Persius/hicric huggingface dataset:
Weight and height percentile
Weight and height percentiles are determined by growth charts and body mass index charts to compare a child's measurements with those of other children in the same age group. By doing this, doctors can track a child's growth over time and monitor how a child is growing in relation to other children. There are different charts for boys and girls because their growth rates and patterns differ. For both boys and girls there are two sets of charts: one for infants ages 0 to 36 months and another for children ages 2 to 20 years old.
Children with failure to thrive usually have a weight that is below the 3rd or 5th percentile for their age and a declining growth velocity (meaning they are not gaining weight as expected) and/or a shift downward in their growth percentiles, crossing two or more percentiles on their growth charts.
Recently it has come to light that current growth charts for infants under 24 months overstate the expected weight of babies and lead to potentially obese children. This is because the original charts produced in 1977 were based on samples of middle class white American babies on high protein bottle fed diets in Ohio. The World Health Organisation has altered these targets in 2006 to represent a more healthy weight.
Wellcome Trust Genome Campus
The Wellcome Trust Genome Campus is a scientific research campus located in the village of Hinxton, Cambridgeshire.
It is owned by the Wellcome Trust, and its largest component is the Wellcome Trust Sanger Institute. It also is the site of the European Bioinformatics Institute (EBI), the bioinformatics outstation of the European Molecular Biology Laboratory.
The site hosted the MRC Rosalind Franklin Center for Genomics Research until its closure in 2005.
In addition to the research institutions, there are facilities on the campus dedicated to training and conferences; these include the former Hinxton Hall buildings.
Zhang Ji (Chinese physician)
Zhang Ji (Template:Zh-stp, 150 - 219), style name Zhang Zhongjing (Template:Zh-stpw), an Eastern Han (Template:Zh-tp) physician and author of the Shanghan Zabing Lun (Template:Zh-tp, lit. "Treatise on Cold Pathogenic and Miscellaneous Diseases"), was one of the most eminent Chinese physicians during the later years of the Eastern Han era.  He lived in today's Nanyang in Henan Province. During his time, with warlords fighting for their own territories, many people were infected with febrile disease. Zhang's family was no exception. He learned medicine by studying from his townsfellow Zhang Bozu, assimilating from previous medicinal literature, and collecting many prescriptions elsewhere, finally writing the medical masterpiece Shanghan Zabing Lun. Unfortunately, shortly after its publication the book was lost during wartime. Due to Zhang's contribution to Traditional Chinese medicine he is often regarded as the sage of Chinese medicine.
Zhang's masterpiece was collected by later people and compiled into two books, namely the Shanghan Lun (in full, Shanghan Zabing Lun or "Treatise on Febrile Diseases") which was a discourse on how to treat epidemic infectious diseases causing fevers prevalent during his era, and the other, highly influential doctrine Jingui yaolue (, "Synoptic Essentials from the Golden Cabinet"), a compendium of his clinical experiences. He established medication principles and summed up the medicinal experience up until the Han Dynasty, thus making a great contribution to the development of Traditional Chinese Medicine.
Though extremely well known in modern Chinese medicine and considered one of the finest Chinese physicians in history very little is known of his life. According to later sources he was born in Nie-Yang (Template:Zh-tp, modern day Nanyang), held an official position in Changsha and lived from approximately 150 to 219CE. Exact dates regarding his birth, death and works vary; an upper limit of 220CD is generally accepted.
Revered for authoring the Shang Han Za Bing Lun, Zhang Ji is considered to have founded the Cold Damage or "Cold Disease" school of Chinese medicine and is widely considered the seminal expert to this day. For more information on Zhong Ji it is best to refer directly to the Shang Han Lun.
Zidovudine drug interactions

# Drug Interactions

## Antiretroviral Agents
Stavudine: Concomitant use of zidovudine with stavudine should be avoided since an antagonistic relationship has been demonstrated in vitro.
Nucleoside Analogues Affecting DNA Replication: Some nucleoside analogues affecting DNA replication, such as ribavirin, antagonize the in vitro antiviral activity of RETROVIR against HIV-1; concomitant use of such drugs should be avoided.

