Persius/hicric huggingface dataset:
Kendra's Law
Kendra's Law is a New York State law concerning involuntary outpatient commitment. This piece of legislation grants judges the authority to issue orders that require people receiving mental health services to take psychiatric drugs, regularly undergo psychiatric treatment, or both. Failure to comply could result in commitment for up to 72 hours.

# Background
Two similar subway assaults occurred in the New York City subway in 1999. In each, a man diagnosed with schizophrenia pushed a person into the path of an oncoming train. An assault by Julio Perez, age 43, caused the amputation of Edgar Rivera's legs. The assault by Andrew Goldstein, age 29, killed Kendra Webdale. Both men had been dismissed by psychiatric facilities with little or no medication. One of the men was homeless and the other had repeatedly sought a supervised living arrangement.
Kendra's law, introduced by Governor George E. Pataki, was created as a response to these incidents.  In 2005, the law was extended for 5 years. 

# Support
E. Fuller Torrey, founder of the Treatment Advocacy Center, lobbied heavily in support of of Kendra's Law.

# Opposition
Kendra's law is opposed for different reasons by many groups, most notably the Anti-Psychiatry movement and the New York Civil Liberties Union. Opponents say that the law has harmed the mental health system, because it can scare patients away from seeking treatment.  The implementation of the law is also criticized as being racially and socioeconomically biased.
Kennel cough
Kennel cough or tracheobronchitis is a highly contagious canine illness characterized by inflammation of the upper respiratory system.  It can be caused by viral infections such as canine distemper, canine adenovirus, canine parainfluenza virus, or canine respiratory coronavirus, or bacterial infections such as Bordetella bronchiseptica.  It is so named because the infection can spread quickly among dogs, such as in the close quarters of a kennel.

# Infection
Both viral and bacterial causes of kennel cough are spread through the air by infected dogs sneezing and coughing.  It can also spread through contact with contaminated surfaces and through direct contact.  It is highly contagious, even days or weeks after symptoms disappear.  Exposure occurs in environments where there are other dogs in proximity, such as pet stores, kennels, dog shows, and groomers.  Symptoms begin usually 3 to 5 days after exposure.  The disease can progress to pneumonia.

# Symptoms
Symptoms can include a harsh, dry hacking/coughing, retching, sneezing, snorting or gagging;in response to light pressing of the trachea or after excitement or exercise.  The presence of a fever varies from case to case.  The disease can last from 10-20 days.  Diagnosis is made by seeing these symptoms and having a history of exposure.

# Treatment and prevention
Antibiotics are given to treat any bacterial infection present.  Cough suppressants are used if the cough is not productive (nothing is being coughed up).  The prognosis is good.  Prevention is by vaccinating for canine adenovirus, distemper, parainfluenza, and Bordetella.  In kennels, the best prevention is to keep all the cages disinfected.  Most kennels will not board dogs without proof of vaccination.
Keratinocyte
The keratinocyte is the major cell type of the epidermis, making up about 90% of epidermal cells. The epidermis is divided into four or five layers (depending on the type of skin) based on keratinocyte morphology:
- stratum basale (at the junction with the dermis)
- stratum spinosum
- stratum granulosum
- stratum lucidum (only present in thick skin - i.e. palms of hand and soles of feet)
- stratum corneum
Keratinocytes originate in the basal layer from the division of keratinocyte stem cells. They are pushed up through the layers of the epidermis, undergoing gradual differentiation until they reach the stratum corneum where they form a layer of enucleated, flattened, highly keratinized cells called squamous cells. This layer forms an effective barrier to the entry of foreign matter and infectious agents into the body and minimises moisture loss.
Keratinocytes are shed and replaced continuously from the stratum corneum. The time of transit from basal layer to shedding is approximately one month. Although that approximate time frame can be accelerated in conditions of keratinocyte hyperproliferation, such as psoriasis.

# See Also
- Amphiregulin
de:Keratinozyt
lt:Keratinocitas
Keratoglobus
Keratoglobus (from Greek: kerato- horn, cornea; and globus round), is a degenerative non-inflammatory disorder of the eye in which structural changes within the cornea cause it to become extremely thin and change to a more globular shape than its normal gradual curve. It causes corneal thinning, primarily at the margins, resulting in a spherical, slightly enlarged eye.

