Persius/hicric huggingface dataset:
kappa Opioid receptor
The -Opioid receptors are a class of opioid receptors with dynorphins as the primary endogenous ligands, and ketazocine as a potent selective exogenous ligand. There are three variants: 1, 2, and 3. The -opioid receptor mediates the action of the dissociative hallucinogenic drug and highly selective agonist salvinorin A and the hallucinogenic side effects of opioids such as pentazocine.

# Effects
It has long been believed that kappa-opioid receptor agonists are dysphoric. This misconception traces back to early articles in the 1980s about human tests with -opioid receptor agonists. It was stated that:
"Both doses of ketocyclazocine substantially elevated scores on the LSD subscale of the ARCI as did the high dose of cyclazocine (fig. 2C). Morphine failed to increase scores significantly on this scale which measures dysphoria."
It is now widely accepted that -opioid receptor (partial) agonists have hallucinogenic ("psychotomimetic") effects, as exemplified by salvinorin A. These effects are generally undesirable in medicinal drugs and could have had frightening or disturbing effects in the tested humans, but they are not per se dysphoric. It is thought that the hallucinogenic effects of drugs such as butorphanol, nalbuphine, and pentazocine serve to limit their opiate abuse potential. In the case of salvinorin A, a structurally novel neoclerodane diterpene -opioid receptor agonist, these hallucinogenic effects are sought after.  While salvinorin A is considered a hallucinogen, its effects are qualitatively different than those produced by the classical psychedelic hallucinogens such as LSD or mescaline.
Activation of the -opioid receptor appears to antagonize many of the effects of the  opioid receptor.
Kappa ligands are also known for their characteristic diuretic effects, due to their negative regulation of antidiuretic hormone (ADH).
Kappa agonism is neuroprotective against hypoxia/ischemia; as such, kappa receptors may represent a novel therapeutic target.

# Location
 receptors are located in the periphery by pain neurons, in the spinal cord and in the brain.

# Reversal
Non-specific opioid receptor antagonists (e.g., naloxone) as well as the mixed opioid agonist/antagonist buprenorphine can be used to reverse the effects of kappa agonists.
Kappa opioid receptor
The -Opioid receptors are a class of opioid receptors with dynorphins as the primary endogenous ligands, and ketazocine as a potent selective exogenous ligand. There are three variants: 1, 2, and 3.

# Effects
It has long been believed that kappa-opioid receptor agonists are dysphoric. This misconception traces back to early articles in the 1980s about human tests with -opioid receptor agonists. It was stated that:
"Both doses of ketocyclazocine substantially elevated scores on the LSD subscale of the ARCI as did the high dose of cyclazocine (fig. 2C). Morphine failed to increase scores significantly on this scale which measures dysphoria."
It is now widely accepted that -opioid receptor (partial) agonists have hallucinogenic ("psychotomimetic") effects, as exemplified by salvinorin A. These effects are generally undesirable in medicinal drugs and could have had frightening or disturbing effects in the tested humans, but they are not per se dysphoric. It is thought that the hallucinogenic effects of drugs such as butorphanol, nalbuphine, and pentazocine serve to limit their opiate abuse potential. In the case of salvinorin A, a structurally novel neoclerodane diterpene -opioid receptor agonist, thes hallucinogenic effects are sought after.  While salvinorin A is considered a hallucinogen, its effects are qualitatively different than those produced by the classical psychedelic hallucinogens such as LSD or mescaline. 
These receptors are involved with analgesia.
Kappa ligands are also known for their characteristic diuretic effects, due to their negative regulation of antidiuretic hormone (ADH).
Kappa agonism is neuroprotective against hypoxia/ischemia; as such, kappa receptors may represent a novel therapeutic target.

# Location
 receptors are located in the periphery by pain neurons, in the spinal cord and in the brain.

# Reversal
Non-specific opioid receptor antagonists (e.g., naloxone) as well as the mixed opioid agonist/antagonist buprenorphine can be used to reverse the effects of kappa agonists.
Kato-Katz thick smear

# Overview
Kato-Katz thick smear is the classic and most commonly used method for identification of schistosome eggs in stool.

# Procedure
- In Kato-Katz thick smear technique, a stool sample is obtained and a small amount is passed through a screen.
- Approximately 50 mg of sieved stool is placed on a slide and covered with a glycerin-soaked cellophane cover slip.
- Schistosome eggs, if present, are counted and multiplied by 20 to obtain the number of eggs per gram of stool.
Kayser-Fleischer ring

# Overview
Kayser-Fleischer rings are dark rings that appear to encircle the iris of the eye. Synonyms include Gowers' chorea, hepatolenticular degeneration, or Westphal-Struempell pseudosclerosis.

