall of microvessels) as well as intrinsic components of the cytokines that are released through the process. Drug toxicities are among the causes and processes strongly associated with vascular injury.
Normally, quinolone vasculitis appears some time after exposure, and is a link in the chain of adverse events that take place for months on end. All of the vasculitides are likely secondary to some form of
inflammatory stimulus, usually infectious or toxic, as in our case. In quinolone vasculitis the real underlying cause either cannot be identified (no doctor is willing to admit that quinolones are the direct cause of vascular disorders) or has long since been cleared by the host, leaving only a chronic or recurrent inflammation focused on the vasculature.
Then, there is the issue of diagnosis. The diagnosis of vasculitis is fundamentally an invasive process (biopsy). A critical feature is the identification of inflammatory cells that diminish the delivery of blood to tissue. Furthermore, the numerous causes that may result in vasculitis can often be distinguished only at the cellular level. Histological studies characterizing injuries on the basis of the infiltrating cells may provide information on both the mechanisms inducing inflammation and predict the sequelae of the injuries. There is an urgent need to determine the underlying mechanism for appropriate treatment.
For most floxed persons the blood studies may be entirely normal. There is no serological test that confirms or excludes a vasculitis. Quinolone-vasculitis is:
 Seronegative (non-ANCA, negative SSA, SSB, anti-Sm, normal anticardiolipine, antiphospholipid, soft muscle markers, halotypes....). This alone convinces all doctors that floxed persons do not have any alteration in their inmune system.
 Drug-induced, non-abating with drug withdrawal, delayed-onset, and typically reaches its acute phase many months after drug discontinuation, when the ischemic process has managed to kill enough nerves or cells. This is considered impossible by almost all doctors, although is a proven fact.
 Not responsive to any known treatment; very long lasting or permanent, because many nerves die and cannot be regenerated.
Being non-ANCA, the floxing vasculitis is normally classified by some advanced doctors as drug-induced immuno-complex vasculitis that shares similarities with other immuno-complex vasculitides like systemic lupus erithematosus, rheumatoid arthritis and Sjögren’s disease.

Could it be that this loss of tolerance to medicines that we previously tolerated, particularly, in my experience, those that I have taken together with moxifloxacin, is due to a fight response of our immune system, which, after having suffered a toxic reaction from a drug, rejects anything exogenous that it considers a threat in a context of immune deregulation, so many people after taking cipro, levo etc... develop IgE-mediated drug allergies, mast cell syndromes and greater susceptibility to suffer side effects from the drugs....
Molecules smaller than 1000 daltons do not have the capacity to provoke an immune response per se (what are known as haptens), but when they bind to plasma proteins, they form a new molecule of greater weight, that is, an antigen, and It does have the ability to stimulate immune cells by producing antibodies by B cells or stimulate T cells that in turn secrete inflammatory cytokines and chemokines.
Quinolones and other drugs could bind to albumin or other proteins, generating a cellular memory response that would be activated every time that substance was taken, generating the same symptoms typical of the chronic phrase of quinolone syndrome without it having to be a quinolone per se. .
Would it make sense then that some patients would have benefited from biologic therapies such as infliximab, immunomodulatory drugs like IVIG etc...?
This should be investigated by those who screwed up our lives with these drugs. Until there is real interest on the part of the entire medical community to clarify what is behind quinolone toxicity syndrome, everything will be unknowns and unresolved questions.
It's just my theory, assumptions, I'm not a scientist nor do I claim to be.
And forgive me for my poor English, I'm trying to improve it without using the translator :)

Greetings, 33m here 5'10 167lbs. Went to the ER for what I felt were kidneys stones / infection emerging due to the pain I was feeling in my back flank both sides for a few days and urinary change (increased output) (no diabetes). Mentioned chest pain as well as i was feeling tightness and shortness of breath. I ended up getting a CT with contrast from my chest through abdomen / pelvis. The doctor was slammed and obviously busy and didn't have much time to go over my CT results, he basically told me I had stones but they haven't dropped yet, blood work looked great and sent me on my way.
It's been difficult to find a pcp in network in my area, 8/10 aren't taking new patients and those that are the doctor can only be seen like 6 months down the road and you just see a nurse practioner.
That said there are some results here I don't understand and haven't been able to really look up regarding liver and pelvis. I would think with contrast there would be more accurate detail. Any opinion /feedback is greatly appreciated.
EXAM: KH CT ANGIOGRAM CHEST WITH IV CONTRAST - PE PROTOCOL(CREATININE DRAW IF NEEDED), KH CT ABDOMEN/PELVIS WITH IV CONTRAST(CREATININE DRAW IF NEEDED)
CLINICAL INDICATION: Shortness of breath. Flank pain
TECHNIQUE: Following IV administration of 99 mL Omnipaque, CT scan of the pulmonary arteries with multiplanar reformatted images including MIPs generated from the data set and CT scan of the abdomen and pelvis with multiplanar reformatted images generated from the data set. Dose reduction techniques were utilized.
COMPARISON: Chest radiograph 8/29/2023
FINDINGS:
Chest:
Vascular: The pulmonary arteries enhance normally. The aorta is normal in size. No evidence of dissection.
Cardiomediastinum: Heart is normal in size.. No CT evidence of right heart strain. No adenopathy.
Soft tissues: Peripheral soft tissues are normal.
Lungs: No abnormal opacities identified.
Bones: No destructive osseous lesion.
Abdomen/pelvis:
Liver: Subcentimeter hypodensities throughout the liver, too small to accurately characterize, but probably represent benign lesions such as cysts.
Gallbladder: Normal.
Pancreas: Normal.
Spleen: Normal.
Adrenals: Normal.
Kidneys: A few punctate nonobstructing renal calculi measuring 1 to 2 mm are noted bilaterally. No hydronephrosis. Symmetric renal enhancement. No stones identified in the ureters. No hydroureter.
Gastrointestinal: The stomach, small bowel, and colon appear normal. The appendix is normal in appearance.
Pelvis: Prostate and seminal vesicles are normal. Decompressed urinary bladder not well evaluated on this exam. No stones identified in the bladder. Tiny bilateral fat-containing inguinal hernias.
Vasculature: Abdominal and pelvic vasculature appears normal.
Lymph nodes: No enlarged lymph nodes.
Bones: No destructive osseous lesion.
Bloodwork Sodium 137 Potassium 4.3 Glucose 93 Bun 10 Creatine .88 Protein 7.4 Albumin 4.9 Calcium 10.2 Bilirubin. 5 Ast 25 Alt 29 Alkaline phosphate 65 Globulin 2.5 Platelet 315 Lipase 40 EGFR >90

Introduction:

Pediatric nephrology is a specialized medical field that focuses on the diagnosis, treatment, and management of kidney diseases in children. As a branch of medicine, it addresses various conditions affecting the kidneys and their associated structures in pediatric patients, including infants, children, and adolescents. This article aims to provide an overview of pediatric nephrology, its significance in children's healthcare, and the key aspects related to this field.

Understanding Pediatric Nephrology:

Pediatric nephrologists are medical professionals who specialize in the care of children with kidney-related conditions. They possess expertise in evaluating and treating a wide range of kidney disorders specific to the pediatric population. These conditions may include congenital anomalies of the kidney and urinary tract (CAKUT), urinary tract infections (UTIs), nephrotic syndrome, acute and chronic kidney diseases, renal tubular disorders, and kidney transplantation, among others.

Significance of Pediatric Nephrology:

Pediatric nephrology plays a crucial role in ensuring the optimal health and well-being of children with kidney diseases. The kidneys are vital organs responsible for maintaining fluid and electrolyte balance, regulating blood pressure, and filtering waste products from the bloodstream. When these functions are compromised in children, it can have severe consequences on their growth, development, and overall health. Pediatric nephrologists work collaboratively with other healthcare professionals to diagnose kidney conditions early, provide appropriate treatments, and monitor long-term outcomes, thus improving the quality of life for affected children.

Common Conditions in Pediatric Nephrology:

Nephrotic Syndrome: Nephrotic syndrome is the most common glomerular disease in childhood, characterized by abnormal glomerular membrane permeability leading to massive proteinuria, hypoalbuminemia, and edema. Various treatment approaches, including corticosteroids, immunosuppressive therapy, and emerging therapies like rituximab and mycophenolate mofetil, have shown promise in managing this condition.
Congenital Anomalies of the Kidney and Urinary Tract (CAKUT): CAKUT refers to a diverse group of structural abnormalities affecting the kidneys, ureters, bladder, and urethra in newborns. It can lead to urinary tract obstruction, vesicoureteral reflux (VUR), or renal dysplasia. Early detection and intervention are essential to preserve kidney function and prevent complications.
Acute and Chronic Kidney Diseases: Children can develop acute kidney injury (AKI) due to various causes such as infections, medications, or systemic illnesses. Chronic kidney disease (CKD) in children may result from congenital abnormalities, hereditary conditions, or acquired kidney diseases. Timely management is crucial to slow disease progression and prevent long-term complications.
Renal Tubular Disorders: Renal tubular disorders encompass a group of genetic conditions that affect the renal tubules' ability to reabsorb or excrete specific substances. Examples include renal tubular acidosis, Bartter syndrome, and Gitelman syndrome. Treatment aims to manage electrolyte imbalances and optimize renal function.

Dr. Sidharth Kumar Sethi

Kidney & Urology Institute

He was trained as a Fellow (International Pediatric Nephrology Association Fellowship) and Senior Resident in Pediatric Nephrology at All India Institute of Medical Sciences and Division of Pediatric Nephrology and Transplant Immunology, Cedars Sinai Medical Centre, Los Angeles, California. He has been actively involved in the care of children with all kinds of complex renal disorders, including nephrotic syndrome, tubular disorders, urinary tract infections, hypertension, chronic kidney disease, and renal transplantation. He has been a part of an 8-member writing committee for the guidelines of Steroid Sensitive Nephrotic Syndrome and an Expert committee involved in the formulation of guidelines for Pediatric Renal Disorders including Steroid Resistant Nephrotic Syndrome and urinary tract infections. He has more than 30 indexed publications in Pediatric Nephrology and chapters in reputed textbooks including Essential Pediatrics (Editors O.P. Ghai) and “Pediatric Nephrology” (Editors A Bagga, RN Srivastava). He is a part of the Editorial Board of “The World Journal of Nephrology” and “eAJKD- Web version of the American Journal of Kidney Diseases”. He is a reviewer of Pediatric Nephrology related content for various Pediatric and Nephrology journals.

Nephrotic Syndrome

Most people have two kidneys, one on either side of the body just beneath the ribcage. Healthy kidneys filter the blood and allow small particles of waste products and water to be excreted as urine. Kidneys also play an important role in the control of blood pressure, maintenance of bone health, and formation of red blood cells.

What is nephrotic syndrome?

Nephrotic syndrome occurs when the kidneys leak large amounts of protein (especially albumin) into the urine. It is these proteins which is mainly responsible for holding water in the blood vessels, and when they are lost in urine, their level decreases in the blood which causes the water to come out of the blood vessels and cause swelling (edema).

What causes Nephrotic Syndrome?

In most cases, the exact cause of the nephrotic syndrome is not known. There is no relationship between diet or socioeconomic status of the family. It is non-infectious and does not transfer to other family members.

What are the symptoms?

The most common symptom is swelling (edema). It first appears on the face, especially around the eyes which is most prominent in the morning when the child gets up and decreases by the evening.
Other symptoms include Frothy urine, weakness, and tiredness, passing less urine than usual, recurrent infections, diarrhea.

What is the treatment?

Prednisolone (steroid) is the drug of choice when the child is first diagnosed. Most children respond to this drug with the disappearance of the protein in the urine and loss of swelling within 1-2 weeks (we call this REMISSION). Other drugs like diuretics, ACE inhibitors, etc may be required for symptomatic treatment.
Those who do not respond to steroids are given second-line drugs like Cyclophosphamide, MMF, Levamisole, and other immunomodulators as decided by your doctor according to the individual patient profile.

Conclusion:

Pediatric nephrology is a specialized medical field dedicated to diagnosing, treating, and managing kidney diseases in children. By focusing on early detection, comprehensive evaluation, and appropriate interventions, pediatric nephrologists play a crucial role in improving the health outcomes and quality of life for children with kidney conditions. Collaborative efforts between healthcare providers, ongoing research, and advancements in therapeutic approaches continue to advance the field of pediatric nephrology and benefit young patients with kidney diseases.

To schedule an appointment with Dr. Sidharth Sethi, please contact:

Name: Pediatric Nephrology India Address: Division of Pediatric Nephrology, Kidney Institute, Medanta, The Medicity, Gurgaon, Haryana, India, 122001 Phone: 0124-4141414 Website: www.pediatricnephrologyindia.com

