Persius/hicric huggingface dataset:
Greek citron
The Greek citron is called "Citrus Medica variety etrog" because of its major use for the Jewish ritual during the Feast of Tabernacles. Initially, it was mainly grown on the island of Corfu, but nowadays not one citron tree is found on that island. As of today, it is the leading variety in Israel.
The variety is best selling for the religious ritual, because of its natural beauty, and usually persistent style and stigma. It could still be found in some Greek Islands for e.g. Crete and Naxos where they are distilling it into certain special liqueurs, but for the ritual use it is mostly cultivated only in Israel.
This Greek Citron got into use for the Ashkenazic community during the wars of Napoleon, when the Yanova Citron import was ceased due to the battles. The use of a newly imported citron was questioned during decades, regarding the poor information about grafting or hybridization.
Rabbi Efraim Zalman Margalioth in his response Beis Efraim (volume 1;56) verified in his time that no grafted trees are found on the grounds of Corfu. This certification as well as the lenient position of many other authorities eventually permitted the Esrog.
While the Greek market expanded, citrons were also imported from the shores of Greece itself, especially from the regions of Parga, Rapiza and Agia. Several conflicts arose if those plantations are in the same state of kashrus each to another, and to the ones of the Corfu Island.

# Introduction to Israel
At the same time (about 1850) effort was done by Sir Moshe Montifuri to establish Esrog plantation in Israel, in order to help the Jewish settlers to survive from hunger and pain. As the Beladdi of Palestine was not so greatful in shape, color etc., with almost no persistent style, the Sephardic settlers who were always lenient about the Corfu, planted their seeds into coastal region of Israel, especially in region of Jaffa.
During days, the Arabic farmers imported cutting from Greece which were budded onto lemon rootstock. Besides, the Corfu variety which they called Kabbud abu Nunia (-the citron with persistent style) suffered difficulties to acclimatize in the Palestinian land, and grafting started to be practiced in a large scale.
The Sephardic rabbis, as well as some Ashkenazic, permitted the citrons of Jaffa upon inspection prior to pick each and every citron. The major Ashkenazic authorities of Jerusalem permitted only the Beladdi which was mainly grown around the towns of Safed, Sh'khem or the Arabic village Um el-Fahm. Also the plantations near Tiberias were accepted.
According to the Hebrew writer "Osof Gur", in his work named Toldos Hoesrog Beretz Yisroel, the variety is distinct by crispiness and slight sweetness in the inner rind. The pulp is high Acid.
Guanethidine

# Overview
Guanethidine is an antihypertensive drug that reduces the release of catecholamines, such as norepinephrine. Guanethidine is transported across the sympathetic nerve membrane by the same mechanism that transports norepinephrine itself (NET, uptake 1), and uptake is essential for the drug's action. Once guanethidine has entered the nerve, it is concentrated in transmitter vesicles, where it replaces norepinephrine.It may also inhibit the release of granules by decreasing norepinephrine.

# Side effects
Side effects include orthostatic and exercise hypotension, sexual dysfunction (delayed or retrograde ejaculation), and diarrhea.

# Pharmacology
Guanethidine is transported by uptake 1 into the presynaptic terminal transported by Norepinephrine transporter (NET). (In this it competes with norepinephrine so can potentiate exogenously applied norepinephrine.) It becomes concentrated in norepinephrine transmitter vesicles, replacing norepinephrine in these vesicles. This leads to a gradual depletion of norepinephrine stores in the nerve endings. 
Once inside the terminal it blocks the release of norepinephrine in response to arrival of an action potential. Spontaneous release is not affected.

# Uses
Guanethidine was once a mainstay for hypertension resistant to other agents, and was often used safely during pregnancy, but it is no longer used in the US due to lack of availability. It is still licensed in some countries, e.g., UK, for the rapid control of blood pressure in a hypertensive emergency.
Intravenous nerve block (Bier block) using guanethidine has been used to treat chronic pain caused by complex regional pain syndrome.