# Differential Diagnosis
Ceruloplasmin deficiency (synonyms include Ferroxidase deficiency, Aceruloplasminemia, Caeruloplasmin deficiency)

# Physical Examination

## Eye
The rings, which consist of copper deposits where the cornea meets the sclera, in Descemet's membrane, first appear as a crescent at the top of the cornea. Eventually, a second crescent forms below, at 6 o'clock, and ultimately completely encircles the cornea.
In later stages, the brownish rings can be seen with the naked eye. In earlier stages, an optometrist's or ophthalmologist's slit lamp reveals the golden brown or greenish-yellow crescents.

# Associations
Kayser-Fleischer rings are a sign of Wilson's disease, which involves abnormal copper handling by the liver resulting in copper accumulation in the body and is characterised by cerebral degenerative changes, liver cirrhosis, splenomegaly, involuntary movements, muscle rigidity, psychic disturbances, and dysphagia.
Kayser-Fleischer rings also appear in cases of chronic copper poisoning, as sometimes happens when children are fed milk warmed in copper or brass pots or when drinking water contains high levels of dissolved copper.
Chronic copper poisoning causes symptoms similar to Wilson's disease, including anemia and liver and kidney damage.
Symptoms of acute copper toxicity include nausea, vomiting, and diarrhea and can result in anemia, severe liver damage and death.
Kearns-Sayer syndrome
Synonyms and Key Words: Kearns Syndrome,  Kearn-Sayre Mitochondrial Cytopathy,  Kearns' Syndrome,  Kearns-Sayre-Shy-Daroff Syndrome

# Overview
Kearns-Sayer syndrome is a mitochondrial disorder featuring the triad of: 
- Chronic progressive external ophthalmoplegia
- Cardiomyopathy with heart block
- Retinitis pigmentosa

# Diagnosis
Disease onset is in the first or second decade.
Diagnostic features include:
- Elevated CSF protein
- Sensorineural deafness
- Seizures
- Pyramidal signs
- Ragged-red fibers are found on muscle biopsy.
-  Adams et al., Principles of Neurology, 6th ed, p984
Kearns-Sayre syndrome
Kearns-Sayre syndrome (abbreviated KSS) is a disease caused by a 5,000 base deletion in the mitochondrial DNA. As such, it is a rare genetic disease in that it can be heteroplasmic, that is, more than one genome can be in a cell at any given time.  As with all mitochondrial diseases, it can only be maternally inherited.
Kearnes-Sayre syndrome starts before the age of 20.

# Presentation
Its expression is systemic, but many of the most common expressions are in the eyes, with ophthalmoplegia and retinal degeneration, specifically retinitis pigmentosa, common features.
Other characteristic features of are dysphagia, proximal weakness, hearing loss, cerebellar ataxia and cardiac conduction defects.

# Prognosis
There is no treatment for Kearnes-Sayre syndrome as of now.
In general, only palliative medications are available to sufferers in order to help relieve the symptoms of the disease.

# Eponym
It is named for Thomas Kearns and George Sayre.
Ketoacidosis overview

# Overview
Ketoacidosis is a type of metabolic acidosis which is caused by high concentrations of ketone bodies, formed by the deamination of amino acids, and the breakdown of fatty acids.

# Pathophysiology
Ketoacidosis occurs when cells do not have sufficient glucose to meet their metabolic demands.  Instead, ketone bodies are produced for energy via the metabolism of fatty acids.  Acidity results from the dissociation of the H+ ion at physiological pH of metabolic ketone bodies such as acetoacetate, and -hydroxybutyrate.

# Differentiating Ketoacidosis from other Diseases
Ketoacidosis should not be confused with ketosis, which is one of the body's normal processes for the metabolism of body fat. In ketoacidosis, the accumulation of keto acids is so severe that the pH of the blood is substantially decreased.
Kleine-Levin syndrome

# Overview
Kleine-Levin Syndrome, or KLS, is a rare disorder characterized by the need for excessive amounts of sleep (hypersomnia), (e.g. up to 20 hours a day); excessive food intake (compulsive hyperphagia); and an abnormally uninhibited sexual drive. Adolescent males are the predominant victims of the disorder.

# Presentation
Individual sufferers may often become irritable, lethargic, and/or apathetic. KLS patients may appear disoriented and report hallucinations. Symptoms are cyclical; with days to weeks (even up to months) of suffering interspersed by weeks or months (even up to years) symptom-free. Although resolution of the disorder may occur for some in later life, this is not universal.

