Persius/hicric huggingface dataset:
Anterior cerebral artery
In human anatomy, the anterior cerebral artery supplies oxygen to most medial portions of frontal lobes and superior medial parietal lobes.  It arises from the internal carotid artery and is part of the Circle of Willis.
The left and right anterior cerebral arteries are connected by the anterior communicating artery.

# Areas supplied
Areas supplied by the anterior cerebral artery include:
- The medial surface of the frontal and parietal lobes
- The anterior four- fifths of the corpus callosum
- Approximately 1 inch of the frontal and parietal cortex
- Anterior portions of the basal ganglia and internal capsule

# Occlusion
Occlusion of the anterior cerebral artery may result in the following defects:
- Paralysis of the contralateral foot and leg
- Sensory loss in the contralateral foot and leg
- Urinary incontinence which usually occurs with bilateral damage

# Branches
The anterior cerebral artery branches into e.g. the following arteries:
- Ophthalmic artery

# Additional images
- Diagram showing the origins of the main branches of the carotid arteries.
- The arteries of the base of the brain.
- Medial surface of cerebral hemisphere, showing areas supplied by cerebral arteries.
- Location of the cerebral cortex

# External link
- Template:LoyolaMedEd
- Template:SUNYAnatomyLabs
- UMichAtlas|n3a8p1
- Template:RocheLexicon
- Template:RocheLexicon
- Blood supply at neuropat.dote.hu
de:Arteria cerebri anterior
no:Arteria cerebri anterior
Tibialis anterior muscle

# Overview
In human anatomy, the tibialis anterior is a muscle in the shin that spans the length of the tibia. It originates in the upper two-thirds of the lateral surface of the tibia and inserts into the medial cuneiform and first metatarsal bones of the foot. Its acts to dorsiflex and invert the foot.
It is situated on the lateral side of the tibia; it is thick and fleshy above, tendinous below.
This muscle overlaps the anterior tibial vessels and deep peroneal nerve in the upper part of the leg.
The tibialis anterior muscle is the source of the common pain of 'shin splints' affecting many runners, either because they are underconditioned or have not yet warmed up properly.

# Function
The tibialis anterior muscle is the most medial muscle of the anterior compartment of the leg. It functions to stabilise the ankle as the foot hits the ground during the contact phase of walking and acts later to pull the foot clear of the ground during the swing phase.  It also functions to 'lock' the ankle, as in toe-kicking a ball, when held in an isometric contraction.
Antagonists are plantar-flexors of the posterior compartment such as soleus and gastrocnemius.
Essentially, the movements of tibialis anterior are dorsiflexion and inversion of the foot. However, actions of tibialis anterior are dependent on whether the foot is weight-bearing or not (closed or open kinetic chain). When the foot is on the ground the muscle helps to balance the leg and talus on the other tarsal bones so that the leg is kept vertical even when walking on uneven ground. But, if you're walking on the beach it stays relaxed. This is because of less preasure pushing on it.

# Origin and insertion
It arises from the lateral condyle and upper half or two-thirds of the lateral surface of the body of the tibia; from the adjoining part of the interosseous membrane; from the deep surface of the fascia; and from the intermuscular septum between it and the Extensor digitorum longus.
The fibres of this fusiform muscle are relatively parallel to the plane on insertion, ending in a tendon, apparent on the anteriomedial dorsal aspect of the foot close to the ankle.
After passing through the most medial compartments of the  jkllj transverse and cruciate crural ligaments, it is inserted into the medial and under surface of the first cuneiform bone, and the base of the first and second metatarsal bone.

# Variations
A deep portion of the muscle is rarely inserted into the talus, or a tendinous slip may pass to the head of the first metatarsal bone or the base of the first phalanx of the great toe.
The Tibiofascialis anterior, a small muscle from the lower part of the tibia to the transverse or cruciate crural ligaments or deep fascia.

