Persius/hicric huggingface dataset:
Hyoscine-pentothal
Hyoscine-pentothal  is a fictional pain-inducing drug that appears in the television series 24. It has been exclusively used by CTU agents as part of their time-sensitive interrogation procedure.
Its name may have been a hasty script-writer's concoction from the name of the two real drugs hyoscine and sodium pentothal, which the CIA sometimes uses as  "truth drugs". Although perhaps intended to imply a mixture of the two real drugs, the fictional drug has no apparent relationship to the effects of either of the two real drugs in the real world.
The drug first appeared in Day 4 when it was administered on Richard Heller, Sarah Gavin and Behrooz Araz during interrogation. It was used again for interrogation  Day 5, when Christopher Henderson, a terrorist captured by CTU, is tortured by an agent who repeatedly injects him with the drug several times. Ultimately, however, the torture proves ineffective, despite the session lasting for over an hour. Agent Tony Almeida is later stabbed with a syringe containing an apparent overdose of the drug.
In Day 6, Jack Bauer uses hyoscine-pentothal to interrogate his brother Graem in a similar manner, and the session proves somewhat fruitful, as he reveals his connection to the death of David Palmer. Phillip Bauer later uses it to kill Graem.

# Effects
A number of characters have described the effects of the drug. CTU Agent Curtis Manning claims that it makes every nerve ending in one's body "feel like it is on fire". Other characters comment that Christopher Henderson withstood "an inhuman amount of pain" during his interrogation session.
Jack, a past victim of torture, further reveals that a 7cc dose of hyoscine-pentothal will result in "indescribable pain", while an 8cc dose is enough to run the risk of inducing cardiac arrest. However the actual mechanisms that describe how the drug actually works have not been revealed yet.
Jack summarizes the drug to his brother Graem Bauer as a "neural inflammatory."
Hyper IgM syndrome
Hyper IgM syndrome is a family of genetic disorders in which the level of Immunoglobulin M (IgM) antibodies is relatively high. The disorder causes immunodeficiencies, including a higher than normal susceptibility to various types of infections.  Individuals with hyper-IgM syndrome typically also have a low number of infection-fighting neutrophil cells.

# Pathophysiology
IgM is the form of antibody that all B cells produce initially, before they undergo class switching due to exposure to a recognized antigen. Healthy B cells efficiently switch to other types of antibodies as needed to attack invading bacteria, viruses, and other pathogens.  Generally, in people with hyper IgM syndromes, the B cells keep making IgM antibodies because they can't switch to a different kind of antibody.  This results in an overproduction of IgM antibodies and an underproduction of all other types.  Some hyper-IgM syndromes are actually deficiencies of the other immunoglobulin classes:  IgA, IgG, and IgE.

# Types
Five types have been characterized:
- Hyper-IgM syndrome type 1, characterized by mutations of the CD40LG gene. In this type, T cells cannot tell B cells to switch classes.
- Hyper-IgM syndrome type 2, characterized by mutations of the AICDA gene.  In this type, B cells cannot recombine genetic material to change heavy chain production, which is a required step in switching classes.
- Hyper-IgM syndrome type 3, characterized by mutations of the CD40 gene. In this type, B cells cannot receive the signal from T cells to switch classes.
- Hyper-IgM syndrome type 4, which is a defect in class switch recombination downstream of the AICDA gene that does not impair Somatic Hyper Mutation.
- Hyper-IgM syndrome type 5, characterized by mutations of the UNG gene.

# Differentiating Hyper IgM Syndrome From Other Diseases
Hyper IgM syndrome should be differentiated from other disorders leading to defects of humoral immunity. The following conditions may be considered as differentials:
- Malignancy: can cause the reduction in the immunoglobulin production.
- Viral infections: such as Epstein-Barr virus, HIV, cytomegalovirus are other causes of hypogammaglobulinemia..
- Side effect of certain medications: Some drugs include systemic glucocorticoids, phenytoin, and carbamazepine, have been associated with IgG deficiency.
- Other causes of primary humoral immunodeficiencies.
- Smoking: may cause IgG2 subclass deficiency.
Hyperopia overview

