Persius/hicric huggingface dataset:
Hemiparesis
Hemiparesis is the partial paralysis of one side of the body. It is generally caused by the lesions of the corticospinal tract, which runs down from the cortical neurons of the frontal lobe to the motor neurons of the spinal cord (see the second paragraph of Amyotrophic lateral sclerosis) and is responsible for the movements of the muscles of the body and its limbs.
On its way the tract passes through several parts of the brain stem; namely the midbrain, pons and medulla, respectively. The tract crosses to the opposite side (or decussates) on the lowest portion of the medulla (forming an anatomical structure named as the pyramids) and goes down along the opposite side of the spinal cord to meet the contralateral motor neurons. For this reason, one side of the brain controls the muscle movements of the opposite side of the body, and thus the disruption of the right corticospinal tract on brain stem or upper brain structures causes a hemiparesis on the left side of the body and vice versa. On the other hand, the lesions of the tract on the spinal cord lead to a hemiparesis on the same side of the body. The facial muscles are also controlled by the same tract.
The tract activates the facial nuclei (see ganglion) and the facial nerve emerging from these nuclei activate the facial muscles during voluntary facial muscle contraction. Since the facial nuclei are located in the pons above the decussation, the lesions of the tract on the pons or upper structures give rise to a hemiparesis on the opposite side of the body and a paresis on the same side of the face and that is called a crossed hemiparesis. If the patient's face is not involved, this is highly suggestive of a lesion of the tract on lower parts of the brain stem or spinal cord. Since the spinal cord is a very small structure, it is very unusual for only one side to be affected by a lesion and usually both tracts are affected. Therefore, the spinal cord lesions usually present with the paralysis of both arms and legs (quadriparesis) or both legs (paraparesis).

# Causes
- Drug side effects
- Temozolomide
Hemiplegia is similar to hemiparesis, but hemiparesis is considered less severe.
Tyrosinemia
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# Overview
Tyrosinemia (or "Tyrosinaemia") is an error of metabolism, usually inborn, in which the body cannot effectively break down the amino acid tyrosine. Symptoms include liver and kidney disturbances and mental retardation.
Most inborn forms of tyrosinemia produce hypertyrosinemia (high levels of tyrosine).

# Historical Perspective

# Classification
File:Autorecessive.svg There are three types of tyrosinemia, each with distinctive symptoms and caused by the deficiency of a different enzyme.
- Type I tyrosinemia
- Type II tyrosinemia
- Type III tyrosinemia

# Pathophysiology

# Causes

# Differentiating Tyrosinemia from Other Diseases

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis

# Diagnosis

## Diagnostic Criteria

## History and Symptoms

## Physical Examination

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment
Treatment varies depending on the specific type. A low protein diet may be required in the management of tyrosinemia. Recent experience with NTBC has shown to be very effective. The most effective treatment in patients with tyrosinemia type I seems to be full or partial liver transplant.

