Persius/hicric huggingface dataset:
40S ribosomal protein S3a
40S ribosomal protein S3a is a protein that in humans is encoded by the RPS3A gene.
Ribosomes, the organelles that catalyze protein synthesis, consist of a small 40S subunit and a large 60S subunit. Together these subunits are composed of 4 RNA species and approximately 80 structurally distinct proteins. This gene encodes a ribosomal protein that is a component of the 40S subunit. The protein belongs to the S3AE family of ribosomal proteins. It is located in the cytoplasm. Disruption of the gene encoding rat ribosomal protein S3a, also named v-fos transformation effector protein, in v-fos-transformed rat cells results in reversion of the transformed phenotype. Transcript variants utilizing alternative transcription start sites have been described. This gene is co-transcribed with the U73A and U73B small nucleolar RNA genes, which are located in its fourth and third introns, respectively. As is typical for genes encoding ribosomal proteins, there are multiple processed pseudogenes of this gene dispersed through the genome.

# Interactions
RPS3A has been shown to interact with DNA damage-inducible transcript 3.
60S ribosomal protein L21
60S ribosomal protein L21 is a protein that in humans is encoded by the RPL21 gene.
Ribosomes, the organelles that catalyze protein synthesis, consist of a small 40S subunit and a large 60S subunit. Together these subunits are composed of 4 RNA species and approximately 80 structurally distinct proteins. This gene encodes a ribosomal protein that is a component of the 60S subunit. The protein belongs to the L21E family of ribosomal proteins. It is located in the cytoplasm. As is typical for genes encoding ribosomal proteins, there are multiple processed pseudogenes of this gene dispersed through the genome.

# Clinical relevance
Mutations in the RPL21 gene result in Hypotrichosis simplex of the scalp.
60S ribosomal protein L22
60S ribosomal protein L22 is a protein that in humans is encoded by the RPL22 gene on Chromosome 1.

# Function
Ribosomes, the organelles that catalyze protein synthesis, consist of a small 40S subunit and a large 60S subunit. Together these subunits are composed of 4 RNA species and approximately 80 structurally distinct proteins. This gene encodes a cytoplasmic ribosomal protein that is a component of the 60S subunit. The protein belongs to the L22E family of ribosomal proteins. Its initiating methionine residue is post-translationally removed. The protein can bind specifically to EpsteinBarr virus-encoded small RNAs (EBERs) 1 and 2. The mouse protein has been shown to be capable of binding to heparin. Transcript variants utilizing alternative polyA signals exist. As is typical for genes encoding ribosomal proteins, there are multiple processed pseudogenes of this gene dispersed through the genome. It was previously thought that this gene mapped to 3q26 and that it was fused to the acute myeloid leukemia 1 (AML1) gene located at 21q22 in some therapy-related myelodysplastic syndrome patients with 3;21 translocations; however, these fusions actually involve a ribosomal protein L22 pseudogene located at 3q26, and this gene actually maps to 1p36.3-p36.2.
Together with RPL4, RPL22 forms the narrowest constriction of the ribosomal exit tunnel (the grove through which a growing protein chain exits the ribosome), and consequently mutations in RPL22 are believed to alter the efficiency with which protein synthesis proceeds.

# Insects
The gene may play a role in Insect toxicity resistance. In culex mosquitos, it was one of several ribosomal proteins which were overexpressed in strains resistant to the insecticide deltamethrin.  More focused analysis revealed that resistant mosquitoes expressed RPL22 at a level more than 2.5x higher than susceptible strains; however, the same study found that over-expression of RPL22 in transfected cells caused a down-regulation of a different deltamethrin-resistance gene (CYP6A1) and made these cells overall less resistant to the insecticide. Less ambiguously, multiple studies indicate that mutations in RPL22 confer erythromycin resistance on E. coli bacteria.
60S ribosomal protein L38
60S ribosomal protein L38 is a protein that in humans is encoded by the RPL38 gene.

# Gene
The human RPL38 gene resides on the long arm of chromosome 17 at 17q25.1.  It consists of five exons spread out over a distance of 6223 bp.  The 213 nucleotide open reading frame encodes a 70 amino acid protein. Alternative splice variants have been identified, both encoding the same protein. As is typical for genes encoding ribosomal proteins, there are multiple processed pseudogenes of this gene dispersed through the genome, including one located in the promoter region of the angiotensin II receptor type 1 gene.