# Overview
Hyperopia, also known as farsightedness, longsightedness or hypermetropia, is a defect of vision caused by an imperfection in theeye (often when the eyeball is too short or when the lens cannot become round enough), causing inability to focus on near objects, and in extreme cases causing a sufferer to be unable to focus on objects at any distance. As an object moves toward the eye, the eye must increase its power to keep the image in focus on the retina. If the power of the cornea and lens is insufficient, as in hyperopia, the image will appear blurred.
People with hyperopia can experience blurred vision, asthenopia, accommodative dysfunction, binocular dysfunction, amblyopia, and strabismus.
Hyperopia is often confused with presbyopia, another condition that frequently causes blurry near vision. Presbyopes who report good far vision typically experience blurry near vision because of a reduced accommodative amplitude brought about by natural aging changes with the crystalline lens. It is also sometimes referred to as farsightedness, since in otherwise normally-sighted persons it makes it more difficult to focus on near objects than on far objects.

# Classification
Hyperopia is typically classified according to clinical appearance, its severity, or how it relates to the eye's accommodative status.

# Diagnosis

## History and Symtpoms
Visual acuity is affected according to the amount of hyperopia, as well as the patient's age, visual demands, and accommodative ability. Mild farsightedness may not cause any problems except for a need for reading glasses.

# Treatment

## Surgery
Various eye care professionals, including ophthalmologists, optometrists, orthoptists, and opticians, are involved in the treatment and management of hyperopia. At the conclusion of an eye examination, an eye doctor may provide the patient with an eyeglass prescription for corrective lenses.
Minor amounts of hyperopia are sometimes left uncorrected, however, larger amounts may be corrected with convex lenses in eyeglassesorcontact lenses. Convex lenses have a positive dioptric value, which causes the light to focus closer than its normal range. 
Hyperopia is sometimes correctable with various refractive surgery procedures (LASIK). It can also be corrected with special concave lenses.
Hypervitaminosis A

# Overview
Hypervitaminosis A refers to the effects of excessive vitamin A (specifically retinoid) intake.

# Presentation
Effects include:
- birth defects
- liver problems,
- reduced bone mineral density that may result in osteoporosis
- coarse bone growths
- hair loss
- excessive skin dryness/peeling

# Signs
Signs of acute toxicity include nausea and vomiting, headache, dizziness, blurred vision, and loss of muscular coordination.

# Pathophysiology
Hypervitaminosis A occurs when the maximum limit for liver stores of retinoids is exceeded. The excess vitamin A enters the circulation causing systemic toxicity. Vitamin A in the form of betacarotene is only selectively converted into retinoids, and hence does not cause toxicity.
Although hypervitaminosis A can occur when large amounts of liver are regularly consumed, most cases of vitamin A toxicity result from an excess intake of vitamin A in the form of vitamin supplements. Toxic symptoms can also arise after consuming very large amounts of preformed vitamin A over a short period of time.

# Recommended supplement limits
The Institute of Medicine has established Daily Tolerable Upper Levels (UL) of intake for vitamin A from supplements that apply to healthy populations, in order to help prevent the risk of vitamin A toxicity. These levels for preformed vitamin A in micrograms (g) and International Units (IU) are:
- 0-3 years: 600 g or 2000 IU
- 4-8 years: 900 g or 3000 IU
- 9-13 years: 1700 g or 5665 IU
- 14-18 years: 2800 g or 9335 IU
- 19+ years: 3000 g or 10,000 IU
The dose over and above the RDA is among the narrowest of the vitamins and minerals. Possible pregnancy, liver disease, high alcohol consumption, and smoking are indications for close monitoring and limitation of vitamin A administration. However, vitamin A has also been repeatedly tested and used therapeutically over several decades in larger amounts, 100,000 - 400,000 IU total dosage, for treatment of severe pediatric measles in areas where vitamin A deficiency may be present, in order to reduce childhood mortality.

# Toxicity from eating liver
The liver of certain animals  including the polar bear, seal, and husky  is unsafe to eat because it is extraordinarily high in vitamin A. This danger has long been known to the Inuit and has been recognized by Europeans since at least 1597 when Gerrit de Veer wrote in his diary that, while taking refuge in the winter in Nova Zembla, he and his men became gravely ill after eating polar-bear liver.  In 1913, Antarctic explorers Douglas Mawson and Xavier Mertz were both poisoned, the latter fatally, from eating the liver of their sled dogs.
Vitamin A itself was not discovered until 1917.
The livers of many other animals have lower levels of vitamin A and are commonly eaten.
Hypervitaminosis D
Hypervitaminosis D is a state of Vitamin D toxicity.