# Additional images
- Bones of the right leg. Anterior surface.
- Bones of the right foot. Plantar surface.
- Anatomical terms of motion
- Cross-section through middle of leg.
- The mucous sheaths of the tendons around the ankle. Medial aspect.
- The mucous sheaths of the tendons around the ankle. Lateral aspect.
Anti-lymphocyte globulin
Anti-lymphocyte globulin (ALG) is an infusion of horse-derived antibodies against human T cells which is used in the treatment of acute rejection in organ transplantation, especially in kidney transplants.
It is less commonly used than the similar anti-thymocyte globulin (ATG), and like ATG it is associated with cytokine release syndrome in the short term and an increased risk of post-transplant lymphoproliferative disorder in the long term. ALG is more likely to cause side effects than ATG, but is safer than OKT3.
At one point in the mid 1990s, the world's entire supply of ALG came from a horse called Volcano, who lived in South America.
Antidepressants in Japan
The number of new psychiatric drugs, and especially antidepressants on the market in Japan,  has significantly lagged behind Western countries.  Although large epidemiological studies have not been done in Japan, It is thought that up to 6 million Japanese suffer from depression, with a lifetime prevalence of 13 to 17.3%, which is similar to that seen in Western countries. 
While the market has seen the entry of the Selective Serotinin Reuptake Inhibitors (SSRIs) fluvoxamine (Luvox-Fujisawa, Depromel-Meiji Seika), paroxetine (Paxil-GSK), sertraline (Zoloft-Pfizer), and the SNRI milnacipran (Toledomin-Asahi Kasei-Janssen), other block-buster antidepressants including citalopram/escitalopram (Cipramil/Cipralex-Lundbeck, Celexa/Lexapro-Forest), fluoxetine (Prozac- Eli Lilly), venlafaxine (Effexor-Wyeth), mirtazapine (Remeron-Organon), and others are either still in development in Japan or have basically "given-up" on gaining entry into the Japanese market. 
While none of the antidepressants on the market in Japan have been studied using placebo controls, this is changing since the beginning of the 2000s. Prior clinical developments have pitted the new drug against a drug already on the market using a non-inferiority method of comparison, however, this method is known to be subject to placebo effects, e.g. depressive symptoms lifting due to effects other than pharmacologic drug effect (see reference 2).
There are a number of other hints that Japan remains behind the majority of Western countries in the treatment of depression and other mood disorders. Sertraline (Pfizer) received approval in April of 2006 after over 15 years of clinical trial development in Japan.  The Japan algorithm for mood disorders does not include many of the post-tricyclic antidepressants used as first-line antidepressants in Western countries for almost two decades, and recent studies are still comparing SSRIs and tricyclic antidepressants, even though tricylics are clearly 2nd or 3rd line treatments in the West.  On a positive note, (Organon) and Meiji Seika have filed an application for approval of mirtazapine in Japan, a drug on the market in many Western countries since 1994. 
Citalopram (Lundbeck), an SSRI on the market since the late 1980s is not available in Japan, however escitalopram (the S-isomer Enantiomer of citalopram), approved in the early 2000s in the West is still in ongoing clinical trials in Japan . There is little news, however, on the status of bupropion (
Glaxo Smith-Kline), used widely in Western countries since the early 1990s and long in clinical trials in Japan.
One of the biggest barriers to antidepressants coming to the market is that the medical insurance system in Japan is national, and the authorities are keen to contain a potentially explosive market for drugs like antidepressants that could be used for persons in many types of distress (see reference 2).
Coronary ostial stenosis
Synonyms and keywords: Ostial lesion, ostial stenosis, aorto-ostial stenosis

# Overview
Coronary ostial stenosis refers to the narrowing of the ostium part of the coronary arteries.  An ostial lesion is defined as a lesion which begins within 3-5 mm of the origin of a major epicardial artery. Ostial lesions represent a challenge to the interventional cardiologist because they often involve the wall of the aorta, they are often calcified, they may not fully dilate and they are prone to restenosis. A key issue in the treatment of an ostial lesion is to assure that the stent is inserted proximal enough to fully cover the aorto-ostial junction (particularly in the right coronary artery). Essentially the operator must realize that the aortic wall is being stented as well.

# Causes
- Atherosclerosis
- Syphilis

# Diagnosis

## Angiography

# PCI in The Ostial Lesion

## Technical Considerations

### Pre-Dilation
Direct stenting confers many benefits in lesions other than the ostial lesion. Pre-dilation is critical in the ostial lesion for may reasons:
1. Assurance that the aorto-ostial junction will dilate. The aorto-ostial junction may be more refractory to dilation and may have greater recoil. If the aorto-ostial junction will not dilate, it may not be a good idea to insert a stent because you may not be able to fully expand the stent.
"Following stent placement with a residual lesion I once ruptured three balloons trying to dilate the stent at high pressures." C. Michael Gibson, M.S., M.D.
2. Use a Low Pressure Inflation to define the extent of the lesion proximally.
"I like to inflate the balloon to 1-2 atmosphere and see how for the lesion extends proximally. While doing this I spin the gantry to gauge the proximal extent of the lesion in multiple angles. Any one view may underestimate the proximal extent of the lesion." C. Michael Gibson, M.S., M.D.

