Persius/hicric huggingface dataset:
Hepatic artery proper
The hepatic artery proper (also proper hepatic artery), arises from the common hepatic artery and joins the portal vein and the common bile duct to form the portal triad. It subsequently gives off the cystic artery which feeds the gallbladder before bifurcating into the right and left hepatic arteries.

# Additional images
- The celiac artery and its branches; the stomach has been raised and the peritoneum removed.
- The portal vein and its tributaries.
- Abdominal portion of the sympathetic trunk, with the celiac and hypogastric plexuses.
- Horizontal disposition of the peritoneum in the upper part of the abdomen.
- Section across portal canal of pig. X 250.
- The pancreatic duct.
- Liver and gallbladder

# External link
- Proper hepatic artery - Washington Hospital Center.
- Template:EMedicineDictionary
- Template:SUNYAnatomyLabs - "Stomach, Spleen and Liver: Contents of the Hepatoduodenal ligament"
- Template:SUNYAnatomyImage
- Template:NormanAnatomy
Hepatic portal system

# Overview
In human anatomy, the hepatic portal system is the system of veins that comprises the hepatic portal vein and its tributaries. It is also called the portal venous system, although it is not the only example of a portal venous system.

# Function
The portal venous system is responsible for directing blood from parts of the gastrointestinal tract to the liver.  Things absorbed in the small intestine, for example, would be taken to the liver for processing before being sent to the heart.  Many drugs that are absorbed through the GI tract are substantially metabolized by the liver before reaching general circulation.  This is known as the first pass effect.
Not all of the gastrointestinal tract is part of this system.  The system extends from about the lower portion of the esophagus to the upper part of the anal canal.  It also includes venous drainage from the spleen and pancreas.  This explains why certain drugs can only be taken via certain routes.  For example, nitro-glycerin cannot be swallowed, but it can be taken under the tongue. The detoxification powers of the liver are strong enough to inactivate the medication before it reaches the heart.  Therefore, nitroglycerin is given in a way that bypasses the portal venous system.
Blood flow to the liver is unique in that it receives both oxygenated and deoxygenated blood. As a result, portal blood has lower pO2 and perfusion pressure than the other organs of the body. Blood passes from branches of the portal vein through cavities between "plates" of hepatocytes called sinusoids. Blood also flows from branches of the hepatic artery and mixes into the sinusoids to supply the hepatocytes with oxygen. This mixture percolates through the sinusoids and collects in a central vein which drains into the hepatic vein. The hepatic vein subsequently drains into the inferior vena cava.
Large veins that are considered part of the portal venous system are the:
- Hepatic portal vein
- Splenic vein
Roughly, the portal venous system corresponds to areas supplied by the celiac trunk, the superior mesenteric artery, and the inferior mesenteric artery.

# Pathology
Portal hypertension is a condition in which the blood pressure of the portal venous system is too high.  It is often the result of cirrhosis of the liver.
Ramsay Hunt syndromes
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# Overview
At least three separate neurological syndromes carry the name of Ramsay Hunt syndrome (RHS), their only connection being that they were all first described by James Ramsay Hunt (1872-1937):
- Ramsay Hunt syndrome type I
- Ramsay Hunt syndrome type II
- Ramsay Hunt syndrome type III, a less commonly referenced condition, a neuropathy of the deep palmar branch of the ulnar nerve.
Heterocyclic compound

# Overview
Heterocyclic compounds are organic compounds that contain a ring structure containing atoms in addition to carbon, such as sulfur, oxygen or nitrogen, as part of the ring. They may be either simple aromatic rings or non-aromatic rings. Some examples are pyridine (C5H5N), pyrimidine (C4H4N2) and dioxane (C4H8O2).
Note that compounds such as cyclopropane, an anaesthetic with explosive properties, and cyclohexane, a solvent, are not heterocyclic, they are merely cycloalkanes. The suffix '-cyclic' implies a ring structure, while 'hetero' refers to an atom other than carbon, as above.  Many heterocyclic compounds, including some amines, are carcinogenic.
Heterocyclic chemistry is the chemistry branch dealing exclusively with synthesis, properties and applications of heterocycles especially vital to drug design.