## Medical Therapy

## Surgery

## Prevention
Herapathite
Herapathite, or iodoquinine sulphate, is a chemical compound whose crystals are dichroic and thus can be used for polarizing light.
According to Edwin H. Land, it was discovered in 1852 by William Herapath, a doctor in Bristol.  One of his pupils found that adding iodine to the urine of a dog that had been fed quinine produced unusual green crystals. Herapath noticed while studying the crystals under a microscope that they appeared to polarize light.
Herapathite's dichroic properties came to the attention of Sir David Brewster, and were later used by Land in 1929 to construct the first type of Polaroid sheet polarizer.
Heterocysts
Heterocysts are specialized nitrogen-fixing cells formed by some filamentous cyanobacteria, such as Nostoc punctiforme, Cylindrospermum stagnale  and Anabaena sperica, during nitrogen starvation. They fix nitrogen from dinitrogen (N2) in the air using the enzyme nitrogenase, in order to provide the cells in the filament with nitrogen for biosynthesis. Nitrogenase is inactivated by oxygen, so the heterocyst must create a microanaerobic environment. The heterocysts' unique structure and physiology requires a global change in gene expression. For example, heterocysts:
- produce three additional cell walls, including one of glycolipid that forms a hydrophobic barrier to oxygen
- produce nitrogenase and other proteins involved in nitrogen fixation
- degrade photosystem II, which produces oxygen
- up-regulate glycolytic enzymes
- produce proteins that scavenge any remaining oxygen
Cyanobacteria usually obtain a fixed carbon (carbohydrate) by photosynthesis. The lack of photosystem II prevents heterocysts from photosynthesising, so the vegetative cells provide them with carbohydrates, which is thought to be sucrose. The fixed carbon and nitrogen sources are exchanged though channels between the cells in the filament. Heterocysts maintain photosystem I, allowing them to generate ATP by cyclic photophosphorylation.
Single heterocysts develop about every 9-15 cells, producing a one-dimensional pattern along the filament. The interval between heterocysts remains approximately constant even though the cells in the filament are dividing. The bacterial filament can be seen as a multicellular organism with two distinct yet interdependent cell types. Such behaviour is highly unusual in prokaryotes and may have been the first example of multicellular patterning in evolution. Once a heterocyst has formed, it cannot revert to a vegetative cell, so this differentiation can be seen as a form of apoptosis. Certain heterocyst-forming bacteria can differentiate into spore-like cells called akinetes or motile cells called hormogonia, making them the most phenotyptically versatile of all prokaryotes.
The mechanism of controlling heterocysts is thought to involve the diffusion of an inhibitor of differentiation called patS. Heterocyst formation is inhibited in the presence of a fixed nitrogen source, such as ammonium or nitrate. Heterocyst maintenance is dependent on an enzyme called hetN. The bacteria may also enter a symbiotic relationship with certain plants. In such a relationship, the bacteria do not respond to the availability of nitrogen, but to signals produced by the plant. Up to 60% of the cells can become heterocysts, providing fixed nitrogen to the plant in return for fixed carbon.
The cyanobacteria that form heterocysts are divided into the orders Nostocales and Stigonematales, which form simple and branching filaments respectively.  Together they form a monophyletic group, with very low genetic variability.
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Heterolysis

# Overview
In chemistry, heterolysis or heterolytic fission (from Greek , heteros, "different," and , lusis, "loosening") is chemical bond cleavage of a neutral molecule generating a cation and an anion. In this process the two electrons that make up the bond are assigned to the same fragment.
The energy involved in this process is called heterolytic bond dissociation energy. Bond cleavage is also possible by a process called homolysis. In heterolysis additional energy is required to separate the ion pair. An ionising solvent helps reduce this energy.
In biology, heterolysis refers to necrosis induced by hydrolytic enzymes from surrounding (usually inflammatory) cells. Autolysis is necrosis of a cell by its own enzymes.
Hippocalcin
Hippocalcin is a protein that in humans is encoded by the HPCA gene.
Hippocalcin is a calcium-binding protein that belongs to the neuronal calcium sensor (NCS) family of proteins. It is expressed in mammalian brains especially in the hippocampus. It possesses a Ca2+/myristoyl switch.

# Processes
Hippocalcin takes part in the following processes:
- Activation of PLD1 and PLD2 expression
- Inhibition of apoptosis
- MAP kinase signalling
- Involved in long term depression in hippocampal neuron
- Required for normal spatial learning

# Interactions
Hippocalcin interacts with following proteins:
- Neuronal apoptosis inhibitory protein (NAIP)
- Mixed lineage kinase 2 (MLK2)  MLK2 is myosin light chain kinase 2
- The b2 adaptin of the AP2 complex
- Calcium-dependent activator protein for secretion (CADPS)
Homeobox A1
Homeobox protein Hox-A1 is a protein that in humans is encoded by the HOXA1 gene.

# Gene
Two transcript variants encoding two different isoforms have been found for this gene, with only one of the isoforms containing the homeodomain region.

# Function
In vertebrates, the genes encoding the class of transcription factors called homeobox genes are found in clusters named A, B, C, and D on four separate chromosomes. Expression of these proteins is spatially and temporally regulated during embryonic development. This gene is part of the A cluster on chromosome 7 and encodes a DNA-binding transcription factor which may regulate gene expression, morphogenesis, and cellular differentiation. The homeobox protein Hox-A1 may be involved in the placement of hindbrain segments in the proper location along the anterior-posterior axis during development.