It seems like all my comments are being deleted. I will post answer at the end of the message.
From the late 2000s to the mid-2010s, I worked as a molecular biologist for a national security contractor in a program to study Exo-Biospheric-Organisms (EBO). The aim of the program was to elucidate the genome and proteome basis of these organisms. Although the study of OBCs has been going on for decades in other programs, the new high-throughput DNA sequencing technologies of the late 90s unblocked stagnant research in this area. Since then, several breakthroughs have led to significant advances in our understanding of the genome and proteome of these beings. What we've learned so far has enabled us to outline some disconcerting perspectives about our place in this universe. Briefly, we've discovered that the EBO genome is a chimera of genomes from our biosphere and from an unknown one. They are artificial, ephemeral and disposable organisms created for a purpose that still partially eludes us. I'll be substantiating my statements after a brief introduction.
The reason for disclosing these secrets is quite simple. I believe that every human being has the right to know the truth, and that to progress, humanity needs to divest itself of certain institutions and organizations that will probably not survive these revelations in the long term. I'm aware that I'll have very little impact in this regard, but I still believe that small leaks are necessary to break the dam of misinformation on this subject. When the governments will eventually reveal these secrets, there will undoubtedly be a societal upheaval, but in my opinion, the longer we wait, the worse it will be. I choose to divulge what I know anonymously out of selfishness for the well-being of myself and my family. I'm aware that this diminishes the reach and credibility of my message, but it's the furthest I am willing to go. I chose this forum because it offers a good compromise between anonymity and popularity. In order to protect my anonymity, I will be purposely vague or even contradictory about any information that could identify me (date, education, role etc.). I'll even introduce red herrings in this respect. I want to make it clear that any information related to the subject of the research will not be treated in this way.
Before going any further, please excuse me if you find it difficult to understand what I'm explaining. Some parts of my text are very technical. It's difficult to find the right balance between vulgarization and scientific explanation. I'll continue by talking about myself. What's the point of talking about me knowing that the information will necessarily be misleading? I simply want to introduce a perspective on the type of people who work there, normal scientists. I have a Ph.D. in molecular biology. I didn't actively seek to be part of this program, rather it was a stroke of luck that introduced me to one of the senior scientists. I met this person at a conference where I was presenting a poster on my Ph.D. research. When I think back, I don't believe he was impressed by what I was presenting, because it was quite frankly a project that wasn't going anywhere. I think it was rather the most important aspect of a professional life: the attitude and the ease with which you make connections. Shortly afterwards, I graduated and received a call from this person offering me a position. At the time, everything pointed to me working in a regular laboratory.
I did a series of three increasingly suspicious interviews, each in a different location, where my scientific background and knowledge became less and less relevant. The first was with two of the senior scientists, the second and third with people I've never seen again and who were obviously not interested in science. Sometime after the interview, I was asked to go to a fourth location where what seemed like a corporate lawyer presented me with an NDA. He made sure not only to explain every detail, but also that I understood the consequence of not respecting it.
The first Employment weeks were by far the most memorable, although I spent most of that time in a depressing archive room. It consists almost exclusively of reading about the subject of study and to get us up to speed. There's no secret Wikipedia or even a reference book to guide us. There are only dry reports, memos, presentations, procedures and SOPs. These documents are almost exclusively about the biology of EBOs, but there are also a few that deal with other subjects such as their food, religion or culture. There were no documents on their technology.
As mentioned above, the aim of the project is to gain a better understanding of the EBO genome and proteome. To achieve this, a team of around twenty scientists, four senior scientists and a director was involved. The scientists, like myself, had as their main responsibility to carry out the technical work. As each scientist had to my knowledge a Ph.D., we were all somewhat overqualified for what is ultimately a technician's job. The senior scientists, who make full use of their diplomas, had the task of designing the assays and had a supervisory responsibility. They were also in charge of training new employees, and sometimes even came in to do technical work. The director, of course, was the person in charge who dictated priorities to the senior scientists. He was rarely on site, and the few times he was, it was to attend meetings. Other than the scientific staff, there were security guards working for one subcontractor or another. There were no support staff such as janitors or maintenance workers. Scientists were responsible for this kind of work. In addition, logistical constraints ensure that every scientist is capable of carrying out any technical activity.
The laboratory itself is located in Fort Detrick, Maryland, in a building used for legitimate biomedical research. The clandestine operations are carried out in a restricted part of the basement, out of sight from regular workers. Contrary to what one might imagine, the biosafety level is not maximal for this type of research. Indeed, the lab containing EBO samples or derived cell cultures is BSL3, while the lab where assays are conducted are only BSL2. The BSL3 area of the facility includes a freezer room and a cell culture lab and is only accessible through an antechamber from the BSL2 section. EBO carcasses are preserved in horizontal freezers at a temperature of -80°C nominal. To maximize the preservation of these carcasses, they are preserved in vacuum bags and the air in the room is controlled to minimize humidity. There are only four bodies and none of them are complete. It's obvious that these creatures have died as a result of major trauma. I've never witnessed a motorcycle accident fatality, but it probably looks similar to this. It is acknowledged that there are more EBOs caracasses at other locations. The cell culture laboratory, as its name suggests, is where cell lines derived from EBOs are grown and related activities are performed. I'll talk in more detail about these specific cell lines later on. The BSL2 part is mainly used for assays, immunohistochemistry, genetic engineering, immunocytochemistry, storage etc. There's also a cell culture lab, but this is used for more traditional cell lines. Other than the labs, there are all the amenities you could find in an office. Note that the internet access is limited to senior staff and up. There is, however, an intranet for bioinformatics needs.
On the subject of the biology of these beings, I'll start by discussing genetics, then their gross anatomy and finally their biological systems. For the sake of clarity, the information that I provide here is an aggregation of what I have observed and what I have read. I will make many comparisons with human anatomy because it is the most logical reference.
Genetics:
First, I'd like to discuss their genetics. Their genetics are like ours, based on DNA. This fact was very puzzling for me when I first learned about it. We imagine that beings from an alternate biosphere would have genetics based on a completely foreign biochemical system and surprisingly, this is not the case. Several conclusions can be drawn from this surprising revelation. The one that immediately comes to mind is that our biosphere and theirs share a common ancestry. They're eukaryotes, which means their cells have nuclei containing genetic material. Which suggests that their biosphere would have been separated from ours sometime after the appearance of this type of organism. The term Exo-Biospheric-Organism is actually a misnomer, but as it's a historical term, it's still used. Their genetics are not only based on the same genetic system, but they’re also even compatible with our own cellular machinery. This means that you can take a human gene and insert it into an EBO cell, and that gene will be translated into protein, and this of course works in reverse with a human gene inserted into an EBO cell. There are important differences in post-translational modifications that will make the final protein non-functional, but I'll discuss these later. Their genome consists of 16 circular chromosomes.
You're probably familiar with the concept of intergenic region or "junk DNA". These are basically DNA sequences that don't code for proteins. These are evolutionary residues, transposons, inactivated genes and so on. To give you an idea, in humans, intergenic regions represent approximately 99% of our genome. I'm aware that these sequences aren't completely useless, they can be used as histone anchors, as buffers to protect coding DNA from radiation or even as alternative open reading frames, but that's rather peripheral.
What's particularly striking about the EBO genome is the uniformity of these intergenic regions. We see the same sequences repeated everywhere, and the distance in bp between the genes is virtually the same throughout their genome. The result is a minimalist, highly condensed genome. In fact, it's much smaller than ours. Moreover, the quantity of protein-coding genes is even significantly lower than ours, probably due to genetic refinement but also to biological processes that are absent in EBO. The uniformity of these sequences is a major indication of the artificiality of these beings. There is no complex organism on earth that has such elegance in its sequences. There is no evolutionary pressure that can lead to this kind of characteristic other than genetic engineering.
Speaking of genetic engineering, following sequencing of their genomes, we noticed a troubling and universal characteristic in the 5' of the regulatory sequence of each gene which we call the Tri-Palindromic Region. The TPR are 134bp sequences containing, as its name suggests, 3 palindromes. In genetics, a palindrome is a DNA sequence that when read in the same direction, gives the same sequence on both DNA strands. They serve both as a flag and as a binding site for proteins. The three palindromes in the TPR are distinct from one another and have been poetically named "5'P TPR", "M TPR" and "3' TPR". The TPR is composed (in 5' - 3' order) of 5'P TPR, 12bp spacer, Chromosomal address, 12bp spacer, M TPR, 12bp spacer, Gene address, 12pb spacer and 3' TPR. The chromosomal address is composed of 4 bp and is identical in each TPR of the same chromosome, but distinct between each of the 16 chromosomes of the genome. The Gene address is a 64bp sequence that is unique for each gene in the whole genome. It's therefore understandable that the TPR serves as a unique address not only for numerically identifying a gene, but also for identifying its chromosomal location. For those with only a basic knowledge of genetics, this is completely unheard of. No living thing in our biosphere has this kind of precise address in its genome. Once again, the presence of TPR cannot be explained by evolutionary pressure but only by genetic engineering on a genomic scale.
TPR opens the door to several possibilities. One of them suggests that EBO geneticists can insert or remove a gene from a cell in a way that is far more targeted and efficient than our technology allows. No proteins have been identified in the EBO genome that interacts with TPR. Rather, we believe that these proteins are exclusively targeted by external genetic engineering tools, probably used at the zygotic stage of embryonic development. The nature of these tools is unclear, but we definitely don't have anything like them. The probable absence of these proteins from the genome is a further indication of their artificiality. Given the high probability of artificiality of their genome and the apparent ease of modifying it with biomolecular tools, it's not out of the question that there could be polymorphism between individuals depending on their role and function. In other words, an individual could be genetically designed to have characteristics that give it an advantage in performing a given task, like soldier ants and worker ants in an anthill. Note that these previous statements are speculation. To my knowledge only one individual genome has been sequenced, I can't make a definitive statement on genetic variation between individuals.
I've talked a lot about intergenic regions, now I'll briefly discuss intragenic sequences. Briefly, because there's not a lot less to say despite its obvious importance. Much like ours, their genes have silencers, enhancers, promoters, 5'UTRs, exons, introns, 3' UTRs etc. There are many genes analogous to ours, which is not surprising given the compatibility of our cellular machinery. What's disturbing is that some genes correspond directly, nucleotide by nucleotide, with known human genes or even some animal genes. For these genes, there doesn't seem to be any artificial refinement but rather a crude copying and pasting. Why they do it is nebulous and still subject to conjecture. There are also many genes which are not found in our biosphere whose role has not been identified. Finding the purpose of these novel genes is one of the aims of the program. I'd like to note before going any further that this heterogeneity of genes of known and unknown origin is an undeniable proof of the artificiality of EBOs.
To conclude with genetics, the mitochondrial genome, at the time I was working there, had not yet been sequenced. It's safe to assume that this genome would also be streamlined and possibly has some version of TPR.
Transcription and translation and protein expression.
I briefly introduced the differences in post-translational modifications between human and EBO. This is hardly a surprise, as we often see the same thing between different terrestrial species. Obtaining a viable protein from a DNA sequence is a complex process involving hundreds of protein intermediates, each with a precise and essential role. A minor variation in this assembly line can lead to functional irregularities in the final product. So, it's no surprise that there are setbacks along the way when the first EBO gene transfection attempts failed to produce the desired functional protein in human cell lines. Fortunately for us, the work of what I imagine to be another team at another site has led to the development of an EBO cell line named EPI-G11 derived from epithelial tissues. With this tool in our hands, we were able to transfect and overexpress proteins of interest in order to eventually purify and study them. For your information, we use a biological ballistics delivery system (AKA gene gun) for our transfection needs because other methods are not very effective with cells of this line. For example, the viral vectors tested cannot be internalized by EPI-G11 and lipofection is too lethal. EPI-G11, like most eukaryotic cell lines, enters a phase of exponential growth when exposed to Fetal Bovine Serum. It's only half surprising that a cell line from such an exotic source should be sensitive to the growth factors present in FBS. In my opinion, this can be explained by the addition of animal genes to the genome, such as growth receptors.
Gross anatomy:
They are morphologically very similar to the grey aliens that are part of modern folklore. Their height is about 150cm, they have two arms, two legs and a head. Still, there are some notable differences.
Skin: The grey skin that is often described in folklore is in fact a biosynthetic film which, likely, serves to protect the EBO from a hostile environment. It doesn't provide effective protection against temperature changes, but it does offer adequate protection against the passage of liquids. It's possible that this film confers other advantages but my knowledge on the subject is limited. Under the grey film, the epidermis is rather white, and the texture is very regular and without any hair. We do not see any defect other than the folds near the joints. It's described as greasy in one report, but that's not something I've observed. The same report states that a strong, lingering smell of burnt hair and ammonia is present when the film is removed. There are a lot of pores on the skin, crossing from the epidermis to a gland in the hypodermis. These glands and pores are the terminal part of the excretory-sudoriferous system, which could explain the previously mentioned smell.
Head: The head contains two large, oversized eyes, two nostrils without protuberance, a narrow mouth without lips and two ear canals without auricles. There is a mandible, but the musculature is vestigial. There are no teeth or tongue in the oral cavity. The nasal cavity where the nostrils meet is compact and does not rise cranially but extends axially. There appears to be no equivalent to the olfactory bulb in the nasal cavity. The mouth leads directly to the esophagus and the nasal cavity to the trachea. The trachea and esophagus do not communicate.
Eye: Like the skin, the eyes are covered with a semi-transparent biosynthetic film that offers the same environmental protection, while providing protection against certain wavelengths and light intensity. When the film is removed, a more traditional eye is revealed. It's about three times larger than a human eye and there are no eyelids. The size of their eyes suggests they have excellent night vision. It seems paradoxical to cover them with a semi-opaque film. Perhaps they only need to wear it in a bright environment. Their sclera is the same color as their skin, the iris is pale grey, and the pupil is black and oversized. The lens is rounder than a human, and the musculature used to adjust focus is more developed. On the retina, there are at least 6 types of cone cells. The responsiveness of each of these 6 types of cone is specific to a wavelength band, with a minimum of overlap between each other. The result is a broader visible spectrum.
Ear: As mentioned, the outer ear has no auricle and the ear canal is unremarkable. The inner ear has all the characteristics of a typical vestibular and cochlear system, although the curvature of the cochlea is more pronounced than a human. This probably results in greater hearing acuity for low frequencies.
Brain: The brain is tetraspheric, i.e. composed of four major sections. The sections are separated by transverse and longitudinal fissures and are connected to the central lobe, which acts as brainstem and cerebellum. The volume of the brain is around 20% superior to that of a man of the same height. It has a much more pronounced level of gyrication than an average human. Moreover, the ratio of glial cells to neurons is also slightly higher than in humans. It is important to mention the presence of nodules on the central lobe. Histological analysis of these structures reveals a kind of intricate biological circuitry. It is speculated that these nodules are essential to interact with their technology. Consequently, determining the proteome of these structures is an absolute priority for the program.
Neck: The neck is proportionally longer than that of a human, and at the same time relatively thin. As mentioned, the esophagus and trachea are separate. There are no vocal cords in this region.
Thorax: The musculature of the thorax is underdeveloped. Muscles equivalent to the pectoralis major can be seen. We can also see the trapezius and deltoid muscles. The sternocleidomastoids are well defined. The ribs and sternum are clearly visible. There are no nipples.
Abdomen: The abdomen is wider than the thorax and bulges slightly forward. There is no navel.
Pelvis: The pelvic bones are apparent. There are no genitals or anus.
Hands and feets: Their hands have four digits, including an opposable thumb on the medial side. They have no nails, and the texture of their fingerprints is composed of concentric circles. Fingers are proportionally much longer than in humans. Unlike humans, finger musculature is entirely intrinsic to the hand. In other words, the muscles used to move the fingers are not in the forearms but entirely located in the hands. At first glance, the feet consist of just two digits, but a necropsy soon determined that each toe was made of two fused digits. The medial toe is marginally longer than the distal toe. The feet are relatively longer and narrower than in a human. Their musculature, however, is vestigial.
The EBOs endoskeleton is very similar to ours, at least in terms of composition. There's collagen, hydroxyapatite but also copper oxide crystals where marrow would normally be found. The role of these crystals has not been established, but it is not a crystalopathic condition. The blood cells of the myeloid lineage (or the equivalent for these creatures) therefore mature in a different location than in humans i.e. in the thymus like organ. A transverse section of the bone reveals osteon and osteocytes. There appear to be few osteoblasts and no osteoclasts. This indicates that the bones are no longer growing and cannot absorb the minerals present or adapt mechanically to changes in posture.
Biological system:
Respiratory system: Their cellular respiration is equivalent to ours, i.e. they need to oxidize organic components to produce energy. Their lungs have no reciprocating action, but rather have a unidirectional flow of air, similar to those seen in birds, which is more efficient than ours. It is speculated that this is in response to the brain's elevated metabolic needs. Vocalization is produced by vibration of the wall membrane at the junction between the two air sacs.
The Circulatory system of EBOs is rather analogous to ours. The heart is located in the mediastanum, but in a more medial position, directly beneath the sternum. The heart has two ventricles and two atria. There is an aorta, a pulmonary vein, a pulmonary artery and a vena cava. Blood flowing to the pulmonary capillaries via the pulmonary artery is pumped against the flow of air, maximizing gas exchange efficiency. The blood gas barrier is relatively narrow in these capillaries, at least compared to a human. Then oxygen-rich blood is returned to the heart and then expelled into the aorta and the rest of the body. Before returning to the heart, the blood will pass through the hepatorenal organ which, among other things, filters and controls osmotic pressure of the blood.
The blood itself is also analogous to that of a human. However, the proportion of plasma is much higher, albumin is in similar proportion ,hormone levels are much lower, metal ion levels are much higher (particularly copper) and glucose levels are significantly higher. The color of the blood is brownish, given the higher proportion of plasma and concentration of metal ions. On the cellular side, there are erythrocytes which, in addition to hemoglobin for binding oxygen, display several complexes capable of binding copper ions. It's not clear what role these copper ions play but we believe it neutralizes blood ammonia, among other things. Several cell types with leukocyte characteristics have been observed, but no comprehensive knowledge of them exists. Platelets are present, but in smaller proportions than in humans.
Excreto-sudoriferous system: This system is completely different from what I've seen. As mentioned earlier, there is no large orifice, like an anus or urethra, to get rid of biological waste. Instead, there are countless small pores on the surface of the skin. There's a large medial organ called the hepatorenal organ, which acts as both kidney and liver and is central to maintaining homeostasis. This organ is highly vascularized and the blood must pass through it before returning to the heart. Its role is, among other things, to purify the blood of metabolic waste. Waste is excreted into the equivalent of a ureter, which branches out into four. Each branch flows towards one of the four limbs and in turn these branches divide until they end up as thousands of excretory pores. The motility of this excretory system is mediated by a weak peristalsis at the proximal level and on the four main branches. Peristalsis ceases around the first distal junction. As there is no urea cycle, the ammonia concentration at the exit of the hepatorenal organ is very high. This ammonia is carried to the pores and gives the distinct odor I mentioned earlier. The rationale behind this unusual excretory system is directly related to this excreted ammonia, which enables thermoregulation by evaporating on the skin's surface. The greater the physical effort, the greater the metabolism. This in turn leads to a rise in temperature, and a corresponding increase in metabolic waste via amino acid catabolism. This leads to an increase in filtration and ammonia excretion, which ultimately lowers body temperature.
Digestive system: The digestive system is extremely underdeveloped. There's no there is no stomach in the familiar sense. However, there is a pseudo-stomach located at the transition between the thoracic and abdominal cavities. This organ is not involved in digestion, but only serves as a reservoir. A sphincter controls the flow of food into the intestine. The intestine is limited to the equivalent of our small intestine, i.e. it only serves to absorb liquids and nutrients and acts as the main digestion site. It has villi and microvilli like ours. The intestine ends in the hepato-renal organ, where non-digested matter is transported to the ureter and excretory system. Residues are dissolved in the ammonia of metabolic waste for excretion. There's an organ near the pseudostomachal sphincter that secretes digestive enzymes directly into the intestine. This organ is inspirationally called the digestive organ. It secretes mainly proteolytic enzymes and glycoside hydrolases.
Given the absence of teeth, the narrowness and rigidity of the esophagus, the absence of a true stomach and the absence of defecation, it is strongly believed that EBOs can only consume food in liquid form. It is assumed that, given the high metabolic needs of their brains, this food would have a high carbohydrate concentration. In order to meet other metabolic needs, there must also be a high protein content in the food consumed. These two statements are supported by the type of enzyme secreted by the digestive organ. It is therefore speculated that the food consumed is a sort of broth rich in sugar and protein, which probably also has a high copper content. Given the strict limitations on the type of food that they can consume, it's unlikely that this type of creature could survive in our biosphere without technological support.
Endocrine system: Knowledge of the endocrine system is minimal. We know that cells are receptive to bovine growth hormones, so it's assumed that certain functions are regulated by such a system. Endocrine mechanisms are very complex, and it goes without saying that they are best studied on living subjects.
Immune system: The immune system is another unknown. There seems to be an innate immune system but there doesn't seem to be any adaptive immunity, at least not similar to what is known. There's a thymus-like organ near the heart that's proportionally larger than in humans. This organ seems to be where all blood cells mature. Some cells have leukocyte characteristics such as granularity. The immune cells that germinate here have a high copper concentration. The surface receptors of innate immune cells have not yet been characterized, so we might as well say that all the work remains to be done.
Nervous system: The nervous system is also relatively similar. The spinal cord begins at the base of the central lobe of the brain and propagates down the vertebral column. In the vertebrae there are ganglia made of afferent and efferent neurons. In short, other than the CNS, there is nothing out of the ordinary.
Musculoskeletal system: The musculoskeletal system is very ordinary, albeit underdeveloped. Most of the human skeletal muscles have an equivalent. Only the hands, feet and forearms are different. It should be noted that the proportion of type 1 and type 2 muscle fibers is different from that in a human. Indeed, type 1 outnumbers type 2 by about a factor of 10.
Artificial system: We speculate that artificial molecular machines may be present in the body, and that copper, if present, would be essential to their function or assembly. Importantly, no AMMs have been observed.
Question 1: Amazing story. Have you shared this with the Senate Select Commission on Intelligence or with AARO and do you have evidence to back this up?
Thank you, no I haven't and no I won't. It sounds like a honey trap to me. I will not place my life in the hands of politicians. I have no proof other than this message. I know it's not much but it's what I'm prepared to offer
Question 2: Well that was a read ... So they are bio engineered worker bees... Any elemental components that are unutributal to our biome ?
Yes, knowing that they're disposable, unable to live independently without technological support, and that they're ephemeral. The only suitable hypothesis is that they are alive only to accomplish their task. Can you clarify your question about elemental components?
Question 3: I havent read everything in detail but can you expend on the document on their religion?
EBOs believe that the soul is not an extension of the individual, but rather a fundamental characteristic of nature that expresses itself as a field, not unlike gravity. In the presence of life, this field acquires complexity, resulting in negative entropy if that makes sense. This gain in complexity is directly correlated with the concentration of living organisms in a given location. With time, and with the right conditions, life in turn becomes more complex until the appearance of sentient life. After reaching this threshold, the field begins to express itself through these sentient beings, forming what we call the soul. Through their life experiences, sentient beings will in turn influence the field in a sort of positive feedback loop. This in turn further accelerates the complexity of the field. Eventually, when the field reaches a "critical mass", there will be a sort of apotheosis. It's not clear what this means in practical terms, but this quest for apotheosis seems to be the EBOs main motivation.
The author of the document added his reflections and interpretations as an appendix. He specified that, for them, the soul field is not a belief but an obvious truth. He also argues that the soul loses its individuality after death, but that memory and experience persist as part of the field. This fact would influence the philosophy and culture of EBOs, resulting in a society that doesn't fear death but which places no importance or reverence on individuality. This "belief" compels them to seed life, shape it, nurture it, monitor it and influence it for the ultimate purpose of creating this apotheosis. Paradoxically, they have little or no respect for an individual's well-being.
Please be advised that I'm speaking from memory of something I read more than 10 years ago, so take the following with a grain of salt. Also, I'm not a philosopher or an artist, so please excuse my struggle to properly formulate the concepts and my dry terminology. Finally, note that this information comes from a document whose author was directly interacting with an EBO. It is not specified whether it was an ambassador, a crash survivor, a prisoner. The means of communication were not specified either.
Question 4: Wtf he dropped the location of the lab
Battelle National Biodefense Institute. It is on google map

****Note*** This post was published on aliens But the user who posted it has now been suspended from the reddit. I am posting it on StrangeEarth so that we can have it in bulk. aliens mod cannot confirm the user identity but they are trying to contact him. I cannot post all the comments but leaving the link to original post so that you can check it.https://www.reddit.com/aliens/comments/14rp7w9/from_the_late_2000s_to_the_mid2010s_i_worked_as_a/