## Doxorubicin
Concomitant use of zidovudine with doxorubicin should be avoided since an antagonistic relationship has been demonstrated in vitro.

## Hematologic/Bone Marrow Suppressive/Cytotoxic Agents
Coadministration of ganciclovir, interferon alfa, ribavirin, and other bone marrow suppressive or cytotoxic agents may increase the hematologic toxicity of zidovudine.
Zona limitans intrathalamica
The zona limitans intrathalamica (ZLI) is a transverse boundary located between the prethalamus (previously also known as ventral thalamus) and the functional distinct thalamus (dorsal thalamus.
Besides its morphological characteristics, it bears the hallmarks of a signalling centre. Fate mapping experiments in chick have shown that the ZLI is cell lineage restricted at its boundaries and therefore can be termed a true developmental compartment in the forebrain.
Besides morphological characteristics, the ZLI is the only structure in the alar plate of the neural tube that expresses the signalling molecule Sonic hedgehog; Shh. In mouse, the function of Hh signalling at the ZLI has not been addressed directly due to a complete absence of the diencephalon in Shh mutants.
Studies in chick have shown that Shh is necessary and sufficient for both prethalamic expression of Dlx2 and thalamic expression of Gbx2 and Sox14. In zebrafish, the structure corresponding to the Shh expression has been termed as mid-diencephalic boundary (MDB) but subsequently referred to as ZLI, in keeping with pre-existing terminology for other vertebrates. In zebrafish, it was shown that the expression of two shh genes, shh-a and shh-b (formerly described as twhh) mark the ZLI territory, and that ZLI development is accompanied by expression of pro-neural genes: anteriorly of dlx2a, a marker of the prethalamus, and posteriorly of dbx1a, a marker of the thalamus. Shh signalling is sufficient for the molecular differentiation of both the prethalamus and the thalamus but is not required for their maintenance and Shh signalling from the ZLI in the alar plate is sufficient for the maturation of prethalamic and thalamic territory while ventral Shh signals are dispensable.
File:Zona limitans intrathalamica.jpg
The Zona limitans intrathalamica (ZLI) expresses the Sonic-hedgehog (Shh) gene. The picture show a lateral view of the brain of a zebrafish embryo at 42 post fertilisation after double in situ hybridization with a probe against shh-a and dlx2a. The ZLI (red) marks the V-shaped boundary between the two Prethalami (PT; blue) and Thalamus (Th; yellow) in a pseudo-frontal view. by Steffen Scholpp
4-Methylbenzylidene camphor
4-Methylbenzylidene camphor, short 4-MBC, also 3-(4-Methylbenzylidene)bornan-2-one, or 3-(4-Methylbenzylidene)-dl-camphor is an organic camphor derivative that is used in the cosmetic industry for its ability to protect the skin against UV, specifically UV B radiation. As such it is used in sunscreen lotions and deodorants. Its tradename is Eusolex 6300.

# Endocrine disruptor
Studies have raised the issue that 4-MBC acts an endocrine disruptor. There is controversy about the estrogenic effects of 4-MBC and while one study showed only a relatively minor effect, a study in Switzerland showed significant uterine growth in immature rodents. In addition, there is some evidence that 4-MBC may suppress the pituitary-thyroid axis leading to hypothyroidism.
The agent can also lead to a photoallergic dermatitis.

# Approval status
4-MBC is approved for use in Europe by the European Union's Scientific Committee for Cosmetic Products & Non-Food Products but is not approved for use in the USA by the Food and Drug Administration. It is also approved in Canada by Health Canada, in Australia and other countries. It's not permitted in Japan.

# Alternative agents
Alternative agents that block UV by absorption include:
- Avobenzone
- Oxybenzone
- octyl methoxycinnamate (OMC)
- homosalate
5-alpha-reductase inhibitor
5-reductase inhibitors (or 5-alpha-reductase inhibitors) are a group of drugs with antiandrogenic activity, used in the treatment of benign prostatic hyperplasia and androgenic (or androgenetic) alopecia. These drugs decrease the levels of available 5-reductase prior to testosterone binding with the enzyme, thus reducing levels of dihydrotestosterone that derives from such a bond.