# Function
Ribosomes, the organelles that catalyze protein synthesis, consist of a small 40S subunit and a large 60S subunit. Together these subunits are composed of 4 RNA species and approximately 80 structurally distinct proteins. This gene encodes a ribosomal protein that is a component of the 60S subunit. The protein belongs to the L38E family of ribosomal proteins. It is located in the cytoplasm.

# Genetics
An ~18kbp deletion, encompassing the entire Rpl38 locus underlies the phenotype in the Tail-short (Ts) mutant mouse. In homozygous state, Ts mice die at around 34 days of gestation. Ts/+ heterozygous embryos undergo an anemia and develop skeletal malformations. During the perinatal period ~30% of the heterozygotes die.  The surviving heterozygous Ts exhibit great variations of shortened, kinked and otherwise malformed tails. They also weigh less than their wild-type littermates but have otherwise a normal life span.  Additionally, Ts mice develop a conductive hearing loss shortly after the onset of hearing at around 34 weeks of age.  The hearing loss is the result of ectopic ossification along the round window ridge at the outside of the cochlea, massive deposition of cholesterol crystals in the middle ear cavity, an enlarged Eustachian tube and a chronic otitis media with effusion.
In Drosophila melanogaster, loss-of-function alleles of RPL38, cause embryonic lethality in homozygotes and protracted growth and shortened bristles in heterozygotes.  Due to the haplo-insufficient nature of the mutation, the phenotype is inherited as a dominant trait.
In humans, mutations in ribosomal proteins cause Diamond-Blackfan Anemia.  However, no disease has yet been linked to mutations in human RPL38.
Absolute neutrophil count

# Overview
Absolute neutrophil count (ANC) is a measure of the number of neutrophil granulocytes (also known as polymorphonuclear cells, PMN's, polys, granulocytes, segmented neutrophils or segs) present in the blood. Neutrophils are a type of white blood cell that fights against infection. A deficiency of neutrophils, known as neutropenia, may increase chances of infection.
The ANC is calculated from measurements of the total number of white blood cells (WBC) and the numbers of neutrophils and bands, which form a subset of the total number of white blood cells.  A normal ANC is above 1,500.  An ANC less than 500 is defined as neutropenia and significantly increases the risk of infection.  Neutropenia is the condition of a low ANC, and the most common condition where an ANC would be measured is in the setting of chemotherapy for cancer.
ANC = (\%neutrophils + \%bands)\times WBC
The unit of ANC is cells per microlitre of blood.
Neutrophils/granulocytes
Source: NCI CTC Toxicity scale Version 2.0 

# Acknowledgements
The content on this page was first contributed by: C. Michael Gibson, M.S., M.D.
Initial content for this page in some instances may have came from Wikipedia and AskDrWiki
Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources:
1.The Disease Database
2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3
3. Sailer, Christian, Wasner, Susanne.  Differential Diagnosis Pocket.  Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7
List of contributors:

# Suggested Reading and Key General References

# Suggested Links and Web Resources

# For Patients
Abdominal angina overview
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# Overview
- Abdominal angina (a.k.a. bowelgina) is postprandial abdominal pain that occurs in individuals with insufficient blood flow to meet visceral demands. The term angina is used in reference to angina pectoris, a similar symptom due to obstruction of the coronary artery. The American Heritage Stedman's Medical Dictionary defines abdominal angina (bowelgina) as "Intermittent abdominal pain, frequently occurring at a fixed time after eating, caused by inadequacy of the mesenteric circulation. Also called  intestinal angina; bowelgina." 
- Mesenteric ischemia is a type of peripheral vascular disease that occurs when the blood supply can not meet the metabolic demands of visceral organs. Acute mesenteric ischemia is a surgical emergency that presents severe abdominal pain which is described as "pain out of proportion to physical examination." However, chronic mesenteric ischemia (CMI) usually presents with vague abdominal pain that may be difficult to differentiate from other, more common causes of abdominal pain
Accessory cuneate nucleus
The accessory cuneate nucleus is located lateral to the cuneate nucleus in the medulla oblongata at the level of the sensory decussation (the crossing fibers of the posterior column/medial lemniscus tract).
It receives input from cervical spinal nerves and transmits that information to the cerebellum.
These fibers are called cuneocerebellar (cuneate nucleus > cerebellum) fibers.  In this function, the accessory cuneate nucleus is comparable to the upper extremity portion of the posterior spinocerebellar tract.
Accessory digestive gland