# Overview
Overdose occurs at more than 100 times the recommended daily allowance (roughly one bottle of vitamin D tablets per day), over a period of months. Acute overdose requires over 50mg (ten thousand times the RDA). Foods contain low levels, and have not been known to cause overdose. Overdose has occurred due to industrial accidents, for example when incorrectly formulated pills were sold or missing industrial concentrate cans misused as cans of milk.

# Symptoms and presentation
Symptoms of vitamin D poisoning include:
- Dehydration
- Vomiting
- Decreased appetite (anorexia)
- Irritability
- Constipation
- Fatigue
An excess of vitamin D causes abnormally high blood concentrations of calcium (hypercalcemia) which can eventually cause severe damage to the bones, soft tissues, and kidneys. It can also damage the kidney and produce kidney stones.  Ongoing research indicates antagonism with oil soluble menatetrenone,  MK-4, an internally transported natural form of vitamin K2, which is associated with bone formation and calcium retention in the bones.
Note: Hypervitaminosis D symptoms appear several months after excessive doses of vitamin D are administered. In almost every case, a low calcium diet combined with corticosteroid drugs will allow for a full recovery within a month.

### Contraindicated medications
Vitamin D toxicity is considered an absolute contraindication to the use of the following medications:
- calcitriol
- Ergocalciferol

# Comparative safety statistics
Deaths by vitamin poisoning appear to be quite rare in the US, typically none in a given year. However before 1998, several deaths per year were typically associated with pharmaceutical iron-containing supplements, especially brightly-colored, sugar-coated, high-potency iron supplements, and most deaths were children. Unit packaging restrictions on supplements with more than 30 mg iron have since reduced deaths to 0 or 1 per year. These statistics compare with 59 deaths due to aspirin poisoning in , 147 deaths associated with acetaminophen-containing products in , and an average of 54 deaths per year due to lightning for .
Hypervitaminosis Dmust be differentiated from other causes of hypercalcaemia
Hypochondrogenesis
Hypochondrogenesis is a severe genetic disorder causing malformations of bone growth. The condition is characterized by a short body and limbs and abnormal bone formation in the spine and pelvis.
Hypochondrogenesis is a subtype of collagenopathy, types II and XI, and is similar to another skeletal disorder, achondrogenesis type 2, although the spinal changes seen in hypochondrogenesis tend to be somewhat milder.

# Diagnosis
Affected infants have short arms and legs, a small chest with short ribs, and underdeveloped lungs. The spinal bones (vertebrae) in the neck and part of the pelvis (the sacrum) do not harden, or ossify, properly. The face appears flat and oval-shaped, with widely spaced eyes, a small chin, and, in some cases, an opening in the roof of the mouth called a cleft palate. The abdomen is enlarged, and excess fluid may build up in the body before birth (a condition called hydrops fetalis).
As a result of these serious health problems, infants are usually premature and stillborn or die shortly after birth from respiratory failure. Some infants have lived for a time, however, with intensive medical support. Babies who live past the newborn period are usually reclassified as having spondyloepiphyseal dysplasia congenita, a related disorder on the spectrum of abnormal bone growth.

# Pathophysiology
Hypochondrogenesis is one of the most severe conditions in a spectrum of disorders caused by mutations in the COL2A1 gene. The protein made by this gene forms type II collagen, a molecule found mostly in cartilage and in the clear gel that fills the eyeball (the vitreous). Type II collagen is essential for the normal development of bones and other connective tissues (tissues that form the body's supportive framework). Mutations in the COL2A1 gene interfere with the assembly of type II collagen molecules, which prevents bones from developing properly.
This condition is caused by new mutations in the COL2A1 gene. Hypochondrogenesis is considered an autosomal dominant disorder because the affected gene is located on an autosome, and only one copy of the altered gene is necessary to cause the condition. The disorder is not passed on to the next generation, however, because affected individuals do not live long enough to have children.
Inferior vena cava

# Overview
The inferior vena cava (or IVC) is the large vein that carries de-oxygenated blood from the lower half of the body into the heart.
It is posterior to the abdominal cavity and runs along side of the vertebral column on its right side (i.e. it is a retroperitoneal structure). It enters the right atrium at the lower right, back side of the heart.

