Persius/hicric huggingface dataset:
HELLP syndrome overview

# Overview
HELLP syndrome is a life-threatening obstetric complication considered by many to be a variant of pre-eclampsia. Both conditions occur during the later stages of pregnancy, or sometimes after childbirth.
HELLP is an abbreviation of the main findings:Hemolytic anemia, Elevated Liver enzymes, and Low Platelet count

# Historical Perspective
HELLP syndrome was identified as a distinct clinical entity (as opposed to severe preeclampsia) by Dr Louis Weinstein in 1982.

# Pathophysiology
The exact cause of HELLP is unknown, but general activation of the coagulation cascade is considered the main underlying problem. Fibrin forms crosslinked networks in the small blood vessels. This leads to a microangiopathic hemolytic anemia: the mesh causes destruction of red blood cells as if they were being forced through a strainer. Additionally, platelets are consumed. As the liver appears to be the main site of this process, downstream liver cells suffer ischemia, leading to periportal necrosis. Other organs can be similarly affected. HELLP syndrome leads to a variant form of disseminated intravascular coagulation (DIC), leading to paradoxical bleeding, which can make emergency surgery a serious challenge.

# Differentiating HELLP Syndrome from other Diseases
Rarely, post caesarean patients with HELLP may be in shock, which mimics either a pulmonary embolism or hemorrhage.

# Epidemiology and Demographics
The incidence of HELPP is reported to be 0.2-0.6% of all pregnancies. Of women with preeclampsia, 4-12% also develop signs of a "superimposed" HELLP syndrome. HELLP usually begins during the third trimester, and usually in Caucasian women over the age of 25. Rarely, cases have been reported as early as 23 weeks gestation.

# Risk Factors
Often, a patient who develops HELLP syndrome has already been followed up for pregnancy-induced hypertension (gestational hypertension), or is suspected to develop pre-eclampsia (high blood pressure and proteinuria). Up to 8% of all cases present after delivery.

# Diagnosis

## History and Symptoms
Patients who present with symptoms of HELLP can be misdiagnosed in the early stages, increasing the risk of liver failure and morbidity. There is gradual but marked onset of headaches (30%), blurred vision, malaise (90%), nausea/vomiting (30%), "band pain" around the upper abdomen (65%) and tingling in the extremities. Edema may occur but its absence does not exclude HELLP syndrome.  If the patient develops a seizure or coma, the condition has progressed into full-blown eclampsia.

## CT
A CT scan may show bleeding into the liver.

# Treatment

## Medical Therapy
The only effective treatment is delivery of the baby. Several medications have been investigated for the treatment of HELLP syndrome, but evidence is conflicting as to whether magnesium sulfate decreases the risk of seizures and progress to eclampsia. The DIC is treated with fresh frozen plasma to replenish the coagulation proteins, and the anemia may require blood transfusion. In mild cases, corticosteroids and antihypertensives (labetalol, hydralazine, nifedipine) may be sufficient. Intravenous fluids are generally required.
Habit reversal training
Habit reversal training (HRT) is a "multicomponent behavioral treatment package originally developed to address a wide variety of repetitive behavior disorders".
Behavioral disorders treated with HRT include tics, trichotillomania, nail biting, thumb sucking, and skin picking.  It consists of five components:
- awareness training,
- competing response training,
- contingency management,
- relaxation training, and
- generalization training.
In the case of tics, these components are intended to increase tic awareness, develop a competing response to the tic, and build treatment motivation and compliance.  Controlled trials have demonstrated that HRT is an acceptable, tolerable, effective and durable treatment for tics.