# 3-membered rings
Heterocycles with three atoms in the ring are more reactive because of ring strain.  Those containing one heteroatom are generally stable.  Those with two heteroatoms are more likely to occur as reactive intermediates.  Common 3-membered heterocycles are:

# 4-membered rings

# 5-membered rings
With heterocycles containing five atoms, the unsaturated compounds are frequently more stable because of aromaticity.
With two heteroatoms:
- The azoles:
Two N: pyrazole & imidazole
Three N: triazole
Four N: tetrazole
One N and one O: oxazole & isoxazole
One N and one S: thiazole & isothiazole
- Two N: pyrazole & imidazole
- Three N: triazole
- Four N: tetrazole
- One N and one O: oxazole & isoxazole
- One N and one S: thiazole & isothiazole
- Two S: Dithiolane

# 6-membered rings
With two heteroatoms:
- Two N:  Pyridazine, Pyrimidine, and Pyrazine are the 1,2-, 1,3-, and 1,4-isomers, respectively.
- Two N:  Piperazine
- One N and one O: Oxazines
- One N and one S: Thiazine
- Two S: Dithiane
- Two O: Dioxane

# Heterocyclic amines and cancer
Some heterocyclic amines (HCAs) found in cooked meat are known carcinogens.  Research has shown that cooking certain meats at high temperatures creates chemicals that are not present in uncooked meats. For example, heterocyclic amines are the carcinogenic chemicals formed from the cooking of muscle meats such as beef, pork, fowl, and fish. HCAs form when amino acids and creatine (a chemical found in muscles) react at high cooking temperatures. Researchers have identified 17 different HCAs resulting from the cooking of muscle meats that may pose human cancer risk.  NCI's Division of Cancer Epidemiology and Genetics found a link between individuals with stomach cancer and the consumption of cooked meat, and other studies for colorectal, pancreatic, and breast cancer is associated with high intakes of well-done, fried, or barbecued meats.  Other sources of protein (milk, eggs, tofu, and organ meats such as liver) have very little or no HCA content naturally or when cooked.
Hippocampal sclerosis
Formaida Sclerosis or Ammon's horn sclerosis (AHS) is the most common type of neuropathological damage seen in individuals with temporal lobe epilepsy (TLE). This type of neuron cell loss, primarily in the hippocampus, can be observed in approximately 65% of people suffering from this form of epilepsy.
Histopathological hallmarks of hippocampal sclerosis include segmental loss of pyramidal neurons, granule cell dispersion and reactive gliosis.
Hippocampal sclerosis was first described in 1880 by Sommer.
A long and ongoing debate addresses the issue of whether hippocampal sclerosis is the cause or the consequence of chronic, pharmacoresistant seizure activity.
Hippocampal sclerosis is nowadays easy to detect with MRI.
Histamine H1 receptor
The H1 receptor is a histamine receptor belonging to the family of rhodopsin-like G-protein-coupled receptors. This receptor is activated by the biogenic amine histamine. It is expressed in smooth muscles, on vascular endothelial cells, in the heart, and in the central nervous system. The H1 receptor is linked to an intracellular G-protein (Gq) that activates phospholipase C and the inositol triphosphate (IP3) signalling pathway. Antihistamines, which act on this receptor, are used as anti-allergy drugs. The crystal structure of the receptor has been determined (shown on the right) and used to discover new histamine H1 receptor ligands in structure-based virtual screening studies.

# Role in inflammation
The expression of NF-B, the transcription factor that regulates inflammatory processes, is promoted by the constitutive activity of the H1 receptor as well as by agonists that bind at the receptor. H1-antihistamines have been shown to attenuate NF-B expression and mitigate certain inflammatory processes in associated cells.

