Persius/hicric huggingface dataset:
Choroideremia
Choroideremia is an X-linked recessive retinal degenerative disease that leads to the degeneration of the choriocapillaris, the retinal pigment epithelium, and the photoreceptor of the eye.

# Pathophysiology
Choroideremia is caused by the deletion of the Rab escort protein 1 (REP1). Rab escort protein 2 (REP2) is 75% identical and can almost compensate for the loss of REP1. The REPs are essential for the prenylation of  Rab proteins. Studies have shown that there is a build up of unprenylated Rab27 in lymphoblasts from Choroideremia patients.

# Presentation
Generally, only men show symptoms of this disease, although in rare cases some women also acquire it.  Initially a person suffering from choroideremia has night blindness, which begins in youth.  As the disease progresses, a CHM sufferer loses their peripheral vision and depth perception, eventually losing all sight by middle age.  In some cases, a severe loss of acuity and color perception become evident as the disease progresses.
The link between the loss of REP1 and the build up of unprenylated Rab27 and the degeneration of the eye is unknown as yet.

# Prognosis
At this time, there is no treatment or cure for this disease.
Chromhidrosis

# Overview
Chromhidrosis is a rare condition characterized by the secretion of colored sweat. It is caused by the deposition of lipofuscin in the sweat glands. Cases of red, blue, green, yellow and black sweat have been reported. Usually chromhydrosis affects the apocrine glands. Chromhydrosis of the eccrine glands is rare, it occurs mainly after the ingestion of certain dyes or drugs.
Two glands produce sweat: eccrine and apocrine glands. Eccrine glands secrete a clear, odorless fluid that serves to regulate body temperature. Apocrine glands secrete a thick, milky sweat that, once broken down by bacteria, is the main cause of body odor.
Chromhidrosis is apocrine in origin. Although apocrine glands are found in the genital, axillary, areolar, and facial skin, chromhidrosis is reported only on the face, axillae, and breast areola. Lipofuscin pigment is responsible for the colored sweat. This pigment is produced in the apocrine gland, and its various oxidative states account for the characteristic yellow, green, blue, or black secretions observed in apocrine chromhidrosis.
In contrast, eccrine chromhidrosis is rare and occurs with ingestion of certain dyes or drugs, and pseudochromhidrosis occurs when clear eccrine sweat becomes colored on the surface of the skin as a result of extrinsic dyes, paints, or chromogenic bacteria.
Approximately 10% of people without the disease have colored sweat that is regarded as acceptable and within the normal range.
Pathophysiology: Lipofuscin is a yellowish brown pigment that is normally found in the cytoplasm of relatively nondividing cells (eg, neurons). In chromhidrosis, lipofuscins are found in a higher-than-normal concentration or a higher-than-normal state of oxidation in apocrine glands. However, why some glands experience these changes is unclear. This increased level of oxidation results in the green, blue, and even black sweat seen in chromhidrosis.
The yellow, green, and blue apocrine secretions produce a yellow fluorescence under a Wood lamp (UV 360 nm), whereas the dark brown and black apocrine secretions seldom autofluoresce. Substance P is also postulated to be an important neurotransmitter in this process.
Pseudochromhidrosis is of an extrinsic etiology in which a chemical on the surface of the skin reacts with eccrine secretions and produces the color transformation.
Frequency:
In the US: Incidence statistics are not available; the disease is rare. 
Internationally: Incidence statistics are not available; the disease is rare. 
Race: Apocrine chromhidrosis appears to be more common in blacks than in whites, but facial chromhidrosis is described only in whites.
Sex: No sexual predilection is reported.
Age: Chromhidrosis is noted after puberty, when the apocrine glands are activated.