# Causes
While some researchers speculate of a hereditary predisposition; others believe the condition may be the result of an autoimmune disorder. Both proposals need not be mutually exclusive with the result being a malfunction of the portion of the brain that helps to regulate functions such as sleep, appetite, and body temperature (hypothalamus).
Similarities between KLS and Kluver-Bucy syndrome (another rare condition characterized by hyperphagia, hypersexuality, and emotional blunting) may warrant further attention.

# Treatment
There is no definitive treatment for Kleine-Levin syndrome. Stimulants, including amphetamines, methylphenidate, imipramine and modafinil, administered orally, are used to treat sleepiness. Because of similarities between Kleine-Levin syndrome and certain mood disorders, lithium and carbamazepine may be prescribed. Responses to treatment have often been limited. This disorder needs to be differentiated from cyclic re-occurrence of sleepiness during the premenstrual period in teenage girls that may be controlled with hormonal contraception. 

# Eponym
It is named for Willi Kleine and Max Levin.
Klippel-Feil syndrome

# Overview
Klippel-Feil syndrome is a rare disorder, initially reported in 1912 by Maurice Klippel and Andre Feil from France, characterized by the congenital fusion of any 2 of the 7 cervical vertebrae.

# Causes
It is caused by a failure in the normal segmentation or division of the cervical vertebrae during the early weeks of fetal development.

# Presentation
The most common signs of the disorder are short neck, low hairline at the back of the head, and restricted mobility of the upper spine. Associated abnormalities may include scoliosis (curvature of the spine), spina bifida, anomalies of the kidneys and the ribs, cleft palate, respiratory problems, and heart malformations. The disorder also may be associated with abnormalities of the head and face, skeleton, sex organs, muscles, brain and spinal cord, arms, legs, and fingers.

# Classification
A classification scheme for Klippel-Feil syndrome was proposed in 1919 by Andre Feil, which accounted for cervical, thoracic, and lumbar spine malformations. 
However, recently, Dino Samartzis and colleagues in 2006 proposed 3 classification-types that specifically addressed the cervical spine anomalies and their associated cervical spine-related symptoms, with additional elaboration on various time-dependent factors regarding this syndrome. 

# Treatment
Treatment for Klippel-Feil syndrome is symptomatic and may include surgery to relieve cervical or craniocervical instability and constriction of the spinal cord, and to correct scoliosis. Physical therapy may also be useful.

# Prognosis
The prognosis for most individuals with KFS is good if the disorder is treated early and appropriately.  Activities that can injure the neck should be avoided. Anomalies associated with the syndrome can be fatal if not treated, or if found too late to be treatable.

# Notable cases
The 18th Dynasty Egyptian pharaoh Tutankhamun is believed by some to have suffered from Klippel-Feil syndrome, though others dispute this claim.
Ligase chain reaction

# Overview
The ligase chain reaction (LCR) is a nucleic acid amplification technique. While the better-known PCR carries out the amplification by polymerizing nucleotides, LCR instead amplifies the nucleic acid used as the probe. For each of the two DNA strands, two partial probes are ligated to form the actual one; thus, LCR uses two enzymes: a DNA polymerase and a DNA ligase. Each cycle results in a doubling of the target nucleic acid molecule. A key advantage of LCR is greater specificity as compared to PCR..

# Target conditions
It has been widely used for the detection of single base mutations, as in genetic diseases.
LCR and PCR may be used to detect gonorrhea and chlamydia, and may be performed on first-catch urine samples, providing easy collection and a large yield of organisms. Endogenous inhibitors limit the sensitivity, but if this effect could be eliminated, LCR and PCR would have clinical advantages over any other methods of diagnosing gonorrhea and chlamydia.
Loey's Dietz syndrome
Synonyms and keywords: LDS

# Overview
Loeys-Dietz syndrome is a recently-discovered autosomal dominant genetic syndrome which has many features similar to Marfan syndrome, but which is caused by mutations in the genes encoding transforming growth factor beta receptor 1 (TGFBR1) or 2 (TGFBR2).

# Historical Perspective
It was identified and characterized by American physician Harry C. Dietz and Belgian physician Bart L. Loeys, for whom it is named.