# Clinical use

## Indications
5-reductase inhibitors are clinically used in the treatment of conditions which are exacerbated by dihydrotestosterone. Specifically, these indications may include: (Rossi, 2004)
- mild-to-moderate benign prostatic hyperplasia
- androgenic (or androgenetic) alopecia

## Adverse drug reactions
Adverse drug reactions (ADRs) experienced with 5-reductase inhibitors are generally dose-dependent. Common ADRs include impotence, decreased libido, decreased ejaculate volume. Rare ADRs include: breast tenderness and enlargement, and allergic reaction. (Rossi, 2004)

# Pharmacology
The enzyme 5-reductase is involved in the conversion of testosterone to the active form dihydrotestosterone by reducing the 4,5 double-bond. In benign prostatic hyperplasia, dihydrotestosterone acts as a potent cellular androgen and promotes prostate growth - inhibiting the enzyme reduces the excessive prostate growth. In alopecia, pattern-baldness is one of the effects of androgenic receptor activation. Reducing the levels of dihydrotestosterone thus reduces alopecia.

# Examples
- finasteride (Proscar, Propecia)
- dutasteride (Avodart)
- FCE 28260, an experimental compound
Alpha-2 adrenergic receptor
The 2 receptor is a type of adrenergic receptor.

# Effect
The 2 receptor has several, general, functions in common with other -receptors, but also has individual effects.

## General
Common (or still unspecified) effects include:
- Vasoconstriction of arteries to heart (coronary artery).
- Vasoconstriction of veins
- Decrease motility of smooth muscle in gastrointestinal tract
- Contraction of male genitalia during ejaculation

## Individual
Individual actions of the 2 receptor include:
- Mediates synaptic transmission in pre- and postsynaptic nerve terminals.
Decrease release of acetylcholine
Decrease release of noradrenaline
Inhibit noradrenaline system in brain
- Decrease release of acetylcholine
- Decrease release of noradrenaline
Inhibit noradrenaline system in brain
- Inhibit noradrenaline system in brain
- Inhibition of lipolysis in adipose tissue.
- inhibition of insulin release in pancreas.
- induction of glucagon release from pancreas.
- platelet aggregation
- contraction of sphincters of the gastrointestinal tract
-  Secretion from salivary gland

# Mechanism
A G protein - Gi renders adenylate cyclase inactivated, resulting in decrease of cAMP.
The relaxation of gastrointestinal tract motility is by presynaptic inhibition, where transmitters inhibit further release  by homotropic effects.

# Agonists
adrenaline has higher affinity for the alpha-2 receptor than has noradrenaline, which, in turn, has much higher affinity than has isoprenaline. Other agonists include:
- clonidine- (antihypertensive)
- lofexidine (antihypertensive)
- xylazine (veterinary)
- tizanidine (in spasms, cramping)
- guanfacine (antihypertensive)
- clenbuterol- (decongestant and bronchodilator)
- denotes selective agonists to the receptor.

# Antagonists
(Alpha blockers)
- yohimbine- (purported aphrodisiac)
- mirtazapine (NaSSA)
- mianserin (tetracyclic antidepressant)
- idazoxan*
- denotes selective agonists to the receptor.