# References and notes
-  Jump up to: 1.0 1.1 1.2 1.3 Piacentini JC, Chang SW. Behavioral treatments for tic suppression: habit reversal training.  Adv Neurol. 2006;99:227-33. PMID 16536370
-  Azrin NH, Nunn RG. Habit-reversal: a method of eliminating nervous habits and tics. Behav Res Ther. 1973 Nov;11(4):619-28. PMID 4777653 As reported in Piacentini JC, Chang SW. Behavioral treatments for tic suppression: habit reversal training.  Adv Neurol. 2006;99:227-33. PMID 16536370
Height and intelligence
A positive correlation exists between human IQ and height within national populations. Correlation coefficients of the effect observed in these studies are typically about 0.2, meaning that variation in height explains about 4% of the variation in IQ.
The correlation between the two factors is therefore weak, although statistically significant, and these studies do not imply that there are no short people who are highly intelligent, or that changes in physical height have a direct effect on cognitive ability.
Indeed, intelligence is believed to be influenced by many different factors, and individuals with a wide range of intelligence can be observed at any given height. Similar strength correlations have been found in early and late childhood and adulthood in both developed and developing countries, and the correlation continues to exist after controlling for social class and parental education.

# Explanations of the correlation
The reasons for the association between height and intelligence remain unclear, but possible explanations include that height may be a marker of nutritional status, prenatal maternal stress, or general mental and physical health during development.  Studies have shown however, that common genetic factors influence variation in both height and intelligence, and are responsible for some of the effect, or that both height and intelligence may be affected by adverse early environmental exposures. A large recent twin pair study of the height-intelligence relationship showed that both shared environment (59%) and shared genetics (35%) are responsible for significant portions of the observed correlation between intelligence and height.
Another suggested reason for the correlation between height and intelligence may stem from the correlation between height and self esteem. The theory is that height indirectly affects intelligence because height during teenage years boosts self esteem, and higher self esteem in turn leads to better performance academically. More importantly, it is not a person's full-grown adult height that matters, but a person's height while in high school. Income-wise, it has been discovered that tall men who were short in high school earn like short men, while short men who were tall in high school earn like tall men.  This seems to rule out discrimination as a factor, since it would be hard for employers to know their employees' heights in the past. It suggests that another factor is at play.
Henry Street Settlement
Assistant Editor-In-Chief: Michelle Lew

# Overview
Henry Street Settlement was one of the first settlement homes founded in the United States. It provided assistance services, particularly health care services, for new immigrants and the poor. It was designated a National Historic Landmark in 1989, and continues to provide support services to residents of New York City's Lower East Side.
The Henry Street Settlement was founded in 1895 by nurses Lillian Wald and Mary Maud Brewster at 265 Henry Street (Manhattan) in the Lower East Side of Manhattan, New York City, New York, United States.

# History
Lillian Wald, a nursing student at Women's Medical College in New York City, was asked to develop programs to help the poor.  She went to the Lower East Side, which she described as a vast crowded area, a foreign city within our own, .  Two years later, she founded the Henry Street Settlement in order to provide better nursing care and other aid to the poor and immigrants.
In 1915, the Neighborhood Playhouse was created nearby.
The Settlement was designated a National Historic Landmark in 1989.
In 2007, it was among over 530 New York City arts and social service institutions to receive part of a $30 million grant from the Carnegie Corporation, which was made possible through a donation by New York City mayor Michael Bloomberg.

# Architecture
Wald established the Henry Street Settlement in a federal-era town house. Several more such houses were subsequently purchased and maintained as part of the Settlement. This had the consequence of preserving part of the 1820s streetscape amid what later became a crowded tenement district.  The block of Henry Street between Montgomery and [[Grand Street (Manhattan)

# Legacy
The Settlement continues to provide support services to residents of the Lower East Side, and offers programs in 11 facilities including the Abrons Arts Center. Programs include arts classes for children and adults, shelter services, health services, senior services, a workforce development center, day care centers, and after school and summer youth programs.

# Clients
The Settlement had many clients who went on to become successful in their fields.  Among these was Aaron Rabinowitz, noted New York City commercial real estate practitioner.
Hepatotoxicity overview
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# Overview
Hepatotoxicity implies chemical-driven liver damage. The liver plays a central role in transforming and clearing chemicals and is susceptible to the toxicity from these agents. Certain medicinal agents when taken in overdoses and sometime even when introduced within therapeutic ranges may injure the organ. Other chemical agents such as those used in laboratories and industries, natural chemicals (e.g. microcystins) and herbal remedies can also induce hepatotoxicity. Chemicals that cause liver injury are called hepatotoxins.