### Debulking
Debulking in the calcified ostial right coronary artery may be necessary using rotational atherectomy before stenting.

### Use of a Longer Stent
Use a longer stent than you anticipate:
1. It is often tempting to use a short 8 mm stent to cover such a short lesion. However, use of a longer stent will reduce the "rocking" of the stent that occurs during systole and diastole during stent deployment.
2. It will also reduce the risk of "watermelon seeding".
3. It increases the chances that sufficient stent is available to cover the aortic wall.

# 2011 ACCF/AHA/SCAI Guidelines for Percutaneous Coronary Intervention (DO NOT EDIT)

## Aorto-Ostial Stenoses (DO NOT EDIT)
Artesunate suppositories
Artesunate suppositories are used for the treatment of malaria. Artesunate is an antimalarial water-soluble derivative of dihydroartemisinin. Artemisinins are sesquiterpene lactones isolated from Artemisia annua, a Chinese traditional medicine.
The risk of death from severe malaria is largely dependent on the time lag between the onset of symptoms and treatment. Rapid access to effective treatment is therefore essential. For many patients, readily available oral drugs cannot be taken because of their symptoms (e.g. vomiting, convulsions, coma), and hospitals providing alternative, non-oral treatment are often inaccessible. The drug artesunate, given in suppository form, provides a potential solution to this problem: it can be made available in remote areas and thus can be given at the onset of symptoms.
Artesunate is one of a number of artemisinin derivatives discovered and developed by Chinese scientists and registered in China in the 1980s. Since the 1990s, UNICEF/UNDP/World Bank/WHO Special Programme for Research and Training in Tropical Diseases (TDR) supported studies to assess the properties of the drug. There were already indications that artesunate, given rectally, was effective in severe malaria. Significant work with artemisinin suppositories in severe malaria was conducted in Viet Nam in the early 1990s,  and clinical trials of rectal artesunate followed by mefloquine treatment in moderately severe malaria were conducted in Thailand.
1. Hien et al, Trans R Soc Trop Med Hyg, 1992, 86: 582-583
2. Vinh et al, Trans R Soc Trop Med Hyg, 1997, 91: 465-457
3. Ashton et al, Clin Pharmacol Ther, 1998, 63 (4): 482-493
4. Looareesuwan et al, Ann Trop Med Parasitol, 1995, 89 (5): 469-475
5. Looareesuwan, Am J Trop Med Hyg, 1997, 57(3): 348-353
Association (statistics)

# Overview
In statistics, an association comes from two variables that are related and is often confused with causation though association does not imply a causal relationship. In formal statistics, correlation and association are related but not entirely overlapping concepts.
For example, the United Nations studied governmental failurewhen governments fall or are overthrown and found that the best indicator of a government about to fall was the infant mortality rate. Causally, it may seem as though the dying children cause the government to fall but their mere association does not imply this.
Another example is the rates of ice cream consumption and murder, which exhibit a strong positive association. Which causes which; does eating ice cream cause murder or does murder make people eat ice cream? The answer is neitherincreases in both ice cream consumption and murder are associated with hot weather.
Another perspective on the relationship between association and causality is that association does not imply a direct causal connection between the associated variables. If, however, association is nonrandom (i.e., not due purely to chance), then it implies that some causal mechanism is operative. Often, the nature of the causal mechanism underlying an association is the joint influence of one or more common causes operating on the variables in question. For example, both the increase in ice cream consumption and murder may occur during warm weather (a conclusion that would require further information to confirm or fail to confirm).  If this were so, then the occurrence of the association between ice cream consumption and murder would be a manifestation of causation, but not in the simple, linear fashion that one initially might be tempted to assume. Associations of this sort, involving a third variable that jointly causes the association between the two original variables, is often termed "spurious association."
Several tests can be used to determine association. Computation of any of several versions of the correlation coefficient, the P test, t-test, and chi-squared test are the most common.
Atherosclerosis overview

# Overview
Atherosclerosis is a disease affecting arterial blood vessels. It is a chronic inflammatory response in the walls of arteries, in large part due to the deposition of lipoproteins (plasma proteins that carry cholesterol and triglycerides). It is commonly referred to as a "hardening" or "furring" of the arteries. It is caused by the formation of multiple plaques within the arteries.