# Diagnosis

## Physical Examination

### Skin
- Chromhidrosis. Adapted from Dermatology Atlas.
- Chromhidrosis. Adapted from Dermatology Atlas.
Chronotherapy

# Overview
People who suffer from Delayed Sleep Phase Syndrome are generally unable to reset their circadian rhythm by moving their bedtime and rising time earlier. In chronotherapy an attempt is made to move bedtime and rising time later and later each day, around the clock, until these times reach the number of hours of sleep per night an individual needs to be fully functional.  According to Michael B Russo, MD, the number of hours of sleep per night necessary for an individual to be fully functional is still unknown because the function of sleep has yet to be fully determined.  Some people claim full effectiveness with only 3-5 hours of sleep per night, while others admit to needing 8 (or more) hours of sleep per night to perform effectively.
While Chronotherapy has been successful for some, it is necessary to rigidly maintain the desired sleep/wake cycle thenceforth. Any deviation in schedule tends to allow the body clock to shift later again.
Here's an example of how Chronotherapy could work over a week's course of treatment, with the patient going to sleep three hours later every day until the desired sleep and waketime is reached.  This technique assumes that an individual can perform effectively with 8 hours of sleep per night. Shifting the sleep phase by 3 hours per day may not always be possible. Shorter increments of 1-2 hours are needed in such cases.
Example:
Whilst this technique can provide temporary respite from sleep deprivation, patients often find the desired sleep and waketimes soon slip, returning them to a state of delayed sleep onset within a few weeks or even days.  The desired pattern can be maintained - to a degree - by following a strictly disciplined timetable for sleeping and rising, but all too often this cannot be maintained, as the body returns to its previous pattern of late sleep onset, regardless of when the patient rises.
A modified chronotherapy (Thorpy et al in J Adolesc Health Care, 1988;9) is called controlled sleep deprivation with phase advance, SDPA. One stays awake one whole night and day, then goes to bed 90 minutes earlier than usual and maintains the new bedtime for a week. This process is repeated weekly until the desired bedtime is reached.

# Reverse chronotherapy
Sometimes, although extremely infrequently, "reverse" chronotherapy - i.e., gradual movements of bedtime and rising time earlier each day - has been used in treatment of patients with abnormally short circadian rhythms, in an attempt to move their bedtimes to later times of the day.  Because circadian rhythms substantially shorter than 24 hours are extremely rare, this type of chronotherapy has remained largely experimental, with very little large-scale study.
Clinical site

# Overview
A clinical site is a medical facility staffed with a clinical investigator (MD) and qualified for performing clinical research. To be qualified as a clinical site, strict regulations are to be adhered to. The foundations for these regulations are defined by the International Conference on Harmonisation of Technical Requirements for Registration of Pharmaceuticals for Human Use (ICH) and regulatory authorities, which set the guidelines for good clinical practice (GCP) at clinical sites.
Per ICH GCP 4.1.1 the investigator(s) should be qualified by education, training, and experience to assume responsibility for the proper conduct of the clinical trial, should meet all the qualifications specified by the applicable regulatory requirement(s), and should provide evidence of such qualifications through up-to-date curriculum vitae and/or other relevant documentation requested by the sponsor, the institutional review board/independent ethics committee (IRB/IEC), and/or the regulatory authority(ies).
Per ICH GCP 4.1.2 the investigator should be thoroughly familiar with the appropriate use of the investigational product(s), as described in the clinical protocol, in the current Investigator's Brochure, in the product information and in other information sources provided by the sponsor.
Per ICH GCP 4.1.3 the investigator should be aware of, and should comply with, GCP and the applicable regulatory requirements. Per ICH GCP 4.1.4 the investigator/institution should permit monitoring and auditing by the sponsor, and inspection by the appropriate regulatory authority(ies). Per ICH GCP 4.1.5 the investigator should maintain a list of appropriately qualified persons to whom the investigator has delegated significant trial-related duties.
Clitoromegaly

# Overview
Clitoromegaly (or macroclitoris ) is an abnormal enlargement of the clitoris (not to be confused with the normal enlargement of the clitoris seen during sexual arousal).
Although clitoromegaly denotes just a clitoris larger than expected (thus involving some uncertainty about what can be defined as normal), it is commonly seen as a congenital anomaly of the genitalia.

# Pathophysiology

## Gross Pathology
In Atlas of Human Sex Anatomy (1949) by Dr. Robert Latou Dickinson, the normal clitoris is defined as having a crosswise width of 3 to 4 mm. (0.12 - 0.16 inches) and a lengthwise width of 4 to 5 mm (0.16 - 0.20 inches). On the other hand, in Obstetrics and Gynecology medical literature, a frequent definition of clitoromegaly is when there is a CI of greater than 35 mm2 (0.05 inches2), which is almost twice the size given above for an average sized clitoral hood .