# Historical Perspective

# Classification

# Pathophysiology

# Causes
More than 900 drugs have been implicated in causing liver injury and it is the most common reason for a drug to be withdrawn from the market. Chemicals often cause subclinical injury to liver which manifests only as abnormal liver enzyme tests. Drug induced liver injury is responsible for 5% of all hospital admissions and 50% of all acute liver failures.

# Differentiating Hepatotoxicity from other Diseases

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis

## Natural History

## Complications

## Prognosis

# Diagnosis

## Diagnostic Criteria

## History and Symptoms

## Physical Examination

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Surgery

## Prevention
Hexamethylphosphoramide

# Overview
Hexamethylphosphoramide (abbreviated HMPA) is a colorless organic liquid with the formula 3PO. It is used as a polymer solvent, as a selective solvent for gases, stabilizer in polystyrene against thermal degradation, as a laboratory solvent for organometallic and organic reactions. It has been tested as a fire retardant and as an insect chemosterilant, but there is no known current use of HMPA for these applications. It is useful for improving the selectivity of certain organic reactions.  For instance in some deprotonation reactions HMPA breaks up the oligomers of lithium bases such as butyl lithium.  Also because HMPA solvates cations so well, while not solvating anions, it has been used as a solvent for some difficult SN2 reactions. The basic oxygen atom in HMPA coordinates strongly to lithium cation.  A molybdenum peroxide complex of HMPA is used in synthetic chemistry as an oxidant.
HMPA is the oxide of the highly basic tertiary phosphine P(NMe2)3.  Like other phosphine oxides, e.g. Triphenylphosphine oxide, the molecule has tetrahedral core and the P-O bond is highly polarlized, with significant negative charge residing on oxygen.

# Alternative reagents
Dimethyl sulfoxide can often be used in place of HMPA as a solvent. Both are strong hydrogen bond acceptors, and their oxygen atoms are able to bind to metal cations. Other alternatives to HMPA include the tetraalkylureas.

# Toxicity
HMPA is only mildly toxic but has been shown to cause nasal cancers in rats.
HMPA can be degraded to less toxic compounds by the action of hydrochloric acid. In phosphorus chemistry it is the case in general that the treatment of a compound containing a nitrogen phosphorus single bond with hydrogen chloride will form a protonated amine and a P-chloro compound. For example if P-dimethylamino-P, P-diphenyl phosphine is treated with hydrogen chloride then P-chloro-P, P-diphenyl phosphine and dimethylamine HCl salt will be obtained.
Histidine ammonia-lyase
Histidine ammonia-lyase (or histidase, or histidinase) is an enzyme that in humans is encoded by the HAL gene. Histidase converts histidine into ammonia and urocanic acid.

# Function
Histidine ammonia-lyase is a cytosolic enzyme catalyzing the first reaction in histidine catabolism, the nonoxidative deamination of L-histidine to trans-urocanic acid. The reaction is catalyzed by 3,5-dihydro-5-methyldiene-4H-imidazol-4-one, an electrophilic co-factor which is formed autocatalytically by cyclization of the protein backbone of the enzyme.

# Pathology
Mutations in the gene for histidase are associated with histidinemia and urocanic aciduria.
Histone code hypothesis
The Histone Code is hypothesized to be a code consisting of covalent histone tail modifications. Together with other modifications as DNA methylation it is part of the epigenetic code.
The main role of histones is in associating with DNA to form nucleosomes, which themselves bundle to form chromatin fibers. They are globular proteins with a flexible N-terminus (taken to be the tail) that protrudes from the nucleosome. The chromatin structure plays an important role in regulation of gene expression, while the tail modifications play an important role in the chromatin structure.
For details of gene expression regulation by histone modifications see table.