# Types
There are three types of 2 receptors: ADRA2A, ADRA2B, ADRA2C.
Glucocorticoid deficiency 1

# Overview
Familial glucocorticoid deficiency (FGD or GCCD) is an adrenocortical failure characterized by low levels of plasma cortisol produced by the adrenal gland despite high levels of plasma ACTH.  This is an inherited disorder with several different causes which define the type.
FGD type 1 (FGD1 or GCCD1) is caused by mutations in the ACTH receptor (melanocortin 2 receptor; MC2R).  FGD type 2 is caused by mutations in the MC2R accessory protein (MRAP).  These two types account for 45% of all cases of FGD.
Some cases of FGD type 3 are caused by mutations in the steroidogenic acute regulatory protein (StAR), with similarity to the nonclassic form of lipoid congenital adrenal hyperplasia.  In this case, a general impairment in not just adrenal steroid production, but gonadal steroid production can affect sexual development and fertility.
The causes of other cases of FGD type 3 not due to StAR are currently unknown.
Anti-mitochondrial antibody
Anti-mitochondrial antibodies (AMA) are antibodies (immunoglobulins) formed against mitochondria, primarily mitochondria in cells of the liver. The presence of AMAs in the blood or serum of a person is indicative of a disease called primary biliary cirrhosis (PBC) (a scarring of liver tissue, confined primarily to the bile duct drainage system of the liver). It is present in about 95% of cases.
Primary biliary cirrhosis is seen primarily in middle-aged women, and in those afflicted with other autoimmune diseases. PBC is an autoimmune disorder, a condition in which the human body's immune defense system mistakenly attacks the body's own cells, or in this case parts of the cells.
Cause of AMAs is postulated that xenobiotic-induced and/or oxidative modification of mitochondrial autoantigens is a critical step leading to loss of tolerance. In acute liver failure AMA are found against all major liver antigens.
- pyruvate dehydrogenase, E2 subunits
- 2-oxo-glutarate dehydrogenase
- branched chain 2-oxo-acid dehydrogenase
Anti-cardiolipin antibodies are another type of AMA, cardiolipin is found on the inner mitochondrial membrane.

# Correlation with non-mitochodrial antigens
Fifty seven percent of acute liver failure patients had elevated anti-transglutaminase antibodies (anti-tTG), which correlate with gluten-sensitive
enteropathy (see coeliac disease, Gluten-sensitive enteropathy associated conditions).
The inflammation produced by gluten-sensitive cellular immunity may cause the oxidative stress resulting in the modification of mitochondrial antigens and acute liver failure. Anti-gp210 antibodies are also found in 47% of PBC patients.
Partial thromboplastin time

# Overview
The partial thromboplastin time (PTT) or activated partial thromboplastin time (aPTT or APTT) is a performance indicator measuring the efficacy of both the "intrinsic" (now referred to as the contact activation pathway) and the common (tissue factor pathway) coagulation pathways. Apart from detecting abnormalities in blood clotting, it is also used to monitor the treatment effects with heparin, a major anticoagulant.

# Differential Diagnosis
In alphabetical order:  
Prolonged
- Clotting factor deficiency
- DIC
- Drugs
- Drug side effect: Thrombin human
- Fibrinolytic states
- Fibrinogen deficiency
- Heparin
- Hypoalbuminemia
- Impaired fibrin polymerization
- Liver Disease
- Subcutaneous heparin injection
- Therapy with unfractionated heparin
- Thrombolytics
- Vitamin K deficiency
- Von Willenbrand's Disease
- Warfarin

# Methodology
Blood is collected, by a phlebotomist, with oxalate or citrate which arrest coagulation by binding calcium. This specimen is delivered to the laboratory.  In order to activate the intrinsic pathway, phospholipid, an activator (such as silica, celite, kaolin, ellagic acid), and calcium (to reverse the anticoagulant effect of the oxalate) are mixed into the plasma sample . The time is measured until a thrombus (clot) forms.  This testing is performed by a medical technologist.
The test is termed "partial" due to the absence of tissue factor from the reaction mixture.

# Interpretation
Values below 25 seconds or over 39 s (depending on local normal ranges) are generally abnormal. Shortening of the PTT has little clinical relevance. Prolonged aPTT may indicate:
- use of heparin (or contamination of the sample)
- antiphospholipid antibody (especially lupus anticoagulant, which paradoxically increases propensity to thrombosis)
- coagulation factor deficiency (e.g. hemophilia)
To distinguish the above causes, mixing studies are performed, in which the patient's plasma is mixed (initially at a 50:50 dilution) with normal plasma. If the abnormality does not disappear, the sample is said to contain an "inhibitor" (either heparin, antiphospholipid antibodies or coagulation factor specific inhibitors), while if it does correct a factor deficiency is more likely. Deficiencies of factors VIII, IX, XI and XII and rarely von Willebrand factor (if causing a low factor VIII level) may lead to a prolonged aPTT correcting on mixing studies.