# Pathophysiology
Atherogenesis is the developmental process of atheromatous plaques. It is characterized by a remodeling of arteries involving the concomitant accumulation of fatty substances called plaques. One recent theory suggests that for unknown reasons, leukocytes such as monocytes or basophils begin to attack the endothelium of the artery lumen in cardiac muscle. The ensuing inflammation leads to formation of  atheromatous plaques in the arterial tunica intima, a region of the vessel wall located between the endothelium and the tunica media and tunica adventitia. The bulk of these lesions are made of excess fat, collagen, and elastin. Initially, as the plaques grow only wall thickening occurs without any narrowing, stenosis of the artery opening, called the lumen; stenosis is a late event which may never occur and is often the result of repeated plaque rupture and healing responses, not the just atherosclerosis process by itself.

# Diagnosis

## History and Symptoms
According to United States data for the year 2004, for about 65% of men and 47% of women, the first symptom of atherosclerotic cardiovascular disease is heart attack or sudden cardiac death (death within one hour of onset of the symptom).

## Laboratory Findings
Cardiac stress testing, traditionally the most commonly performed non-invasive testing method for blood flow limitations generally only detects lumen narrowing of ~75% or greater, although some physicians advocate that nuclear stress methods can detect as little as 50%.

# Treatment

## Medical Therapy
If atherosclerosis leads to symptoms, some symptoms such as angina pectoris can be treated. Non-pharmaceutical means are usually the first method of treatment, such as cessation of smoking and practicing regular exercise. If these methods do not work, medicines are usually the next step in treating cardiovascular diseases, and with improvements, have increasingly become the most effective method over the long term. However, medicines are criticized for their expense, patented control and occasional undesired effects.

## Future or Investigational Therapies
Since about 2002, progress in understanding and developing techniques for modulating immune system function so as to significantly suppress the action of macrophages to drive atherosclerotic plaque progression are being developed with considerable success in reducing plaque development in both mice and rabbits. Plans for human trials, hoped for by about 2008, are in progress. Generally these techniques are termed immunomodulation of atherosclerosis.
Autoimmune heart disease
Autoimmune heart diseases are the effects of the body's own immune defense system mistaking cardiac antigens as foreign and attacking them leading to inflammation of the heart as a whole, or in parts. The commonest form of autoimmune heart disease is rheumatic heart disease or rheumatic fever.

# Mechanism and Etiology
These are the typical mechanisms of autoimmunity. Autoantibodies or auto-toxic T lymphocyte mediated tissue destruction. The process is aided by neutrophils, the complement system, tumor necrosis factor alpha, etc.
Etiologically, these are most commonly seen in children with a history of sore throat caused by a streptococcal infection. This is similar to the post-streptococcal glomerulonephritis. Here, the anti-bacterial antibodies cross react with the heart antigens causing inflammation.
Inflammatory damage leads to the following:
- Pericarditis: Here the pericardium gets inflamed. Acutely, it can cause pericardial effusion leading tocardiac tamponade and death. After healing, there may be fibrosis and adhesion of the pericardium with the heart leading to constriction of the heart and reduced cardiac function.
- Myocarditis: Here the muscle bulk of the heart gets inflamed. Inflamed muscles have reduced functional capacity. This may be fatal, if left untreated as is in a case of pancarditis. On healing, there will be fibrosis and reduced functional capacity.
- Endocarditis: Here the inner lining of the heart is inflamed, including the heart valves. This may cause a valve prolapse, adhesion of the adjacent cusps of these valves and occlusion of the flow tracts of blood through the heart causing diseases called valve stenosis.

# Specific Clinical Manifestations
These depend on the amount of inflammation. These are covered in their relevant articles.
- Acute: Heart failure; pericardial effusion; etc
- Chronic: Valve diseases as noted above; Reduced cardiac output; Exercise intolerance.