# Causes
Clitoromegaly is otherwise a rare condition and can be either present by birth or acquired later in life.
If present at birth, congenital adrenal hyperplasia can be one of the causes, since in this condition the adrenal gland of the female fetus produces additional androgens and the newborn baby has ambiguous genitalia which are not clearly male or female.

## Common Causes
In acquired clitoromegaly, the main cause is due to hormonal imbalance affecting the adult women, as in polycystic ovarian syndrome (PCOS) , arrhenoblastoma and Fraser syndrome.
Clitoromegaly may be acquired through use of anabolic steroids or testosterone supplements, both of which can cause enlargement of the clitoris. This occurs in Female to Male Transsexuals (FtM) after a period of hormone replacement therapy.  Like FtM transsexuals, female body-builders who use androgens may also experience enlargement of the clitoris and increases in libido.  Women who use testosterone for therapeutic reasons (treating low libido, averting osteoporosis, as part of an anti-depressant regimen, etc) may also experience some enlargement of the clitoris although the dosages warranted for these conditions is much lower.
Deliberately induced clitoris enlargement, as form of female genital body modification, is reported to be achieved through testosterone injections directly in the clitoris shaft.

# Diagnosis

## Symptoms
In the most pronounced cases, clitoromegaly is a symptom of intersexuality since the large clitoris resembles a penis (the different grade of genital ambiguity is commonly measured by the Prader classification  ranging, in ascending order of masculinisation, from 1: Female external genitalia with clitoromegaly through 5: Pseudo-Phallus looking like normal male external genitalia ).
Clomethiazole

# Overview
Clomethiazole (also called Chlormethiazole) is a sedative and hypnotic that is widely used in treating and preventing symptoms of acute alcohol withdrawal. It is a drug which is structurally related to thiamine (vitamin B1) but acts like a sedative, hypnotic, muscle relaxant and anticonvulsant. It is also used for the management of agitation, restlessness, short-term insomnia and Parkinson's disease in the elderly. In the U.S, it is sold under the brand, Distraneurin (AstraZeneca Pharmaceuticals) and in the U.K, Heminevrin (AstraZeneca Pharmaceuticals). Another brand name includes Nevrin (in Romania). The drug is marketed either a the freebase in an oily suspension containing 192mg (presumably 3 grains) as capsules or clomethiasole edisylate (ethane disulfonate) syrup.

# Pharmacology
Chlormethiazole acts on GABA receptors, which cause the release of the neurotransmitter GABA. GABA is a major inhibitory chemical in the brain involved in causing sleepiness and controlling anxiety and panic attacks. It acts by increasing the activity of GABA, thereby reducing the functioning of certain areas of the brain. This results in sleepiness, a decrease in anxiety and relaxation of muscles.  It also inhibits the enzyme alcohol dehydrogenase, which is responsible for breaking down alcohol in the body. This slows the rate of elimination of alcohol from the body, which helps to relieve the sudden effects of alcohol withdrawal in alcoholics.

# Adverse effects
When misused, chlormethiazole can cause tolerance and physical dependence. Abrupt withdrawal may result in symptoms similar to those of sudden withdrawal of alcohol.

# Trivia
-The Who drummer, Keith Moon, died from an overdose of chlormethiazole. The coroner discovered 32 partially digested capsules in his stomach.
-Abuse of this drug involves the freebase being placed in a syringe and injected. This must be done quickly as the freebase is known to melt plastic.
de:Clomethiazol
Clonorchiasis

# Overview
Clonorchiasis is an infectious disease caused by the Chinese liver fluke, Clonorchis sinensis.
Clonorchiasis is a known risk factor for the development of cholangiocarcinoma, a neoplasm of the biliary system.