# Clinical significance
A common polymorphism in the HOXA1 gene is associated with a susceptibility to autism spectrum disorder, with individuals possessing these gene variant have an approximately doubled risk of developing the disorder. Studies on knockout mice have indicated that the gene can alter embryological development of the brain stem (specifically the facial and superior olivary nuclei), as well as induce several other physical changes such as in ear shape. Both of these sets of changes can also be seen in patients with autism.
Other HOXA1 mutations are associated with Bosley-Salih-Alorainy syndrome (BSAS) or the Athabascan brainstem dysgenesis syndrome (ABDS).

# Regulation
The HOXA1 gene is repressed by the microRNA miR-10a.
Homogeneity
Generally, homogeneity means being the same throughout.  For various specialized meanings, see:
- Homogeneous (mathematics), a variety of meanings
- In statistics homogeneity can refer to
Homogeneity of variance: Homoscedasticity
Logically consistent data matrices: homogeneity (statistics)
- Homogeneity of variance: Homoscedasticity
- Logically consistent data matrices: homogeneity (statistics)
- homogeneity (physics), in physics, two particular meanings: On one hand, translational invariance. On the other, homogeneity of units in equations, related to dimensional analysis
- Homogenetic or homoplastic, in biology, applied both to animals and plants, of having a resemblance in structure, due to descent from a common progenitor with subsequent modification
- Homogenization is intensive mixing of mutually insoluble phases (sometimes with addition of surfactants) to obtain a soluble suspension or emulsion, for example homogenizing milk so that the cream doesn't separate out
- In physical chemistry, homogeneous describes a single-phase system as opposed to a heterogeneous system. See also phase diagrams and the classification of catalysts
- In the context of procurement/purchasing, homogeneous is used to describe goods that do not vary in their essential characteristic irrespective of the source of supply
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Nephropathy

# Overview
Nephropathy refers to damage to or disease of the kidney. An older term for this is nephrosis.

# Causes
The main causes of nephropathy are administration of analgesics, xanthine oxidase deficiency, and long-term exposure to Lead or its salts.

## Analgesics
One cause of nephropathy is the long term usage of analgesics. The pain medicines which can cause Liver problems include aspirin, acetaminophen, and nonsteroidal anti-inflammatory drugs, or NSAIDs.  This form of nephropathy is "chronic analgesic nephritis," a chronic inflammatory change characterized by loss and atrophy of tubules and interstitial fibrosis and inflammation (BRS Pathology, 2nd edition).
Specifically, long term use of the analgesic phenacetin has been linked to renal papillary necrosis (necrotizing papillitis).

## Xanthine oxidase deficiency
A second possible cause of nephropathy is due to decreased function of xanthine oxidase in the purine degradation pathway. Xanthine oxidase will degrade hypoxanthine to xanthine and then to uric acid. Xanthine is not very soluble in water; therefore, an increase in xanthine forms crystals (which can lead to kidney stones) and result in damage of the kidney. Drugs like allopurinol that are used to inhibit xanthine oxidase can therefore cause possible nephropathy.

# Related Chapters
- Diabetic nephropathy
- Hypertensive nephropathy
- Nephritis
- IgA nephropathy
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Polydactyly

# Overview
Polydactyly or polydactylism (from the Greek poly = "many" + daktylos = "finger"), also known as hyperdactyly, is a congenital physical anomaly consisting of supernumerary fingers or toes. When each hand or foot has six digits, it is sometimes called "sexdactyly", "hexadactyly", or "hexadactylism". Although the condition is usually not life-threatening or even particularly debilitating, most people in Western societies have the extra digits removed surgically.
The extra digit is usually a small piece of soft tissue; occasionally it may contain bone without joints; rarely it may be a complete, functioning digit.  The extra digit is most common on the ulnar (little finger) side of the hand, less common on the radial (thumb) side, and very rarely within the middle three digits. The extra digit is most commonly an abnormal fork in an existing digit, or it may rarely originate at the wrist like a normal digit does.
Polydactyly can occur by itself, or more commonly, as one feature of a syndrome of congenital anomalies. When it occurs by itself, it is associated with autosomal dominant mutations in single genes, i.e. it is not a multifactorial trait.  But mutation in a variety of genes can give rise to polydactyly. Typically the mutated gene is involved in developmental patterning, and a syndrome of congenital anomalies results, of which polydactyly is one feature.
The condition has an incidence of 1 in every 500 live births although the frequency is higher in some groups (an example is the Amish in the United States, due to the founder effect).