# Therapy
Intensive cardiac care and immuno-supressives including corticosteroids are helpful in the acute stage of the disease. Chronic phase has, mainly debility control and supportive care options.
Azithromycin description

# Description
ZITHROMAX (azithromycin for injection) contains the active ingredient azithromycin, an azalide, a subclass of macrolide antibiotics, for intravenous injection. Azithromycin has the chemical name (2R,3S,4R,5R,8R,10R,11R,12S,13S,14R)-13--2-ethyl-3,4,10-trihydroxy-3,5,6,8,10,12,14-hepta-methyl-11-oxy]-1-oxa-6-azacyclopentadecan-15-one. Azithromycin is derived from erythromycin; however, it differs chemically from erythromycin in that a methyl-substituted nitrogen atom is incorporated into the lactone ring. Its molecular formula is C38H72N2O12, and its molecular weight is 749.00. Azithromycin has the following structural formula:
Azithromycin, as the dihydrate, is a white crystalline powder with a molecular formula of C38H72N2O12- 2H2O and a molecular weight of 785.0.
ZITHROMAX (azithromycin for injection) consists of azithromycin dihydrate and the following inactive ingredients: citric acid and sodium hydroxide. ZITHROMAX (azithromycin for injection) is supplied in lyophilized form in a 10-mL vial equivalent to 500 mg of azithromycin for intravenous administration. Reconstitution, according to label directions, results in approximately 5 mL of ZITHROMAX for intravenous injection with each mL containing azithromycin dihydrate equivalent to 100 mg of azithromycin.
Bruton's tyrosine kinase
Bruton's tyrosine kinase (abbreviated Btk or BTK) also known as tyrosine-protein kinase BTK is an enzyme that in humans is encoded by the BTK gene. BTK is a kinase that  plays a crucial role in B-cell development.

# Function
BTK plays a crucial role in B cell maturation as well as mast cell activation through the high-affinity IgE receptor.
Btk contains a PH domain that binds phosphatidylinositol (3,4,5)-trisphosphate (PIP3). PIP3 binding induces Btk to phosphorylate phospholipase C, which in turn hydrolyzes PIP2, a phosphatidylinositol, into two second messengers, inositol triphosphate (IP3) and diacylglycerol (DAG), which then go on to modulate the activity of downstream proteins during B-cell signalling.

# Clinical significance
Mutations in the BTK gene are implicated in the primary immunodeficiency disease X-linked agammaglobulinemia (Bruton's agammaglobulinemia); sometimes abbreviated to XLA. Patients with XLA have normal pre-B cell populations in their bone marrow but these cells fail to mature and enter the circulation. The Btk gene is located on the X chromosome. At least 400 mutations of the BTK gene have been identified.

## BTK inhibitors
Approved drugs that inhibit BTK :
- Ibrutinib (PCI-32765), a selective Bruton's tyrosine kinase inhibitor.
- Acalabrutinib, approved in October 2017 for relapsed Mantle Cell Lymphoma
Various drugs that inhibit BTK are in clinical trials:
- Phase 3:
Acalabrutinib, for relapsed CLL, 95% overall remission reported.
- Acalabrutinib, for relapsed CLL, 95% overall remission reported.
- Phase 2:
- Phase 1:
ONO-4059 for Non-Hodgkin's Lymphoma and/or CLL. Renamed GS-4059 and now in trial NCT02457598.
spebrutinib (AVL-292, CC-292) 
BGB-3111 for CLL. It can be taken orally.
HM71224 for autoimmune diseases, under development by Hanmi Pharmaceutical and Lilly as of 2015
- ONO-4059 for Non-Hodgkin's Lymphoma and/or CLL. Renamed GS-4059 and now in trial NCT02457598.
- spebrutinib (AVL-292, CC-292) 
- BGB-3111 for CLL. It can be taken orally.
- HM71224 for autoimmune diseases, under development by Hanmi Pharmaceutical and Lilly as of 2015

# Discovery
Bruton's tyrosine kinase was discovered in 1993 and is named for Ogden Bruton, who first described XLA in 1952.

# Interactions
Bruton's tyrosine kinase has been shown to interact with:
- ARID3A
- BLNK,
- CAV1,
- GNAQ,
- GTF2I,
- PLCG2,
- PRKD1,  and
- SH3BP5.