# Drainage patterns
The IVC is formed by the joining of the left and right common iliac veins and brings blood into the right atrium of the heart. It also anastomoses with the azygos vein system (which runs on the right side of the vertebral column) and the venous plexuses next to the spinal cord.
Because the IVC is not centrally located, there are some asymmetries in drainage patterns. The gonadal veins and suprarenal veins drain into the IVC on the right side, but into the renal vein on the left side, which in turn drains into the IVC.
By contrast, all the lumbar veins and hepatic veins usually drain directly into the IVC.
Note that the vein that carries de-oxygenated blood from the upper half of the body is the superior vena cava.

# Pathologies associated with the IVC
Health problems attributed to the IVC are most often associated with it being compressed (ruptures are rare because it has a low intraluminal pressure). Typical sources of external pressure are an enlarged aorta (abdominal aortic aneurysm), the gravid uterus (aortocaval compression syndrome) and abdominal malignancies, such as colorectal cancer, renal cell carcinoma and ovarian cancer.  Since the inferior vena cava is primarily a right-sided structure, unconscious pregnant females should be turned on to their left side (the recovery position), to relieve pressure on it and facilitate venous return.  In rare cases, straining associated with defecation can lead to restricted blood flow through the IVC and result in syncope (fainting).
Occlusion of the IVC is rare, but considered life-threatening and is an emergency.  It is associated with deep vein thrombosis, IVC filters, liver transplantation and instrumentation (e.g. catheter in the femoral vein).

# Embryology
In the embryo, the IVC and right atrium are separated by the Eustachian valve, also known in Latin as the valvula venae cavae inferiore (valve of the inferior vena cava).  In the adult, this structure typically has totally regressed or remains as a small endocardial fold.

# Additional images
- Diagram showing completion of development of the parietal veins.
- Base and diaphragmatic surface of heart.
- The arch of the aorta, and its branches.
- Superior vena cava, inferior vena cava, azygos vein and their tributaries.
- The position and relation of the esophagus in the cervical region and in the posterior mediastinum. Seen from behind.
- Transverse section of human embryo eight and a half to nine weeks old.
- Liver and gallbladder
Ibuprofen overdose

# Overdosage topics
Infants
Children
Adults
Acute overdosage

## Infants
Approximately 112 hours after the reported ingestion of from 7 to 10 Ibuprofen tablets (400 mg), a 19-month old child weighing 12 kg was seen in the hospital emergency room, apneic and cyanotic, responding only to painful stimuli. This type of stimulus, however, was sufficient to induce respiration. Oxygen and parenteral fluids were given; a greenish-yellow fluid was aspirated from the stomach with no evidence to indicate the presence of Ibuprofen. Two hours after ingestion the child's condition seemed stable; she still responded only to painful stimuli and continued to have periods of apnea lasting from 5 to 10 seconds. She was admitted to intensive care and sodium bicarbonate was administered as well as infusions of dextrose and normal saline. By four hours post-ingestion she could be aroused easily, sit by herself and respond to spoken commands. Blood level of Ibuprofen was 102.9 g/mL approximately 812 hours after accidental ingestion. At 12 hours she appeared to be completely recovered. Return to top

## Children
In two other reported cases where children (each weighing approximately 10 kg) accidentally, acutely ingested approximately 120 mg/kg, there were no signs of acute intoxication or late sequelae. Blood level in one child 90 minutes after ingestion was 700 g/mLabout 10 times the peak levels seen in absorption-excretion studies.Return to top

## Adults
A 19-year old male who had taken 8,000 mg of Ibuprofen over a period of a few hours complained of dizziness, and nystagmus was noted. After hospitalization, parenteral hydration and three days bed rest, he recovered with no reported sequelae. Return to top

## Acute overdosage
In cases of acute overdosage, the stomach should be emptied by vomiting or lavage, though little drug will likely be recovered if more than an hour has elapsed since ingestion. Because the drug is acidic and is excreted in the urine, it is theoretically beneficial to administer alkali and induce diuresis. In addition to supportive measures, the use of oral activated charcoal may help to reduce the absorption and reabsorption of Ibuprofen tablets.Return to top
Adapted from the FDA Package Insert.
Icthyosis acquista

# Overview
Ichthyosis acquisita (or "acquired ichthyosis") is a disorder clinically and histologically similar to ichthyosis vulgaris.:565

# Associated conditions
The development of ichthyosis in adulthood can be a manifestation of systemic disease, and it has been described in association with malignancies, drugs, endocrine and metabolic disease, HIV, infection, and autoimmune conditions.:494
It usually is associated with people who have Hodgkin's disease but it is also occurs in people with mycosis fungoides, other malignant sarcomas, Kaposi's sarcoma and visceral carcinomas. It can occur in people suffering from leprosy, AIDS, tuberculosis, and typhoid fever.