# The Hypothesis
The hypothesis is that chromatin-DNA interactions are guided by combinations of histone modifications.  While it is accepted that modulations (such as methylation, acetylation, ADP-ribosylation, ubiquitination and phosphorylation) to histone tails alter chromatin structure, a complete understanding of the precise mechanisms by which these alterations to histone tails influence DNA-histone interactions remains elusive.  However, some specific examples have been worked out in detail.  For example, phosphorylation of serine residues 10 and 28 on histone H3 is a marker for chromosomal condensation.  Similarly, the combination of phosphorylation of serine residue 10 and acetylation of a lysine residue 14 on histone H3 is a tell-tale sign of active transcription.

## Modifications
Possible modifications to the tails are:
- Acetylation - by HAT (Histone Acetyl Transferase); deactylation - by HDAC (Histone Deacetlyase)
Deacetylation allows tight arrangement of chromatin, preventing gene expression, while acetylation may occur to open up the chromatin.
- Methylation
- Phosphorylation
- Ubiquitination
- Ribosylation
Horizontal transmission
Horizontal transmission is the transmission of a bacterial, fungal, or viral infection between members of the same species that are not in a parent-child relationship.
There are two types of horizontal transmission, anterior station and posterior station.
In anterior station, transmission occurs via the bite of an infected organism, like in malaria, dengue fever, and bubonic plague. Posterior station is transmission via contact with infected feces. Examples are rickettsiae driven diseases (like typhus), which are contracted by a body louse's fecal material being scratched into the bloodstream.
Horizontal transmission tends to evolve virulence.  It is therefore a critical concept for evolutionary medicine.
HtrA serine peptidase 2
Serine protease HTRA2, mitochondrial is an enzyme that in humans is encoded by the HTRA2 gene. This protein is involved in caspase-dependent apoptosis and in Parkinson's disease.

# Structure

## Gene
The gene HTRA2 encodes a serine protease. The human gene has 8 exons and locates at chromosome band 2p12.

## Protein
Protein HtrA2, also known as Omi, is a mitochondrially-located serine protease. The human protein Serine protease HTRA2, mitochondrial is 49kDa in size and composed of 458 amino acids. The peptide fragment of 1-31 amino acid is the mitochondrial transition sequence, fragment 32-133 amino acid is propertied, and 134-458 is the mature protein Serine protease HTRA2, mitochondrial, and its theoretical pI of this protein is 6.12. HtrA2 shows similarities with DegS, a bacterial protease present in the periplasm of gram-negative bacteria. Structurally, HtrA2 is a trimeric molecule with central protease domains and a carboxy-terminal PDZ domain, which is characteristic of the HtrA family. The PDZ domain  preferentially binds C-terminus of the protein substrate and modulate the proteolytic activity of the trypsin-like protease domain.

# Function
The high-temperature requirement (HtrA) family are conserved evolutionarily and these oligomeric serine proteases has been classified in family S1B of the PA protease clan in the MEROPS protease database. The protease activity of the HtrA member HtrA2/Omi is required for mitochondrial homeostasis in mice and humans and inactivating mutations associated with neurodegenerative disorders such as Parkinson's disease. Moreover, HtrA2/Omi is released in the cytosol from the mitochondria during apoptosis and uses its four most N-terminal amino acids to mimic a caspase and be recruited by inhibitor of apoptosis protein (IAP) caspase inhibitors such as XIAP and CIAP1/2.  Once bound, the serine protease cleaves the IAP, reducing the cell's inhibition to caspase activation. In summary, HTRA2/Omi contributes to apoptosis through both caspase-dependent and -independent pathways.

# Clinical significance
The members of the HtrA family of proteases have been shown playing critical roles in cell physiology and being involved in several pathological processes including cancer and neurodegenerative disease. Strong evidences supported of HtrA2's involvement in oncogenesis. This protein is widely expressed in a variety of cancer cell lines, Analysis of biopsy samples showed changes in expression of HtrA2 in cancer tissues compared with normal tissues.
HtrA2 has recently been identified as a gene related to Parkinson's disease. Mutations in Htra2 have been found in patients suffering from Parkinson's disease. Additionally, mice lacking HtrA2 have a parkinsonian phenotype. This suggests that HtrA2 is linked to Parkinson's disease progression in humans and mice.

