Persius/hicric huggingface dataset:
CMR in Cardiac Sarcoidosis
Cardiac involvement is found at autopsy in 20-30% of patients diagnosed with sarcoid and is felt to play a role in sudden death.  Recent research has shown that one can find evidence of cardiac sarcoid on MRI in patients with normal echocardiograms.
Echocardiography in cardiac sarcoid shows septal thinning, systolic and diastolic LV dysfunction.  There are multiple findings on MR in patients with cardiac sarcoidosis.  MR may help with early diagnosis of cardiac sarcoidosis.

# ACC/AHA Guidelines- ACCF/ACR/AHA/NASCI/SCMR 2010 Expert Consensus Document on Cardiovascular Magnetic Resonance (DO NOT EDIT)

# Delayed hyperenhancement
Delayed hyperenhancement is consistent with inflammatory or fibrotic areas.  Specifically, the regions of hyperenhancement in patients with sarcoidosis do not correspond to a coronary artery territory.
IMAGE
In a study by Patel et al of 58 consecutive patients with biopsy proven systemic sarcoidosis patients had a two fold higher rate of cardiac involvement by CMR diagnosis than by the Japanese Ministry of Health clinical criteria.
- Hyperenhancement was found in the mid-myocardial wall or epicardium (ie non-ischemic)
It has also been shown that contrast enhancement decreases in these patients following steroid therapy. (Shimada et al.)

# LV dysfunction
IMAGE

# Contrast accumulation
This typically occurs in the intramyocardial and subepicardial layers
IMAGE

# Transmural scarring and thinning of the basal septum
Transmural scarring and thinning of the basal septum is a common finding in patients with cardiac sarcoidosis.
IMAGE
Javier Sanz reported on a 47 year old woman with recent diagnosis of sarcoidisis.  She underwent cardiac MR which revealed transmural scarring.
Pubmed image1 - reference Sanz, Javier in Eur Heart Jour
Endomyocardial biopsy subsequently showed areas of focal necrosis that could explain the MR findings.

# Ventricular Tachycardia and Cardiac Sarcoidosis
A clinical vignette published by Redheuil and collegues showed the association of ventricular tachycardia and cardiac sarcoidosis using MR to show the relationship.
A 44 year old female with histologically proven pulmonary and mediastinal sarcoidosis who presented with palpitations followed by syncope.
MR findings were as follows:
- Marked delayed enhancement of the basal lateral wall of the RV, basal anteroseptal and basal, mid LV and apical anterior epicardium of the LV.
- Endocavitary ventricular stimulation induced 2 VT morphologies.  The first was compatible with VT originating from the basal lateral wall of the RV and the second was compatible with VT originating from teh basal anteroseptal and or anterior segments of the LV.
California Ground Squirrel
The California Ground Squirrel, Spermophilus beecheyi (referred to in some older sources as Otospermophilus beecheyi or Citellus beecheyi), is a common and easily observed ground squirrel of the western United States and the Baja California peninsula; it is common in Oregon and California and its range has relatively recently extended into Washington.
The squirrel's upperparts are mottled, the fur containing a mixture of gray, light brown and dusky hairs; the underside is lighter, buff or grayish yellow.  The fur around the eyes is whitish, while that around the ears is black.  Head and body are about 30 cm long and the tail an additional 15 cm.  The tail is relatively bushy for a ground squirrel, and at a quick glance the squirrel might be mistaken for a Fox Squirrel.
As is typical for ground squirrels, California Ground Squirrels live in burrows which they excavate themselves.  Some burrows are occupied communally.  Although they readily become tame in areas used by humans, and quickly learn to take food left or offered by picnickers, they spend most of their time within 25 m of their burrow, and rarely go further than 50 m from it.
California Ground Squirrels are frequently preyed on by rattlesnakes.  They are also preyed on by eagles, raccoons, red foxes, badgers, and weasels.  Interdisciplinary research at the University of California, Davis since the 1970s has shown that the squirrels use a variety of techniques to reduce rattlesnake predation.  Some populations of California Ground Squirrels have varying levels of immunity to rattlesnake venom as adults.  Female squirrels with pups also chew on the skins shed by rattlesnakes and then lick themselves and their pups (who are never immune to venom before one month of age) to disguise their scent.  Sand-kicking and other forms of harassment provoke the snake to rattle its tail, which allows a squirrel to assess the size and friskiness (dependent on blood temperature) of the snake.
Another strategy is for a squirrel to super-heat and swish around its tail.  When hunting, rattlesnakes primarily rely on their pit organ, which detects infra-red.  The hot-tail-swishing appears to convey the message "I am not a threat, but I am too big and swift-moving for it to be worth trying to hunt me."  These two confrontational techniques also distract the snake from any nearby squirrel burrows containing pups.
In the colder parts of their range, California Ground Squirrels hibernate for several months, but where winters are mild some squirrels are active year round.  In those parts where the summers are hot they may also estivate for periods of a few days.
California Ground Squirrels are often regarded as a pest in gardens and parks, since they will feed off ornamental plants and trees.
Williams-Campbell syndrome
Synonyms and keywords: Cartilage deficiency