# Classification
There are currently two forms of Loeys-Dietz syndrome which are further subdivided into another two forms based upon the genetic abnormality as shown in the table below:

# Pathophysiology

## Associated Conditions
- Congenital heart diseases including patent ductus arteriosus (connection between the aorta and the lung circulation) and atrial septal defect (connection between heart chambers)
- Abnormal junction of the brain and medulla (Arnold-Chiari malformation)
- Bicuspid aortic valves

# Differentiating Loey's Dietz Syndrome from other Disorders
Many of the physical findings typical in Loeys-Dietz syndrome are also found in Marfan syndrome cases, including increased risk of ascending aortic aneurysm and aortic dissection, abnormally long limbs and fingers, and dural ectasia (a gradual stretching and weakening of the dura mater that can cause abdominal and leg pain).  However, it also has some additional traits not typical of Marfan patients, including widely spaced eyes, a split uvula in the back of the throat, and skin findings such as easy bruising or abnormal scars.

# Diagnosis

## Physical Examination

### General Appearance
- Scoliosis

### Skin
- Translucency of the skin with velvety texture

### Head
- Widely spaced eyes (orbital hypertelorism)
- Cleft palate or bifid uvula (a split in the tissue that hangs down in the back of the throat)

### Cardiac
- Indented or protruding chest wall (pectus excavatum or pectus carinatum)

### Extremities
- Contractures of fingers and toes (camptodactyly)
- Long fingers and lax joints
- Club foot
- Premature fusion of the skull bones (craniosynostosis)
- Joint hypermobility

## Imaging Findings
Aortic and arterial aneurysms/dissections with tortuosity (corkscrew structure) of the arteries.

# Treatment
As there is no known cure, Loeys-Dietz syndrome is a lifelong condition. Due to the high risk of death from aortic aneurysm rupture, patients should be followed closely to monitor aneurysm formation, which can then be corrected with vascular surgery.
Previous research in laboratory mice has suggested that the angiotensin II receptor antagonist losartan, which appears to block TGF-beta activity, can slow or halt the formation of aortic aneurysms in Marfan syndrome. A large clinical trial sponsored by the National Institutes of Health is currently underway to explore the use of losartan to prevent aneurysms in Marfan syndrome patients. Both Marfan syndrome and Loeys-Dietz syndrome are associated with increased TGF-beta signaling in the vessel wall. Therefore, losartan also holds promise for the treatment of Loeys-Dietz syndrome.
Ladislaus Bortkiewicz

# Overview
Ladislaus Josephovich Bortkiewicz (August 7, 1868 - July 15, 1931) was a Russian economist and statistician of Polish descent. Some of his works in German language are published using the name Ladislaus von Bortkewitsch
Bortkiewicz was born in St. Petersburg, Imperial Russia (today Russia) where he graduated in law in 1890.
In 1898 he published a book about the Poisson distribution, titled The Law of Small Numbers. In this book he first noted that events with low frequency in a large population follow a Poisson distribution even when the probabilities of the events varied. It was that book that made the Prussian cavalry horse-kick data famous. The data give the number of soldiers killed by being kicked by a horse each year in each of 14 cavalry corps over a 20-year period.  Bortkiewicz showed that those numbers follow a Poisson distribution. The book also examined data on child-suicides.  Some historians of mathematics have even argued that the Poisson distribution should have been named the "Bortkiewicz distribution."
Bortkiewicz attempted to predict how many pieces of artillery would overheat in an intensive battle. He failed in this because of his limited knowledge of thermodynamics and metallic composition of cannons.
In political economy, Bortkiewicz is important for his analysis of Karl Marx's reproduction schema in the last two volumes of Capital. Bortkiewicz identified a transformation problem in Marx's work which, if proven, would profoundly undermine Marx's claim to have provided a consistent account of capitalist economics. This work provided the basis of major elaborations by Joseph Schumpeter and Paul Sweezy among others.
Bortkiewicz died in Berlin, Germany.

# Major publications
- Die mittlere Lebensdauer. Die Methoden ihrer Bestimmung und ihr Verhaltnis zur Sterblichkeitsmessung. Gustav Fischer, Jena 1893 (Gottinger Digitalisierungszentrum)
- "Review of Leon Walras, Elements d'economie politique pure, 2e edit.", 1890, Revue d'economie politique
- Das Gesetz der kleinen Zahlen, 1898
- "Wertrechnung und Preisrechnung im Marxschen System", 1907, Archiv fur Sozialwissenschaft und Sozialpolitik.
- "On the Correction of Marx's Fundamental Theoretical Construction in the Third Volume of Capital."
- Die Iterationen, spanish version 1917
- "Value and Price in the Marxian System", 1952, IEP.
Laing distal myopathy
Synonyms and keywords: Distal myopathy type 1; Laing early-onset distal myopathy; MPD1.

# Overview
Laing distal myopathy is characterized by early-onset selective weakness of the great toe and ankle dorsiflexors, and a very slowly progressive course.