# Epidemiology
It is a much rarer condition than keratoconus, which is the most common dystrophy of the cornea. Similar to keratoconus it is typically diagnosed in the patient's adolescent years and attains its most severe state in the twenties and thirties.

# Pathophysiology
Keratoglobus is a little-understood disease with an uncertain cause, and its progression following diagnosis is unpredictable. If afflicting both eyes, the deterioration in vision can affect the patient's ability to drive a car or read normal print. It does not however lead to blindness per se.

# Prognosis
Keratoglobus continues to be a somewhat mysterious disease, but it can be successfully managed with a variety of clinical and surgical techniques. The patient is at risk for globe perforation because the thinned out cornea is extremely weak.

# Surgical treatment
Further progression of the disease usually leads to a need for surgery because of extreme thinning of the cornea.  Primarily, large size penetrating keratoplasty has been advocated. Recent additions of techniques specifically for keratoglobus include the "tuck procedure", whereby a 12 mm corneo-scleral donor graft is taken and trimmed at its outer edges. A host pocket is formed at the limbal margin and the donor tissue is "tucked" into the host pocket.
Kerley lines

# Overview
Kerley lines are a sign seen on chest x-rays with interstitial pulmonary edema. They are thin linear pulmonary opacities caused by fluid or cellular infiltration into the interstitium of the lungs. They are suggestive for the diagnosis of congestive heart failure, but are also seen in various non-cardiac conditions such as pulmonary fibrosis, interstitial deposition of heavy metal particles or carcinomatosis of the lung. Chronic Kerley B lines may be caused by fibrosis or hemosiderin deposition caused by recurrent pulmonary oedema.

# Kerley A lines
Kerley A lines are longer (at least 2 cm) unbranching lines coursing diagonally from the periphery toward the hila in the inner half of the lungs. They are caused by distension of anastomotic channels between peripheral and central lymphatics of the lungs. Kerley A lines are less commonly seen than Kerley B lines. Kerley A lines are never seen without Kerley B or C lines also present.

# Kerley B lines
Kerley B lines are short parallel lines at the lung periphery. These lines represent distended interlobular septa, which are usually less than 1 cm in length and parallel to one another at right angles to the pleura. They are located peripherally in contact with the pleura, but are generally absent along fissural surfaces.  They may be seen in any zone but are most frequently observed at the lung bases at the costophrenic angles on the PA radiograph, and in the substernal region on lateral radiographs.

# Kerley C lines
Kerley C lines are the least commonly seen of the Kerley lines. They are short, fine "spider web" polygonal opacities distributed primarily in a peripheral and subpleural location. They may represent thickening of anastomotic lymphatics or superimposition of many Kerley B lines. Keyley C lines may be associated with conditions such as pulmonary fibrosis and hypersensitivity pneumonitis.

# Diagnostic Findings
- Plain film: Mitral stenosis, Kerley B lines
- Plain film: Mitral stenosis, Kerley B lines
- Plain film: Mitral stenosis, Kerley B lines
- Acute heart failure due to atrial fibrillation with Kerley B lines. (Image courtesy of Radiopaedia.org)
- Pulmonary edema with Kerley B lines. (Image courtesy of Radiopaedia.org)
- Heart failure with Kerley B lines. (Image courtesy of Radiopaedia.org)
- Pulmonary congestion in heart failure with Kerley B lines. (Image courtesy of Radiopaedia.org)
Kernel trick
In machine learning, the kernel trick is a method for using a linear classifier algorithm to solve a non-linear problem by mapping the original non-linear observations into a higher-dimensional space, where the linear classifier is subsequently used; this makes a linear classification in the new space equivalent to non-linear classification in the original space.
This is done using Mercer's theorem, which states that any continuous, symmetric, positive semi-definite kernel function K(x, y) can be expressed as a dot product in a high-dimensional space.
More specifically, if the arguments to the kernel are in a measurable space X, and if the kernel is positive semi-definite  i.e.
for any finite subset  {x1, ..., xn} of X and subset {c1, ..., cn} of objects (typically real numbers)  then there exists a function (x) whose range is in an inner product space of possibly high dimension, such that
The kernel trick transforms any algorithm that solely depends on the dot product between two vectors. Wherever a dot product is used, it is replaced with the kernel function. Thus, a linear algorithm can easily be transformed into a non-linear algorithm. This non-linear algorithm is equivalent to the linear algorithm operating in the range space of . However, because kernels are used, the  function is never explicitly computed. This is desirable, because the high-dimensional space may be infinite-dimensional (as is the case when the kernel is a Gaussian).
The kernel trick was first published by Aizerman et al.
It has been applied to several kinds of algorithm in machine learning and statistics, including:
- Perceptrons
- Support vector machines
- Principal components analysis
- Canonical correlation analysis
- Fisher's linear discriminant analysis
- Clustering
The origin of the term kernel trick is not known.
Ketobemidone