# Diagnosis

## Physical Examination

### Skin
- Acquired Ichthyosis-Clofazimine. Adapted from Dermatology Atlas.
- Acquired Ichthyosis-Clofazimine. Adapted from Dermatology Atlas.
- Acquired Ichthyosis-Clofazimine. Adapted from Dermatology Atlas.
Imidazole syndrome
Synonyms and keywords: Bessman-baldwin syndrome

# Overview
Imidazole syndrome is a familial disorder of imidazole metabolism described by Samuel bessman and Ruth baldwin. It is characterised by cerebromacular degenration with convulsions, retinitis pigentosa, mental retardation and excessive urinary excretion of carnosine, anserine and histidine.

# Historical prospective
Imidazole syndrome is a familial disorder of imidazole metabolism described by Samuel bessman and Ruth baldwin.

# Diagnosis

## Symptoms
It is characterised by cerebromacular degenration with convulsions, retinitis pigentosa, mental retardation.

## Laboratory findings
Excessive urinary excretion of carnosine, anserine and histidine is characteristic laboratory finding of imidazole syndrome.
Indicator bacteria
Each gram of human feces contains approximately 10 billion (109) bacteria, among them may include pathogenic bacteria, such as Salmonella, associated with gastroenteritis. In addition, feces may contain pathogenic viruses, protozoa and parasites. If ingested, these organisms could cause disease. When testing drinking water for contamination, the variety and often low concentrations of pathogens makes them difficult to test for individually. Health authorities therefore use the presence of other more abundant and more easily detected fecal bacteria as indicators of the presence of fecal contamination.
Indicator bacteria are not themselves dangerous to the health but are used to indicate the presence of a health risk.
The most popularized known indicator bacteria are fecal coliforms, which are found in the intestinal tracts of warm blooded animals. Another less commonly used group of indicator organisms are hydrogen sulfide producing bacteria, which are also found in humans as well as the intestinal tracts of birds and reptiles - known carriers of Salmonella.
WHO Guidelines for Drinking Water Quality state that as an indicator organism Escherichia coli provides conclusive evidence of recent fecal pollution and should not be present in water meant for human consumption. It is generally assumed that higher the number of coliform organisms found in a 100ml sample, the higher the risk for waterborne disease.
Indicator organism
Indicator organisms are used to measure potential fecal contamination of environmental samples.  The presence of coliform bacteria, such as E. coli, in surface water is a common indicator of fecal contamination.  Coliform bacteria in water samples may be quantified using the most probable number (MPN) method, a probabilistic test which assumes cultivable bacteria meet certain growth and biochemical criteria.  If preliminary tests suggest that coliform bacteria are present at numbers in excess of an established cut-off (the Coliform Index), fecal contamination is suspected and confirmatory assays such as the Eijckman test are conducted.
Coliform bacteria selected as indicators of fecal contamination must not persist in the environment for long periods of time following efflux from the intestine, and their presence must be closely correlated with contamination by other fecal organisms.  Indicator organisms need not be pathogenic.
Non-coliform bacteria, such as Streptococcus bovis and certain clostridia may also be used as an index of fecal contamination.
Inductive transfer
Inductive transfer, or transfer learning, is the machine learning process of storing and applying knowledge gained from one problem or task to a different but related problem or task. For example, learning to walk could be used in learning to run, or learning to recognize  cars could be used in learning to recognize trucks.
This terminology was developed in reference to machine learning, although the underlying idea of transfer of learning has been studied in cognitive psychology for more than a century. The process is typically most effective in machine learning when learned knowledge is stored in relational or heirarchical structures.
Algorithms have been developed to apply transfer learning in Markov logic networks and Bayesian networks. Applications that have been studied include text classification, spam filtering, and urban combat simulation.

# See Also
Multi-task learning