# Pathophysiology
The pathological features vary, although atrophic type I muscle fibres are found in half the patients. MPD1 is transmitted as an autosomal dominant trait. It is caused by mutation of the MYH7 gene (14q11) that encodes the myosin heavy chain of type 1 fibers of skeletal muscle and cardiac ventricles (mutations have been identified in approximately 50% of individuals with MPD1).

# Differentiating Laing distal myopathy from other Diseases
Differential diagnoses include milder congenital myopathies (central core disease and centronuclear myopathy) and distal myopathies (Udd distal myopathy, Nonaka distal myopathy, Markesbery-Griggs distal myopathy) (see these terms). Genetically related (allelic) disorders are familial hypertrophic cardiomyopathy 1 and myosin storage myopathy, however, the clinical picture of MPD1 is distinct from that of these conditions.

# Epidemiology and Demographics
MPD1 is rare, the prevalence is unknown. Age at onset varies from 4 to 5 years to the early twenties.

# Diagnosis
- The disease initially involves the dorsiflexors of the ankles and great toes and then the finger extensors, especially those of the third and fourth fingers.
- Early weakness of neck flexion is present in all patients.
- Mild involvement of the facial musculature (particularly of the orbicularis oculi and oris muscles) is often present. Mild proximal weakness develops more than ten years after the onset of the disease.
- Diagnosis is based on clinical findings.
- The pathological findings are variable.
- Serum creatine kinase concentration is usually normal but is sometimes increased by up to 3-fold.
- Electromyographic findings are nonspecific, muscle biopsy is not diagnostic.
- Molecular genetic testing is available on a research basis only. \
- Prenatal testing may be available for families in which the disease-causing mutation has been identified in an affected family member.

# Treatment
- Management includes physiotherapy and lightweight splinting of the ankle.
- Monitoring (electrocardiogram and echocardiogram) for symptoms of cardiac insufficiency is recommended. Life expectancy is normal.
Lansoprazole overdose

# Overdose Topics
Manifestations
Panic disorder
Lansoprazole overdose

## Manifestations
Significant naproxen overdosage may be characterized by drowsiness, heartburn, indigestion, nausea
-r vomiting. In the event that ANAPROX/ANAPROX-DS, ALEVE, or naproxen sodium is taken with
Lansoprazole , earlier and higher blood levels may be anticipated due
to the rapid absorption of naproxen sodium. A few patients have experienced seizures, but it is not
clear whether or not these were drug-related. It is not known what dose of the drug would be lifethreatening. Return to top

## Oral LD50
The oral LD50 of the drug is 543 mg/kg in rats, 1234 mg/kg in mice, 4110 mg/kg in
hamsters, and greater than 1000 mg/kg in dogs.
Should a patient ingest a large number of tablets, accidentally or purposefully, the stomach may
be emptied and usual supportive measures employed. In animals 0.5 g/kg of activated charcoal was
effective in reducing plasma levels of naproxen. Hemodialysis does not decrease the plasma
concentration of naproxen because of the high degree of its protein binding. Return to top

## Lansoprazole overdose
Oral doses up to 5000 mg/kg in rats (approximately 1300 times the 30 mg human dose based on body
surface area) and mice (about 675.7 times the 30 mg human dose based on body surface area) did not
produce deaths or any clinical signs.
LANSOPRAZOLE IS NOT REMOVED FROM THE CIRCULATION BY HEMODIALYSIS. IN ONE
REPORTED CASE OF OVERDOSE, THE PATIENT CONSUMED 600 MG OF LANSOPRAZOLE WITH NO
ADVERSE REACTION. Return to top
Adapted from the FDA Package Insert.
Lateral sacral artery
The lateral sacral arteries arise from the posterior division of the internal iliac artery; there are usually two, a superior and an inferior.

# Superior
The superior, of large size, passes medialward, and, after anastomosing with branches from the middle sacral, enters the first or second anterior sacral foramen, supplies branches to the contents of the sacral canal, and, escaping by the corresponding posterior sacral foramen, is distributed to the skin and muscles on the dorsum of the sacrum, anastomosing with the superior gluteal.

# Inferior
The inferior runs obliquely across the front of the piriformis and the sacral nerves to the medial side of the anterior sacral foramina, descends on the front of the sacrum, and anastomoses over the coccyx with the middle sacral and opposite lateral sacral artery.
In its course it gives off branches, which enter the anterior sacral foramina; these, after supplying the contents of the sacral canal, escapes by the posterior sacral foramina, and are distributed to the muscles and skin on the dorsal surface of the sacrum, anastomosing with the gluteal arteries.