# Overview
Ketobemidone is a powerful opioid analgesic. Its potency is equal to morphine, and it also has some NMDA-antagonist properties. This makes it useful for some types of pain that don't respond well to other opioids.
It is used for all types of severe pain, such as postoperative, cancer, kidney stones and fractures.

# History
It was first synthesized in 1942 by Eisleb. The first study of it in man was published in 1946, and it was introduced in clinical medicine shortly after.

# Chemistry
Ketobemidone is 1-methyl-4-(3-hydroxyphenyl)-4-propionylpiperidine.  It is usually available as the hydrochloride, which is a white powder. It is synthesized by alkylating (3-methoxyphenyl)acetonitrile with bis(2-chloroethyl)methylamine, followed by reaction with ethylmagnesiumbromide, and finally O-demethylation with hydrobromic acid.

# Pharmacology
Experiments on former addicts indicated it was more addictive than other opioids, so in 1954 the Economic and Social Council took a resolution urging governments to stop manufacture and use of ketobemidone
. As a result ketobemidone is mostly used in the Scandinavian countries, with Denmark topping the statistics
. This result was not in agreement with clinical observations, and another study in 1958 didn't find it more addictive than morphine. That study noticed that while for morphine the dose for euphoria is the same as that for analgesia, for ketobemidone the analgesic dose was well below the euphoric dose.
Analgesia after 5-10 mg orally or 5-7.5 mg intravenously lasts 3-5 hours. Ketobemidone is also available in preparations with a spasmolytic, which can improve the analgesia.
Ketobemidone is mainly metabolised by conjugation of the phenolic hydroxyl group, and by N-desmethylation. Only about 16% is excreted unchanged.
Pfizer manufactures ketobemidone under the tradenames Ketogan and Ketorax. It is available as tablets, suppositories and injection fluid. A sustained release formulation exists sold as Ketodur in some countries containing 10 or 25 mg ketobemidone.
Killip class

# Overview
The Killip classification is a system used in individuals with an acute myocardial infarction (heart attack), in order to risk stratify them.  Individuals with a low Killip class are less likely to die within the first 30 days after their myocardial infarction than individuals with a high Killip class.

# The study
The study was a case series with unblinded, unobjective outcomes, not adjusted for confounding factors, nor validated in an independent set of patients. The setting was the coronary care unit of a university hospital in the USA.
250 patients were included in the study (aged 28 to 94; mean 64, 72% male) with a myocardial infarction. Patients with a cardiac arrest prior to admission were excluded.
Patients were ranked by Killip class in the following way:
- Killip class I includes individuals with no clinical signs of heart failure.
- Killip class II includes individuals with rales or crackles in the lungs, an S3 gallop, and elevated jugular venous pressure.
- Killip class III describes individuals with frank acute pulmonary edema.
- Killip class IV describes individuals in cardiogenic shock or hypotension (measured as systolic blood pressure lower than 90 mmHg), and evidence of peripheral vasoconstriction (oliguria, cyanosis or sweating).

# Conclusions
Within a 95% confidence interval the patient outcome was as follows:
- Killip class I: 81/250 patients; 32% (27 to 38%). Mortality rate was found to be at 6%.
- Killip class II: 96/250 patients; 38% (32 to 44%). Mortality rate was found to be at 17%.
- Killip class III: 26/250 patients; 10% (6.6 to 14%). Mortality rate was found to be at 38%.
- Killip class IV: 47/250 patients; 19% (14 to 24%). Mortality rate was found to be at 81%.
The Killip-Kimball classification has played a fundamental role in classic cardiology, having been used as a stratifying criteria for many other studies. Worsening Killip class has been found to be independently associated with increasing mortality in several studies.
Killip class 1 and no evidence of hypotension or bradycardia, in patients presenting with acute coronary syndrome, should be considered for immediate IV beta blocker therapy.
Koilocytosis

# Overview
Koilocytosis (a.k.a koilocytotic atypia) is cell changes caused by HPV. By microscopic observation, the cells have halo nuclei. These changes are neither precancerous nor dangerous in and of themselves. Koilocytosis often co-exists with dysplasia, and it's the dysplasia that could lead to cancer, and thus, needs treatment.