# Overview
An accessory digestive gland is a gland of the digestive system that is not a part of the digestive tract.
An example of an accessory digestive gland is the exocrine pancreas.
A closely related term is "accessory digestive organ". This can include structures that play a direct role in digestion, but are not glands, such as teeth.
Accessory hemiazygos vein
The accessory hemiazygos vein (vena azygos minor superior) is a vein on the left side of the vertebral column that generally drains the fifth through eighth intercostal spaces on the left side of the body.

# Structure
The accessory hemiazygos vein varies inversely in size with the left superior intercostal vein.
It receives the posterior intercostal veins from the 4th, 5th, 6th, and 7th intercostal spaces between the left superior intercostal vein and highest tributary of the hemiazygos vein; the left bronchial vein sometimes opens into it.
It either crosses the body of the eighth thoracic vertebra to join the azygos vein or ends in the hemiazygos.
When this vein is small, or altogether absent, the left superior intercostal vein may extend as low as the fifth or sixth intercostal space.
Acute mesenteric ischemia
Synonyms and keywords: Intestinal ischemia; intestinal ischaemia; bowel ischemia; bowel ischaemia

# Overview

# Classification

# Pathophysiology

# Causes

# Differentiating Acute mesenteric ischemia from other Diseases

# Epidemiology and Demographics

# Risk Factors

# Natural History, Complications and Prognosis

# Diagnosis
Guidelines for Diagnosis | History and Symptoms | Physical Examination | Laboratory Findings | Angiography | CT | MRA

# Treatment
Guidelines for Treatment | Medical Therapy | Surgery | Primary Prevention

# Case Studies
Case #1

# Related Chapters
This article concerns ischemia of the small bowel. See ischemic colitis for ischemia of the large bowel
CME Category::Cardiology
Aflatoxin total synthesis
Aflatoxin total synthesis concerns the total synthesis of a group of organic compounds called aflatoxins. These compounds occur naturally in several fungi. As with other chemical compound targets in organic chemistry, the organic synthesis of aflatoxins serve different purposes. Traditionally it served to prove the structure of a complex biocompound in addition to evidence obtained from spectroscopy. It also demonstrates new concepts in organic chemistry (reagents, reaction types) and it also opens the way to molecular derivatives not found in nature. Last but not least a synthetic biocompound is a commercial alternative to isolating the compound from natural resources. Aflatoxins in particular add another dimension because it is suspected that they have been mass produced in the past from biological sources as part of a biological weapons program.
The group of Barry Trost of Stanford University is responsible for the stereoselective total synthesis of  (+)-Aflatoxin B1 and B2a in 2003. In 2005 the group of E. J. Corey of Harvard University presented the enantioselective synthesis of Aflatoxin B2.

# Aflatoxin B2 synthesis
The total synthesis of Aflatoxin B2 (11) is a multistep sequence that kicks off with a cycloaddition between the quinone 1 and the enol ether 2. This reaction is catalyzed by a CBS catalyst and is enantioselective. The next step is the orthoformylation of reaction product 3 in a Duff reaction. The hydroxyl group in 4 is esterified with triflic anhydride which adds a triflate protecting group. This step enables a Grignard reaction of the aldehyde group in 5 with methylmagnesiumbromide to the alcohol 6 which is then oxidized with the Dess-Martin periodinane to the ketone 7. A Baeyer-Villiger oxidation converts the ketone to an ester (8) and a reduction with Raney nickel converts the ester into an alcohol and removes the triflic acid group. In the final step the coumarin skeleton is added to 9 by a combined coupling reaction with zinc carbonate of the vinyl bromide in 10 and a transesterification step between the phenol group and the ethyl ester group.
Aging-associated diseases
An aging-associated disease is a disease that is seen with increasing frequency with increasing senescence. Age-associated diseases are to be distinguished from the ageing process itself  because all adult animals age, but not all adult animals experience all age-associated diseases. Aging-associated diseases do not refer to age-specific diseases, such as the childhood diseases chicken pox and measles. "Aging-associated disease" is used here to mean "diseases of the elderly". Nor should aging-associated diseases be confused with accelerated aging diseases, all of which are genetic disorders.
Examples of aging-associated diseases are cardiovascular disease, cancer, arthritis, cataract, osteoporosis, type 2 diabetes, hypertension and Alzheimer's disease. The incidence of all of these diseases increases rapidly with aging (increases exponentially with age, in the case of cancer).