# Chemical synthesis
Guanethidine is synthesized beginning with the alkylation of azocine with chloroacetonitrile.  This reaction which forms 1-azocinylacetonitrile, which can be reduced into 1-(2-aminoethyl)azocine by using lithium aluminium hydride as a reductant.  This compound reacts with S-methylthiourea forming guanethidine.
Gubernaculum
The paired gubernacula are folds of peritoneum that attach to the caudal end of the gonads (testes in males and ovaries in females).

# Function during development
As the scrotum and labia majora form in males and females, respectively, the gubernaculum aids in the descent of the gonads (both testes and ovaries).
The testis descends to a greater degree than the ovary and ultimately pass through the inguinal canal.

# Adult structures
The gubernaculum is present only during the development of the urinary and reproductive organs, being replaced by distinct vestiges in males and females.

## Males
In males:
- The upper part of the gubernaculum degenerates.
- The lower part persists as the gubernaculum testis ("scrotal ligament"). This ligament secures the testis to the most inferior portion of the scrotum, tethering it in place and limiting the degree to which the testis can move within the scrotum.

## Females
In females:
- The upper part of the gubernaculum, together with the ovarian artery and vein form the suspensory ligament of the ovary, which suspends the ovary from the pelvic wall.
- The lower gubernaculum has two vestigial remnants in females, the ovarian ligament and the round ligament of the uterus (ligamentum teres uteri) which respectively serve to support the ovaries and uterus in the pelvis.
H3F3B (gene)
H3 histone, family 3B (H3.3B) is a protein in humans that is encoded by the H3F3B gene.

# Function
Histones are basic nuclear proteins that are responsible for the nucleosome structure of the chromosomal fiber in eukaryotes. Two molecules of each of the four core histones (H2A, H2B, H3, and H4) form an octamer, around which approximately 146 bp of DNA is wrapped in repeating units, called nucleosomes. The linker histone, H1, interacts with linker DNA between nucleosomes and functions in the compaction of chromatin into higher order structures.

# Gene
This gene contains introns and its mRNA is poyadenylated, unlike most histone genes. The protein encoded is a member of the histone H3 family. Unlike most histone genes, H3F3B is not located in a cluster, but rather is isolated in the telomeric region of chromosome 17.

# Clinical significance
Somatic mutations in the H3F3B gene are associated with chondroblastoma.  A rare de novo germline mutation of the H3F3B gene (A30P) has been linked to a syndrome with a range of developmental and behavioral abnormalities including microcephaly, mild strabismus, seizure disorder, autistic continuum, hypothyroidism, global developmental delay, and low muscle tone.
Hemoglobin C

# Overview
Hemoglobin C (abbreviated as Hb C or HbC) is an abnormal hemoglobin in which substitution of a glutamic acid residue with a lysine residue at the 6th position of the -globin chain has occurred (E6K substitution). In those who are heterozygous for the mutation, about 2844% of total hemoglobin (Hb) is HbC, and no anemia develops. In homozygotes, nearly all Hb is in the HbC form, resulting in moderate normocytic hemolytic anemia.  Individuals heterozygous for both HbC and Hb S (Hb SC disease) or for HbC and thalassemia are known, and have atypical hemolytic anemias; sickling is enhanced in Hb SC disease. Hemoglobin C is found predominantly in West Africa and has been shown to protect against severe malaria.
The "C" designation for HbC is from the name of the city where it was discoveredChristchurch, New Zealand.

# Clinical significance
This mutated form reduces the normal plasticity of host erythrocytes causing a hemoglobinopathy. In those who are heterozygous for the mutation, about 2844% of total hemoglobin (Hb) is HbC, and no anemia develops.
In homozygotes, nearly all Hb is in the HbC form, resulting in mild hemolytic anemia.

# Presentation
Target cells, microspherocytes and HbC crystals are found in a blood smear from a homozygous patient.

# Combinations with other conditions
Individuals with sickle cellhemoglobin C (HbSC), have the gene for HbS inherited from one parent and the gene for HbC is inherited from the other parent: they are "heterozygous".  Since HbC does not polymerize as readily as HbS, there is less sickling (fewer sickle cells). The peripheral smear demonstrates mostly target cells and only a few sickle cells.  There are fewer acute vaso-occlusive events. However, persons with hemoglobin SC disease (HbSC) have more significant retinopathy, ischemic necrosis of bone, and priapism than those with pure SS disease.  