# Diagnosis
A distinctive abnormality in the appearance of the cells of the skin of the cervix, in which some of the nuclei are surrounded by tiny "halos."
Most commonly, these changes occur in the presence of HPV (Human Papilloma Virus) but occasionally are associated with more serious problems such a cervical dysplasia or even early malignancy.
Patients demonstrating koilocytosis who previously had normal Pap smears are ideally evaluated with colposcopy and cervical biopsies to determine the source of the koilocytes, although such evaluation can usually safely wait for weeks to a few months if necessary because of operational requirements.
Kunjin virus

# Overview
Kunjin virus (KUNV) is a zoonotic virus of the family Flaviviridae and the genus Flavivirus.  It is a subtype of West Nile virus endemic to Oceania.

# History
The virus was first isolated from Culex annulirostris mosquitoes in Australia in 1960.
The name of Kunjin virus derives from an Aboriginal clan living on the Mitchell River close to where the virus was first isolated in Kowanyama, northern Queensland.

# Virology
Kunjin virus is a zoonotic virus of the family Flaviviridae and the genus Flavivirus. It is an arbovirus which is transmitted by mosquitoes and is part of the Japanese encephalitis serological complex. It is antigenically and genetically very similar to West Nile virus and in 1999 was reclassified as a subtype of WNV. Its genome is positive-sense single stranded RNA made up of 10,644 nucleotides.

# Symptoms and Prognosis
Infection with the virus often causes no symptoms, but it can lead to either an encephalitic disease or a non-encephalitic disease. Non-encephalitic Kunjin virus disease can cause symptoms including acute febrile illness, headache, arthralgia, myalgia, fatigue and rash. Kunjin virus encephalitis features acute febrile meningoencephalitis.
Both forms of Kunjin virus disease are milder than the diseases caused by West Nile virus and Murray Valley encephalitis virus.

# Transmission and control
Kunjin virus is transmitted by mosquito vectors, especially the Culex annulirostris. They pass the virus to waterbird reservoir hosts; a major example is the nankeen night heron. It is also passed to horses and humans. The virus been isolated in mosquitoes in South East Asia but in humans, only in Australia. It has been found all over Australia and is particularly prevalent in areas near wetlands and rivers.
The control of Kunjin virus is achieved in the same ways as other mosquito-borne diseases. These include individuals using insect repellent, wearing long-sleeved clothes and avoiding areas where mosquitoes are particularly prevalent. Habitat control by government agencies can take the form of reducing the amount of water available for mosquitoes to breed in, and the use of insecticides. There is no available vaccine against Kunjin virus.

# Use in medicine
In 2005, scientists at the Queensland Institute of Medical Research and the University of Queensland found that modified Kunjin virus particles injected into mice were able to deliver a gene into the immune system targeting cancer cells. This research may lead to vaccines  for cancer and HIV.
Kupffer cell