It seems like all my comments are being deleted. I will post answer at the end of the message.
From the late 2000s to the mid-2010s, I worked as a molecular biologist for a national security contractor in a program to study Exo-Biospheric-Organisms (EBO). The aim of the program was to elucidate the genome and proteome basis of these organisms. Although the study of OBCs has been going on for decades in other programs, the new high-throughput DNA sequencing technologies of the late 90s unblocked stagnant research in this area. Since then, several breakthroughs have led to significant advances in our understanding of the genome and proteome of these beings. What we've learned so far has enabled us to outline some disconcerting perspectives about our place in this universe. Briefly, we've discovered that the EBO genome is a chimera of genomes from our biosphere and from an unknown one. They are artificial, ephemeral and disposable organisms created for a purpose that still partially eludes us. I'll be substantiating my statements after a brief introduction.
The reason for disclosing these secrets is quite simple. I believe that every human being has the right to know the truth, and that to progress, humanity needs to divest itself of certain institutions and organizations that will probably not survive these revelations in the long term. I'm aware that I'll have very little impact in this regard, but I still believe that small leaks are necessary to break the dam of misinformation on this subject. When the governments will eventually reveal these secrets, there will undoubtedly be a societal upheaval, but in my opinion, the longer we wait, the worse it will be. I choose to divulge what I know anonymously out of selfishness for the well-being of myself and my family. I'm aware that this diminishes the reach and credibility of my message, but it's the furthest I am willing to go. I chose this forum because it offers a good compromise between anonymity and popularity. In order to protect my anonymity, I will be purposely vague or even contradictory about any information that could identify me (date, education, role etc.). I'll even introduce red herrings in this respect. I want to make it clear that any information related to the subject of the research will not be treated in this way.
Before going any further, please excuse me if you find it difficult to understand what I'm explaining. Some parts of my text are very technical. It's difficult to find the right balance between vulgarization and scientific explanation. I'll continue by talking about myself. What's the point of talking about me knowing that the information will necessarily be misleading? I simply want to introduce a perspective on the type of people who work there, normal scientists. I have a Ph.D. in molecular biology. I didn't actively seek to be part of this program, rather it was a stroke of luck that introduced me to one of the senior scientists. I met this person at a conference where I was presenting a poster on my Ph.D. research. When I think back, I don't believe he was impressed by what I was presenting, because it was quite frankly a project that wasn't going anywhere. I think it was rather the most important aspect of a professional life: the attitude and the ease with which you make connections. Shortly afterwards, I graduated and received a call from this person offering me a position. At the time, everything pointed to me working in a regular laboratory.
I did a series of three increasingly suspicious interviews, each in a different location, where my scientific background and knowledge became less and less relevant. The first was with two of the senior scientists, the second and third with people I've never seen again and who were obviously not interested in science. Sometime after the interview, I was asked to go to a fourth location where what seemed like a corporate lawyer presented me with an NDA. He made sure not only to explain every detail, but also that I understood the consequence of not respecting it.
The first Employment weeks were by far the most memorable, although I spent most of that time in a depressing archive room. It consists almost exclusively of reading about the subject of study and to get us up to speed. There's no secret Wikipedia or even a reference book to guide us. There are only dry reports, memos, presentations, procedures and SOPs. These documents are almost exclusively about the biology of EBOs, but there are also a few that deal with other subjects such as their food, religion or culture. There were no documents on their technology.
As mentioned above, the aim of the project is to gain a better understanding of the EBO genome and proteome. To achieve this, a team of around twenty scientists, four senior scientists and a director was involved. The scientists, like myself, had as their main responsibility to carry out the technical work. As each scientist had to my knowledge a Ph.D., we were all somewhat overqualified for what is ultimately a technician's job. The senior scientists, who make full use of their diplomas, had the task of designing the assays and had a supervisory responsibility. They were also in charge of training new employees, and sometimes even came in to do technical work. The director, of course, was the person in charge who dictated priorities to the senior scientists. He was rarely on site, and the few times he was, it was to attend meetings. Other than the scientific staff, there were security guards working for one subcontractor or another. There were no support staff such as janitors or maintenance workers. Scientists were responsible for this kind of work. In addition, logistical constraints ensure that every scientist is capable of carrying out any technical activity.
The laboratory itself is located in Fort Detrick, Maryland, in a building used for legitimate biomedical research. The clandestine operations are carried out in a restricted part of the basement, out of sight from regular workers. Contrary to what one might imagine, the biosafety level is not maximal for this type of research. Indeed, the lab containing EBO samples or derived cell cultures is BSL3, while the lab where assays are conducted are only BSL2. The BSL3 area of the facility includes a freezer room and a cell culture lab and is only accessible through an antechamber from the BSL2 section. EBO carcasses are preserved in horizontal freezers at a temperature of -80°C nominal. To maximize the preservation of these carcasses, they are preserved in vacuum bags and the air in the room is controlled to minimize humidity. There are only four bodies and none of them are complete. It's obvious that these creatures have died as a result of major trauma. I've never witnessed a motorcycle accident fatality, but it probably looks similar to this. It is acknowledged that there are more EBOs caracasses at other locations. The cell culture laboratory, as its name suggests, is where cell lines derived from EBOs are grown and related activities are performed. I'll talk in more detail about these specific cell lines later on. The BSL2 part is mainly used for assays, immunohistochemistry, genetic engineering, immunocytochemistry, storage etc. There's also a cell culture lab, but this is used for more traditional cell lines. Other than the labs, there are all the amenities you could find in an office. Note that the internet access is limited to senior staff and up. There is, however, an intranet for bioinformatics needs.
On the subject of the biology of these beings, I'll start by discussing genetics, then their gross anatomy and finally their biological systems. For the sake of clarity, the information that I provide here is an aggregation of what I have observed and what I have read. I will make many comparisons with human anatomy because it is the most logical reference.
Genetics:
First, I'd like to discuss their genetics. Their genetics are like ours, based on DNA. This fact was very puzzling for me when I first learned about it. We imagine that beings from an alternate biosphere would have genetics based on a completely foreign biochemical system and surprisingly, this is not the case. Several conclusions can be drawn from this surprising revelation. The one that immediately comes to mind is that our biosphere and theirs share a common ancestry. They're eukaryotes, which means their cells have nuclei containing genetic material. Which suggests that their biosphere would have been separated from ours sometime after the appearance of this type of organism. The term Exo-Biospheric-Organism is actually a misnomer, but as it's a historical term, it's still used. Their genetics are not only based on the same genetic system, but they’re also even compatible with our own cellular machinery. This means that you can take a human gene and insert it into an EBO cell, and that gene will be translated into protein, and this of course works in reverse with a human gene inserted into an EBO cell. There are important differences in post-translational modifications that will make the final protein non-functional, but I'll discuss these later. Their genome consists of 16 circular chromosomes.
You're probably familiar with the concept of intergenic region or "junk DNA". These are basically DNA sequences that don't code for proteins. These are evolutionary residues, transposons, inactivated genes and so on. To give you an idea, in humans, intergenic regions represent approximately 99% of our genome. I'm aware that these sequences aren't completely useless, they can be used as histone anchors, as buffers to protect coding DNA from radiation or even as alternative open reading frames, but that's rather peripheral.
What's particularly striking about the EBO genome is the uniformity of these intergenic regions. We see the same sequences repeated everywhere, and the distance in bp between the genes is virtually the same throughout their genome. The result is a minimalist, highly condensed genome. In fact, it's much smaller than ours. Moreover, the quantity of protein-coding genes is even significantly lower than ours, probably due to genetic refinement but also to biological processes that are absent in EBO. The uniformity of these sequences is a major indication of the artificiality of these beings. There is no complex organism on earth that has such elegance in its sequences. There is no evolutionary pressure that can lead to this kind of characteristic other than genetic engineering.
Speaking of genetic engineering, following sequencing of their genomes, we noticed a troubling and universal characteristic in the 5' of the regulatory sequence of each gene which we call the Tri-Palindromic Region. The TPR are 134bp sequences containing, as its name suggests, 3 palindromes. In genetics, a palindrome is a DNA sequence that when read in the same direction, gives the same sequence on both DNA strands. They serve both as a flag and as a binding site for proteins. The three palindromes in the TPR are distinct from one another and have been poetically named "5'P TPR", "M TPR" and "3' TPR". The TPR is composed (in 5' - 3' order) of 5'P TPR, 12bp spacer, Chromosomal address, 12bp spacer, M TPR, 12bp spacer, Gene address, 12pb spacer and 3' TPR. The chromosomal address is composed of 4 bp and is identical in each TPR of the same chromosome, but distinct between each of the 16 chromosomes of the genome. The Gene address is a 64bp sequence that is unique for each gene in the whole genome. It's therefore understandable that the TPR serves as a unique address not only for numerically identifying a gene, but also for identifying its chromosomal location. For those with only a basic knowledge of genetics, this is completely unheard of. No living thing in our biosphere has this kind of precise address in its genome. Once again, the presence of TPR cannot be explained by evolutionary pressure but only by genetic engineering on a genomic scale.
TPR opens the door to several possibilities. One of them suggests that EBO geneticists can insert or remove a gene from a cell in a way that is far more targeted and efficient than our technology allows. No proteins have been identified in the EBO genome that interacts with TPR. Rather, we believe that these proteins are exclusively targeted by external genetic engineering tools, probably used at the zygotic stage of embryonic development. The nature of these tools is unclear, but we definitely don't have anything like them. The probable absence of these proteins from the genome is a further indication of their artificiality. Given the high probability of artificiality of their genome and the apparent ease of modifying it with biomolecular tools, it's not out of the question that there could be polymorphism between individuals depending on their role and function. In other words, an individual could be genetically designed to have characteristics that give it an advantage in performing a given task, like soldier ants and worker ants in an anthill. Note that these previous statements are speculation. To my knowledge only one individual genome has been sequenced, I can't make a definitive statement on genetic variation between individuals.
I've talked a lot about intergenic regions, now I'll briefly discuss intragenic sequences. Briefly, because there's not a lot less to say despite its obvious importance. Much like ours, their genes have silencers, enhancers, promoters, 5'UTRs, exons, introns, 3' UTRs etc. There are many genes analogous to ours, which is not surprising given the compatibility of our cellular machinery. What's disturbing is that some genes correspond directly, nucleotide by nucleotide, with known human genes or even some animal genes. For these genes, there doesn't seem to be any artificial refinement but rather a crude copying and pasting. Why they do it is nebulous and still subject to conjecture. There are also many genes which are not found in our biosphere whose role has not been identified. Finding the purpose of these novel genes is one of the aims of the program. I'd like to note before going any further that this heterogeneity of genes of known and unknown origin is an undeniable proof of the artificiality of EBOs.
To conclude with genetics, the mitochondrial genome, at the time I was working there, had not yet been sequenced. It's safe to assume that this genome would also be streamlined and possibly has some version of TPR.
Transcription and translation and protein expression.
I briefly introduced the differences in post-translational modifications between human and EBO. This is hardly a surprise, as we often see the same thing between different terrestrial species. Obtaining a viable protein from a DNA sequence is a complex process involving hundreds of protein intermediates, each with a precise and essential role. A minor variation in this assembly line can lead to functional irregularities in the final product. So, it's no surprise that there are setbacks along the way when the first EBO gene transfection attempts failed to produce the desired functional protein in human cell lines. Fortunately for us, the work of what I imagine to be another team at another site has led to the development of an EBO cell line named EPI-G11 derived from epithelial tissues. With this tool in our hands, we were able to transfect and overexpress proteins of interest in order to eventually purify and study them. For your information, we use a biological ballistics delivery system (AKA gene gun) for our transfection needs because other methods are not very effective with cells of this line. For example, the viral vectors tested cannot be internalized by EPI-G11 and lipofection is too lethal. EPI-G11, like most eukaryotic cell lines, enters a phase of exponential growth when exposed to Fetal Bovine Serum. It's only half surprising that a cell line from such an exotic source should be sensitive to the growth factors present in FBS. In my opinion, this can be explained by the addition of animal genes to the genome, such as growth receptors.
Gross anatomy:
They are morphologically very similar to the grey aliens that are part of modern folklore. Their height is about 150cm, they have two arms, two legs and a head. Still, there are some notable differences.
Skin: The grey skin that is often described in folklore is in fact a biosynthetic film which, likely, serves to protect the EBO from a hostile environment. It doesn't provide effective protection against temperature changes, but it does offer adequate protection against the passage of liquids. It's possible that this film confers other advantages but my knowledge on the subject is limited. Under the grey film, the epidermis is rather white, and the texture is very regular and without any hair. We do not see any defect other than the folds near the joints. It's described as greasy in one report, but that's not something I've observed. The same report states that a strong, lingering smell of burnt hair and ammonia is present when the film is removed. There are a lot of pores on the skin, crossing from the epidermis to a gland in the hypodermis. These glands and pores are the terminal part of the excretory-sudoriferous system, which could explain the previously mentioned smell.
Head: The head contains two large, oversized eyes, two nostrils without protuberance, a narrow mouth without lips and two ear canals without auricles. There is a mandible, but the musculature is vestigial. There are no teeth or tongue in the oral cavity. The nasal cavity where the nostrils meet is compact and does not rise cranially but extends axially. There appears to be no equivalent to the olfactory bulb in the nasal cavity. The mouth leads directly to the esophagus and the nasal cavity to the trachea. The trachea and esophagus do not communicate.
Eye: Like the skin, the eyes are covered with a semi-transparent biosynthetic film that offers the same environmental protection, while providing protection against certain wavelengths and light intensity. When the film is removed, a more traditional eye is revealed. It's about three times larger than a human eye and there are no eyelids. The size of their eyes suggests they have excellent night vision. It seems paradoxical to cover them with a semi-opaque film. Perhaps they only need to wear it in a bright environment. Their sclera is the same color as their skin, the iris is pale grey, and the pupil is black and oversized. The lens is rounder than a human, and the musculature used to adjust focus is more developed. On the retina, there are at least 6 types of cone cells. The responsiveness of each of these 6 types of cone is specific to a wavelength band, with a minimum of overlap between each other. The result is a broader visible spectrum.
Ear: As mentioned, the outer ear has no auricle and the ear canal is unremarkable. The inner ear has all the characteristics of a typical vestibular and cochlear system, although the curvature of the cochlea is more pronounced than a human. This probably results in greater hearing acuity for low frequencies.
Brain: The brain is tetraspheric, i.e. composed of four major sections. The sections are separated by transverse and longitudinal fissures and are connected to the central lobe, which acts as brainstem and cerebellum. The volume of the brain is around 20% superior to that of a man of the same height. It has a much more pronounced level of gyrication than an average human. Moreover, the ratio of glial cells to neurons is also slightly higher than in humans. It is important to mention the presence of nodules on the central lobe. Histological analysis of these structures reveals a kind of intricate biological circuitry. It is speculated that these nodules are essential to interact with their technology. Consequently, determining the proteome of these structures is an absolute priority for the program.
Neck: The neck is proportionally longer than that of a human, and at the same time relatively thin. As mentioned, the esophagus and trachea are separate. There are no vocal cords in this region.
Thorax: The musculature of the thorax is underdeveloped. Muscles equivalent to the pectoralis major can be seen. We can also see the trapezius and deltoid muscles. The sternocleidomastoids are well defined. The ribs and sternum are clearly visible. There are no nipples.
Abdomen: The abdomen is wider than the thorax and bulges slightly forward. There is no navel.
Pelvis: The pelvic bones are apparent. There are no genitals or anus.
Hands and feets: Their hands have four digits, including an opposable thumb on the medial side. They have no nails, and the texture of their fingerprints is composed of concentric circles. Fingers are proportionally much longer than in humans. Unlike humans, finger musculature is entirely intrinsic to the hand. In other words, the muscles used to move the fingers are not in the forearms but entirely located in the hands. At first glance, the feet consist of just two digits, but a necropsy soon determined that each toe was made of two fused digits. The medial toe is marginally longer than the distal toe. The feet are relatively longer and narrower than in a human. Their musculature, however, is vestigial.
The EBOs endoskeleton is very similar to ours, at least in terms of composition. There's collagen, hydroxyapatite but also copper oxide crystals where marrow would normally be found. The role of these crystals has not been established, but it is not a crystalopathic condition. The blood cells of the myeloid lineage (or the equivalent for these creatures) therefore mature in a different location than in humans i.e. in the thymus like organ. A transverse section of the bone reveals osteon and osteocytes. There appear to be few osteoblasts and no osteoclasts. This indicates that the bones are no longer growing and cannot absorb the minerals present or adapt mechanically to changes in posture.
Biological system:
Respiratory system: Their cellular respiration is equivalent to ours, i.e. they need to oxidize organic components to produce energy. Their lungs have no reciprocating action, but rather have a unidirectional flow of air, similar to those seen in birds, which is more efficient than ours. It is speculated that this is in response to the brain's elevated metabolic needs. Vocalization is produced by vibration of the wall membrane at the junction between the two air sacs.
The Circulatory system of EBOs is rather analogous to ours. The heart is located in the mediastanum, but in a more medial position, directly beneath the sternum. The heart has two ventricles and two atria. There is an aorta, a pulmonary vein, a pulmonary artery and a vena cava. Blood flowing to the pulmonary capillaries via the pulmonary artery is pumped against the flow of air, maximizing gas exchange efficiency. The blood gas barrier is relatively narrow in these capillaries, at least compared to a human. Then oxygen-rich blood is returned to the heart and then expelled into the aorta and the rest of the body. Before returning to the heart, the blood will pass through the hepatorenal organ which, among other things, filters and controls osmotic pressure of the blood.
The blood itself is also analogous to that of a human. However, the proportion of plasma is much higher, albumin is in similar proportion ,hormone levels are much lower, metal ion levels are much higher (particularly copper) and glucose levels are significantly higher. The color of the blood is brownish, given the higher proportion of plasma and concentration of metal ions. On the cellular side, there are erythrocytes which, in addition to hemoglobin for binding oxygen, display several complexes capable of binding copper ions. It's not clear what role these copper ions play but we believe it neutralizes blood ammonia, among other things. Several cell types with leukocyte characteristics have been observed, but no comprehensive knowledge of them exists. Platelets are present, but in smaller proportions than in humans.
Excreto-sudoriferous system: This system is completely different from what I've seen. As mentioned earlier, there is no large orifice, like an anus or urethra, to get rid of biological waste. Instead, there are countless small pores on the surface of the skin. There's a large medial organ called the hepatorenal organ, which acts as both kidney and liver and is central to maintaining homeostasis. This organ is highly vascularized and the blood must pass through it before returning to the heart. Its role is, among other things, to purify the blood of metabolic waste. Waste is excreted into the equivalent of a ureter, which branches out into four. Each branch flows towards one of the four limbs and in turn these branches divide until they end up as thousands of excretory pores. The motility of this excretory system is mediated by a weak peristalsis at the proximal level and on the four main branches. Peristalsis ceases around the first distal junction. As there is no urea cycle, the ammonia concentration at the exit of the hepatorenal organ is very high. This ammonia is carried to the pores and gives the distinct odor I mentioned earlier. The rationale behind this unusual excretory system is directly related to this excreted ammonia, which enables thermoregulation by evaporating on the skin's surface. The greater the physical effort, the greater the metabolism. This in turn leads to a rise in temperature, and a corresponding increase in metabolic waste via amino acid catabolism. This leads to an increase in filtration and ammonia excretion, which ultimately lowers body temperature.
Digestive system: The digestive system is extremely underdeveloped. There's no there is no stomach in the familiar sense. However, there is a pseudo-stomach located at the transition between the thoracic and abdominal cavities. This organ is not involved in digestion, but only serves as a reservoir. A sphincter controls the flow of food into the intestine. The intestine is limited to the equivalent of our small intestine, i.e. it only serves to absorb liquids and nutrients and acts as the main digestion site. It has villi and microvilli like ours. The intestine ends in the hepato-renal organ, where non-digested matter is transported to the ureter and excretory system. Residues are dissolved in the ammonia of metabolic waste for excretion. There's an organ near the pseudostomachal sphincter that secretes digestive enzymes directly into the intestine. This organ is inspirationally called the digestive organ. It secretes mainly proteolytic enzymes and glycoside hydrolases.
Given the absence of teeth, the narrowness and rigidity of the esophagus, the absence of a true stomach and the absence of defecation, it is strongly believed that EBOs can only consume food in liquid form. It is assumed that, given the high metabolic needs of their brains, this food would have a high carbohydrate concentration. In order to meet other metabolic needs, there must also be a high protein content in the food consumed. These two statements are supported by the type of enzyme secreted by the digestive organ. It is therefore speculated that the food consumed is a sort of broth rich in sugar and protein, which probably also has a high copper content. Given the strict limitations on the type of food that they can consume, it's unlikely that this type of creature could survive in our biosphere without technological support.
Endocrine system: Knowledge of the endocrine system is minimal. We know that cells are receptive to bovine growth hormones, so it's assumed that certain functions are regulated by such a system. Endocrine mechanisms are very complex, and it goes without saying that they are best studied on living subjects.
Immune system: The immune system is another unknown. There seems to be an innate immune system but there doesn't seem to be any adaptive immunity, at least not similar to what is known. There's a thymus-like organ near the heart that's proportionally larger than in humans. This organ seems to be where all blood cells mature. Some cells have leukocyte characteristics such as granularity. The immune cells that germinate here have a high copper concentration. The surface receptors of innate immune cells have not yet been characterized, so we might as well say that all the work remains to be done.
Nervous system: The nervous system is also relatively similar. The spinal cord begins at the base of the central lobe of the brain and propagates down the vertebral column. In the vertebrae there are ganglia made of afferent and efferent neurons. In short, other than the CNS, there is nothing out of the ordinary.
Musculoskeletal system: The musculoskeletal system is very ordinary, albeit underdeveloped. Most of the human skeletal muscles have an equivalent. Only the hands, feet and forearms are different. It should be noted that the proportion of type 1 and type 2 muscle fibers is different from that in a human. Indeed, type 1 outnumbers type 2 by about a factor of 10.
Artificial system: We speculate that artificial molecular machines may be present in the body, and that copper, if present, would be essential to their function or assembly. Importantly, no AMMs have been observed.
Question 1: Amazing story. Have you shared this with the Senate Select Commission on Intelligence or with AARO and do you have evidence to back this up?
Thank you, no I haven't and no I won't. It sounds like a honey trap to me. I will not place my life in the hands of politicians. I have no proof other than this message. I know it's not much but it's what I'm prepared to offer
Question 2: Well that was a read ... So they are bio engineered worker bees... Any elemental components that are unutributal to our biome ?
Yes, knowing that they're disposable, unable to live independently without technological support, and that they're ephemeral. The only suitable hypothesis is that they are alive only to accomplish their task. Can you clarify your question about elemental components?
Question 3: I havent read everything in detail but can you expend on the document on their religion?
EBOs believe that the soul is not an extension of the individual, but rather a fundamental characteristic of nature that expresses itself as a field, not unlike gravity. In the presence of life, this field acquires complexity, resulting in negative entropy if that makes sense. This gain in complexity is directly correlated with the concentration of living organisms in a given location. With time, and with the right conditions, life in turn becomes more complex until the appearance of sentient life. After reaching this threshold, the field begins to express itself through these sentient beings, forming what we call the soul. Through their life experiences, sentient beings will in turn influence the field in a sort of positive feedback loop. This in turn further accelerates the complexity of the field. Eventually, when the field reaches a "critical mass", there will be a sort of apotheosis. It's not clear what this means in practical terms, but this quest for apotheosis seems to be the EBOs main motivation.
The author of the document added his reflections and interpretations as an appendix. He specified that, for them, the soul field is not a belief but an obvious truth. He also argues that the soul loses its individuality after death, but that memory and experience persist as part of the field. This fact would influence the philosophy and culture of EBOs, resulting in a society that doesn't fear death but which places no importance or reverence on individuality. This "belief" compels them to seed life, shape it, nurture it, monitor it and influence it for the ultimate purpose of creating this apotheosis. Paradoxically, they have little or no respect for an individual's well-being.
Please be advised that I'm speaking from memory of something I read more than 10 years ago, so take the following with a grain of salt. Also, I'm not a philosopher or an artist, so please excuse my struggle to properly formulate the concepts and my dry terminology. Finally, note that this information comes from a document whose author was directly interacting with an EBO. It is not specified whether it was an ambassador, a crash survivor, a prisoner. The means of communication were not specified either.
Question 4: Wtf he dropped the location of the lab
Battelle National Biodefense Institute. It is on google map

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Age: 33
Sex: Female
Height: 5’ 6”
Weight: 140 lbs
Race: White
Duration of complaint: New
Location: Kidney
Any existing relevant medical issues: Thyroid Cancer and Bilateral Duplex Kidneys
Current medications: Synthroid 150
Friday I was sent for a CT for an unrelated issue and the results indicated birth defect of my kidneys I was unaware of and a small low-attenuation lesion involving my right kidney. My primary care doctor (who I just started seeing in April) told me it was nothing to worry about. However, I feel like I may need a second opinion based on my personal and family health history.
History: I was diagnosed with Thyroid cancer in 2017 when I was 27. Upon my surgery to remove my thyroid they discovered it had spread to my lymph nodes. At 6 months they discovered the surgery and first dose of radio active iodine did not get everything and I did another, large dose, of RAI. Since 2018 there has been no evidence of reoccurrence.
I’m 2021 my mom was diagnosed with stage 2 Renal Cell Carcinoma at 56. Her father also had a genetic kidney disease he passed on to her.
Test details: CT ABDOMEN PELVIS W CONTRAST IOPAMIDOL 61 % INTRAVENOUS SOLUTION (SINGLE USE VIAL) Given:100 mL
Kidneys: Symmetric enhancement. Duplicated bilateral renal collecting systems. Subcentimeter low-attenuation lesion involving the right kidney image 46 which is too small to characterize. No hydronephrosis.
Additional Information: Non-smoker, social drinker, physically active 60+ mins 5-7 days a week
Labs as of Friday 6/23 Creatinine was 1.07 mmol/L Total Protein was 8.0 mmol/L Fasted Glucose was 103 mmol/L Sodium was 135 mmol/L Albumin was 4.9 mmol/L GFR value 70 RBC 5.18 million/uL Platelets 442 thousand/uL BP was 124/76