# Overview
WilliamsCampbell syndrome is a disease of the airways where cartilage in the bronchi is defective. This leads to collapse of the airways and bronchiectasis.
WilliamsCampbell syndrome is deficiency of the bronchial cartilage distally.

# Historical Perspective
It was described in 1960 by Howard Williams and Peter Campbell.

# Symptoms
- Persistent cough
- Wheeze
- Impaired lung function

# Diagnosis
Radiologically, the lungs are overinflated and on bronchoscopy, bronchomalacia is demonstrated.
Cefoxitin clinical studies

# CLINICAL STUDIES
A prospective, randomized, double-blind, placebo-controlled clinical trial was conducted to determine the efficacy of short-term prophylaxis with cefoxitin in patients undergoing cesarean section who were at high risk for subsequent endometritis because of ruptured membranes. Patients were randomized to receive either three doses of placebo (n=58), a single dose of cefoxitin (2 g) followed by two doses of placebo (n=64), or a three-dose regimen of cefoxitin (each dose consisting of 2 g) (n=60), given intravenously, usually beginning at the time of clamping of the umbilical cord, with the second and third doses given 4 and 8 hours post-operatively. Endometritis occurred in 16/58 (27.6%) patients given placebo, 5/63 (7.9%) patients given a single dose of cefoxitin, and 3/58 (5.2%) patients given three doses of cefoxitin. The differences between the two groups treated with cefoxitin and placebo with respect to endometritis were statistically significant (p<0.01) in favor of cefoxitin. The differences between the one-dose and three-dose regimens of cefoxitin were not statistically significant.
Two double-blind, randomized studies compared the efficacy of a single 2 gram intravenous dose of cefoxitin to a single 2 gram intravenous dose of cefotetan in the prevention of surgical site-related infection (major morbidity) and non-site-related infections (minor morbidity) in patients following cesarean section. In the first study, 82/98 (83.7%) patients treated with cefoxitin and 71/95 (74.7%) patients treated with cefotetan experienced no major or minor morbidity. The difference in the outcomes in this study (95% CI: -0.03, +0.21) was not statistically significant. In the second study, 65/75 (86.7%) patients treated with cefoxitin and 62/76 (81.6%) patients treated with cefotetan experienced no major or minor morbidity. The difference in the outcomes in this study (95% CI: -0.08, +0.18) was not statistically significant.
In clinical trials of patients with intra-abdominal infections due to Bacteroides fragilis group microorganisms, eradication rates at 1 to 2 weeks post-treatment for isolates were in the range of 70% to 80%. Eradication rates for individual species are listed below
Cerebellar stroke syndrome

# Overview
Cerebellar stroke syndrome is a condition in which the circulation to the cerebellum is impaired due to a lesion of the superior cerebellar artery, anterior inferior cerebellar artery or the posterior inferior cerebellar artery.
Cardinal signs include vertigo, headache, vomiting, and ataxia.
Cerebellar strokes account for only 2-3% of the 600 000 strokes that occur each year in the United States. They are far less common than strokes which occur in the cerebral hemispheres. In recent years mortality rates have decreased due to advancements in health care which include earlier diagnosis through MRI and CT scanning. Advancements have also been made which allow earlier management for common complications of cerebellar stroke such as brainstem compression and hydrocephalus.
Research is still needed in the area of cerebellar stroke management; however, it has been proposed that several factors may lead to poor outcomes in individuals who suffer from cerebellar stroke. These factors include:
- Declining levels of consciousness
- New signs of brainstem involvement
- Progressing Hydrocephalus
- Stroke to the midline of the cerebellum (aka. the vermis)
Cerebral aneurysm overview
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# Overview
A cerebral aneurysm or brain aneurysm is a cerebrovascular disorder in which weakness in the wall of a cerebral artery or vein causes a localized dilation or ballooning of the blood vessel.
A common location of cerebral aneurysms is on the arteries at the base of the brain, known as the Circle of Willis. Approximately 85% of cerebral aneurysms develop in the anterior part of the Circle of Willis, and involve the internal carotid arteries and their major branches that supply the anterior and middle sections of the brain. The most common sites include  the anterior communicating artery (30-35%), the bifurcation of the internal carotid and posterior communicating artery (30-35%), the  bifurcation of the middle cerebral artery (20%), the bifurcation of the basilar artery, and the remaining posterior circulation arteries (5%).