# Neurophysiology
Histamine H1 receptors are activated by endogenous histamine, which is released by neurons that have their cell bodies in the tuberomammillary nucleus of the hypothalamus. The histaminergic neurons of the tuberomammillary nucleus become active during the 'wake' cycle, firing at approximately 2 Hz; during slow wave sleep, this firing rate drops to approximately 0.5 Hz. Finally, during REM sleep, histaminergic neurons stop firing altogether. It has been reported that histaminergic neurons have the most wake-selective firing pattern of all known neuronal types.
The tuberomammillary nucleus is a histaminergic nucleus that strongly regulates the sleep-wake cycle.  H1-antihistamines that cross the blood-brain barrier inhibit H1 receptor activity on neurons that project from the tuberomammillary nucleus. This action is responsible for the drowsiness effect associated with these drugs.
Histamine H4 receptor
The histamine H4 receptor is, like the other three histamine receptors, a member of the G protein-coupled receptor superfamily.

# Discovery
Unlike the histamine receptors discovered earlier, H4 was found in 2000 through a search of the human genomic DNA data base.

# Tissue distribution
H4 is highly expressed in bone marrow and white blood cells and regulates neutrophil release from bone marrow and subsequent infiltration in the  zymosan-induced pleurisy mouse model. It is also expressed in the colon, liver, lung, small intestine, spleen, testes, thymus, tonsils, and trachea. It was also found that H4R exhibits a uniform expression pattern in the human oral epithelium. 

# Function
The Histamine H4 receptor has been shown to be involved in mediating eosinophil shape change and mast cell chemotaxis. This occurs via the  subunit acting at phospholipase C to cause actin polymerisation and eventually chemotaxis.

# Structure
The 3D structure of the H4 receptor has not been solved yet due to the difficulties of GPCR crystallization. Some attempts have been made to develop structural models of the H4 receptor for different purposes. The first H4 receptor model was built by homology modelling based on the crystal structure of bovine rhodopsin. This model was used for the interpretation of site-directed mutagenesis data, which revealed the crucial importance of Asp94 (3.32) and Glu182 (5.46) residues in ligand binding and receptor activation.
A second rhodopsin based structural model of the H4 receptor was successfully used for the identification of novel H4 ligands.
Recent advancements in GPCR crystallization, in particular the determination of the human histamine H1 receptor in complex with doxepin will likely increase the quality of novel structural H4 receptor models.

# Ligands

## Agonists
- 4-Methylhistamine
- VUF-8430 (2-ethyl carbamimidothioic acid ester)
- OUP-16
- Clozapine
- JNJ 28610244

## Antagonists
- Thioperamide
- JNJ 7777120
- VUF-6002 (1--4-methylpiperazine)
- A987306
- A943931
- Pimozide

## Therapeutic potential
By inhibiting the H4 receptor, asthma and allergy may be treated.
The highly selective histamine H4 antagonist VUF-6002 is orally active and inhibits the activity of both mast cells and eosinophils in vivo, and has antiinflammatory and antihyperalgesic effects.
Histone deacetylase 5
Histone deacetylase 5 is an enzyme that in humans is encoded by the HDAC5 gene.

# Function
Histones play a critical role in transcriptional regulation, cell cycle progression, and developmental events. Histone acetylation/deacetylation alters chromosome structure and affects transcription factor access to DNA. The protein encoded by this gene belongs to the class II histone deacetylase/acuc/apha family. It possesses histone deacetylase activity and represses transcription when tethered to a promoter. It coimmunoprecipitates only with HDAC3 family member and might form multicomplex proteins. It also interacts with myocyte enhancer factor-2 (MEF2) proteins, resulting in repression of MEF2-dependent genes. This gene is thought to be associated with colon cancer. Two transcript variants encoding different isoforms have been found for this gene.
AMP-activated protein kinase regulation of the glucose transporter GLUT4 occurs by phosphorylation of HDAC5.
HDAC5 is involved in memory consolidation and suggests that development of more selective HDAC inhibitors for the treatment of Alzheimer's disease should avoid targeting HDAC5. Its function can be effectively examined by siRNA knockdown based on an independent validation.

# Interactions
Histone deacetylase 5 has been shown to interact with:
- BCL6,
- CBX5,
- GATA1,
- HDAC3,
- IKZF1,
- MEF2A,
- NRIP1,
- NCOR1,
- NCOR2,
- YWHAQ, and
- ZBTB16.
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Human herpesvirus six
Human Herpesvirus Six (HHV-6) is one of the eight known viruses that are members of the human herpesvirus family.