Introduction Nephrotic syndrome is a complex kidney disorder characterized by a specific set of symptoms, including edema (swelling), proteinuria (excessive protein in urine), hypoalbuminemia (low levels of albumin in the blood), and hyperlipidemia (elevated levels of lipids in the blood). It can affect both children and adults, with varying causes and treatment approaches. In this blog post, we will delve into the details of nephrotic syndrome, exploring its causes, symptoms, and management options. Our expert for this discussion is Dr. Sidharth Kumar Sethi, a renowned pediatric nephrologist specializing in the treatment of nephrotic syndrome. Understanding Nephrotic Syndrome Nephrotic syndrome occurs when the kidneys' filtering units, known as nephrons, become damaged, leading to a disruption in their normal function. This damage can result from various underlying conditions or diseases. The most common cause of nephrotic syndrome in children is minimal change disease, which typically responds well to corticosteroid treatment. However, some cases, such as those associated with focal segmental glomerulosclerosis, may be resistant to corticosteroids and may progress to kidney failure, potentially requiring renal transplantation. Symptoms and Diagnosis The hallmark symptoms of nephrotic syndrome include swelling in various parts of the body, particularly the legs and around the eyes, due to fluid retention. Proteinuria, which causes foamy urine, is another key indicator. Hypoalbuminemia and hyperlipidemia can be detected through blood tests. To diagnose nephrotic syndrome, a thorough evaluation is necessary, including a medical history assessment, physical examination, and laboratory tests. A kidney biopsy may also be performed to determine the underlying cause of the condition. Management and Treatment The management of nephrotic syndrome involves addressing the underlying cause, relieving symptoms, and preventing complications. Dr. Sidharth Kumar Sethi emphasizes the importance of individualized treatment plans based on the patient's age, medical history, and specific condition. For children with minimal change disease, corticosteroids are commonly prescribed and have shown significant success in achieving remission of proteinuria. However, some children may experience relapses and require further treatment. In cases of steroid-resistant nephrotic syndrome, alternative treatment options may be explored, including immunosuppressive medications and other targeted therapies. Dr. Sidharth Kumar Sethi's expertise in pediatric nephrology enables him to develop comprehensive treatment plans that prioritize the well-being and long-term outcomes of his patients.
Dr. Sidharth Kumar Sethi Kidney & Urology Institute He was trained as a Fellow (International Pediatric Nephrology Association Fellowship) and Senior Resident in Pediatric Nephrology at All India Institute of Medical Sciences and Division of Pediatric Nephrology and Transplant Immunology, Cedars Sinai Medical Centre, Los Angeles, California. He has been actively involved in the care of children with all kinds of complex renal disorders, including nephrotic syndrome, tubular disorders, urinary tract infections, hypertension, chronic kidney disease, and renal transplantation. He has been a part of an 8-member writing committee for the guidelines of Steroid Sensitive Nephrotic Syndrome and an Expert committee involved in the formulation of guidelines for Pediatric Renal Disorders including Steroid Resistant Nephrotic Syndrome and urinary tract infections. He has more than 30 indexed publications in Pediatric Nephrology and chapters in reputed textbooks including Essential Pediatrics (Editors O.P. Ghai) and “Pediatric Nephrology” (Editors A Bagga, RN Srivastava). He is a part of the Editorial Board of “The World Journal of Nephrology” and “eAJKD- Web version of the American Journal of Kidney Diseases”. He is a reviewer of Pediatric Nephrology related content for various Pediatric and Nephrology journals Conclusion Nephrotic syndrome is a complex kidney disorder characterized by specific symptoms and underlying causes. Early diagnosis and appropriate management are crucial for achieving remission, preventing complications, and ensuring the best possible outcomes for patients. Dr. Sidharth Kumar Sethi, an esteemed pediatric nephrologist, brings extensive knowledge and expertise to the field of nephrotic syndrome treatment. His individualized approach and focus on evidence-based practices make him a trusted resource for patients and their families. Name: Pediatric Nephrology India Address: Division of Pediatric Nephrology, Kidney Institute, Medanta, The Medicity, Gurgaon, Haryana, India, 122001 Phone: 0124-4141414 Website: www.pediatricnephrologyindia.com

29F, 5'7", 135lbs, white - below is a very detailed overview of my health. I am looking for anybody who can potentially lead me in which direction I should turn to next.
Current Medications: Trazodone 150mg 1x per night, Pregabalin 200mg 2x per day
Short Version: I've had the same chronic pain in my left upper abdominal quadrant for 3 years, since March 2020. The pain is primarily located anteriorly just underneath the rib cage in the mid-clavicular line. The pain seems to be gradual throughout the day, with it being pretty severe at night, depending on what I am doing or how I am sitting. The pain will occasionally radiate to the back, up towards the sternum, and down towards the pubis and the groin on the left side. The pain is mostly positional, meaning I can relieve it by standing up, walking around, or lying down because it is most severe when I am sitting, whether that be driving, on the couch, at a table, etc. There is nothing that takes my pain away other than adjusting positions, but mostly laying down. No pain medications relieve my pain. (a detailed list of things I've tried for pain will be at the bottom) I have had multiple imaging studies including a CTA of the abdomen/pelvis that showed possible Nutcracker syndrome with a 17 degree angle between the aorta and SMA with dilation of the left renal vein. I was evaluated by UW Madison for consideration of an autotransplant of my left kidney. However, after I underwent a venogram which showed equal pressures between the renal vein and IVC, Dr. Foley did not want to offer the surgery. I also have had irregular menstrual cycles since I began having periods. Within the last few years, I feel like I almost get the "period flu" or have more PMDD symptoms before I'm about to get it.
Long Version: This all started in March 2020, my office had just moved to working from home with the Coronavirus outbreak. I hadn't gotten a desk/office chair for home yet, so I started out by sitting on my couch with my laptop in my lap for a couple of weeks. After about 3 weeks in I started to notice a bad pain in my left side. It was like a pinching/burning pain and it seemed to come on slowly the more I sat in the same position. My immediate thought was that it was like a "side stitch" or a cramp from the way I was kind of slouching and not sitting upright in a chair. I quickly made sure to get a desk and chair to see if it helped resolve the pain. Unfortunately, it did not. The more the days went on, the worse the pain was getting and it only seemed to be when I was sitting for longer periods of time. I had to start getting up more frequently and walking around or switching positions. I went to a chiropractor which did not alter the pain in any sort of way. The same chiropractor also tried a few laser therapy sessions over the affected area as well, with no relief. The pain was gradually becoming a permanent thing, and it became painful to wear a bra due to the pressure it caused around my ribs/where the pain is. I was trying everything I could think of to relieve the pain. At first I tried ibuprofen, Tylenol, heat, ice, heating pad, icy hot, cbd muscle rub, cannabis, The pain continued on and I started talking to my then primary doctor, I had an x-ray done of my ribs 04/2020 - which showed normal. I then had a chest x-ray and chest CT done 05/2020 - also normal. The pain continued through that fall and into 2021. I had c*v*d for the first time 11/22/2020. In spring of 2021 I had c*v*d again in March, so almost right at 90 days since first infection. I then started to get more serious about finding out what was wrong because I started to have a new pain in my left collarbone. It seemed like the whole bone would ache and the more I moved my arms(I had started cosmetology school in the fall of 2020) the worse the pain got. Sometimes the lightest touch from my shirt, a tank top, my cosmetology apron, or even my seat belt resting on my collarbone would cause immense pain. This lasted about a couple weeks at first, then it would go away for weeks/months, then it would come back randomly. I went to the emergency room one day in 03/2021 because I was so tired of being in so much pain, and had more chest x-rays done, which came back clear and normal. The collarbone pain has not bothered me for about 6 months now, but I have also been pretty sedentary since then. Fast forward to 06/15/2022 after my third round of c*v*d the beginning part of June, I started having the following symptoms for a month straight. I was physically so unwell, I could barely get up from laying down most of the time and could not go outside due to not being able to tolerate the heat, until I finally asked my doctor to run more labs, which all came back normal: dizziness, night sweats, severe intolerance to heat, severe loss of appetite and nausea, and new body odor(previously never had an issue with body odor). Since then, I have had periodic episodes that last weeks with severe loss of appetite(cannabis is the only way I can eat most of the time), some mild nausea(never any vomiting), lethargy, feeling hopeless, very mild night sweats, hotter body temperature while sleeping. And then I'll have weeks where I feel fine except my usual pain. On 01/26/2023 I traveled to Punta Cana for my sisters wedding. I suffered through the pain of sitting for an extended period of time on the plane ride. While there, I virtually had no appetite my first night and the next morning/afternoon. And then my appetite came back and my pain went almost completely away for almost 4 days, until I went back home. I ate Taco Bell at the airport and had almost immediate pain from sitting on the plane again, and the pain has been present every day since.
01/25/2023 Urology consult: CHIEF COMPLAINT: left sided pain; concern for Nutcracker syndrome. Impression: 29 FEMALE with pain that has been difficult to identify a cause and treat. She does have a narrow angle between the SMA and aorta with slight dilation of the left renal vein. However, there is no pressure difference between the left renal vein and IVC indicating that while there may be slight anatomic abnormality, this doesn't necessarily indicatee Nutcracker syndrome which would be characterized by left flank pain due to elevated pressure in the left renal vein (and kidney) due to compression of the vein. Additionally, her pain is not classic kidney pain based on description (stabbing/burning and anterior). Additionally, she has several indicators for possible Ehlers-Danlos and her pain may have a myofascial componenent.
10/25/2022 I saw an Integrative Health Practitioner who ran some tests for celiac disease. deamidated gliadin abs, IgA - 4 deamidated gliadin abs, IgG - 1 T-transglutaminase (ttg) IgA <2 T-transglutaminase (ttg) IgG <2 endomysial antibody IgA: negative immunoglobulin A, qn, serum: 51 amylase: 73 lipase: 20
11/07/2022 GI Consult outside of the VA, Impression: "does not sound GI related in the slightest. I recommend trying Elavil. Also might not be a bad idea to go back and look for multiple sclerosis with a spinal MRI"
List of things I have tried, nothing on the list has successfully helped my pain

• ibuprofen
• Tylenol
• acetaminophen with codeine
• Norco
• Prednisone
• tramadol
• lidocaine patches
• topical analgesics
• chiropractic care
• multiple rounds of physical therapy
• dry needling
• acupuncture
• basic exercise and stretching
• nerve block injections into 9, 10, & 11 intercostal
• left inferior costal margin trigger-point injection with 0.5% Marcaine and Celestone on the border of the 11th an 12th rib.
• CBD
• Cannabis

Below is a list of my imaging/diangnostic procedure history: - 4/25/2020 Seen for left chest wall pain. Left Rib xray: negative. - 5/1/2020 Chest CT w/o contrast: no abnormality in left anterior lower lateral rib/chest wall. Benign calcified left lower lobe granuloma adn left hilar lymph node consistent with prior granulomatous infection. - 5/13/2020 thoracic spine xray: minimal S shaped scoliosis of thoracolumbar spine. - 3/11/21 Seen at ER for collarbone and "left rib pain" Also fatigue, weakness, sensitivity to cold, weight loss. Labs normal. EKG normal. No significant abnl findings on exam. Notes state - Suspect underlying personality/mood disorder. Given ibuprofen and tramadol for pain. CXR 3-11-21: normal. - 7/8/21 CT - impression: Hepatic and left renal low density attenuation lesions suspicious for cyst. Ultrasound may be beneficial for further evaluation. - 09/07/2021 MRI Thoracic Spine WO Contrast, Impressions: small area of bright T1 & T2 signal suggest intraosseous hemangioma in the lower thoracic vertebra. Essentially unremarkable. - 4/28/22 Ultrasound Liver, Kidneys, Bladder: Liver measurement-18.56 cm with smooth contour however with coarse echotexture concern for hepatocellular disease. Previous CT study of the abdomen demonstrated 4.0 mm lesion of the liver not seen on today's ultrasound examination, likely too small to visualize. -05/04/2022 MRI ABDOMEN W/O & W CONTRAST: Impression:

1. Incidental small hepatic segment 7 cyst corresponding with low density focus on CT 7/8/2021. No additional follow up imaging is needed for this finding.
2. Findings compatible with small involuting cyst at left kidney corresponding with low density focus on CT 7/8/2021. No additional follow up imaging is needed for this finding.
3. Narrowing of left renal vein between reduced angle at aorta and SMA. Please correlate for Nutcracker syndrome.
4. Narrowing of duodenum between reduced angle at aorta and SMA. Please correlate for superior mesenteric artery syndrome. Vasculature: Patency at hepatic and portal venous system, superior mesenteric vein, splenic vein, IVC, renal veins. No significant collateral vessel formation. Redemonstration narrowing at left renal vein between aorta and SMA (narrow aortomesenteric angle). Otherwise, aorta and branching vessels unremarkable. -06/30/2022 CTA (AP) ABDOMEN/PELVIS W CONTRAST Impression:
5. There is a reduced aortic to celiacomesentery angle resulting in narrowing of the left renal vein, however there are no CT findings to suggest left renal vein obstruction.
6. Sclerosis at the right femoral head may reflect minimal osteonecrosis. -08/17/2022 MRI BRAIN W/WO CONTRAST - unremarkable -09/21/2022 Renal Artery Duplex Impression: Normal study, no evidence of hemodynamically significant stenosis in bilateral kidneys. Bilateral veins are patent -10/03/2022 Venogram Left Renal Vein Impressions: Left Renal - venous pressure 12mmHg segmental/distal, 11 mmHg in proximal, 11 mmHg inferior vena cava. Left External iliac - 6 mmHg in external iliac/distal, 5 mmHg in proximal. -11/04/2022 US ABDOMENT LTD - unremarkable, no gallstones, no gallbladder wall thickening, no free fluid -11/04/2022 US PELVIS NON OB TRANSVAGINAL Impressions: bicornuate uterus, small 0.9x0.8cm echogenic non shadowing focus in the right ovary, possible small dermoid, small complex left ovarian cyst measuring 1.8x1.3cm -11/10/2022 CT PELLVIS W CONTRAST Impressions: normal CT of pelvis. Right ovarian lesions not shown on CT 03/17/2023 Colonoscopy - unremarkable

Most recent lab results:
1/15/2023 WBC 8.51 RBC 4.20 HGB 11.7 HCT 37.6 MCV 89.5 MCH 30.7 MCHC 34.3 Platelets 303 sodium 138 potassium 3.6 chloride 101 CO2 20 Glucose 138 BUN 13 Creatine 0.86 Calcium 9.7 total protein 7.5 Albumin 5.0 Biliruben total 0.5 Alaline phosphatase 50 AST 16 ALT <5 Anion gap 17 BUN/Creatine Ratio 15.1 Osmolality Calculated 288 Globulin 2.5 A/G Ratio 2.0 Creatine Based eGFR >90
10/13/2022 CBC: WBC: 7.9 K/uL RBC: 4.53 M/uL HGB: 13.6 g/dL HCT: 41.4 % MCV: 91.4 fL MCH: 30.0 pg MCHC: 32.9 g/dL MPV: 12.3 fL RDW: 12.1 % PLT: 281 K/uL BMP: Sodium: 139 mmol/L Potassium: 4.2 mmol/L Chloride: 109 mmol/L CO2: 24.4 mmol/L Glucose: 84 mg/dL Urea Nitrogen: 13 mg/dL Creatinine: 0.72 mg/dL Calcium: 9.3 mg/dL
10/3/22 Creatinine: 0.81mg/dL e-GFR: 101 Prothrombin Time/INR 0.9
08/12/22 Serotonin: 113/ng/mL ACTH: 26.7pg/mL Aldosterone: 13.5 Cortisol AM: 11.5ug/mL Metanephrine: 0.13nmol/L Normetanephrine: 0.32nmol/L
07/18/22 TSH Reflex Free T4: 1.16 Vitamin D: 42.7ng/mL Vitamin B12: 452pg/mL Folate: 11.9ng/mL A1C: 4.6 Glucose: 85 Ferritin: 66 Iron: 92ug/dL TIBC: 297ug/dL Iron Saturation: 31% UIBC: 205 ug/dL Peripheral Blood Smear - no significant abnormalities Lyme disease IGG/IGM: Negative Normal EKG sinus rhythm
If anyone has suggestions, please do not hesitate to leave them below.

Current Medications: Trazodone 150mg 1x per night, Pregabalin 200mg 2x per day
29F, 5'7", 135lbs, white - below is a very detailed overview of my health. I am looking for anybody who can potentially lead me in which direction I should turn to next.
Short Version: I've had the same chronic pain in my left upper abdominal quadrant for 3 years, since March 2020. The pain is primarily located anteriorly just underneath the rib cage in the mid-clavicular line. The pain seems to be gradual throughout the day, with it being pretty severe at night, depending on what I am doing or how I am sitting. The pain will occasionally radiate to the back, up towards the sternum, and down towards the pubis and the groin on the left side. The pain is mostly positional, meaning I can relieve it by standing up, walking around, or lying down because it is most severe when I am sitting, whether that be driving, on the couch, at a table, etc. There is nothing that takes my pain away other than adjusting positions, but mostly laying down. No pain medications relieve my pain. (a detailed list of things I've tried for pain will be at the bottom) I have had multiple imaging studies including a CTA of the abdomen/pelvis that showed possible Nutcracker syndrome with a 17 degree angle between the aorta and SMA with dilation of the left renal vein. I was evaluated by UW Madison for consideration of an autotransplant of my left kidney. However, after I underwent a venogram which showed equal pressures between the renal vein and IVC, Dr. Foley did not want to offer the surgery. I also have had irregular menstrual cycles since I began having periods. Within the last few years, I feel like I almost get the "period flu" or have more PMDD symptoms before I'm about to get it.
Long Version: This all started in March 2020, my office had just moved to working from home with the Coronavirus outbreak. I hadn't gotten a desk/office chair for home yet, so I started out by sitting on my couch with my laptop in my lap for a couple of weeks. After about 3 weeks in I started to notice a bad pain in my left side. It was like a pinching/burning pain and it seemed to come on slowly the more I sat in the same position. My immediate thought was that it was like a "side stitch" or a cramp from the way I was kind of slouching and not sitting upright in a chair. I quickly made sure to get a desk and chair to see if it helped resolve the pain. Unfortunately, it did not. The more the days went on, the worse the pain was getting and it only seemed to be when I was sitting for longer periods of time. I had to start getting up more frequently and walking around or switching positions. I went to a chiropractor which did not alter the pain in any sort of way. The same chiropractor also tried a few laser therapy sessions over the affected area as well, with no relief. The pain was gradually becoming a permanent thing, and it became painful to wear a bra due to the pressure it caused around my ribs/where the pain is. I was trying everything I could think of to relieve the pain. At first I tried ibuprofen, Tylenol, heat, ice, heating pad, icy hot, cbd muscle rub, cannabis, The pain continued on and I started talking to my then primary doctor, I had an x-ray done of my ribs 04/2020 - which showed normal. I then had a chest x-ray and chest CT done 05/2020 - also normal. The pain continued through that fall and into 2021. I had c*v*d for the first time 11/22/2020. In spring of 2021 I had c*v*d again in March, so almost right at 90 days since first infection. I then started to get more serious about finding out what was wrong because I started to have a new pain in my left collarbone. It seemed like the whole bone would ache and the more I moved my arms(I had started cosmetology school in the fall of 2020) the worse the pain got. Sometimes the lightest touch from my shirt, a tank top, my cosmetology apron, or even my seat belt resting on my collarbone would cause immense pain. This lasted about a couple weeks at first, then it would go away for weeks/months, then it would come back randomly. I went to the emergency room one day in 03/2021 because I was so tired of being in so much pain, and had more chest x-rays done, which came back clear and normal. The collarbone pain has not bothered me for about 6 months now, but I have also been pretty sedentary since then. Fast forward to 06/15/2022 after my third round of c*v*d the beginning part of June, I started having the following symptoms for a month straight. I was physically so unwell, I could barely get up from laying down most of the time and could not go outside due to not being able to tolerate the heat, until I finally asked my doctor to run more labs, which all came back normal: dizziness, night sweats, severe intolerance to heat, severe loss of appetite and nausea, and new body odor(previously never had an issue with body odor). Since then, I have had periodic episodes that last weeks with severe loss of appetite(cannabis is the only way I can eat most of the time), some mild nausea(never any vomiting), lethargy, feeling hopeless, very mild night sweats, hotter body temperature while sleeping. And then I'll have weeks where I feel fine except my usual pain. On 01/26/2023 I traveled to Punta Cana for my sisters wedding. I suffered through the pain of sitting for an extended period of time on the plane ride. While there, I virtually had no appetite my first night and the next morning/afternoon. And then my appetite came back and my pain went almost completely away for almost 4 days, until I went back home. I ate Taco Bell at the airport and had almost immediate pain from sitting on the plane again, and the pain has been present every day since.
01/25/2023 Urology consult: CHIEF COMPLAINT: left sided pain; concern for Nutcracker syndrome. Impression: 29 FEMALE with pain that has been difficult to identify a cause and treat. She does have a narrow angle between the SMA and aorta with slight dilation of the left renal vein. However, there is no pressure difference between the left renal vein and IVC indicating that while there may be slight anatomic abnormality, this doesn't necessarily indicatee Nutcracker syndrome which would be characterized by left flank pain due to elevated pressure in the left renal vein (and kidney) due to compression of the vein. Additionally, her pain is not classic kidney pain based on description (stabbing/burning and anterior). Additionally, she has several indicators for possible Ehlers-Danlos and her pain may have a myofascial componenent.
10/25/2022 I saw an Integrative Health Practitioner who ran some tests for celiac disease. deamidated gliadin abs, IgA - 4 deamidated gliadin abs, IgG - 1 T-transglutaminase (ttg) IgA <2 T-transglutaminase (ttg) IgG <2 endomysial antibody IgA: negative immunoglobulin A, qn, serum: 51 amylase: 73 lipase: 20
11/07/2022 GI Consult outside of the VA, Impression: "does not sound GI related in the slightest. I recommend trying Elavil. Also might not be a bad idea to go back and look for multiple sclerosis with a spinal MRI"
List of things I have tried, nothing on the list has successfully helped my pain