# Medical Therapy

## Surgery
Emergency treatment for individuals with a ruptured cerebral aneurysm generally includes restoring deteriorating respiration and reducing intracranial pressure. Currently there are two treatment options for brain aneurysms.  Either surgical clipping or endovascular coiling is usually performed within the first three days to occlude the ruptured aneurysm and reduce the risk of rebleeding.
Cholecystokinin A receptor
The Cholecystokinin A receptor is a human protein, also known as CCKAR or CCK1, with CCK1 now being the IUPHAR-recommended name.

# Function
This gene encodes a G-protein coupled receptor that binds sulfated members of the cholecystokinin (CCK) family of peptide hormones. This receptor is a major physiologic mediator of pancreatic enzyme secretion and smooth muscle contraction of the gallbladder and stomach. In the central and peripheral nervous system this receptor regulates satiety and the release of beta-endorphin and dopamine.
The extracellular, N-terminal, domain of this protein adopts a tertiary structure consisting of a few helical turns and a disulfide-cross linked loop. It is required for interaction of the cholecystokinin A receptor with its corresponding hormonal ligand.

# Selective Ligands

## Agonists
- Cholecystokinin
- Gastrin
- CCK-4
- SR-146,131
- A-71623 - modified tetrapeptide, potent and selective CCKA agonist, IC50 3.7nM, 1200x selectivity over CCKB, CAS# 130408-77-4

## Antagonists
- Proglumide
- Lorglumide
- Devazepide
- Dexloxiglumide
- Asperlicin
- SR-27897
- IQM-95333
- JNJ-17156516
Cholecystokinin B receptor
The cholecystokinin B receptor also known as CCKBR or CCK2 is a protein that in humans is encoded by the CCKBR gene.
This gene encodes a G protein-coupled receptor for gastrin and cholecystokinin (CCK), regulatory peptides of the brain and gastrointestinal tract. This protein is a type B gastrin receptor, which has a high affinity for both sulfated and nonsulfated CCK analogs and is found principally in the central nervous system and the gastrointestinal tract. A misspliced transcript variant including an intron has been observed in cells from colorectal and pancreatic tumors.

# CNS effects
CCK receptors significantly influence neurotransmission in the brain, regulating anxiety, feeding, and locomotion. CCK-B expression may correlate parallel to anxiety and depression phenotypes in humans. CCK-B receptors possess a complex regulation of dopamine activity in the brain. CCK-B activation appears to possess a general inhibitory action on dopamine activity in the brain, opposing the dopamine-enhancing effects of CCK-A. However, the effects of CCK-B on dopamine activity vary depending on location. CCK-B antagonism enhances dopamine release in rat striatum. Activation enhances GABA release in rat anterior nucleus accumbens. CCK-B receptors modulate dopamine release, and influence the development of tolerance to opioids. CCK-B activation decreases amphetamine-induced DA release, and contributes to individual variability in response to amphetamine.
In rats, CCK-B antagonism prevents the stress-induced reactivation of cocaine-induced conditioned place preference, and prevents the long-term maintenance and reinstatement of morphine-induced CPP. Blockade of CCK-B potentiates cocaine-induced dopamine overflow in rat striatum.  CCK-B may pose a modulatory role in parkinson's disease. Blockade of CCK-B in dopamine-depleted squirrel monkeys induces significant enhancement of locomotor response to L-DOPA. One study shows that visual hallucinations in Parkinson's disease are associated with cholecystokinin 45C>T polymorphism, and this association is still observed in the presence of the cholecystokinin-A receptor TC/CC genotype, indicating a possible interaction of these two genes in the visual hallucinogenesis in Parkinson's disease.

# Gastrointestinal Tract
The cholecystokinin B receptor is stimulated by CCK and gastrin in the stomach during digestion.