# Overview
Kupffer cells, also  known as Browicz-Kupffer cells, are specialized macrophages located in the liver that form part of the reticuloendothelial system (aka: mononuclear phagocyte system). The cells were first observed by Karl Wilhelm von Kupffer in 1876. The scientist called them "sternzellen" (star cells or stellate cells) but thought falsely that they were an integral part of the endothelium of the liver blood vessels and that they originated from it. In 1898, after several years of research, Tadeusz Browicz, a polish sciencist, identified them correctly as macrophages. 
Their development begins in the bone marrow with the genesis of promonocytes and monoblasts into monocytes and then on to peripheral blood monocytes completing their differentiation into Kupffer cells.
The primary function of Kupffer cells is to recycle old red blood cells that no longer are functional. The red blood cell is broken down by phagocytic action and the hemoglobin molecule is split.  The globin chains are reutilized while the iron containing portion or heme is further broken down into iron which is reutilized and bilirubin, which is conjugated with glucuronic acid within hepatocytes and secreted into the bile.
Helmy et al. identified a receptor present in Kupffer cells, the complement receptor of the immunoglobulin family (CRIg). Mice without CRIg could not clear complement system-coated pathogens. CRIg is conserved in mice and humans and is a critical component of the innate immune system.
Kynureninase
Kynureninase or L-Kynurenine hydrolase (KYNU) (EC 3.7.1.3) is a PLP dependent enzyme that catalyses the cleavage of kynurenine (Kyn) into anthranilic acid (Ant). It can also act on 3hKyn (to produce 3hAnt) and some other (3-arylcarbonyl)-alanines. Humans express one kynureninase enzyme that is encoded by the KYNU gene located on chromosome 2.
KYNU is part of the pathway for the catabolism of Trp and the biosynthesis of NAD cofactors from tryptophan (Trp).
Kynureninase catalyzes the following reaction:
- L-kynurenine + H2O = anthranilate + L-alanine

# Structure
Kynureninase belongs to the class V group of aspartate aminotransferase superfamily of structurally homologous pyridoxal 5'-phosphate (PLP) dependent enzymes. To date, two structures of human kynureninase have determined by X-ray diffraction with resolutions of 2.0 and 1.7 A. Forty percent of the amino acids are arranged in an alpha helical and twelve percent are arranged in beta sheets. Docking of the kynurenine substrate into the active site suggests that Asn-333 and His-102 are involved in substrate binding.

# Function
In KYNU reaction, PLP facilitates C-C bond cleavage. The reaction follows the same steps as the transamination reaction but does not hydrolyze the tautomerized Schiff base. The proposed reaction mechanism involves an attack of an enzyme nucleophile on the carbonyl carbon (C) of the tautomerized 3hKyn-PLP Schiff base. This is followed by C-C bond cleavage to generate an acyl-enzyme intermediate together with a tautomerized Ala-PLP adduct. Hydrolysis of the acyl-enzyme then yields 3hAnt.
LOC100287387
LOC100287387 is a protein that in humans is encoded by the gene LOC100287387. The function of the protein is not yet understood in the scientific community. The gene is located on the q arm of chromosome 2.

# Gene
The human LOC100287387 gene is located on the minus strand of the q arm of chromosome 2 at 2q37.3. It overlaps the TWIST2 gene family on the plus strand of chromosome 2. The gene is formed by three exons, with two introns near the start codon.

# mRNA
There are no alternative splicings of the LOC100287387 gene (isoforms).

# Protein
The LOC100287387 protein is formed by a 423 amino acid peptide sequence.  The molecular mass is 44.4 kdal, and the isoelectric point is 10.77.  There is a G-patch domain and a short domain of unknown function within the peptide sequence. There are many predicted modification sites within the amino acid sequence including cAMP- dependent phosphorylation sites (CampP), casein kinase 2 (CK2), and protein kinase C (PKC) phosphorylation sites, O-linked beta-N-acetylglucosamine sites, and a sumoylation site. The predicted secondary structure of the protein includes 8 short alpha-helices (15.6% of the protein), 14 short extended strands (12.1%), and the rest as random coils (72%).

# Expression
In humans, there is low expression of LOC100287387 in all tissues. Highest expression is in the skin and central nervous system tissue such as the pons, superior cervical ganglion, trigeminal ganglion, and globus pallidus. However, expression was inconsistent among patients.

# Regulation
The promoter region of the LOC100287387 gene contains binding sites for many transcription factors which affect transcription levels of the gene. Within the promoter region, there are three TFIIB binding sites (initiates transcription), a cysteine-serine-rich nuclear protein 1 site (an activator), a Kruppel-like zinc finger protein 219 site (repressor), a stimulating protein 1 site (activator), and many more.

# Homology
Orthologs to the human LOC100287387 gene are found only in mammals, and the protein sequence is not highly conserved. Conservation is highest in primates, and falls drastically among other mammals. Conservation between species is highest at the nuclear localization signal and towards the end of the coding sequence at the G Patch domain and DUF308 which indicates these are the most functionally important parts of the sequence.
There are no paralogs of the human gene LOC100287387.

# Function
The protein contains a nuclear localization signal, and most likely acts in the nucleus. There are no confirmed protein interactions or associations to diseases.