• ibuprofen
• Tylenol
• acetaminophen with codeine
• Norco
• Prednisone
• tramadol
• lidocaine patches
• topical analgesics
• chiropractic care
• multiple rounds of physical therapy
• dry needling
• acupuncture
• basic exercise and stretching
• nerve block injections into 9, 10, & 11 intercostal
• left inferior costal margin trigger-point injection with 0.5% Marcaine and Celestone on the border of the 11th an 12th rib.
• CBD
• Cannabis

Below is a list of my imaging/diangnostic procedure history: - 4/25/2020 Seen for left chest wall pain. Left Rib xray: negative. - 5/1/2020 Chest CT w/o contrast: no abnormality in left anterior lower lateral rib/chest wall. Benign calcified left lower lobe granuloma adn left hilar lymph node consistent with prior granulomatous infection. - 5/13/2020 thoracic spine xray: minimal S shaped scoliosis of thoracolumbar spine. - 3/11/21 Seen at ER for collarbone and "left rib pain" Also fatigue, weakness, sensitivity to cold, weight loss. Labs normal. EKG normal. No significant abnl findings on exam. Notes state - Suspect underlying personality/mood disorder. Given ibuprofen and tramadol for pain. CXR 3-11-21: normal. - 7/8/21 CT - impression: Hepatic and left renal low density attenuation lesions suspicious for cyst. Ultrasound may be beneficial for further evaluation. - 09/07/2021 MRI Thoracic Spine WO Contrast, Impressions: small area of bright T1 & T2 signal suggest intraosseous hemangioma in the lower thoracic vertebra. Essentially unremarkable. - 4/28/22 Ultrasound Liver, Kidneys, Bladder: Liver measurement-18.56 cm with smooth contour however with coarse echotexture concern for hepatocellular disease. Previous CT study of the abdomen demonstrated 4.0 mm lesion of the liver not seen on today's ultrasound examination, likely too small to visualize. -05/04/2022 MRI ABDOMEN W/O & W CONTRAST: Impression:

1. Incidental small hepatic segment 7 cyst corresponding with low density focus on CT 7/8/2021. No additional follow up imaging is needed for this finding.
2. Findings compatible with small involuting cyst at left kidney corresponding with low density focus on CT 7/8/2021. No additional follow up imaging is needed for this finding.
3. Narrowing of left renal vein between reduced angle at aorta and SMA. Please correlate for Nutcracker syndrome.
4. Narrowing of duodenum between reduced angle at aorta and SMA. Please correlate for superior mesenteric artery syndrome. Vasculature: Patency at hepatic and portal venous system, superior mesenteric vein, splenic vein, IVC, renal veins. No significant collateral vessel formation. Redemonstration narrowing at left renal vein between aorta and SMA (narrow aortomesenteric angle). Otherwise, aorta and branching vessels unremarkable. -06/30/2022 CTA (AP) ABDOMEN/PELVIS W CONTRAST Impression:
5. There is a reduced aortic to celiacomesentery angle resulting in narrowing of the left renal vein, however there are no CT findings to suggest left renal vein obstruction.
6. Sclerosis at the right femoral head may reflect minimal osteonecrosis.

-08/17/2022 MRI BRAIN W/WO CONTRAST - unremarkable -09/21/2022 Renal Artery Duplex Impression: Normal study, no evidence of hemodynamically significant stenosis in bilateral kidneys. Bilateral veins are patent -10/03/2022 Venogram Left Renal Vein Impressions: Left Renal - venous pressure 12mmHg segmental/distal, 11 mmHg in proximal, 11 mmHg inferior vena cava. Left External iliac - 6 mmHg in external iliac/distal, 5 mmHg in proximal. -11/04/2022 US ABDOMENT LTD - unremarkable, no gallstones, no gallbladder wall thickening, no free fluid -11/04/2022 US PELVIS NON OB TRANSVAGINAL Impressions: bicornuate uterus, small 0.9x0.8cm echogenic non shadowing focus in the right ovary, possible small dermoid, small complex left ovarian cyst measuring 1.8x1.3cm -11/10/2022 CT PELLVIS W CONTRAST Impressions: normal CT of pelvis. Right ovarian lesions not shown on CT 03/17/2023 Colonoscopy - unremarkable
Most recent lab results:
1/15/2023 WBC 8.51 RBC 4.20 HGB 11.7 HCT 37.6 MCV 89.5 MCH 30.7 MCHC 34.3 Platelets 303 sodium 138 potassium 3.6 chloride 101 CO2 20 Glucose 138 BUN 13 Creatine 0.86 Calcium 9.7 total protein 7.5 Albumin 5.0 Biliruben total 0.5 Alaline phosphatase 50 AST 16 ALT <5 Anion gap 17 BUN/Creatine Ratio 15.1 Osmolality Calculated 288 Globulin 2.5 A/G Ratio 2.0 Creatine Based eGFR >90
10/13/2022 CBC: WBC: 7.9 K/uL RBC: 4.53 M/uL HGB: 13.6 g/dL HCT: 41.4 % MCV: 91.4 fL MCH: 30.0 pg MCHC: 32.9 g/dL MPV: 12.3 fL RDW: 12.1 % PLT: 281 K/uL BMP: Sodium: 139 mmol/L Potassium: 4.2 mmol/L Chloride: 109 mmol/L CO2: 24.4 mmol/L Glucose: 84 mg/dL Urea Nitrogen: 13 mg/dL Creatinine: 0.72 mg/dL Calcium: 9.3 mg/dL
10/3/22 Creatinine: 0.81mg/dL e-GFR: 101 Prothrombin Time/INR 0.9
08/12/22 Serotonin: 113/ng/mL ACTH: 26.7pg/mL Aldosterone: 13.5 Cortisol AM: 11.5ug/mL Metanephrine: 0.13nmol/L Normetanephrine: 0.32nmol/L
07/18/22 TSH Reflex Free T4: 1.16 Vitamin D: 42.7ng/mL Vitamin B12: 452pg/mL Folate: 11.9ng/mL A1C: 4.6 Glucose: 85 Ferritin: 66 Iron: 92ug/dL TIBC: 297ug/dL Iron Saturation: 31% UIBC: 205 ug/dL Peripheral Blood Smear - no significant abnormalities Lyme disease IGG/IGM: Negative Normal EKG sinus rhythm
If anyone has suggestions, please do not hesitate to leave them below.

29 year old female - below is a very detailed overview of my health. I am looking for anybody who can potentially lead me in which direction I should turn to next.
Short Version: I've had the same chronic pain in my left upper abdominal quadrant for 3 years, since March 2020. The pain is primarily located anteriorly just underneath the rib cage in the mid-clavicular line. The pain seems to be gradual throughout the day, with it being pretty severe at night, depending on what I am doing or how I am sitting. The pain will occasionally radiate to the back, up towards the sternum, and down towards the pubis and the groin on the left side. The pain is mostly positional, meaning I can relieve it by standing up, walking around, or lying down because it is most severe when I am sitting, whether that be driving, on the couch, at a table, etc. There is nothing that takes my pain away other than adjusting positions, but mostly laying down. No pain medications relieve my pain. (a detailed list of things I've tried for pain will be at the bottom) I have had multiple imaging studies including a CTA of the abdomen/pelvis that showed possible Nutcracker syndrome with a 17 degree angle between the aorta and SMA with dilation of the left renal vein. I was evaluated by UW Madison for consideration of an autotransplant of my left kidney. However, after I underwent a venogram which showed equal pressures between the renal vein and IVC, Dr. Foley did not want to offer the surgery. I also have had irregular menstrual cycles since I began having periods. Within the last few years, I feel like I almost get the "period flu" or have more PMDD symptoms before I'm about to get it.
Long Version: This all started in March 2020, my office had just moved to working from home with the Coronavirus outbreak. I hadn't gotten a desk/office chair for home yet, so I started out by sitting on my couch with my laptop in my lap for a couple of weeks. After about 3 weeks in I started to notice a bad pain in my left side. It was like a pinching/burning pain and it seemed to come on slowly the more I sat in the same position. My immediate thought was that it was like a "side stitch" or a cramp from the way I was kind of slouching and not sitting upright in a chair. I quickly made sure to get a desk and chair to see if it helped resolve the pain. Unfortunately, it did not. The more the days went on, the worse the pain was getting and it only seemed to be when I was sitting for longer periods of time. I had to start getting up more frequently and walking around or switching positions. I went to a chiropractor which did not alter the pain in any sort of way. The same chiropractor also tried a few laser therapy sessions over the affected area as well, with no relief. The pain was gradually becoming a permanent thing, and it became painful to wear a bra due to the pressure it caused around my ribs/where the pain is. I was trying everything I could think of to relieve the pain. At first I tried ibuprofen, Tylenol, heat, ice, heating pad, icy hot, cbd muscle rub, cannabis, The pain continued on and I started talking to my then primary doctor, I had an x-ray done of my ribs 04/2020 - which showed normal. I then had a chest x-ray and chest CT done 05/2020 - also normal. The pain continued through that fall and into 2021. I had c*v*d for the first time 11/22/2020. In spring of 2021 I had c*v*d again in March, so almost right at 90 days since first infection. I then started to get more serious about finding out what was wrong because I started to have a new pain in my left collarbone. It seemed like the whole bone would ache and the more I moved my arms(I had started cosmetology school in the fall of 2020) the worse the pain got. Sometimes the lightest touch from my shirt, a tank top, my cosmetology apron, or even my seat belt resting on my collarbone would cause immense pain. This lasted about a couple weeks at first, then it would go away for weeks/months, then it would come back randomly. I went to the emergency room one day in 03/2021 because I was so tired of being in so much pain, and had more chest x-rays done, which came back clear and normal. The collarbone pain has not bothered me for about 6 months now, but I have also been pretty sedentary since then. Fast forward to 06/15/2022 after my third round of c*v*d the beginning part of June, I started having the following symptoms for a month straight. I was physically so unwell, I could barely get up from laying down most of the time and could not go outside due to not being able to tolerate the heat, until I finally asked my doctor to run more labs, which all came back normal: dizziness, night sweats, severe intolerance to heat, severe loss of appetite and nausea, and new body odor(previously never had an issue with body odor). Since then, I have had periodic episodes that last weeks with severe loss of appetite(cannabis is the only way I can eat most of the time), some mild nausea(never any vomiting), lethargy, feeling hopeless, very mild night sweats, hotter body temperature while sleeping. And then I'll have weeks where I feel fine except my usual pain. On 01/26/2023 I traveled to Punta Cana for my sisters wedding. I suffered through the pain of sitting for an extended period of time on the plane ride. While there, I virtually had no appetite my first night and the next morning/afternoon. And then my appetite came back and my pain went almost completely away for almost 4 days, until I went back home. I ate Taco Bell at the airport and had almost immediate pain from sitting on the plane again, and the pain has been present every day since.
01/25/2023 Urology consult: CHIEF COMPLAINT: left sided pain; concern for Nutcracker syndrome. Impression: 29 FEMALE with pain that has been difficult to identify a cause and treat. She does have a narrow angle between the SMA and aorta with slight dilation of the left renal vein. However, there is no pressure difference between the left renal vein and IVC indicating that while there may be slight anatomic abnormality, this doesn't necessarily indicatee Nutcracker syndrome which would be characterized by left flank pain due to elevated pressure in the left renal vein (and kidney) due to compression of the vein. Additionally, her pain is not classic kidney pain based on description (stabbing/burning and anterior). Additionally, she has several indicators for possible Ehlers-Danlos and her pain may have a myofascial componenent.
10/25/2022 I saw an Integrative Health Practitioner who ran some tests for celiac disease. deamidated gliadin abs, IgA - 4 deamidated gliadin abs, IgG - 1 T-transglutaminase (ttg) IgA <2 T-transglutaminase (ttg) IgG <2 endomysial antibody IgA: negative immunoglobulin A, qn, serum: 51 amylase: 73 lipase: 20
11/07/2022 GI Consult outside of the VA, Impression: "does not sound GI related in the slightest. I recommend trying Elavil. Also might not be a bad idea to go back and look for multiple sclerosis with a spinal MRI"
List of things I have tried, nothing on the list has successfully helped my pain

• ibuprofen
• Tylenol
• acetaminophen with codeine
• Norco
• Prednisone
• tramadol
• lidocaine patches
• topical analgesics
• chiropractic care
• multiple rounds of physical therapy
• dry needling
• acupuncture
• basic exercise and stretching
• nerve block injections into 9, 10, & 11 intercostal
• left inferior costal margin trigger-point injection with 0.5% Marcaine and Celestone on the border of the 11th an 12th rib.
• CBD
• Cannabis

Below is a list of my imaging/diangnostic procedure history: - 4/25/2020 Seen for left chest wall pain. Left Rib xray: negative. - 5/1/2020 Chest CT w/o contrast: no abnormality in left anterior lower lateral rib/chest wall. Benign calcified left lower lobe granuloma adn left hilar lymph node consistent with prior granulomatous infection. - 5/13/2020 thoracic spine xray: minimal S shaped scoliosis of thoracolumbar spine. - 3/11/21 Seen at ER for collarbone and "left rib pain" Also fatigue, weakness, sensitivity to cold, weight loss. Labs normal. EKG normal. No significant abnl findings on exam. Notes state - Suspect underlying personality/mood disorder. Given ibuprofen and tramadol for pain. CXR 3-11-21: normal. - 7/8/21 CT - impression: Hepatic and left renal low density attenuation lesions suspicious for cyst. Ultrasound may be beneficial for further evaluation. - 09/07/2021 MRI Thoracic Spine WO Contrast, Impressions: small area of bright T1 & T2 signal suggest intraosseous hemangioma in the lower thoracic vertebra. Essentially unremarkable. - 4/28/22 Ultrasound Liver, Kidneys, Bladder: Liver measurement-18.56 cm with smooth contour however with coarse echotexture concern for hepatocellular disease. Previous CT study of the abdomen demonstrated 4.0 mm lesion of the liver not seen on today's ultrasound examination, likely too small to visualize. -05/04/2022 MRI ABDOMEN W/O & W CONTRAST: Impression:

1. Incidental small hepatic segment 7 cyst corresponding with low density focus on CT 7/8/2021. No additional follow up imaging is needed for this finding.
2. Findings compatible with small involuting cyst at left kidney corresponding with low density focus on CT 7/8/2021. No additional follow up imaging is needed for this finding.
3. Narrowing of left renal vein between reduced angle at aorta and SMA. Please correlate for Nutcracker syndrome.
4. Narrowing of duodenum between reduced angle at aorta and SMA. Please correlate for superior mesenteric artery syndrome. Vasculature: Patency at hepatic and portal venous system, superior mesenteric vein, splenic vein, IVC, renal veins. No significant collateral vessel formation. Redemonstration narrowing at left renal vein between aorta and SMA (narrow aortomesenteric angle). Otherwise, aorta and branching vessels unremarkable. -06/30/2022 CTA (AP) ABDOMEN/PELVIS W CONTRAST Impression:
5. There is a reduced aortic to celiacomesentery angle resulting in narrowing of the left renal vein, however there are no CT findings to suggest left renal vein obstruction.
6. Sclerosis at the right femoral head may reflect minimal osteonecrosis. -08/17/2022 MRI BRAIN W/WO CONTRAST - unremarkable -09/21/2022 Renal Artery Duplex Impression: Normal study, no evidence of hemodynamically significant stenosis in bilateral kidneys. Bilateral veins are patent -10/03/2022 Venogram Left Renal Vein Impressions: Left Renal - venous pressure 12mmHg segmental/distal, 11 mmHg in proximal, 11 mmHg inferior vena cava. Left External iliac - 6 mmHg in external iliac/distal, 5 mmHg in proximal. -11/04/2022 US ABDOMENT LTD - unremarkable, no gallstones, no gallbladder wall thickening, no free fluid -11/04/2022 US PELVIS NON OB TRANSVAGINAL Impressions: bicornuate uterus, small 0.9x0.8cm echogenic non shadowing focus in the right ovary, possible small dermoid, small complex left ovarian cyst measuring 1.8x1.3cm -11/10/2022 CT PELLVIS W CONTRAST Impressions: normal CT of pelvis. Right ovarian lesions not shown on CT 03/17/2023 Colonoscopy - unremarkable

Most recent lab results:
1/15/2023 WBC 8.51 RBC 4.20 HGB 11.7 HCT 37.6 MCV 89.5 MCH 30.7 MCHC 34.3 Platelets 303 sodium 138 potassium 3.6 chloride 101 CO2 20 Glucose 138 BUN 13 Creatine 0.86 Calcium 9.7 total protein 7.5 Albumin 5.0 Biliruben total 0.5 Alaline phosphatase 50 AST 16 ALT <5 Anion gap 17 BUN/Creatine Ratio 15.1 Osmolality Calculated 288 Globulin 2.5 A/G Ratio 2.0 Creatine Based eGFR >90
10/13/2022 CBC: WBC: 7.9 K/uL RBC: 4.53 M/uL HGB: 13.6 g/dL HCT: 41.4 % MCV: 91.4 fL MCH: 30.0 pg MCHC: 32.9 g/dL MPV: 12.3 fL RDW: 12.1 % PLT: 281 K/uL BMP: Sodium: 139 mmol/L Potassium: 4.2 mmol/L Chloride: 109 mmol/L CO2: 24.4 mmol/L Glucose: 84 mg/dL Urea Nitrogen: 13 mg/dL Creatinine: 0.72 mg/dL Calcium: 9.3 mg/dL
10/3/22 Creatinine: 0.81mg/dL e-GFR: 101 Prothrombin Time/INR 0.9
08/12/22 Serotonin: 113/ng/mL ACTH: 26.7pg/mL Aldosterone: 13.5 Cortisol AM: 11.5ug/mL Metanephrine: 0.13nmol/L Normetanephrine: 0.32nmol/L
07/18/22 TSH Reflex Free T4: 1.16 Vitamin D: 42.7ng/mL Vitamin B12: 452pg/mL Folate: 11.9ng/mL A1C: 4.6 Glucose: 85 Ferritin: 66 Iron: 92ug/dL TIBC: 297ug/dL Iron Saturation: 31% UIBC: 205 ug/dL Peripheral Blood Smear - no significant abnormalities Lyme disease IGG/IGM: Negative Normal EKG sinus rhythm
If anyone has suggestions, please do not hesitate to leave them below.

https://docs.google.com/document/d/1pSOMGU_vHBOXeDrlD8MvMNsEO8Kyqye5/edit?usp=sharing&ouid=109474854956598892099&rtpof=true&sd=true
Work Book (Phase - VIII)
Subjective:
Board Type Questions

1. What will be the sequence of bases on mRNA molecule synthesized on the following strand of DNA?
   
2. Aspartame, an artificial sweetener, is a peptide and has the following structure:
   

📷
(i) Identify the four functional groups.
(ii) Write the Zwitterionic structure.
(iii) Write the structure of amino acids obtained from the hydrolysis of aspartame.
(iv) Which of the two amino acids is more hydrophobic?