# Selective Ligands
The cholecystokinin B receptor responds to a number of ligands.

## Agonists
- Cholecystokinin
- CCK-4
- Gastrin
- BBL-454

## Antagonists
- Proglumide
- CI-988
- CI-1015
- L-365,260
- L-369,293
- YF476
- YM-022
- RP-69758
- LY-225,910
- LY-288,513
- PD-135,158
- PD-145,942

## Inverse agonists
- L-740,093
Mucous membrane pemphigoid

# Overview
Mucous membrane pemphigoid, also known as cicatricial pemphigoid (which means scarring pemphigoid) is a skin-blistering autoimmune disease. This is a rare condition with an incidence of approximately one in a million of the population.

# Historical Perspective

# Classification

# Pathophysiology
In mucous membrane pemphigoid, the autoimmune reaction occurs in the skin specifically at the level of the basement membrane, the layer that holds the skin to the underlying tissue. When the condition is active, the basement membrane is dissolved by the antibodies produced, and areas of skin lift away at the base, causing hard blisters which scar if they burst. In other words, this is a desquamating/blistering disease in which the epithelium "unzips" from the underlying connective tissue, allowing fluid to gather that subsequently manifest as bullae, or blisters.

# Causes

# Differentiating Mucous Membrane Pemphigoid from other Diseases

# Epidemiology and Demographics

# Risk Factors

# Natural History, Complications and Prognosis

# Diagnosis

## Diagnostic Criteria

## Symptoms

## Physical Examination
The autoimmune reaction most commonly affects the mouth, causing lesions in the gingiva or gums, but can also affect areas of mucous membrane elsewhere in the body, such as the sinuses, genitals and anus.  When the cornea of the eye is affected, repeated scarring may result in blindness.

### Skin
- Cicatricial pemphigoid. Adapted from Dermatology Atlas.
- Cicatricial pemphigoid. Adapted from Dermatology Atlas.
- Cicatricial pemphigoid. Adapted from Dermatology Atlas.

## Laboratory Findings
antibodies (IgG) precipitates complement (C3) in the lamina lucida of the basement membrane. Circulating auto-antibodies to BP-1 antigen (located in hemidesmosome).  50% have BP-2. Positive Nikolsky sign. IgG, C3 deposition at BM creating smooth line in immunofluorescent analysis.

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Surgery

## Prevention
Ciprofloxacin how supplied
CIPRO (ciprofloxacin hydrochloride) Tablets are available as round, slightly yellowish film-coated tablets containing 250 mg ciprofloxacin. The 250 mg tablet is coded with the word BAYER on one side and CIP 250 on the reverse side. CIPRO is also available as capsule shaped, slightly yellowish film-coated tablets containing 500 mg ciprofloxacin. The 500 mg tablet is coded with the word BAYER on one side and CIP 500 on the reverse side. CIPRO 250 mg and 500 mg are available in bottles of 100.
Store below 30C (86F).
CIPRO Oral Suspension is supplied in 5% and 10% strengths. The drug product is composed of two components (microcapsules containing the active ingredient and diluent) which must be mixed by the pharmacist. See Instructions To The Pharmacist For Use/Handling.
Microcapsules and diluent should be stored below 25C (77F) and protected from freezing.
Reconstituted product may be stored below 30C (86F) for 14 days. Protect from freezing. A graduated teaspoon (5mL) with markings 1/2 and 1/1 is provided for the patient
Circumflex scapular artery
The circumflex scapular artery (scapular circumflex artery, dorsalis scapulae artery) is a branch of the subscapular artery and part of the scapular anastomoses.
It curves around the axillary border of the scapula, traveling through the anatomical "Triangular space" made up of the Subscapularis superiorally, the Teres major inferiorally, and the long head of the Triceps laterally.
It enters the infraspinatous fossa under cover of the Teres minor, and anastomoses with the transverse scapular artery and the descending branch of the transverse cervical.

# Branches
In its course it gives off two branches:
- one (infrascapular) enters the subscapular fossa beneath the Subscapularis, which it supplies, anastomosing with the transverse scapular artery and the descending branch of the transverse cervical.
- the other is continued along the axillary border of the scapula, between the Teres major and minor, and at the dorsal surface of the inferior angle anastomoses with the descending branch of the transverse cervical.
In addition to these, small branches are distributed to the back part of the Deltoideus and the long head of the Triceps brachii, anastomosing with an ascending branch of the profunda brachii.
Clarithromycin description