# Groupings
HHV-6 is a member of the betaherpesviridae (subfamily of the herpesvirinae) which also includes HHV-7 and Cytomegalovirus (HHV-5 or HCMV). There are two subtypes of HHV-6 termed HHV-6A and HHV-6B.

# Occurrence
HHV-6B is responsible for up to 93% of primary infections in Europe and North America. Such infections usually cause fever, with exanthem subitum (Roseola/rash) only being observed in 10% of cases. HHV-6 primary infections account for up to 20% of infant hospitalizations in the United States and are associated with several more severe complications, such as encephalitis, lymphadenopathy, myocarditis and myelosuppression.
After primary infection, latency is established in myeloid and bone marrow progenitors and exists for the life time of the host. The virus periodically re-activates from this latent state, with HHV-6 DNA being detectable in 20-25% of healthy adults in the United States. In the immunocompetent setting, these re-activations are often asymptomatic, but in immunosuppressed, individuals there can be serious complications.
HHV-6 re-activation causes severe disease in transplant recipients and can lead to graft rejection, often in consort with other betaherpesviridae. Likewise in HIV/AIDS, HHV-6 re-activations cause disseminated infections leading to end organ disease and death. Although up to 100% of the population are exposed (seropositive) to HHV-6, most by 3 years of age, there are rare cases of primary infections in adults. In the United States, these have been linked more with HHV-6A, which is thought to be more pathogenic and more neurotropic and has been linked to several central nervous system-related disorders.
HHV-6 has also been found in multiple sclerosis patients and has been implicated as a co-factor in several other diseases, including chronic fatigue syndrome, fibromyalgia, AIDS, and temporal lobe epilepsy but no definitive link has been established.

# Treatment

## Antimicrobial Regimen
- Human herpesvirus 6 treatment
- Preferred regimen: supportive therapy
- Note: If patient is immunocompromised, there are no antiviral regimens stablished as there are no clinical trials to validate their use on these cases. Consider administering Ganciclovir, Acyclovir, Foscarnet OR Cidofovir.
Human biting injuries

# Overview
Injuries from human bites present a particular risk to other humans, with a major risk of sepsis from infection by human oral bacteria and the possibility of transmission of blood-borne diseases including, syphilis and hepatitis.
Involuntary biting injuries due to closed-fist injuries from fists striking teeth are a common consequence of fist fights.  Injuries in which the knuckle joints or tendons of the hand are bitten into tend to be the most serious.
In spite of their name, love bites are not biting injuries (they involve bruising from sucking, and the skin is not broken), although actual biting injuries are sometimes seen as the result of fetishistic activities.

# Treatment
Thorough wound cleaning and management is essential: this involves washing out the wound, the removal of any foreign material and debriding any dead or infected tissue. Surgical consultation may be required.
Antibiotics are an important part of the management of a human bite, but are only effective after cleaning of the wound has been completed.   Amoxicillin/Clavanulate 625mg thrice daily for at least ten days is the optimal prophylaxis for infection.  If the patient is penicillin-allergic, then use doxycycline 100mg twice daily with metronidazole 400mg thrice daily.  Macrolides such as clarithromycin or erythromycin must not be used to treat human bites because many human oral commensals are resistant to these antibiotics.  Clindamycin is also ineffective
Due to the risk of hepatitis B transmission, the non immunized patient should be offered a dose of Hep B immune globulin, followed by an accelerated course of the Hep B series.
Humanistic Geriatrics

# Overview
Humanistic Geriatrics is a branch of geriatrics concerned with the integration of humanistic principles into the practice of medicine, particularly the care of older people.
Humanistic Geriatrics was developed as a response to the overwhelming influence of modern technology, science and evidence based medicine that often treats the patient at the expense of their individuality as a person.
The term was developed from a combination of Humanism and Humanistic Psychology by Dr R Kersh.
Hydrangea arborescens
Hydrangea arborescens, commonly known as Wild Hydrangea or Smooth Hydrangea, is a species of Hydrangea native to eastern North America.