# Patterns of differences
By age 3 about 30% of rats have had cancer, whereas by age 85 about 30% of humans have had cancer. Humans, dogs and rabbits get Alzheimer's disease, but rodents do not. Elderly rodents typically die of cancer or kidney disease, but not of cardiovascular disease.
In humans, the relative incidence of cancer increases exponentially with age for most cancers, but levels-off or may even decline by age 60-75 (although  colon/rectal cancer continues to increase).
Victims of some of the so-called segmental progerias are vulnerable to different sets of diseases. Victims of Werner's syndrome suffer from osteoporosis, cataracts and cardiovascular disease, but not neurodegeneration or Alzheimer's disease. Victim's of Down syndrome suffer type 2 diabetes and Alzheimer's disease, but not high blood pressure, osteoporosis or cataracts. Victims of Bloom syndrome most often die of cancer.

# Theories
Aging (senescence) increases vulnerability to age-associated diseases, whereas genetics determines vulnerability or resistance between species and individuals within species. Some age-related changes (like graying hair) are said to be unrelated to an increase in mortality. But some biogerontologists believe that the same underlying changes that cause graying hair also increase mortality in other organ systems and that understanding the incidence of age-associated disease will advance knowledge of the biology of senescence just as knowledge of childhood disease]]s advanced knowledge of human development.
Agouti signalling peptide
Agouti signalling peptide, a product of the Agouti gene, is a peptide consisting of 131 amino acids. Its discovery was published in 1994 in the scientific journal Nature where its functional properties were described. It acts as an inverse agonist at melanocortin receptors, to be specific MC1.
It is produced by the Agouti gene ASIP.

# Function
In mice, the agouti gene encodes a paracrine signalling molecule that causes hair follicle melanocytes to synthesize the yellow pigment pheomelanin instead of the black or brown pigment eumelanin. Pleiotropic effects of constitutive expression of the mouse gene include adult-onset obesity, increased tumor susceptibility, and premature infertility. This gene is highly similar to the mouse gene and encodes a secreted protein that may (1) affect the quality of hair pigmentation, (2) act as an inverse agonist of alpha-melanocyte-stimulating hormone, (3) play a role in neuroendocrine aspects of melanocortin action, and (4) have a functional role in regulating lipid metabolism in adipocytes.

# Structure
Agouti signalling peptide adopts an inhibitor cystine knot motif.  Along with the homologous Agouti-related peptide, these are the only known mammalian proteins to adopt this fold.
Alphamethylacetylfentanyl
-methylacetylfentanyl is an opioid analgesic that is an analogue of fentanyl.
-methylacetylfentanyl was sold briefly on the black market in the early 1980s, before the introduction of the Federal Analog Act which for the first time attempted to control entire families of drugs based on their structural similarity rather than scheduling each drug individually as they appeared.  -methylacetylfentanyl is made with the same synthetic route as -methylfentanyl, but by substituting the relatively common acetic anhydride for the more difficult to obtain chemical propanoic anhydride in the synthesis.
-methylacetylfentanyl has similar effects to fentanyl. Side effects of fentanyl analogues are similar to those of fentanyl itself, which include itching, nausea and potentially serious respiratory depression which can be life-threatening.
Alstrom syndrome overview

# Overview
Alstrom syndrome is a rare genetic disorder caused by mutations in the gene ALMS1 which is located on the chromosome 2. It is among the rarest genetic disorders.