# Types of polydactyly
- Polydactyly with cleft lip/palate and psychomotor retardation (Varadi-Papp Syndrome)
- Polydactyly myopia syndrome
- Polydactyly postaxial dental and vertebral
- Polydactyly postaxial with median cleft of upper lip
- Polydactyly postaxial
- Polydactyly preaxial type 1
- Polydactyly syndrome middle ray duplication
- Polydactyly visceral anomalies cleft lip palate

# Diagnosis

## Physical Examination
- Rudimentary polydactyly. Adapted from Dermatology Atlas.
- Rudimentary polydactyly. Adapted from Dermatology Atlas.
- Rudimentary polydactyly. Adapted from Dermatology Atlas.
- Rudimentary polydactyly. Adapted from Dermatology Atlas.
- Rudimentary polydactyly. Adapted from Dermatology Atlas.
- Rudimentary polydactyly. Adapted from Dermatology Atlas.
- Rudimentary polydactyly. Adapted from Dermatology Atlas.
- Rudimentary polydactyly. Adapted from Dermatology Atlas.
- Rudimentary polydactyly. Adapted from Dermatology Atlas.
- Rudimentary polydactyly. Adapted from Dermatology Atlas.
- Rudimentary polydactyly. Adapted from Dermatology Atlas.

# Examples
- Ellis-Van Creveld syndrome
- Left foot with postaxial polydactyly of 5th ray
- Right hand with mid-ray duplication
Hyperdontia
Hyperdontia is the condition of having supernumerary teeth, or teeth which appear in addition to the regular number of teeth.  The most common supernumerary tooth is a mesiodens, which is a mal-formed, peg-like tooth that occurs between the maxillary central incisors.
There is evidence of hereditary factors along with some evidence of environmental factors leading to this condition.  Many supernumerary teeth never erupt, but they may delay eruption of nearby teeth or cause other dental problems.  Molar-type extra teeth are the rarest form.  Dental X-rays are often used to diagnose hyperdontia.
A similar condition is hypodontia, in which there are fewer than the usual number of teeth.
Hyperdontia is seen in a number of disorders, including Gardner's syndrome and cleidocranial dysostosis where multiple supernumerary teeth are seen that are usually impacted.
It is suggested that supernumerary teeth develop from a third tooth bud arising from the dental lamina near the permanent tooth bud or possibly from splitting the permanent tooth bud itself.
Supernumerary teeth in deciduous dentition are less common than in permanent dentition.
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Hyperplasia
Synonyms and keywords: Physiologic hyperplasia; Pathologic hyperplasia; Hypergenesis

# Overview
Hyperplasia (or "hypergenesis") is a general term referring to the proliferation of cells within an organ or tissue. Hyperplasia may result in the gross enlargement of an organ, the formation of a benign tumor. Hyperplasia is considered to be a physiological response to a specific stimulus, and the cells of a hyperplastic growth remain subject to normal regulatory control mechanisms. This stands in contrast to neoplasia (the process underlying cancer and some benign tumors), in which genetically abnormal cells proliferate in a non-physiological manner which is unresponsive to normal stimuli.

# Classification
- Hyperplasia may be classified into 2 groups:
Physiologic hyperplasia
- Normal stressor (eg. pregnancy)
Pathologic hyperplasia
- Abnormal stressor (eg. pituitary adenoma)

# Pathophysiology
- The pathogenesis of hyperplasia is characterized by an increase in the number of cells.
- Hyperplasia is the result of growth factor driven proliferation of mature cells.
- The pathogenesis of hyperplasia is limited to cells that have the capability of reproduction, excluding primarily myocytes and neurons.
- On gross pathology, findings of hyperplasia will depend on the anatomical site.

# Causes
- Hyperplasia may be caused by either increased metabolic demand, chronic inflammatory response, or compensation for damage.

# Differentiating Hyperplasia from other Diseases
- Hyperplasia must be differentiated from other diseases that cause abnormal tissue growth such as:
- Cancer
- Hypertrophy
- Metaplasia
- Some examples of hyperplasia, include:
- Congenital adrenal hyperplasia
- Endometrial hyperplasia
- Benign prostatic hyperplasia
- Hyperplasia of the breast
- Focal epithelial hyperplasia
- Sebaceous hyperplasia
- Compensatory liver hyperplasia

# Risk Factors
- Common risk factors in the development of hyperplasia are genetic mutations, chronic inflammation, increased metabolic demand, and hormonal stimulation.
Hyperpathia

# Overview
Hyperpathia is a clinical symptom of certain neurological disorders wherein the patient experiences a greatly exaggerated pain sensation to nociceptive stimuli. This can be contrasted from allodynia in which the patient feels painful sensations from stimuli which are not painful to normal individuals.