# Epidemiology
Hemoglobin C gene is found in 2-3% of US Blacks while 8% of US Blacks have hemoglobin S (Sickle) gene. Thus Hemoglobin SC disease is significantly more common than Hemoglobin CC disease. Hemoglobin C is found predominantly in Yorubas (A profile of sickle cell disease in Nigeria By O.O Akinyanju, Department of Medicine University of Lagos). It is also found in areas of West Africa, such as Ghana, where Yorubas once lived (MAN Volume 56 March 1956 pages 34-36)
Plasmodiidae
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The Plasmodiidae are a family of apicomplexan parasites, including the type genus Plasmodium, which is responsible for malaria.  They are given their own order - the Haemosporida.

# Diagnostic criteria
The diagnostic criteria of this family are:
- macrogametes and microgamonts develop independently
- syzygy absent
- microgametocyte produces 8 flagellated microgametes
- zygote is motile (known as an ookinete)
- conoid present in ookinete stage only
- sporozoites naked in oocyst (that is without a sporocyst)
- heteroxenous: merogony and gamogony occur in vertebrate host and fertilization and sporogony in definitive host (a blood sucking insect)
- hemozoin pigment produced in some genera

# Related genera
Currently there are a number of genera recognised in this family. Like many of the protist groupings these may be significantly revised in light of findings from the DNA sequences. While more complete listings of the vertebrate host species can be found on the genus pages, typical hosts are given here.
Biguetiella - bats 
Billbraya  
Bioccala - bats 
Dionisia - bats 
Haemoproteus - birds 
Hepatocystis - bats, monkeys, hippopotamus, squirrels 
Leukocytozoon - birds 
Mesnilium - fish 
Nycteria - bats 
Plasmodium - mammals, birds and reptiles 
Polchromophilus - bats 
Rayella - flying squirrels 
Saurocytozoon - reptiles

# Related species
Families:
Lankesterellidae
- Lainsonia
- Lankesterella
- Schellackia
Genera:
The hameogregarines: 
Cyrilia
Desseria
Hepatozoon
Hemogregarina
Hemolivia
Karyolysus
Others: 
Chelonplasma
Pirhemocyton
Sauroplasma
Serpentoplasma
Halofantrine

# Overview
Halofantrine is a drug used to treat malaria. Halofantrine's structure contains a substituted phenanthrene, and is related to the antimalarial drugs quinine and lumefantrine. Marketed as Halfan, halofantrine is never used to prevent malaria and its mode of action is unknown, although a crystallographic study showed that it binds to hematin in vitro, suggesting a possible mechanism of action. Halofantrine has also been shown to bind to plasmpesin, a haemoglobin degrading enzyme unique to the malarial parasites.
Halofantrine was developed at SRI International for the Walter Reed Army Institute of Research from 1965 to 1975 by a team led by medicinal chemist William Colwell.

# Adverse reactions
Halofantrine can cause abdominal pain, diarrhea, vomiting, rash, headache, itching and elevated liver enzymes.
It can be associated with cardiotoxicity. The most dangerous side effect is cardiac arrhythmias: halofantrine causes significant QT prolongation, and this effect is seen even at standard doses.  The drug should therefore not be given to patients with cardiac conduction defects and should not be combined with mefloquine. A survey from 2009 suggests that the drug is safe when correctly administered it

# Other adverse reactions
Consumption of grapefruit combined with certain medications can cause serious side effects, even death. Halofantrine combined with this fruit or grapefruit juice is dangerous.  The mechanism of action is inhibition of CYP3A4, which is necessary to metabolize the drug and eliminate it from the body.  Without CYP3A4, levels of the drug will become toxic in the body.

# Pharmacology
The mechanism of action of halofantrine is unknown.  The absorption of halofantrine is erratic, but is increased when taken with fatty food.  Because of fears of toxicity due to increased halofantrine blood levels, halofantrine should be taken on an empty stomach.
Plasma levels peak at 16 hours and the half-life of the drug is about 4 days.