1. Could a copolymer be formed in both condensation or not? Explain with example.
   
2. What are biodegradable polymers write structure of PHBV?
   
3. What is Nylon? Write an equation for the chemistry involved when a drop of hydrochlorine acid makes a hole in a nylon stocking.
   
4. (i) Give the Fischer projection of L-glucose.
   

(ii) Give the products of reaction of L-glucose with Tollen’s reagent.

1. Differentiate between

(a) Nucleotide and Nucleoside
(b) Vitamins and Hormones
(c) DNA and RNA

1. Give the IUAPC names of the following compounds:

(a) 📷
(b) Cr(CO)6
(c) K3[Al(C2O4)3]

1. Combination of Pt(IV), NH3, Cl− and K+ results in the formation of seven complexes and one such complex is 📷. Write the formulae of the other six members of the series.
   
2. What is the number of ionizable chlorine atoms in the complex 📷?
   
3. Complete and balance:
   

📷

1. Compete the following

📷

1. Explain why:

Ferrous salt turns brown in air.

1. Which one of Fe2+ and Fe3+ ions is more paramagnetic and why?
   
2. Which of the following is formed when K2Cr2O7, CaCl2 and conc. H2SO4 is heated?
   

📷

1. Though copper, silver and gold have completely filled sets of d-orbitals yet they are considered as transition metals. Why?
   
2. Why does Mn(II) show maximum paramagnetic character amongst the bivalent ions of the first transition series?
   
3. Why Zn2+ salts are white while Ni2+ salts are blue?
   
4. Why Zn2+ salts are white while Cu2+ salts are blue?
   
5. [Ti(H2O)6]3+ is coloured while [Sc(H2O)6]3+ is colourless. Explain.
   
6. A co-ordination compound has the formula CoCl3.4NH3. It does not liberate ammonia but precipitates chloride ions as silver chloride. Give the IUPAC name of the complex and write its structural formula.
   
7. Arrange the following complexes in order of increasing electrical conductivity:
   

[CoCl3(NH3)3], [CoCl(NH3)5]Cl2, [Co(NH3)6]Cl3, [CoCl2(NH3)4]Cl

1. Which of the two compounds is more stable and why?

[K4[Fe(CN)6], K3[Fe(CN)6]

1. [NiCl4]2− is paramagnetic while [Ni(CO)4] is diamagnetic though both are tetrahedral. Why?
   
2. Name one polymer formed by step growth polymerization. Give names of its monomers.
   
3. Arrange the following polymers in increasing order of their intermolecular forces. Also classify them as addition and condensation polymers:
   

Nylon-66, Buna-S, Nylon – 66

1. Given reason of the following

(i) Aniline does not undergo Friedel-Craft reaction.
(ii) Diazonium salts of aromatic amines are more stable than those of aliphatic amines

1. Given account of the following

(i) Gabriel phthalamide synthesis is preferred for synthesing primary amines.
(ii) Ethylamine is soluble in water whereas aniline is not.

1. Given reason of the following

(i) Methylamine in water reacts with FeCl3 to precipitate hydrated ferric oxide.
(ii) pKb of aniline is more than that of methylamine.

1. Discuss the nature of bonding in the following co-ordinate compound on the basis of valence bond theory.

(i) 📷 (ii) 📷 (iii) 📷 (iv) 📷

1. (i) Draw figure to show splitting of degenerate d-orbital in an octahedral crystal field?

(ii) What is the significance of Δ0 (stabilization energy).

1. (i) Explain inner and outer orbital complexes with suitable example.

(ii) Draw the figure to show splitting of degenerate d-orbitals in an octahedral crystal field?

1. What are class-b-acceptors? What which type of ligands they form stable complexes?
   
2. (i) Classify the following into monosaccharides and disachharides.
   

Ribose, 2-deoxyribose, maltose, galactose, fructose and lactose.
(ii) What do you understand by the term glycosidic linkage?
(iii) What is glycogen? How is it different from starch?

1. (i) What is the basic structural difference between starch and cellulose?

(ii) What happens when D-glucose is treated with the following reagents?
(a) HI (b) Br2 – water (c) HNO3

1. (i) Write the monomers used for getting the following polymers

(a) Polyvinyl chloride (b) Teflon (c) Bakelite
(ii) How can you differentiate between addition and condensation polymerization.

1. (i) How is Dacron obtained from ethylene glycol and terephthalic acid?

(ii) What is a bidegreadable polymer? Give an example of a biodegradable aliphatic polyester.

1. (a) What are the monomeric repeating units of Nylon-6 and Nylon -66?

(b) Write the names and structure of the monomers of the following polymers.
(i) Buna-S (ii) Buna-N (iii) Dacron (iv) Neoprene

1. Indicate the steps in the preparation of

(i) K2Cr2O7 from chromite ore.
(ii) KMnO4 from pyrolusite ore.

1. Describing the oxidizing action of K2Cr2O7 and write the ionic equation for its reaction with

(i) Iodine (ii) Iron (II) solution (iii) H2S
IIT Level Questions

1. How will you carry out the following conversions?

(i) Methylamine to ethylamine
(ii) Ethylamine to methylamine
(iii) Aniline to benzoic acid
(iv) Nitrobenzene to 2, 4, 6-tribromoaniline
(v) Nitrobenzene to benzamide

1. For M2+/M and M3+/M2+ systems the E0 values for same metals are as follows:

📷
📷
📷
📷
Use the above data to comment upon
(i) the stability of Fe3+ in acid solution as compound to that of Cr3+ or Mn2+ and
(ii) the case with which iron can be oxidized as compared to a similar process for either chromium or manganese metal.

1. Arrange the following:

(i) C2H5NH2, (C2H5)2NH, (C2H5)3N and NH3................increasing basic strength in gaseous.
(ii) C2H5NH2, (C2H5)2NH, (C2H5)3N and NH3..................increasing basic strength in water.

1. How will you convert?

(i) Aniline to p-bromoaniline
(ii) Benzyl chloride to 2-phenyl ethanamine
(iii) Aniline to 2, 4, 6-tribromoflurobenzene

1. Complete the following reaction:

(i) 📷
(ii) 📷
(iii) 📷

1. Identification of A, B and C in the following reactions:

(i) 📷
(ii) 📷
(iii) 📷

1. Write the correct formulae for the following co-ordination compounds

(i) CrCl3.6H2O (violet with 3Cl− ions /unit formula)
(ii) CrCl3.6H2O (light green colour, with 2Cl− ions/unit formula)
(iii) CrCl3.6H2O (dark green colour with Cl− ion/unit formula)

1. (i) Briefly outline the drawback of V.B.T.

(ii) Explain the hybridization and magnetic behaviour.
(a) 📷 (b) 📷

1. (a) Explain with example cis-trans geometrical isomerism.

(b) Explain the facial and meridional isomerism.’

1. (i) Define the following as related to proteins.
   (a) Peptide linage (b) Primary structure (iii) Denaturation
   

(ii) What is the difference between a nucleoside and a nucleotide.
Objective:
Multiple choice questions with single correct options

1. Correct order of basicities of the following compounds is

📷
(A) 2 > 1 > 3 > 4 (B) 1 > 3 > 2 > 4
(C) 3 > 1 > 2 > 4 (D) 1 > 2 > 3 > 4

1. The compound that will react most readily with NaOH to form methanol is

(A) 📷 (B) CH3OCH3
(C) 📷 (D) 📷

1. Which of the following is the strongest base?

(A) C6H5NH2 (B) 📷
(C) 📷 (D) 📷

1. In 📷 the order of proton accepting tendency will be

(A) 📷 (B) 📷
(C) 📷 (D) 📷

1. Ions of the two most common isotopes of the transition metal nickel are shown below:

📷
Which one of the following statements is true?
(A) The electron arrangement of both these Ni2+ ions is 1s2, 2s2, 2p6, 3s2, 3p6, 3d6, 4s2.
(B) The 📷 ion will have more protons in its nucleus than the 📷 ion.
(C) In the same strength magnetic field, the 📷 ion will be deflected more than the 📷 ion.
(D) Both 📷ions have the same number of electrons but a different number of neutrons.

1. Which equation does not involve the reduction of a transition metal compound?

(A) 📷 (B) 📷
(C) 📷 (D) 📷

1. Ag+ forms many complexes, some of these are [Ag(NH3)2]+, [Ag(CN)2]–, [Ag(S2O3)2]3–.

Which of the following statements is true?
(A) In these complexes, Ag+ is a Lewis base.
(B) The hybridization of Ag+ is sp2.
(C) The Ag+ complexes are good reducing agents.
(D) These complexes are all linear.

1. The magnetic moment of an iron compound is 5.918 BM, then the oxidation state of iron in this compound will be

(A) 0 (B) 1
(C) 2 (D) 3

1. Which pair of elements can form an alloy?

(A) Zn + Pb (B) Fe + Hg
(C) Fe + C (D) C + Pt

1. Identify the product P in the following reaction.

📷
(A)
📷
(B)
📷
(C)
📷
(D)
📷

1. The product(s) of the Hofmann exhaustive methylation of the following compound is

📷
(A)
📷
(B)
📷
(C)
📷
(D)
All of the above

1. When aniline is heated with benzene diazonium chloride at low temperature in weakly acidic medium, the final product obtained is

(A)
📷
(B)
📷
(C)
📷
(D)
📷
13.
The major product formed in the elimination reaction of
📷
(A)
📷
(B)
📷
(C)
📷
(D)
📷
14.
📷
Hydrocarbon ‘B’ is,
(A) CH4 (B) 📷
(C) 📷 (D) 📷

1. In which of the following compounds chromium shows maximum ionic radius?

(A) K2Cr2O7 (B) CrO2Cl2
(C) Cr2(SO4)3 (D) CrCl2

1. Zinc tarnishes in moist air due to

(A) ZnCO3.3Zn(OH)2 (B) Zn(OH)2
(C) ZnCO3.ZnCl2 (D) None of the above

1. Which compound does not dissolve in hot dilute 📷

(A) HgS (B) PbS
(C) CuS (D) CdS

1. A compound of mercury which is a strong poison and its antidote being the white of an egg, which eliminates it from the system in the form of a coagulated mass, is

(A) Hg2Cl2 (B) HgCl2
(C) HgI2.HgO (D) K2HgI4

1. The product of reaction of an aqueous solution of Bi3+ salt with sodium thiosulphate gives

(A) Bi2S3 (B) Na3[Bi(S2O3)3]
(C) Na[Bi(S2O3)2] (D) [Bi2(S2O3)2]Cl2

1. An aqueous solution of FeSO4.Al2(SO4)3 and chrome alum is heated with excess of X and filtered, a yellow filtrate and a brown residue is obtained. X is

(A) Na2O2 (B) Na2ZnO2
(C) NaCl (D) KCl

1. When H2O2 in ether reacts with acidified K2Cr2O7 solution blue coloured perchromic anhydride is obtained in etheral solution. It is due to:

(A) CrO3 (B) H2CrO4
(C) CrO5 (D) H2CrO7

1. The atomic radius of Cu is greater than that of Cr but ionic radius of Cr2+ is greater than Cu2+:

(A) because Cr+2 has no stable oxidation state of Cr
(B) because (d – d) transition is not easily available in Cr.
(C) because in Cu, (d – d) electron repulsion is larger due to pairing of electron
(D) because of Cu has larger no of protons in nucleus w.r.t. Cr

1. Dicyclopentadienyliron [(C5H5)-]2 Fe2+ is stable molecule because of

(A) resonance (B) not stable
(C) five member ring (D) none

1. Which one of the following would not react with aqueous silver nitrate to produce a precipitate that is soluble in concentrated aqueous ammonia?

(A) CaBr2 (B) [CoCl4]2–
(C) (CH3)4N+I– (D) CH3COCl

1. From the stability constant which one is strongest ligand?

(A) 📷
(B) 📷
(C) 📷
(D) 📷

1. The crystal field splitting energy for Cr3+ ion in an octahedral field increases for the ligands I–, H2O, NH3, CN– and the order is

(A) CN– < I– < H2O < NH3 (B) I– < H2O < NH3 < CN–
(C) CN– < NH3 < H2O < I– (D) NH3 < H2O < I– < CN–

1. Which of the following complex ion is paramagnetic?

(A) [Fe(CN)6]4– (B) [Fe(CN)6]3–
(C) [Fe(CN)5NO]2– (D) [Co(NO2)6]3–

1. IUPAC nomenclature of the complex compound Na3[Cr(O)2(O2)(O2)2(NH3)] where half of the coordination number are occupied by neutral ligands with magnetic moment 📷 must be

(A) Sodium amminedioxodioxygensuperoxochromate (III)
(B) Sodium amminedioxygendioxodisuperoxochromate (III)
(C) Sodium amminebisdioxygendioxoperoxochromate (III)
(D) Sodium amminebisdioxygendioxoperochromium (III)

1. Polymer used in bullet proof glass is

(A) PMMA (B) Lexame
(C) Nomex (D) Kelvar

1. On hydrolysis which of the following carbohydrates gives only glucose?

(A) Sucrose (B) Lactose
(C) Maltose (D) Galactose

1. Grape sugar is

(A) Glucose (B) Fructose
(C) Maltose (D) Lactose

1. Which of the following is fruit sugar?

(A) Sucrose (B) Fructose
(C) Glucose (D) All of these

1. The urine sample of diabetic patients contains

(A) Sucrose (B) fructose
(C) Cane sugar (D) Starch

1. The fibre obtained by the condensation of hexamethylene diamine and adipic acid is

(A) Dacron (B) Nylon 66
(C) Rayon (D) Teflon

1. Natural silk is

(A) Polyester (B) Polyamide
(C) Epoxide (D) Polyurethane

1. Natural rubber is obtained from Latex which is a

(A) mixture of wood, plants and gums
(B) Colloidal dispersion of rubber in water
(C) mixture of chloroprene and carbohydrate
(D) none of these

1. A raw material used in making Nylon is

(A) adipic acid (B) 1, 3-butadiene
(C) ethyne (D) cyclohexanone

1. Which of the following is not a natural polymer?

(A) Wool (B) Silk
(C) Cotton (D) Teflon

1. In the dichromate dianion

(A) 4Cr – O bonds are equivalent
(B) 6-Cr – O bonds are equivalent
(C) All Cr – O bonds are equivalent
(D) All Cr – O bonds are non – equivalent

1. In the standardization of Na2S2O3 using K2Cr2O7 by iodomaety, the equivalent weight of K2Cr2O7 is

(A) Molecular weight/2 (B) Molecular weight/6
(C) Molecular weight/3 (D) Same as molecular weight

1. The chemical composition of ‘slag’ formed during smelting process in the extraction of copper in

(A) Cu2O + FeS (B) FeSiO3
(C) CuFeS2 (D) Cu2S + FeO

1. Amongst the following, identify the species with an atom in +6 oxidation state

(A) MnO4− (B) Cr(CN)6−3
(C) NiF6−2 (D) CrO2Cl2

1. Ammonium dichromate is used in same fire works. The green coloured powder blown in the air is

(A) CrO3 (B) Cr2O3
(C) Cr (D) CrO(O2)

1. Isoprene on polymerization produces

(A) Synthetic rubber (B) Neoprene
(C) Gutta-Percha (D) Cis-poly(2-Methyl-1, 3-butadiene)

1. Example of thermosetting plastic is/are

(A) bakelite (B) PVC
(C) Polyurethane (D) Nylon

1. The repeating units of PTFE are

(A) CH ≡ CH (B) CF3 – CF3
(C) CH2 = CHCN (D) CF2 = CF2

1. Terylene is a condensation polymer of ethylene glycol and

(A) Benzoic acid (B) acetic acid
(C) terephthalic acid (D) salicylic acid

1. Which of the following is used as rocket fuel?

(A) cyanogens + O3 (B) Cyanogen + O2
(C) water gas + O3 (D) Nitrolium + O3

1. The expected spin only magnetic moment for 📷respectively are

(A) 1.73 and 4.82 (B) 5.92 and 4.82 (C) 1.73 and 3.87 (D) 0.00 and 1.73
Multiple choice questions with more than one option correct

1. Aniline and diethylamine can be distinguished by

(A) coupling reaction (B) carbylamine reaction
(C) reaction with HONO (D) Hoffmann bromamide reaction

1. Cyclobutyl amine is treated with nitrous acid. The products may be

(A)
📷
(B)
📷
(C)
📷
(D)
📷

1. Consider the reaction

📷
Which of the following statements is/are correct?
(A) Product B is an orange coloured compound
(B) Product A contain azo linkage
(C) Product B contain azo linkage
(D) Product A is used as dye

1. The low spin complexes are

(A) K3[Fe(CN)6] (B) [Ni(CO)4]
(C) K3[CoF6] (D) Na2[Ni(CN)4]

1. Which of the following statement(s) is/are correct?

(A) Oxidation number of Fe in Na2[Fe(CN)5(NO)] is +2.
(B) [Ag(NH3)2]+ is linear in shape.
(C) In [Fe(H2O)6]3+, Fe is d2sp3 hybridized.
(D) In [Ni(CO)4], oxidation number of Ni is zero.

1. When MnO2 is fused with KOH, a coloured compound is formed then the compound will be

(A) K2MnO4 (B) Mn3O4
(C) purple in colour (D) brown in colour

1. Which of the following statements is/are correct when a mixture of NaCl and K2Cr2O7 is gently warmed with conc. H2SO4?

(A) A deep red vapour is evolved.
(B) The vapour when passed into NaOH solution gives a yellow solution of Na2CrO4.
(C) Chlorine gas is evolved.
(D) Chlomyl chloride is formed.

1. Which of the following gives an optically active compound when reacted with sodium borohydride, NaBH4?

(A)
📷
(B)
📷
(C)
📷
(D)
📷
59.
📷
For the above reaction,
(A)
📷
(B)
📷
(C)
📷
(D)
📷

1. Consider the following three bases of DNA and RNA.

📷
Order of acidic strength on different sites will be
(A) (2) > (1) (B) (3) > (4)
(C) (7) > (6) (D) (6) > (5)

1. Which of the following statement(s) about D(+) glucose is/are true?

(A) Naturally occurring glucose is dextrorotatory
(B) It reduces ammoniacal AgNO3 solution
(C) On polymerisation it forms galactose
(D) It forms cyanohydrin on reaction with HCN
COMPREHENSION - I
Read the following paragraph and answer the questions given below:
The variety of colours among transition metal complexes has always fascinated the observers. For example, aqueous solutions of octahedral [Co(H2O)6]2+ are pink in colour but those of tetrahedral [CoCl4]2– are blue. The green colour of aqueous [Ni(H2O)6]2+ turns blue when ammonia is added to the solution to give [Ni(NH3)6]2+. The reduction of violet [Cr(H2O)6]3+ gives bright blue [Cr(H2O)6]2+. As with all colours, these arise from electronic transitions between levels whose spacing correspond to the wavelength available in visible light. The magnitude of spacing depends upon the factors such as the geometry of the complex, the nature of the ligands present, and the oxidation state of central atom.

1. Identify the complexes which is/are expected to be coloured?

(A) [Ti(NO3)4] (B) [Cu(NCCH3)4]+📷
(C) [Cr(NH3)6]3+3Cl– (D) [Zn(H2O)6]2+

1. Which of the following is π-acid ligand?

(A) NH3 (B) CO
(C) F– (D) Ethylene diamine

1. The complex which has no ‘d’ electrons in the central metal atom is

(A) [MnO4]– (B) [Fe(CN)6]3–
(C) [Co(NH3)6]3+ (D) [Cr(H2O)6]3+

1. Among 📷(atomic numbers of Ti = 22, Co = 27, Cu = 29, Ni = 28), the colourless species are

(A) 📷and 📷 (B) 📷
(C) Cu2Cl2 and 📷 (D) 📷

1. The ferric ion is detected by the formation of a prussian blue precipitate on addition of potassium ferrocyanide solution. The formula of the prussian blue precipitate is

(A) Fe4[Fe(CN)6]3 (B) Fe3[Fe(CN)6]4
(C) KFe[Fe(CN)6] (D) None of the above
COMPREHENSION - II
Read the following paragraph and answer the questions given below:
Molecules of the amino acids that comprise our proteins have the property of being non-super imposable on their mirror images because, they are said to be chiral or possess ‘handedness’. Most of the amino acids are of left handed form, but with no reasons available. Even more interesting, recent experiments have shown that a 7–9% excess of four amino acids is present in Murchison meteorite discovered in 1970. This analysis shows life could arise outside the confines of earth. The origin of unequal distribution is probably because of electromagnetic radiations emitted in a corkscrew fashion from the poles of spinning neutron stars could lead to a bias of one mirror image isomer over another when molecules form in interstellar space.
A stereogenic carbon can be defined as a carbon atom bearing groups of such nature that an interchange of any two groups will produce a stereoisomer. The device that is used for measuring the effect of optically active compounds on plane polarized light is a polarimeter. The analyser in the polarimeter decides the activity of compound present. This is being decided on the basis of angle by which axis of analyser has to be rotated for complete brightness. Left, right or no adjustment decides 📷activity or optical inactivity respectively.