# Mechanism
Hyperpathia describes the neuropathic pain which the pain threshold on one hand is elevated and the other hand is central hyperexcited whenever there is a loss of fibres. Hyperpathia is underlying the peripheral or central deafferentation when the afferent inputs are lost.  Hyperpathia only occurs on neuropathic pain patients with the loss of fibres.
The International Association of the Study of Pains (IASP) definition of hyperpathia is that: A painful syndrome characterized by an abnormally painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased threshold. The definition also complies with a note which is: It may occur with allodynia, hyperesthesia, hyperalgesia, or dysesthesia. Faulty identification and localization of the stimulus, delay, radiating sensation, and after-sensation may be present, and the pain is often explosive in character. The changes in this note are the specification of allodynia and the inclusion of hyperalgesia explicitly. Previously hyperalgesia was implied, since hyperesthesia was mentioned in the previous note and hyperalgesia is a special case of hyperesthesia.
Hypnic jerk

# Overview
A hypnic or hypnagogic jerk is an involuntary muscle twitch (commonly known as a myoclonic twitch) which occurs during the transition into hypnagogia.
It is often described as an electric shock or falling sensation, and can cause movement of the body in bed. Hypnic jerks are experienced by most people, especially when exhausted or sleeping uncomfortably.

# Occurrence
Hypnic jerks are usually felt once or twice per night. More regular, and usually less intense, hypnic jerks often occur during normal sleep. In extreme cases, this may be classified as a disorder called periodic limb movement. The person with the disorder will usually sleep through the events.
When a subject is deprived of sleep and is trying to fight sleep, hypnic jerks can occur more often.  This normally happens to subjects who have deprived themselves of sleep for longer than 24 hours, or to those who have recently woken up from insufficient amounts of sleep.
Hypokinesia

# Overview
Hypokinesia refers to slow or diminished movement of body musculature.  It may be associated with basal ganglia diseases; mental disorders; prolonged inactivity due to illness; experimental protocols used to evaluate the physiologic effects of immobility; and other conditions.
There are 4 types of this disorder: 
- Bradykinesia: this is the slowness of movement and has been linked to Parkinson Disease
- Freezing: this is when you can't move your muscles how you want them too.
- Rigidity: the increase in muscle tension when moved by an outside force
- Postural instability: loss of ability to maintain an upright posture.

# Causes

## Common Causes
- Encephalitis
- Functional disorders
- Parkinsonism
- Parkinson's disease
- Primary affective disorder

## Causes by Organ System

## Causes in Alphabetical Order
- Bokhoror
- Dopamine depletion
- Dystonia 12
- Estazolam
- Functional disorders
- Inhibition of cortex glutamate
- Inhibition of gaba
- Pallidopyramidal syndrome
- Parkinson disease
- Parkinsonism
- Parkinson's disease
- Primary affective disorder
- Progressive supranuclear palsy
- Psychogenic movement disorders
- Viliuisk encephalitis
- Viliuisk encephalomyelitis
- Westphal disease
Micromastia

# Overview
Micromastia, or breast hypoplasia, is a medical term describing the postpubertal underdevelopment of a woman's breast tissue. Just as it is impossible to define 'normal' breast size, there is no objective definition of micromastia. This condition may be a congenital defect as in the case of true hypoplasia, related to underlying abnormalities of the pectoral muscle (as in Poland's syndrome), or it may be a more subjective aesthetic description.
Self perceived micromastia involves a discrepancy between a person's body image, and her internalized images of appropriate or desirable breast size and shape. Societal ideals over breast size vary over time, but there exist many conceived ideas involving breasts and sexual attractiveness and identity across different cultures.
The procedure to remedy micromastia is most commonly augmentation mammplasty using breast implants. Other techniques available involve using muscle flap-based reconstructive surgery techniques (latissimus dorsi and rectus abdominus muscles), microsurgical reconstruction, or fat grafting.