# Uses
Halofantrine is only used to treat malaria.  It is not used to prevent malaria (prophylaxis) because of the risk of toxicity and unreliable absorption.

# Dosing
Adult dose: Three doses of 500 mg six hours apart. Halofantrine should be taken on an empty stomach.

# Manufacturing information and availability
Halfan (GlaxoSmithKline) is available as 250 mg tablets.  A full treatment cost (6 tablets) costs US$1.40 in the developing world.  Halofantrine is not available in the UK or U.S.

# Synthesis
Halonium ion
A halonium ion in organic chemistry is any onium compound (ion) containing a bridged halogen atom carrying a positive charge. This cation has the general structure R-X+-R where X is any halogen and R any organic residue and this structure can be cyclic or an open chain molecular structure.
Halonium ions were first postulated in 1937 by Roberts and Kimball  to account for observed diastereoselectivity in halogen addition reactions to alkenes. They correctly argued that if the initial reaction intermediate in bromination is the open-chain X--C-C+, rotation around the C-C single bond would be possible leading to a mixture of equal amounts of dihalogen cis isomer and trans isomer which is not the case. They also asserted that a positively charged halogen atom is isoelectronic with oxygen and that carbon and bromine have comparable ionization potentials.
In 1970 George A. Olah succeeded in preparing and isolating halonium salts  by adding a methyl halide such as methyl bromide or methyl chloride in sulfur dioxide at -78C to a complex of antimony pentafluoride and tetrafluoromethane in sulfur dioxide. After evaporation of sulfur dioxide this procedure left crystals of CH3-X+-CH3SbF6-, stable at room temperature but not to moisture.
A halonium ion also seems to refer generically to the simpler onium compounds (ions) based on halogens: fluoronium, H2F+; chloronium, H2Cl+; bromonium, H2Br+; iodonium, H2I+.
Hand surgeon

# Overview
Hand surgeons are a surgeons specializing in the care and treatment of problems relating to the hand, wrist, and forearm including trauma and hand infection.  Many hand surgeons also treat the elbow, arm and shoulder. Hand surgeons do not just engage in surgery - they are the primary medical doctors to deal with these issues, and often use non-surgical approaches.
In the US, hand surgery is a subspecialty of surgery.  A hand surgeon must first qualify as a general surgeon, plastic surgeon, or orthopedic surgeon, and then must do a one year long fellowship in hand practice.  Board certified general, plastic, or orthopedics surgeons who have completed approved fellowship training in hand surgery and have met a number of other practice requirements are qualified to take the "Certificate of Added Qualifications in Surgery of the Hand" examination, commonly referred to as the "CAQSH."
The historical context for the three qualifying fields is that both plastic surgery and orthopedic surgery are more recent branches off the general surgery main trunk.  Modern hand surgery began in World War II as a military planning decision. US Army Surgeon General, Major General Norman T. Kirk, knew that hand injuries in World War I had poor outcomes in part because there was no formal system to deal with them. Kirk also knew that his civilian general surgical colleague Dr. Sterling Bunnell had a special interest and experience in hand reconstruction. Kirk tapped Bunnell to train military surgeons in the management of hand injuries to treat the war casualties, and at that time hand surgery became a formal specialty. Orthopedic surgeons continued to develop special techniques to manage small bones, as found in the wrist and hand. Pioneering plastic surgeons developed microsurgical techniques for repairing the small nerves and arteries of the hand. Surgeons from all three specialties have contributed to the development of techniques for repairing tendons and managing a broad range of acute and chronic hand injuries. Hand surgery incorporates techniques from orthopaedics, plastic surgery, general surgery, neurosurgery, vascular and microvascular surgery and psychiatry and is a complex, fascinating specialty.
Two medical societies exist in the United States to provide continuing medical education to hand surgeons: the American Society for Surgery of the Hand and the American Association for Hand Surgery.