# Gallery
- Illustration of the life cycle of Clonorchis sinensis, the causal agent of Clonorchiasis. From Public Health Image Library (PHIL). 
- Micrograph depicts an egg of the parasitic trematode, or flatworm, Clonorchis sinensis. From Public Health Image Library (PHIL). 
- Artifactual finding Clonorchis sinensis (400x mag). From Public Health Image Library (PHIL). 
- An egg from the Oriental, or Chinese liver fluke, Clonorchis sinensis (400x mag). From Public Health Image Library (PHIL). 
- Artifactual finding, which resembles a trematode egg of the Chinese, or oriental liver fluke, Clonorchis sinensis (400x mag). From Public Health Image Library (PHIL). 
- Illustration depicts a number of trematode species eggs, which have been found in human stool specimens. From Public Health Image Library (PHIL). 
- Single egg of a parasitic trematode, or fluke, from the genus, Opisthorchis (500x mag). From Public Health Image Library (PHIL).
Cluster decay
Cluster decay is a type of nuclear decay in which a radioactive atom emits a cluster of neutrons and protons heavier than an alpha particle.  This type of decay happens only in nuclides which decay predominatly by alpha decay, and occurs only a small percentage of the time in all cases.  Cluster decay is limited to heavy atoms which have enough nuclear energy to expel a portion of its nucleus.
Cluster decay was discovered in 1987 when researchers at Oxford University detected that 223Ra emits one 14C nucleus for every billion (109) alpha decays.
Cluster decay has an intermediate position between alpha decay (in which a nucleus spits out a 4He nucleus) and spontaneous fission in which a heavy nucleus splits into two large fragments and a variable number of neutrons.  In cluster decay the emitted particle is a light nucleus and the decay always emits the same particle.  More than 20 nuclei have been found which occasionally decay by emitting clusters.
Tritons and deuterons are also known as radioactive decay products. Helium-6 occasionally decays via deuteron emission and Helium-8 decays a small part of the time with a triton emission. It is possible that other exotic isotopes decay in these methods as helium is studied in particle accelerators to a great degree.
The known cluster emissions are as follows:
Co-amilofruse
Co-amilofruse (BAN) is a non-proprietary name used to denote a combination of amiloride and the formerly named frusemide (now the INN termed furosemide). Co-amilofruse in the treatment of fluid retension (oedema), either in the legs (peripheral edema) or on the lungs (pulmonary oedema). The stronger furosemide loop diuretic has a tendency to cause low potassium levels (hypokalaemia) that may be prevented by the potassium-sparing effects of amiloride.

# Formulation
Two strengths of co-amilofruse are available:
- 2.5 mg amiloride with 20 mg furosemide, BAN of Co-amilofruse 2.5/20 (brand name Frumil LS)
- 5 mg amiloride with 40 mg furosemide, BAN of Co-amilofruse 5/4-0 (brand name Frumil)
Co-fluampicil
Co-fluampicil is the British Approved Name, for the combination of ampicillin and flucloxacillin -lactam antibiotics (trade name Magnapen).

# Indication
Ampicillin is a moderate spectrum penicillin antibiotic with good cover against Group A streptococcal infection whilst Flucloxacillin is a narrow spectrum antibiotic with cover against Staphylococcus aureus. The combination covers the two most likely bacteria in cellulitis infections in the arm or leg.

# Formulations
As Co-fluampicil 250/250 capsules containing 250mg of each component, Co-fluampicil 125/125 syrup or as Co-fluampicil 250/250 powder for reconstruction for intravenous injection.

# Dosage
Typical oral dosage is Co-fluampicil 250/250 four times a day, doubled in severe infection and half the dose for children under 10 years.

# Side-effects
As per the individual components with stomach or bowel upset from the Flucloxacillin being the most common. Both parts are members of the penicillin family of antibiotics, and therefore should not be taken by patients allergic to penicillin. See Flucloxacillin for additional contraindications.
Cobb syndrome

# Overview
Cobb syndrome is a rare congenital disorder characterized by visible skin lesions with underlying spinal angiomas or arteriovenous malformations (AVMs). The skin lesions of Cobb syndrome typically are present as port wine stains or angiomas, but reports exist of angiokeratomas, angiolipomas, and lymphangioma circumscriptum. The intraspinal lesions may be angiomas or AVMs and occur at levels of the spinal cord corresponding to the affected skin dermatomes. They may in turn produce spinal cord dysfunction and weakness or paralysis.

# Historical Perspective
The disorder was first described by Berenbruch in 1890, but became widely known only after Cobb's report in 1915. Cobb syndrome is thought to be more common in males and have no racial prediliction, but only a few dozen cases are known. It is believed to be due to a sporadic mutation, since parents of affected children usually have no evidence of the disease.