# Cultivation
The cultivar "Annabelle" is the best known of this species.  It is one of the most cold hardy of Hydrangeas.
The cultivar Grandiflora has flowers that resemble snowballs, similar to Viburnum plicatum.
- Hills-of-Snow Hydrangea "Grandiflora"
Hills-of-Snow Hydrangea "Grandiflora"
- Wild Hydrangea v. Annabelle Hydrangea arborescens
Wild Hydrangea v. AnnabelleHydrangea arborescens
- Flowers of Smooth Hydrangea
Flowers of Smooth Hydrangea
Somatic hypermutation

# Overview
Somatic hypermutation (or SHM) is a mechanism inside cells that is part of the way the immune system adapts to new foreign elements if it is confronted with (for example, microbes). It serves to diversify the receptors the immune system uses to recognize foreign elements (antigens), and allows the immune system to adapt its response to new threats during the lifetime of an organism. Somatic hypermutation involves a programmed process of mutation affecting  the variable regions of immunoglobulin genes. Unlike many other types of mutation, SHM affects only individual immune cells, and the mutations are not transmitted to offspring.
Mistargetted somatic hypermutation is currently under investigation as a possible mechanism in the development of B-cell lymphomas. 

# Targets
When a B cell recognizes an antigen, it is stimulated to divide (or proliferate). During proliferation, the B cell receptor locus undergoes an extremely high rate of somatic mutation, that is at least 105-106 fold greater than the normal rate of mutation across the genome.   
The mutations that occur are mainly single base substitutions, with occasional insertions and deletions and occur at hotspots located throughout DNA that encodes the immunoglobulin variable region.  This directed hypermutation allows for the selection of B cells that express immunoglobulin receptors possessing an enhanced ability to recognize and bind a specific foreign antigen.

# Mechanism
Experimental evidence supports the view that the mechanism of SHM involves deamination of cytosine to uracil in DNA by an enzyme called Activation-Induced (Cytidine) Deaminase, or AID. A cytosine:guanine pair is thus directly mutated a to a uracil:guanine mismatch. Uracil residues are not normally found in DNA, therefore, to maintain the integrity of the genome most of these mutations must be repaired by high-fidelity DNA mismatch repair enzymes. The uracil bases are removed by the repair enzyme, uracil-DNA glycosylase. Error-prone DNA polymerases are then recruited to fill in the gap and create mutations.
The synthesis of this new DNA involves error-prone DNA polymerases, which often introduce mutations either at the position of the deaminated cytosine itself or neighboring base pairs. During B cell division the immunoglobulin variable region DNA is transcribed and translated. The introduction of mutations in the rapidly-proliferating population of B cells ultimately culminates in the production of thousands of B cells, possessing slightly different receptors and varying specificity for the antigen, from which the B cell with highest affinities for the antigen can be selected. The B cells with the greatest affinity will then be selected to differentiate into long-lived plasma cells producing antibody and memory B cells contributing to enhanced immune responses upon reinfection.
The hypermutation process also utilizes cells that auto-select against the 'signature' of an organism's own cells. It is hypothesized that failures of this auto-selection process may also lead to the development of an auto-immune response.
Hyperosmolar syndrome
Hyperosmolar syndrome or diabetic hyperosmolar syndrome is a medical emergency caused by a very high blood glucose level.
The prefix "hyper" means high, and "osmolarity" is a measure of the concentration of active particles in a solution, so the name of the syndrome simply refers to the high concentration of glucose in the blood.

# Signs & symptoms
Hyperosmolar syndrome may take a long duration - days and weeks - to develop. However, certain signs and symptoms may indicate that such a condition is developing. Some of the signs include the following:
- Excessive thirst despite frequently taking water / other liquids
- Continued high level of blood sugar
- Dry and/ or parched mouth
- Frequency of urination increases
- Pulse rate becomes rapid
- Shortness of breath with exertion
- Skin becomes dry and warm and there is no sweating
- Sleepiness and/ or a condition of confusion