1. For existence of life, amino acids as ingredient of protein exist mainly in

(A) 📷form (B) d–form
(C) Both (D) None of the above

1. EMR emitted in corkscrew fashion from poles of spinning neutrons are biased to

(A) 📷amino acids (B) d–amino acids
(C) Both (D) None of the above

1. Stereogenic carbons can bring

(A) optical activity (B) optical inactivity
(C) Both (D) None of the above

1. Optically inactive isomer possessing chiral centres are categorized as

(A) optical isomers (B) non-optical isomers
(C) mesomers (D) diastereoisomers

1. In one of the experiment performed by two students “Abraham” and “Fienkelstein” for measurement of optical activity of a substance. Result given by “Abraham” was: It is d–form with +30o rotation and by “Fienkelstein”, it was: It is 📷form with –150o rotation. One of them can be correct only as solution can either be d form or, 📷form.

Which of the following is correct measure to come out of this dispute?
(A) Result with acute angle is correct.
(B) Result with obtuse angle is correct.
(C) Students should perform another experiment by varying the concentrations or length of polarimeter tube to which angle of rotation is directly proportional.
(D) Students should perform the experiment again with precaution. They will come on same conclusion as one of them must be committing observational mistake.
COMPREHENSION - III
Formation of amine salts can be used to isolate and characterize amines. Most amines containing more than six carbon atoms are relatively insoluble in water. In dilute aqueous acids, these amines form their corresponding ammonium salts and they dissolve. Formation of soluble salt is one of the characteristic functional group test for amines.
The formation of amine salts is also used to separate amines from less basic compounds. When the solution is made alkaline (by
addition of NaOH) the free amine is regenerated. The purified free amine either separates out of the aqueous solution or is extracted into an organic solvent. Many drugs and other biologically important amines are commonly stored and used as their salts. Amine salts are less prone to decomposition by oxidation and other reactions and they have virtually no fishy odor. The salts are soluble in water and they are easily converted to solution for syrup and injections.

1. Amine form salt with which of the following reagents

(A) NaOH (B) KOH
(C) HBr (D) All of these

1. In the presence of NaOH amines separate out because

(A) amines react with NaOH (B) amines are less basic than NaOH
(C) amines form slat with NaOH (D) None of these

1. Amines are soluble in solution of many transition metal salts because

(A) Amines act as base with transition metal salt
(B) Amines act as ligand with transition metal salts
(C) Amines do not react with transition metal salt
(D) None of these

1. The hybridisation of N-atom in amine salts is

(A) sp2 (B) dsp2
(C) sp (D) sp3

1. Which of the following reaction involves amine salt?

(A) Hoffmann bromamide reaction (B) Hoffmann elimination
(C) Hoffmann rearrangement (D) None of these
COMPREHENSION - IV
Read the following paragraph and answer the questions given below:
Triglycerides are the oils of plants and the fats of animal origin. They include such common substances as peanut oil, soya bean oil, corn oil, butter etc. Triglycerides that are liquid at room temperature are generally called oils; those that are solids are called fats. In simple triglycerides all three acyl groups are same and in mixed triglycerides acyl groups are different. Hydrolysis of oils and fats produces a mixture of fatty acids.
Most natural fatty acids have unbranched chains and because they are synthesized from two carbon units, they have an even number of carbon atoms. In most unsaturated fatty acids double bonds are in cis configuration. Many naturally occurring fatty acids contain two or three double bonds. The fats or oils that these come from are called polyunsaturated fats or oils.
The carbon chain of saturated fatty acids can adopt many conformations but tend to be fully extended because this minimizes steric repulsions between neighbouring methylene groups. Saturated fatty acids pack efficiently into crystals because of larger van der Waals’ forces these have high melting points. The cis configuration of the double bond of an unsaturated fatty acid puts a rigid bend in the carbon chain that interferes with crystal packing causing reduced van der Waals’ attraction between molecules.

1. The hydrolysis of fats or oils with NaOH is called

(A) esterification (B) trans esterification
(C) glycolysis (D) saponification

1. Consider the reaction,

📷
The product A on oxidation with HIO4 gives
(A) only formaldehyde (B) only formic acid
(C) both formaldehyde and formic acid (D) None of the above

1. Unsaturated fatty acids having trans configuration have

(A) higher boiling points than cis isomer
(B) higher melting points than cis isomer
(C) higher molecular mass than cis isomer
(D) All of the above

1. Aliphatic unsaturated fatty acids can be reduced to corresponding unsaturated alcohol by

(A) NaBH4 (B) LiAlH4
(C) H2/Pt (D) All of the above

1. The boiling points of branched chain fatty acids are less than straight chain isomers due to

(A) less steric hindrance (B) less van der Waals’ forces
(C) more van der Waals’ forces (D) None of the above
Match The Following

1. List – 1 (complex ion) List – 2 (number of unpaired electrons)

(A) [CrF6]-4 (1) one
(B) [MnF6]-4 (2) two
(C) [Cr(CN)6]-4 (3) three
(D) [Mn(CN)6]-4 (4) four
(5) five

1. Match List − I with List − II

List − I
List − II
(A)
Amino acid
(p)
Secondary structure
(B)
α-amino acid
(q)
Neutral
(C)
Albumin
(r)
Simple protein
(D)
α-helix structure
(s)
Ninhydrin

1. Match List − I with List − II

List − I
List − II
(A)
Epimers
(p)
Reserve food for animals
(B)
Sorbitol
(q)
Hetrogenous polysaccharides
(C)
Glycogen
(r)
By the reduction of glucose
(D)
Starch
(s)
Glucose and mannose

1. Match the compounds in List-I with their properties in List-II:

List-I List-II
(A) K2MnO4 (P) Transition element in +6 state
(B) KMnO4 (Q) Oxidising agent in acid medium
(C) K2Cr2O7 (R) Manufactured from pyrolusite ore
(D) K2CrO4 (S) Manufactured from chromite ore

1. Match the complexes in List-I with their information in List-II:

List-I List-II
(A) [Cu(NH3)2]SO4 (P) dsp2
(B) [Pt(NH3)2Cl2] (Q) Octahedral
(C) K4[Fe(CN)6] (R) sp3d2
(D) [Fe(H2O)6]Cl3 (S) Square planar
ANSWERS TO WORK BOOK
Objective:
Single Correct Questions

1. B 2. A 3. D 4. C
   
2. D 6. B 7. D 8. D
   
3. C 10. A 11. B 12. C
   
4. D 14. B 15. D 16. A
   
5. A 18. B 19. A 20. A
   
6. C 22. C 23. A 24. C
   
7. B 26. B 27. B 28. B
   
8. C 30. B 31. C 32. A
   
9. B 34. C 35. B 36. B
   
10. B 38. A 39. D 40. B
    
11. B 42. B 43. D 44. B
    
12. A 46. A 47. D 48. C
    
13. A 50. C
    

Multiple Correct Questions

1. A, B, C 52. A, B, C 53. A, C 54. A, B, D
   
2. A, B, D 56. A, C 57. A, B, D 58. B, C, D
   
3. C, D 60. A, B, D 61. A, B, D
   

Comprehension

1. C 63. B 64. A 65. D
   
2. C 67. A 68. A 69. C
   
3. A 71. C 72. C 73. B
   
4. B 75. D 76. B 77. D
   
5. C 79. B 80. B 81. B
   

Match The Following

1. (A) – (4), (B) – (5), (C) – (2), (D) – (1)
   
2. (A) –(q), (B) – (s), (C) – (r), (D) – (p)
   
3. (A) –(s), (B) – (r), (C) – (p), (D) – (q)
   
4. (A-P, R) (B-Q,R) (C-P, Q,S) (D-P,S)
   
5. (A-P,S) (B-P,S) (C-Q) (D-Q,R)
   

Whether you think of it as a dream, or a reality, there is a house building service on the moon. You can find out more about the technology behind this idea by reading this article.

Cost of building a house on the moon

Getting the cost of building a house on the Moon down to earth is a tall order. For starters, the surface of the Moon is far from the Earth's magnetic field and there is no atmosphere. It is constantly bombarded by charged particles, but these particles don't have much penetrating power.
To provide reliable energy for a lunar base, a small nuclear reactor might be required. It would cost $1.3 billion to build one and the technology isn't exactly cheap.
Solar panels could be installed in select locations. They're relatively light and safe, but they can't be used during the night.
Another possible solution to the cost of building a house on the moon is to mine the lunar soil and use the resulting regolith to construct bricks that will retain heat. These can then be used to heat indoor spaces.

Artificial stone from regolith as a building material

Several NASA-backed companies are developing 3D printing technologies that can be used to construct extraterrestrial habitats. They are testing their ability to use regolith as a building material. This is important because crewed missions to Mars face a huge survival risk from the galactic cosmic radiation.
One method is to melt lunar soil using microwaves. Another is to use a solar oven to grow regolith into stone. A third method is to use robots to build structures with the help of a 3D printer.
Scientists are also exploring ways to bind regolith together. They have investigated various biological binders. For instance, researchers from the University of Manchester have discovered that the protein in human serum albumin can be mixed with lunar regolith to produce biocomposites.
Some scientists believe that sulfur could be used as a binding agent in regolith. This would not have the properties of terrestrial concrete, but it could be heated to a temperature of 140 degrees Celsius and set to rock-like solid quickly.

Protection against solar flares

Getting protection against solar flares is crucial if you're planning a future voyage to the moon. As with any space travel, the optimum protection requires more than just a cheap suit. There are many scientific and technological means of reducing radiation, including shielding, rerouting electrical flow paths, and rerouting thermal energy.
The sun produces a lot of electromagnetic waves, including visible light, radio waves, and infrared. These are often combined into an electromagnetic field. This field is known as the "solar wind" and is composed of electrons and helium ions. These particles are able to travel through the sun's magnetic field lines, and can affect communication satellites and other Earthly objects.
A coronal mass ejection is an example of an extreme Sun event. It hurls a massive cloud of charged particles into space. These storms can interact with the atmosphere, and can produce a colorful aurora borealis. These are also capable of causing some damage to electronics and sensitive equipment.

Human adaptation to conditions of long stay in weightlessness

During house building service on the moon , astronauts are exposed to near-weightlessness for long periods. The effects of such exposure are not well understood. While there is an increasing amount of information about the physiological adaptation to this condition, there is also a lack of evidence regarding the effects of prolonged hypogravity exposure.
Several studies have been conducted on board the ISS. These have demonstrated changes in cardiovascular and neurovestibular systems and decreased plasma volume. The decrease in these physiological functions may impair performance and behavior health.
During the first three weeks in space, the brain and higher attention processes are affected. These changes may be the result of a "sensory mismatch" between the various motion sensors of the body. This can lead to space adaptation syndrome. This syndrome is characterized by nausea and vomiting.

Material Science

Nano Research
Title: Recent advances of bioresponsive polymeric nanomedicine for cancer therapy Author: Tu Hong, Xinyuan Shen, Madiha Zahra Syeda, Yang Zhang, Haonan Sheng, Yipeng Zhou, JinMing Xu, Chaojie Zhu, Hongjun Li, Zhen Gu, Longguang Tang Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5002-2 DOI: 10.1007/s12274-022-5002-2
Title: Amplitude-mode spectroscopy of chemically injected and photogenerated charge carriers in semiconducting single-walled carbon nanotubes Author: Shai R. Vardeny, Alan Phillips, Kira A. Thurman, Z. Valy Vardeny, Jeffrey L. Blackburn Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5080-1 DOI: 10.1007/s12274-022-5080-1
Title: Carbonitride MXene Ti3CN(OH)x@MoS2 hybrids as efficient electrocatalyst for enhanced hydrogen evolution Author: Jizhou Jiang, Fangyi Li, Saishuai Bai, Yongjing Wang, Kun Xiang, Haitao Wang, Jing Zou, Jyh-Ping Hsu Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5112-x DOI: 10.1007/s12274-022-5112-x
Title: 2D/2D hierarchical Co3O4/ZnIn2S4 heterojunction with robust built-in electric field for efficient photocatalytic hydrogen evolution Author: Guping Zhang, Xunxun Li, Mengmeng Wang, Xueqing Li, Yaru Wang, Shuting Huang, Dongyun Chen, Najun Li, Qingfeng Xu, Hua Li, Jianmei Lu Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5096-6 DOI: 10.1007/s12274-022-5096-6
Title: Albumin-based multidrug delivery system enriched in Golgi apparatus against metastatic breast cancer Author: Chenqi Guo, Xiong Peng, Ting Zhao, Jiaxing Feng, Zhaofei Guo, Mengying Wu, Rongping Zhang, Xun Sun, Yuan Huang, Zhirong Zhang, Tao Gong Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5141-5 DOI: 10.1007/s12274-022-5141-5
Title: Self-assembly of polysarcosine amphiphilic polymers-tethered gold nanoparticles for precise photo-controlled synergistic therapy Author: Runkai Lv, Zhengzheng Qian, Xiaopeng Zhao, Fei Xiong, Yingjie Xu, Wenpei Fan, Xikuang Yao, Wei Huang Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5184-7 DOI: 10.1007/s12274-022-5184-7
Title: Crown ether interlayer-modulated polyamide membrane with nanoscale structures for efficient desalination Author: Yanyu Zhao, Xiangju Song, Minghua Huang, Heqing Jiang, Arafat Toghan Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5196-3 DOI: 10.1007/s12274-022-5196-3
Title: Hollow tubular conjugated organic polymer for lithium batteries Author: Weijia Zhang, Shibing Zheng, Tao Ma, Tianjiang Sun, Zhanliang Tao Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-4995-x DOI: 10.1007/s12274-022-4995-x
Title: Advance in two-dimensional twisted moiré materials: Fabrication, properties, and applications Author: Han Yang, Liwei Liu, Huixia Yang, Yu Zhang, Xu Wu, Yuan Huang, Hong-Jun Gao, Yeliang Wang Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5025-8 DOI: 10.1007/s12274-022-5025-8
Title: Melatonin and probiotics ameliorate nanoplastics-induced hematopoietic injury by modulating the gut microbiota-metabolism Author: Lei Zhang, Jiaru Jing, Lin Han, Ziyan Liu, Jingyu Wang, Wei Zhang, Ai Gao Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5032-9 DOI: 10.1007/s12274-022-5032-9
Title: Defect engineering of two-dimensional materials towards next-generation electronics and optoelectronics Author: Jie Jiang, Peng Yang, Juin J. Liou, Wugang Liao, Yang Chai Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5016-9 DOI: 10.1007/s12274-022-5016-9
Title: Construction of multi-homojunction TiO2 nanotubes for boosting photocatalytic hydrogen evolution by steering photogenerated charge transfer Author: Jinbo Xue, Shan Jiang, Chengkun Lei, Huan Chang, Jiaqi Gao, Xuguang Liu, Qi Li, Qianqian Shen Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5050-7 DOI: 10.1007/s12274-022-5050-7
Title: Ni3B modified BiVO4 photoanodes for enhanced photoelectrochemical water splitting: The key role of Ni3B on reducing the water oxidation barrier Author: Kehui Xue, Haifeng Zhu, Xingyu Zhao, Liana Alvares Rodrigues, D. Amaranatha Reddy, Yaping Zhang, Lianqing Yu Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5079-7 DOI: 10.1007/s12274-022-5079-7
Title: High-density single antibody electrochemical nanoarrays Author: Khalil Chennit, Yannick Coffinier, Shuo Li, Nicolas Clément, Agnès Anne, Arnaud Chovin, Christophe Demaille Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5137-1 DOI: 10.1007/s12274-022-5137-1
Title: Asymmetrically coordinated single-atom iron nanozymes with Fe-N1C2 structure: A peroxidase mimetic for melatonin detection Author: Lihong Lin, Heng Li, Hongfei Gu, Zhiyi Sun, Juan Huang, Zhenni Qian, Hang Li, Juzhe Liu, Hongyan Xi, Pengfei Wu, Qingqing Liu, Shuhu Liu, Lirong Zheng, Zhuo Chen, Zhengbo Chen, Juanjuan Qi Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5211-8 DOI: 10.1007/s12274-022-5211-8
Title: Black-phosphorus-based junctions and their optoelectronic device applications Author: Kunchan Wang, Zhuoyang He, Xinyue Li, Ke Xu, Qingping Zhou, Xiaowo Ye, Teng Zhang, Shenghao Jiang, Yanming Zhang, Bei Hu, Changxin Chen Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5008-9 DOI: 10.1007/s12274-022-5008-9
Title: The role of CO2 dissociation in CO2 hydrogenation to ethanol on CoCu/silica catalysts Author: Zhongyan Wang, Chengsheng Yang, Xianghong Li, Xiwen Song, Chunlei Pei, Zhi-Jian Zhao, Jinlong Gong Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5092-x DOI: 10.1007/s12274-022-5092-x
Title: High gain, broadband p-WSe2/n-Ge van der Waals heterojunction phototransistor with a Schottky barrier collector Author: Shuo Li, Qiang Wu, Haokun Ding, Songsong Wu, Xinwei Cai, Rui Wang, Jun Xiong, Guangyang Lin, Wei Huang, Songyan Chen, Cheng Li Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5081-0 DOI: 10.1007/s12274-022-5081-0
Title: [(CH3)4N]2Mn0.6Zn0.4Br4: Lead-free MnII-based hybrid halide with high photoluminescence quantum yield for backlight displays Author: Xiaoting Liu, Jiapeng Yang, Wenya Chen, Fan Yang, Yihuang Chen, Xiaojuan Liang, Shuang Pan, Weidong Xiang Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5152-2 DOI: 10.1007/s12274-022-5152-2
Title: A high-loading and cycle-stable solid-phase conversion sulfur cathode using edible fungus slag-derived microporous carbon as sulfur host Author: Hui Li, Xiangjiang Wu, Sijie Jiang, Qian Zhang, Yuliang Cao, Hanxi Yang, Feifei Cao, Xinping Ai Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5156-y DOI: 10.1007/s12274-022-5156-y
Title: Enhanced plasmonic absorption of Pt cuboctahedra-WO3 nanohybrids used as visible light photocatalysts for overall water splitting Author: Qiaoling Chen, Yiwei Tan Volume: Nano Research URL: https://www.sciopen.com/article/10.1007/s12274-022-5175-8 DOI: 10.1007/s12274-022-5175-8
SCIENCE CHINA Materials
Title: CsPbBr3@PbBrOH 3D/1D Molecular Matrix for High Performance Scintillator Author: Guo Heng, Zhu Yizhi, Zhao Qingxian, Jiang Qingsong, Ma Yi, Chen Jinping, Song Lei, Shi Zengliang, Xu Chunxiang Volume: SCIENCE CHINA Materials (2022) URL: https://www.sciengine.com/doi/10.1007/s40843-022-2329-9 DOI: 10.1007/s40843-022-2329-9
Title: Supercompressible conductive hydrogels in harsh environments Author: Antonietti Markus Volume: SCIENCE CHINA Materials (2022) URL: https://www.sciengine.com/doi/10.1007/s40843-022-2333-1 DOI: 10.1007/s40843-022-2333-1

Mathematics

SCIENCE CHINA Mathematics
Title: On $m$-ovoids of finite classical polar spaces with an irreducible transitive automorphism group Author: Feng Tao, Li Weicong, Tao Ran Volume: SCIENCE CHINA Mathematics (2022) URL: https://www.sciengine.com/doi/10.1007/s11425-021-2060-3 DOI: 10.1007/s11425-021-2060-3

Biology

Acta Biochimica et Biophysica Sinica
Title: Circ-BPTF served as miR-486-5p sponge to regulate CEMIP and promoted hypoxic pulmonary arterial smooth muscle cells proliferation in COPD Author: Wang Chang-guo, Liu Ying-ying, Zhang Wei-yun, Huang Jian-an, Jiang Jun-hong, Wang Ran, Zeng Daxiog Volume: Acta Biochimica et Biophysica Sinica (2022) URL: https://www.sciengine.com/doi/10.3724/abbs.2022178 DOI: 10.3724/abbs.2022178

Medicine

Stress and Brain
Title: High-level social support alleviates the negative effect of life stress on postgraduate students' mental health during campus enclosed management of the COVID-19 Omicron pandemic Author: Yuanyuan Yin, Xinyu Cheng, Ziqi Liu, Jianyin Qiu, Ti-Fei Yuan Volume: Stress and Brain URL: https://www.sciopen.com/article/10.26599/SAB.2022.9060022 DOI: 10.26599/SAB.2022.9060022

Computer Science/ Electronic / Communication / AI

SCIENCE CHINA Information Sciences
Title: Energy-efficient trajectory planning and resource allocation in UAVcommunication networks under imperfect channel prediction Author: Min SHENG, Chenxi ZHAO, Junyu LIU, Wei TENG, Yanpeng DAI, Jiandong LI Volume: SCIENCE CHINA Information Sciences 65(12), 222301 (2022) URL: https://www.sciengine.com/doi/10.1007/s11432-021-3332-0 DOI: 10.1007/s11432-021-3332-0