# History
The aPTT was first described in 1953.
Abnormal posturing overview
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# Overview
Abnormal posturing is an involuntary flexion or extension of the arms and legs, indicating severe brain injury.  It occurs when one set of muscles becomes incapacitated while the opposing set is not, and an external stimulus such as pain causes the working set of muscles to contract. The posturing may also occur without a stimulus. Since posturing is an important indicator of the amount of damage that has occurred to the brain, it is used by medical professionals to measure the severity of a coma with the Glasgow Coma Scale (for adults) and the Pediatric Glasgow Coma Scale (for infants).

# Classification
The two types of abnormal posturing are decorticate and decerebrate posturing.  Opisthotonos, in which the head and back are arched backward, is another form of abnormal posturing.

# Causes
Decerebrate and decorticate posturing can indicate that brain herniation is occurring or is about to occur.  Brain herniation is an extremely dangerous condition in which parts of the brain are pushed past hard structures within the skull.  In herniation syndrome, which is indicative of brain herniation, decorticate posturing occurs, and, if the condition is left untreated, develops into decerebrate posturing.

# Natural History, Complications and Prognosis
The presence of posturing indicates a severe medical emergency requiring immediate medical attention.  Decerebrate and decorticate posturing are strongly associated with poor outcome in a variety of conditions.  For example, near-drowning victims that display decerebrate or decorticate posturing have worse outcomes than those that do not.  Changes in the condition of the patient may cause him or her to alternate between different types of posturing.
Acinetobacter calcoaceticus

# Overview
Acinetobacter calcoaceticus is a bacterial species of the genus Acinetobacter. It is a nonmotile, gram negative coccobacillus. It grows under aerobic conditions, is catalase positive and oxidase negative. It is part of the normal human intestinal flora. 
Together with A. baumannii, it is referred to as the A. calcoaceticus-A. baumannii complex, which is relatively simple to identify based on the beforementioned phenotypic characteristics. To identify other Acinetobacter species genotyping is required.

# Habitat
A. calcoaceticus is a soil bacterium. It has been shown to be prevalent in the tiger mosquito Aedes albopictus microflora.

# Metabolism
Phloroglucinol carboxylic acid is a degradation product excreted by A. calcoaceticus grown on (+)-catechin as the sole source of carbon.

# Clinical significance
A. calcoaceticus can be pathogenic and cause an opportunistic infection in patients with multiple underlying diseases.

# Uses
A. calcoaceticus can be used as an alternative to A. baumannii in the laboratory setting. The interchangeability of the two species stems from their extreme degree of similarity and ability to form the A. calcoaceticus-A. baumannii complex. Other contributing factors include the cost-effective nature of A. calcoaceticus compared to A. baumannii and the ability of A. calcoaceticus to readily uptake DNA.
Acute eosinophilic leukemia
Acute eosinophilic leukemia (AEL) is a rare subtype of acute myeloid leukemia with 50 to 80 percent of eosinophilic cells in the blood and marrow. It can arise de novo or may develop in patients having the chronic form of a hypereosinophilic syndrome. Patients with acute eosinophilic leukemia have a propensity for developing bronchospasm and heart failure from endomyocardial fibrosis. Hepatomegaly and splenomegaly are more common than in other variants of AML.

# Diagnosis
A specific histochemical reaction, cyanide-resistant peroxidase, permits identification of leukemic blast cells with eosinophilic differentiation and diagnosis of acute eosinoblastic leukemia in some cases of AML with few identifiable eosinophils in blood or marrow.

# Treatment and Prognosis
Acute eosinophilic leukemia is treated as other subtypes of AML. Response to treatment is approximately the same as in other types of AML.