# Interactions
HtrA serine peptidase 2 has been shown to interact with MAPK14, XIAP and BIRC2.
Hybrid growth disorders
Hybrid growth disorders refer to reduced growth or overgrowth in an organism that is a hybrid of two different species. In some sense, it is a type of hybrid dysgenesis when the growth disorder proves deleterious, thus making it the opposite of heterosis or hybrid vigour.
Hybrid growth disorders may be referred to as a growth dysplasia, especially when resulting in overgrowth, although this terminology may be confusing since the term dysplasia is commonly used to imply an impending cancer. However, a hybrid growth disorder is not caused by cancer.
A study on hybrid mice which investigated the possible causes for hybrid growth disorders revealed gene imprinting to have a major effect. The study also showed that the growth disorder most commonly affected the heterozygous sex, as expected by Haldane's rule. This would also explain why hybrid growth disorders often appear to affect one sex more than the other.
Hyperchloremia overview

# Overview
Hyperchloremia is an electrolyte disturbance in which there is an abnormally elevated level of the chloride ion in the blood.  The normal serum range for chloride is 97 to 107 mEq/L.  Hyperchloremia is defined as a chloride concentration exceeding this level.

# Causes
Elevations in chloride may be associated with diarrhea, certain kidney diseases, and overactivity of the parathyroid glands.  Hyperchloremia is often comorbid with diabetes or hyponatremia.  Certain drugs, especially diuretics such as carbonic anhydrase inhibitors, hormonal treatments, and polypharmacy, may contribute to this disorder.

# Diagnosis

## History and Symptoms
Often hyperchloremia does not produce any symptoms.  However, hyperchloremia is sometimes associated with excess fluid loss such as vomiting and diarrhea.  If the sufferer is a diabetic, hyperchloremia may lead to poor control of blood sugar levels, causing them to become elevated.  Hyperchloremia can be symptomatic with signs of Kussmaul breathing, weakness, and intense thirst.
Pallister-Hall syndrome
Pallister-Hall syndrome is a disorder that affects the development of many parts of the body. Most people with this condition have extra fingers and/or toes (polydactyly), and the skin between some fingers or toes may be fused (cutaneous syndactyly). An abnormal growth in the brain called a hypothalamic hamartoma is characteristic of this disorder. In many cases, these growths do not cause any medical problems; however, some hypothalamic hamartomas lead to seizures or hormone abnormalities that can be life-threatening in infancy. Other features of Pallister-Hall syndrome include a malformation of the airway called a bifid epiglottis, an obstruction of the anal opening (imperforate anus), and kidney abnormalities. Although the signs and symptoms of this disorder vary from mild to severe, only a small percentage of affected people have serious complications.

# Genetics
Mutations in the GLI3 gene cause Pallister-Hall syndrome. The GLI3 gene provides instructions for making a protein that controls gene expression, which is a process that regulates whether genes are turned on or off in particular cells. By interacting with certain genes at specific times during development, the GLI3 protein plays a role in the normal shaping (patterning) of many organs and tissues before birth. Defects in the same gene also cause Greig cephalopolysyndactyly syndrome.
Mutations that cause Pallister-Hall syndrome typically lead to the production of an abnormally short version of the GLI3 protein. Unlike the normal GLI3 protein, which can turn target genes on or off, the short protein can only turn off (repress) target genes. Researchers are working to determine how this change in the protein's function affects early development. It remains uncertain how GLI3 mutations can cause polydactyly, hypothalamic hamartoma, and the other features of Pallister-Hall syndrome.
This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In some cases, an affected person inherits a mutation in the GLI3 gene from one affected parent. Other cases result from new mutations in the gene and occur in people with no history of the disorder in their family.

# Reference
- Pallister-Hall syndrome at NLM Genetics Home Reference