Chemistry

SCIENCE CHINA Chemistry
Title: In situ/operando characterization techniques for electrochemical CO2 reduction Author: Song Xinning, Xu Liang, SUN Xiaofu, Han Buxing Volume: SCIENCE CHINA Chemistry (2022) URL: https://www.sciengine.com/doi/10.1007/s11426-021-1463-6 DOI: 10.1007/s11426-021-1463-6

Engineering

SCIENCE CHINA Technological Sciences
Title: Liquid metal-based textiles for smart clothes Author: Bie Binglin, Xu Weilin, Lv Yonggang Volume: SCIENCE CHINA Technological Sciences (2022) URL: https://www.sciengine.com/doi/10.1007/s11431-022-2266-3 DOI: 10.1007/s11431-022-2266-3
SCIENTIA SINICA Technologica
Title: 齿轨车辆-轨道(齿轨)系统耦合动力学模型及其基本振动特性 Author: chen zhaowei, li shihui, yuan miao, wang lang, li zhanglin, yang jizhong, chen zhihui, yang wu Volume: SCIENTIA SINICA Technologica (2022) URL: https://www.sciengine.com/doi/10.1360/SST-2022-0260 DOI: 10.1360/SST-2022-0260

Earth Science/ Environmental Science/ Ecology

SCIENTIA SINICA Terrae
Title: 华北克拉通下马岭组与龙山组之间存在大型不整合吗？ Author: Kuang Hongwei, peng nan, liu yongqing, wang yuchong, cui mingming, chen xiaoshuai, qiao dawei, qi kening Volume: SCIENTIA SINICA Terrae (2022) URL: https://www.sciengine.com/doi/10.1360/SSTe-2022-0213 DOI: 10.1360/SSTe-2022-0213

Multidisciplinary Sciences

Journal of Shenzhen University Science and Engineering
Title: Influence of impact velocity on dynamic performance of reinforced concrete beams strengthened with CFRP Author: YafangZHANG, LibinDUAN, JuanLU, YongjieHUO Volume: Journal of Shenzhen University Science and Engineering 39(6), 622 (2022) URL: https://www.sciengine.com/doi/10.3724/SP.J.1249.2022.06622 DOI: 10.3724/SP.J.1249.2022.06622
Title: Efficiency investigation of mitigation effect of isolation piles on tunneling-induced ground settlements Author: ZhenjiZHENG, LiqiangCAO, DongSU, XiangshengCHEN Volume: Journal of Shenzhen University Science and Engineering 39(6), 615 (2022) URL: https://www.sciengine.com/doi/10.3724/SP.J.1249.2022.06615 DOI: 10.3724/SP.J.1249.2022.06615
Title: Influence of coherent structure on turbulence characteristics of 0814 strong typhoon Hagupit Author: LixiaoLI, YuqingHUANG, ShangxinCHEN, XiguiHUANG, YiqingXIAO, XianchuanCHEN Volume: Journal of Shenzhen University Science and Engineering 39(6), 629 (2022) URL: https://www.sciengine.com/doi/10.3724/SP.J.1249.2022.06629 DOI: 10.3724/SP.J.1249.2022.06629
Title: Influence of different surface curing materials on pavement concrete properties Author: TianlunLI, YonggenWU, HaoxiangWU Volume: Journal of Shenzhen University Science and Engineering 39(6), 642 (2022) URL: https://www.sciengine.com/doi/10.3724/SP.J.1249.2022.06642 DOI: 10.3724/SP.J.1249.2022.06642
Title: The field measurement of wellhead anti-freezing technology using exhaust wind waste heat Author: MengSUN, GuanjunJIANG, JizheFENG, TianzeMA, LinZHOU Volume: Journal of Shenzhen University Science and Engineering 39(6), 637 (2022) URL: https://www.sciengine.com/doi/10.3724/SP.J.1249.2022.06637 DOI: 10.3724/SP.J.1249.2022.06637
Title: Analysis on the pressure dynamic characteristics of slanted well in dual-porosity and dual-permeability reservoir Author: RenshiNIE, RanJIA, MingjinCAI, HongLI, CongLU, LanYANG Volume: Journal of Shenzhen University Science and Engineering 39(6), 660 (2022) URL: https://www.sciengine.com/doi/10.3724/SP.J.1249.2022.06660 DOI: 10.3724/SP.J.1249.2022.06660
Title: Influence of local thermal non-equilibrium on enhanced geothermal system Author: LinsongCHENG, JunjieSHI, RenyiCAO, ChenxuYANG, XulinDU Volume: Journal of Shenzhen University Science and Engineering 39(6), 649 (2022) URL: https://www.sciengine.com/doi/10.3724/SP.J.1249.2022.06649 DOI: 10.3724/SP.J.1249.2022.06649
Title: Distributed random vector functional link network with subspace-based local connections Author: WanguoYU, ZhenhaoYUAN, JiaqiCHEN, YulinHE Volume: Journal of Shenzhen University Science and Engineering 39(6), 675 (2022) URL: https://www.sciengine.com/doi/10.3724/SP.J.1249.2022.06675 DOI: 10.3724/SP.J.1249.2022.06675
Title: Drilling fluid for stabilizing the wellbore in compound-salt formation based on multiple-synergism-method Author: XinZHAO, HaoSUN, ZhengsongQIU, WeianHUANG, JiafangXU, HanyiZHONG Volume: Journal of Shenzhen University Science and Engineering 39(6), 668 (2022) URL: https://www.sciengine.com/doi/10.3724/SP.J.1249.2022.06668 DOI: 10.3724/SP.J.1249.2022.06668
Title: Improved sine cosine algorithm for large-scale optimization problems Author: ChaoZHANG, YiYANG Volume: Journal of Shenzhen University Science and Engineering 39(6), 684 (2022) URL: https://www.sciengine.com/doi/10.3724/SP.J.1249.2022.06684 DOI: 10.3724/SP.J.1249.2022.06684
Title: A content-location-aware personalized POI recommendation model Author: BiLIANG, DujinLIU, LunXIONG, XiaohongXU Volume: Journal of Shenzhen University Science and Engineering 39(6), 693 (2022) URL: https://www.sciengine.com/doi/10.3724/SP.J.1249.2022.06693 DOI: 10.3724/SP.J.1249.2022.06693
Title: Classification of retinopathy of prematurity based on mixed attention Author: ShaobinCHEN, BaiyingLEI, HaiXIE, GuomingZHANG, YueshanyiDU, XinyuZHAO Volume: Journal of Shenzhen University Science and Engineering 39(6), 701 (2022) URL: https://www.sciengine.com/doi/10.3724/SP.J.1249.2022.06701 DOI: 10.3724/SP.J.1249.2022.06701
Title: Optimal excess of loss reinsurance-barrier dividend strategies with investment Author: ZongqiSUN, PengYANG, JingWU, YangYANG Volume: Journal of Shenzhen University Science and Engineering 39(6), 719 (2022) URL: https://www.sciengine.com/doi/10.3724/SP.J.1249.2022.06719 DOI: 10.3724/SP.J.1249.2022.06719
Title: Fixed and preassigned-time synchronization of drive-response networks with discontinuous activation functions Author: XingruiLI, YuzhuXIAO, XueliSONG, NannanZHAO, DongxinSHI, MeihuaSHAN Volume: Journal of Shenzhen University Science and Engineering 39(6), 709 (2022) URL: https://www.sciengine.com/doi/10.3724/SP.J.1249.2022.06709 DOI: 10.3724/SP.J.1249.2022.06709
Science Bulletin
Title: Cr(VI) detoxification and simultaneous selective recovery of Cr resource from wastewater via photo-chemical extraction using biomass Author: Ling Yao, Zewen Shen, Zhuoyu Ji, Yezi Hu, Duoyue Tang, Guixia Zhao, Xiangke Wang Volume: Science Bulletin 67(21), 2154 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.013 DOI: 10.1016/j.scib.2022.10.013
Title: A distinctive Eocene Asian monsoon and modern biodiversity resulted from the rise of eastern Tibet Author: Songlin He, Lin Ding, Zhongyu Xiong, Robert A. Spicer, Alex Farnsworth, Paul J. Valdes, Chao Wang, Fulong Cai, Houqi Wang, Yong Sun, Deng Zeng, Jing Xie, Yahui Yue, Chenyuan Zhao, Peiping Song, Chen Wu Volume: Science Bulletin 67(21), 2245 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.006 DOI: 10.1016/j.scib.2022.10.006
Title: High-strength super-hydrophobic double-layered PBO nanofiber-polytetrafluoroethylene nanocomposite paper for high-performance wave-transparent applications Author: Lin Tang, Yusheng Tang, Junliang Zhang, Yuhan Lin, Jie Kong, Kun Zhou, Junwei Gu Volume: Science Bulletin 67(21), 2196 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.011 DOI: 10.1016/j.scib.2022.10.011
Title: Solvating power regulation enabled low concentration electrolyte for lithium batteries Author: Linshan Peng, Xiangkun Wu, Mengmin Jia, Weiwei Qian, Xiaoyan Zhang, Na Zhou, Lan Zhang, Cuiying Jian, Suojiang Zhang Volume: Science Bulletin 67(21), 2235 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.008 DOI: 10.1016/j.scib.2022.10.008
Title: Positioning solid-state sodium batteries in future transportation and energy storage Author: Bin Tang, Xinyu Yu, Yirong Gao, Shou-Hang Bo, Zhen Zhou Volume: Science Bulletin 67(21), 2149 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.014 DOI: 10.1016/j.scib.2022.10.014
Title: Maximizing the ion accessibility and high mechanical strength in nanoscale ion channel MXene electrodes for high-capacity zinc-ion energy storage Author: Yongfa Cheng, Yimei Xie, Shuwen Yan, Zunyu Liu, Yanan Ma, Yang Yue, Jianbo Wang, Yihua Gao, Luying Li Volume: Science Bulletin 67(21), 2216 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.003 DOI: 10.1016/j.scib.2022.10.003
Title: Robust carbon nanotube-interwoven KFeSO4F microspheres as reliable potassium cathodes Author: Jiaying Liao, Qiao Hu, Yichen Du, Jianbo Li, Liping Duan, Jianchun Bao, Xiaosi Zhou Volume: Science Bulletin 67(21), 2208 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.012 DOI: 10.1016/j.scib.2022.10.012
Title: Spatiotemporal variation in precipitation-economy correlations in eastern China over the past 1800 years Author: Shiwei Jiang, Xin Zhou, Min Ding, Luyao Tu, Xuanqiao Liu, Wuhong Luo, Juzhong Zhang, Yan'an Shen Volume: Science Bulletin 67(21), 2142 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.09.027 DOI: 10.1016/j.scib.2022.09.027
Title: Trace antibiotics perturb the metabolism of Escherichia coli Author: Dongyang Ye, Chengfei Wang, Xiaowei Li, Liang Zhao, Saiwa Liu, Jingjing Du, Xixi Jia, Zhinan Wang, Lu Tian, Jian Xu, Jing Li, Zuhao Yan, Jiangyi Ding, Jianzhong Shen, Xi Xia Volume: Science Bulletin 67(21), 2158 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.017 DOI: 10.1016/j.scib.2022.10.017
Title: Detection of spectral hardenings in cosmic-ray boron-to-carbon and boron-to-oxygen flux ratios with DAMPE Author: DAMPE Collaboration Volume: Science Bulletin 67(21), 2162 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.002 DOI: 10.1016/j.scib.2022.10.002
Title: Topological π modes and beyond Author: Weiwei Zhu, Jiangbin Gong, Raditya Weda Bomantara Volume: Science Bulletin 67(21), 2145 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.018 DOI: 10.1016/j.scib.2022.10.018
Title: Experimental measurement-device-independent type quantum key distribution with flawed and correlated sources Author: Jie Gu, Xiao-Yu Cao, Yao Fu, Zong-Wu He, Ze-Jie Yin, Hua-Lei Yin, Zeng-Bing Chen Volume: Science Bulletin 67(21), 2167 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.010 DOI: 10.1016/j.scib.2022.10.010
Title: Tailoring electrolyte enables high-voltage Ni-rich NCM cathode against aggressive cathode chemistries for Li-ion batteries Author: Fangyuan Cheng, Xiaoyu Zhang, Peng Wei, Shixiong Sun, Yue Xu, Qing Li, Chun Fang, Jiantao Han, Yunhui Huang Volume: Science Bulletin 67(21), 2225 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.007 DOI: 10.1016/j.scib.2022.10.007
Title: On the chronology of Tibetan ice cores Author: Shugui Hou Volume: Science Bulletin 67(21), 2139 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.009 DOI: 10.1016/j.scib.2022.10.009
Title: Titanium doped kagome superconductor CsV3−xTixSb5 and two distinct phases Author: Haitao Yang, Zihao Huang, Yuhang Zhang, Zhen Zhao, Jinan Shi, Hailan Luo, Lin Zhao, Guojian Qian, Hengxin Tan, Bin Hu, Ke Zhu, Zouyouwei Lu, Hua Zhang, Jianping Sun, Jinguang Cheng, Chengmin Shen, Xiao Lin, Binghai Yan, Xingjiang Zhou, Ziqiang Wang, Hong-Jun Gao Volume: Science Bulletin 67(21), 2176 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.015 DOI: 10.1016/j.scib.2022.10.015
Title: Dynamic metal patterns of wrinkles based on photosensitive layers Author: Shuai Chen, Kaiming Hu, Shuzhen Yan, Tianjiao Ma, Xinlu Deng, Wenming Zhang, Jie Yin, Xuesong Jiang Volume: Science Bulletin 67(21), 2186 (2022) URL: https://www.sciengine.com/doi/10.1016/j.scib.2022.10.016 DOI: 10.1016/j.scib.2022.10.016
Source: https://zhuanlan.zhihu.com/p/585768626

What are the most common kidney diseases in Children?
Our kidneys form an integral part of the urinary system and play a very crucial role in maintaining the required balance between chemicals like potassium and sodium along with water. They do this by eliminating waste products in the blood through urine.
However, if this smooth process is disturbed, it could lead to major complications and this is common for both adults and children.
According to eminent doctors working with Blue Bliss Hospital, the best kidney hospital in Bangalore, Kidney disease can impact children in various ways. It could range from treatable disorders without long-term consequences to life-threatening conditions.
Let us look at some of these disorders that can affect children.
Common Kidney Diseases in Children? As per Nephrology specialists in Bangalore, kidney diseases in children can be either acute or chronic in nature. Some of the commonly observed kidney diseases in children include:
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• Hereditary Diseases Hereditary Diseases are genetic in nature and are usually inherited through parents. Some examples of Hereditary Diseases are Polycystic Kidney Disease (PKD) and Alport Syndrome, which develop quite early in childhood.

Nephrologists associated with Blue Bliss Hospital rated as the best hospital for kidney treatment in Bangalore have said that hereditary diseases can affect even other bodily functions, including hearing and vision.
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• Infections Bacterial and Viral Infections can become the major causes of kidney diseases in children. According to Best Kidney specialists in Bangalore, the most prominent diseases noticed are,

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1. Hemolytic Uremic Syndrome This condition is caused due to bacteria and viruses that enter our body system through contaminated food or processed food. Children who develop hemolytic uremic syndrome become pale, tired, and irritable. Hemolytic uremic syndrome can cause kidney failure in some children.
2. Glomerulonephritis This condition occurs when bacteria impact the child’s immune system and over some time can hurt the kidneys. Any prolonged or untreated infection can cause this condition which can either appear for a short term or remain for a longer duration of time.
3. Nephrictic Syndrome This condition occurs after upper respiratory tract infection and skin infection characterized by haematuria, B/L loin pain, fever and Proteinuria (albumin in Urine)

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• Nephrotic Syndrome Top Nephrologists in Bangalore who form the core team of specialists at Blue Bliss Hospital describe Nephrotic Syndrome as a collection of different symptoms that children experience which can cause kidney damage at a later stage. These can include:
• Elevated Albumin levels
• Elevated Cholesterol levels
• Low Albumin levels
• Inflammation or swelling noticed in the hands, legs, face, ankle or feet
• Trauma Physical or Mental Trauma can lead to variations in blood pressure which can subsequently damage the kidneys. Conditions such as heavy percentage of burns, bleeding, injury and dehydration can lead to physical or mental trauma.
• Blockage of Urine This is a very serious condition, which if not attended to immediately, can cause large- scale damage to the kidneys resulting in serious complications. The free flow of urine out of the body must be restored immediately.

Treatment for Kidney Diseases in Children Blue Bliss Hospital is Bangalore’s most trusted center for kidney failure treatment. With a team of some of the finest and vastly experienced Nephrologists and Pediatric Nephrologists, the hospital has a proven track record of having treated the most complicated cases of kidney diseases in children.
Depending upon the complexity of the situation, doctors at the hospital might recommend simple medications, antibiotics and diet control. In severe cases, dialysis could be an option.

10 Basic Facts To Know About Chronic Kidney Disease.
1. What exactly is chronic kidney disease?
Chronic kidney disease (CKD) is characterized by a gradual decline of kidney function over months or years. Damage to the kidneys means that your kidneys can't do their job and you might become quite ill as a result. Without adequate treatment, which may include dialysis, you might develop kidney failure, which can be fatal.
2. Who is affected by CKD?
The National Kidney Foundation estimates that 30 million Americans have CKD. While this ailment can affect anybody at any age, it is more frequent in African-Americans, Hispanics, Native Americans, and South Asians (those from India, Bangladesh, Sri Lanka, or Pakistan), as well as persons over the age of 60. Furthermore, women are more likely than males to get CKD.
3. What causes chronic kidney disease?
CKD can be caused by a number of causes, the most serious of which are diabetes and high blood pressure. These two disorders account for two-thirds of all instances of CKD. Ironically, those with diabetes are more likely than non-diabetics to have high blood pressure and Kidney damage.
There are various conditions that might cause CKD. These include glomerulonephritis, a kidney inflammation and damage disorder; lupus, an inflammatory illness; polycystic kidney disease; kidney stones; kidney tumors; recurrent urinary tract infections; and kidney deformities.
4. What are the symptoms of CKD?
You may not have any symptoms in the early stages of CKD. Some people, on the other hand, find that they:
• Feeling fatigued and drained of energy
• Have a poor appetite
• Have difficulty concentrating
• Having difficulty sleeping
• Have itchy, dry skin
• Have swelling ankles and feet
• Experience muscular cramps
• Urinate more frequently than normal
• Urine that is pink or dark
5. What tests are used to detect CKD?
Kidney disease is detected using both blood and urine testing. One of the tests looks for creatinine, a waste product produced by muscles and eliminated by the kidneys. Creatinine levels in the blood might rise if the kidneys aren't operating as effectively as they should.
The glomerular filtration rate, or GFR, is an equation that may be used to calculate your kidney function. This indicates to your doctor how effectively your kidneys are functioning. The urine microalbumin, or albumin-to-creatinine ratio, is another easy test. This test determines whether or not there is protein in the urine.
6. What is the treatment for CKD?
CKD, like diabetes, has no cure, although therapies are available. Medication and dietary adjustments are frequently required in the early stages of this condition. If your CKD worsens and your kidneys fail, you will most likely require dialysis to eliminate wastes and extra fluid from your body. Some patients may benefit from a kidney transplant.
7. What diet is good for chronic kidney disease?
CKD, like diabetes, does not have a single diet. What and how much you eat may be affected by how effectively your kidney illness is treated and the stage of kidney disease you are in. Most people, however, need to make some dietary modifications, particularly in terms of how much sodium (salt) they consume. You may also need to reduce your consumption of potassium and phosphorus.
8. Is a low-protein diet required for CKD management?
Until recently, doctors frequently advised persons with CKD to limit their protein intake. Too much protein, such as that found in meat, poultry, or fish, was considered to cause waste buildup in the circulation. However, emerging evidence suggests that, while you should always check your protein intake, a low-protein diet isn't essential and, in some situations, can lead to malnutrition. If you have CKD, you should see your doctor and meet with a nutritionist who specializes in kidney disease to determine the optimal diet for you.
9. Are herbal supplements safe to consume if you have CKD?
It's critical to see your doctor about any supplements you're taking or considering taking. Some supplements are toxic to the kidneys and should be avoided. Creatine (not to be confused with creatinine), licorice root, barberry, yohimbe, and astragalus are among them. Potassium is also found in bitter melon, American ginseng, feverfew, and evening primrose. Phosphorus is also found in several supplements, such as American ginseng, feverfew, and milk thistle. Taking these pills can be extremely harmful, therefore always see your doctor before taking any supplements.
10. Is it possible to prevent CKD?
While there are no guarantees that you will never develop CKD, you can take steps to avoid it. Focus on controlling your blood sugars and A1C levels if you have diabetes. Everyone, especially those at higher risk of CKD, should strive to maintain healthy blood pressure and cholesterol levels. Reaching and maintaining a healthy weight, as well as quitting smoking, are also important steps to take. Finally, discuss CKD with your healthcare team, including your risk factors, screening tests, and specific steps you can take to reduce your risk.
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