# Description
Clarithromycin is a semi-synthetic macrolide antibiotic. Chemically, it is 6-0-methylerythromycin. The molecular formula is C38H69NO13, and the molecular weight is 747.96. The structural formula is:
Clarithromycin is a white to off-white crystalline powder. It is soluble in acetone, slightly soluble in methanol, ethanol, and acetonitrile, and practically insoluble in water.
BIAXIN is available as immediate-release tablets, extended-release tablets, and granules for oral suspension.
Each yellow oval film-coated immediate-release BIAXIN tablet (clarithromycin tablets, USP) contains 250 mg or 500 mg of clarithromycin and the following inactive ingredients:
250 mg tablets: hypromellose, hydroxypropyl cellulose, croscarmellose sodium, D&C Yellow No. 10, FD&C Blue No. 1, magnesium stearate, microcrystalline cellulose, povidone, pregelatinized starch, propylene glycol, silicon dioxide, sorbic acid, sorbitan monooleate, stearic acid, talc, titanium dioxide, and vanillin.
500 mg tablets: hypromellose, hydroxypropyl cellulose, colloidal silicon dioxide, croscarmellose sodium, D&C Yellow No. 10, magnesium stearate, microcrystalline cellulose, povidone, propylene glycol, sorbic acid, sorbitan monooleate, titanium dioxide, and vanillin.
Each yellow oval film-coated BIAXIN XL tablet (clarithromycin extended-release tablets) contains 500 mg of clarithromycin and the following inactive ingredients: cellulosic polymers, D&C Yellow No. 10, lactose monohydrate, magnesium stearate, propylene glycol, sorbic acid, sorbitan monooleate, talc, titanium dioxide, and vanillin.
After constitution, each 5 mL of BIAXIN suspension (clarithromycin for oral suspension, USP) contains 125 mg or 250 mg of clarithromycin. Each bottle of BIAXIN granules contains 1250 mg (50 mL size), 2500 mg (50 and 100 mL sizes) or 5000 mg (100 mL size) of clarithromycin and the following inactive ingredients: carbomer, castor oil, citric acid, hypromellose phthalate, maltodextrin, potassium sorbate, povidone, silicon dioxide, sucrose, xanthan gum, titanium dioxide and fruit punch flavor.
Cluster of differentiation

# Overview
The cluster of differentiation (CD) is a protocol used for the identification and investigation of cell surface molecules present on leukocytes. CD molecules can act in numerous ways, often acting as receptors or ligands (the molecule that activates a receptor) important to the cell. A signal cascade is usually initiated, altering the behavior of the cell (see cell signaling). Some CD proteins do not play a role in cell signalling, but have other functions, such as cell adhesion.

# Nomenclature
The CD nomenclature was proposed and established in the 1st International Workshop and Conference on Human Leukocyte Differentiation Antigens (HLDA), which was held in Paris in 1982. This system was intended for the classification of the many monoclonal antibodies (mAbs) generated by different laboratories around the world against epitopes on the surface molecules of leukocytes (white blood cells). Since then, its use has expanded to many other cell types, and more than 320 CD unique clusters and subclusters have been identified. The proposed surface molecule is assigned a CD number once two specific monoclonal antibodies (mAb) are shown to bind to the molecule. If the molecule has not been well characterized, or has only one mAb, it is usually given the provisional indicator "w" (as in "CDw186").

# Uses as cell markers
The CD system is commonly used as cell markers; this allows cells to be defined based on what molecules are present on their surface. These markers are often used to associate cells with certain immune functions or properties. While using one CD molecule to define populations is uncommon (though a few examples exist), combining markers has allowed for cell types with very specific definitions within the immune system.
CD molecules are utilized in cell sorting using various methods including flow cytometry.  Cell populations are usually defined using a '+' or a '' symbol to indicate whether a certain cell fraction expresses or lacks a CD molecule. For example, a "CD34+, CD31" cell is one that expresses CD34, but not CD31.  This CD combination typically corresponds to a stem cell, opposed to a fully differentiated endothelial cell.
Two commonly used CD molecules are CD4 and CD8, which are generally used as markers for helper and cytotoxic T cells, respectively. When defining T cells, these molecules are defined in combination with CD3+, as some other leukocytes also express these CD molecules (some macrophages express low levels of CD4, dendritic cells express high levels of CD8). CD4 is also an essential receptor during HIV infection, allowing the HIV to bind to the helper T cell and destruction of CD4+ T cells.  The relative abundance of CD4+ and CD8+ T cells is often used to monitor the progression of an HIV infection.

# Other uses
It is important to note that while CD molecules are very useful in defining leukocytes, they are not merely markers on the cell surface.  While only a fraction of known CD molecules have been thoroughly characterised, most of them have an important function. In the example of CD4 & CD8, these molecules are critical in antigen recognition.