# Diagnosis

## History and Symptoms
The disease is present at birth, but clinical manifestations are often not seen until later in life. Patients typically experience the sudden onset of pain, numbness, or weakness in their extremities as children or young adults. These symptoms may remit or remain stable and often can be localized below a specific dermatome. Symptoms tend to worsen over time either by discrete steps or continuously. Early development of weakness may portend a more aggressive course. Less commonly, weakness or bowel and bladder dysfunction may be presenting symptoms.
The major debility from Cobb syndrome is the onset of weakness, paresis, sensory loss, and loss of bowel and bladder control. A possible complication if treatment is delayed is Foix-Alajouanine disease or subacute necrotic myelopathy due to thrombosis in the spinal angioma.

## Physical Examination
Cutaneous lesions may be distributed anywhere in the dermatome, from midline back to abdomen. Midline back lesions may be associated with spina bifida. The cutaneous lesion may be very faint and may be more pronounced when the patient performs a Valsalva maneuver which increases abdominal pressure and causes preferential filling of the cutaneous angioma. Neurological examination will reveal weakness or paralysis and numbness or decreased sensation with a sharp upper cutoff.

# Related Chapters
- Klippel-Trenaunay-Weber syndrome
Cognitive map
Cognitive maps, mental maps, mind maps, cognitive models, or mental models are a type of mental processing (cognition) composed of a series of psychological transformations by which an individual can acquire, code, store, recall, and decode information about the relative locations and attributes of phenomena in their everyday or metaphorical spatial environment.
Tolman (1948) is generally credited with the introduction of the term 'cognitive map'. Here, 'cognition' can be used to refer to the mental models, or belief systems, that people use to perceive, contextualize, simplify, and make sense of otherwise complex problems. Cognitive maps have been studied in various fields, such as psychology, education, archaeology, planning, geography and management. As a consequence, these mental models are often referred to, variously, as cognitive maps, mental maps, scripts, schemata, and frames of reference.
Put more simply, cognitive maps are a method we use to structure and store spatial knowledge, allowing the "mind's eye" to visualize images in order to reduce cognitive load, and enhance recall and learning of information. This type of spatial thinking can also be used as a metaphor for non-spatial tasks, where people performing non-spatial tasks involving memory and imaging use spatial knowledge to aid in processing the task.
These can be abstract, flat or spatial representations of cognitive spaces. When these cognitive spaces are combined they can form a cognitive panorama. We can distinguish cognitive maps or cognitive spaces as being either "workbenches of the mind" (Baars) or "externally related workbenches of the mind" (Benking) as representations of the inside or outside.
The oldest known formal method of using spatial locations to remember data is the "method of loci". This method was originally used by students of rhetoric in ancient Rome when memorizing speeches. To use it one must first memorize the appearance of a physical location (for example, the sequence of rooms in a building).  When a list of words, for example, needs to be memorized, the learner visualizes an object representing that word in one of the pre-memorized locations. To recall the list, the learner mentally "walks through" the memorized locations, noticing the objects placed there during the memorization phase.
Cognitive maps may also be represented and assessed on paper or screen through various practical methods such as a concept map, sketch map, spider diagram, Hasse diagram or any variety of spatial representation.
A fuzzy cognitive map (FCM) is a cognitive map which can be processed based on fuzzy logic.
The neural correlates of a cognitive map (at least in rodents') brains has been speculated to be the place cell system in the hippocampus or the recently discovered grid cells in the entorhinal cortex.
Cohen's kappa

# Overview
Cohen's kappa coefficient is a statistical measure of inter-rater reliability.  It is generally thought to be a more robust measure than simple percent agreement calculation since  takes into account the agreement occurring by chance.  Cohen's kappa measures the agreement between two raters who each classify N items into C mutually exclusive categories.
The equation for  is:
where Pr(a) is the relative observed agreement among raters, and Pr(e) is the probability that agreement is due to chance.  If the raters are in complete agreement then  = 1.  If there is no agreement among the raters (other than what would be expected by chance) then   0.
The seminal paper introducing kappa as a new technique was published by Jacob Cohen in the journal Educational and Psychological Measurement in 1960.
Note that Cohen's kappa measures agreement between two raters only.  For a similar measure of agreement (Fleiss' kappa) used when there are more than two raters, see Fleiss (1981).

# Significance
Landis and Koch gave the following table for interpreting  \kappa values. This table is however by no means universally accepted;  Landis and Koch supplied no evidence to support it, basing it instead on personal opinion. It has been noted that these guidelines may be more harmful than helpful, as the number of categories and subjects will affect the magnitude of the value. The kappa will be higher when there are fewer categories.