# Historical Perspective
Alstrom syndrome was first described by Carl-Henry Alstrom in Sweden in 1959.

# Epidemiology and Demographics
It is among the rarest genetic disorders in the world, as currently it has only 266 reported cases in medical literature and only 800 known cases in 54 countries.

# Diagnosis

## Diagnostic Criteria
It is possible to clinically detect Alstrom syndrome in infancy, but more frequently, it is detected much later, as doctors tend to detect symptoms as separate problems. Currently, Alstrom syndrome is only diagnosed clinically, since genetic testing is still rare and only available on a limited basis.

## Imaging

### Other Imaging Findings
Electroretinogram is used for ophthalmologic evaluation.  Screening esophagogastroduodenoscopy can be used to diagnose varices.  Similarly upper GI endoscopy can aid in the diagnosis of gastroesophageal reflux.

## Other Diagnostic Studies
The diagnosis of Alstrom syndrome relies primarily on clinical findings and/or family history.  In some instances the diagnosis can be confirmed by molecular genetic testing. Sequence analysis of the coding region should be performed: tiered testing with sequencing of select exons first, followed by analysis of the entire gene.  The frequency of deletions is unknown but deletion/duplication analysis may be clinically indicated in some instances.
Ambulatory blood pressure

# Overview
Ambulatory blood pressure monitoring (ABPM) measures blood pressure at regular intervals throughout the day and night. It is believed to be able to reduce the white coat hypertension effect in which a patient's blood pressure is elevated during the examination process due to nervousness and anxiety caused by being in a clinical setting. Out-of-office measurements are highly recommended as an adjunct to office measurements by almost all hypertension organizations..

# Nocturnal Hypertension
Ambulatory blood pressure monitoring allows blood pressure to be continually monitored during sleep, and is useful to determine whether the patient is a dipper or non-dipper, that is to say whether or not blood pressure falls at night compared to daytime values.  A night time fall is normal. It correlates with relationship depth but other factors such as sleep quality, age, hypertensive status, marital status, and social network support. Absence of a night time dip is associated with poorer health outcomes, including increased mortality in one recent study. In addition, nocturnal hypertension is associated with end organ damage and is a much better indicator than the daytime blood pressure reading.

# Target Organ Damage
It has been shown that end-organ damages related to hypertension, such as left ventricular hypertrophy, narrowing of the retinal arteries are more strongly associated with ABPM than with a clinical BP measurement, the reason being clinical BP measurement are referred to the marked variability of BP measurement and white coat effect .

# Morning Surge
Optimal blood pressure fluctuates over a 24-hour sleep-wake cycle, with values rising in the daytime and falling after midnight.  The reduction in early morning blood pressure compared with average daytime pressure is referred to as the night-time dip.   Ambulatory blood pressure monitoring may reveal a blunted or abolished overnight dip in blood pressure.  This is clinically useful information because non-dipping blood pressure is associated with a higher risk of left ventricle hypertrophy and cardiovascular mortality.  By comparing the early morning pressures with average daytime pressures, a ratio can be calculated which is of value in assessing relative risk.  Dipping patterns are classified by the percent of drop in pressure, and based on the resulting ratios a person may be clinically classified for treatment as a "non-dipper" (with a blood pressure drop of less than 10%), a "dipper," an "extreme dipper," or a "reverse dipper," as detailed in the chart below.  Additionally, ambulatory monitoring may reveal an excessive morning blood pressure surge; which is associated with increased risk of stroke in elderly people with high blood pressure.
Classification of dipping in blood pressure is based on the American Heart Association's calculation, using systolic blood pressure (SBP) as follows:

# Blood Pressure Variability
24-hour, non-invasive ambulatory blood pressure monitoring allows estimates of BP variability.
American Headache Society
The American Headache Society (AHS) is a professional society of health care providers dedicated to the study and treatment of headache and facial pain..
AHS has presented an annual headache symposium since 1970 as well as two teaching symposia a year.
The American Council for Headache Education (ACHE), was founded by AHS in 1990.  It is a partnership between patients and health care professionals devoted to enhancing public understanding of headaches.
The society publishes a peer-reviewed journal, HEADACHE The Journal of Head and Face Pain.