# Notes
-  "Why Visit a Hand Surgeon", American Society for Surgery of the Hand. Retrieved on 2008-11-20.
-  "About Physician Specialties", American Board of Medical Specialties. Retrieved on 2008-11-20.
-  Stern, Peter J, "Subspecialty certification in hand surgery." Clinical orthopaedics and related research 2006; 449: 165-8. PMID 16735880
-  "Certificate of Added Qualifications in Surgery of the Hand" The American Board of Orthopaedic Surgery. Retrieved on 2008-11-20.
-  American Society for Surgery of the Hand. (1995). The First Fifty Years. "The Second World War to 1971: The Founding," pp. 1-17. New York: Churchill Livingstone Inc. ISBN 0-443-07761-4
hu:Kezsebesz
Hazard ratio

# Overview
The hazard ratio in survival analysis is the effect of an explanatory variable on the hazard or risk of an event.  For a less technical definition than is provided here, consider hazard ratio to be an estimate of relative risk and see the explanation on that page.
The instantaneous hazard rate is the limit of the number of events per unit time divided by the number at risk as the time interval decreases.
where N(t) is the number at risk at the beginning of an interval.
The hazard ratio is the effect on this hazard rate of a difference, such as group membership (for example, treatment or control, male or female), as estimated by regression models which treat the log of the hazard rate as a function of a baseline hazard h_0(t) and a linear combination of explanatory variables:
Such models are generally classed proportional hazards regression models (they differ in their treatment of h_0(t), the underlying pattern the hazard rate over time), and include the Cox semi-parametric proportional hazards model, and the exponential, Gompertz and Weibull parametric models.
For two individuals who differ only in the relevant membership (e.g. treatment vs control) their predicted log-hazard will differ additively by the relevant parameter estimate, which is to say that their predicted hazard rate will differ by e^\beta, i.e. multiplicatively by the anti-log of the estimate. Thus the estimate can be considered a hazard ratio, that is, the ratio between the predicted hazard for a member of one group and that for a member of the other group, holding everything else constant.
For a continuous explanatory variable, the same interpretation applies to a unit difference.
Other hazard rate models have different formulations and the interpretation of the parameter estimates differs accordingly.
Heat syncope
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# Overview
Heat syncope another stage in the same process as heat stroke, occurs under similar conditions as heat stroke and is not distinguished from the latter by some authorities.  The basic symptom of heat syncope is a body temperature above 40C (104F) with fainting, or  without mental confusion, which does occur in heat stroke. Heat syncope is caused by mild overheating with inadequate water or salt.  In young persons, it is far more common than true sunstroke.
Heat syncope occurs when blood pressure is lowered as the body dilates (widens) capillaries (small blood vessels) in the skin to radiate heat.  Also, water is evaporated from the blood, reducing the blood's volume and therefore lowering blood pressure further.  The result is less blood to the brain, causing light-headedness and fainting.
The basic treatment for heat syncope is like fainting: the patient is positioned in a seating or supine position with legs raised.  Water and oral rehydration salt are administered slowly, and the patient is moved to a cooler area.
Hegar's sign

# Overview
Hegar's sign is an indication of pregnancy in a woman, specifically the compressibility and softening of the cervical isthmus (the portion of the cervix between the uterus and the vaginal portion of the cervix) and the uterine cervix appearing bluish and engorged.
The sign is usually present during second and third months of pregnancy from the fourth to sixth week. It is not a positive indicator of pregnancy, and its absence does not exclude pregnancy.
The indicator was originally described by Ernst Ludwig Alfred Hegar, a German gynecologist, in 1895. Hegar credits one of his students for discovering the sign.
Hepatic vein

# Overview
In human anatomy, the hepatic veins are the blood vessels that drain de-oxygenated blood from the liver and blood cleaned by the liver (from the stomach, pancreas, small intestine and colon) into the inferior vena cava.
They arise from the substance of the liver, more specifically the central vein of the liver lobule.
None of the hepatic veins have valves.

# Groups
They can be differentiated into two groups, the upper group and lower group.
- The upper group typically arises from the posterior aspect of the liver, are three in number, and drain the quadrate lobe and left lobe.
- The lower group arise from the right lobe and caudate lobe, are variable in number, and are typically smaller than those in the upper group.

# Pathology
Occlusion of the hepatic veins is known as Budd-Chiari syndrome.