Persius/hicric huggingface dataset:
Aspartate transaminase

# Overview
Aspartate transaminase (AST) also called serum glutamic oxaloacetic transaminase (SGOT) or aspartate aminotransferase (ASAT/AAT) (EC 2.6.1.1) is similar to alanine transaminase (ALT) in that it is another enzyme associated with liver parenchymal cells.

# Function
It facilitates the conversion of aspartate and alpha-ketoglutarate to oxaloacetate and glutamate.

# Isozymes
Two isoenzymes are present in humans. They have high similarity.
- GOT1, the cytosolic isoenzyme derives mainly from red blood cells and heart.
- GOT2, the mitochondrial isoenzyme is predominantly present in liver.

# Clinical significance
It is raised in acute liver damage. It is also present in red blood cells and cardiac muscle.
AST was defined as a biochemical marker for the diagnosis of acute myocardial infarction in 1954. However the use of AST for such a diagnosis is now redundant and has been superseded by the cardiac troponins.
AST / ALT is commonly measured clinically as a part of a diagnostic liver function test, to determine liver health. This is because of hepatic deficiency of pyrodoxal-6-phosphate in alcoholics, which is a cofactor for the enzymatic activity of ALT.

# Differential Diagnosis of Causes of Elevated AST
- Acute hepatitis
- Alcoholic hepatopathy
- Cholangitis
- Cholestasis
- Chronic active hepatitis
- Cirrhosis
- Dermatomyositis
- Drugs
Amoxicillin
Anidulafungin
Artemether and lumefantrin
Asparaginase Erwinia Chrysanthemi
Asenapine maleate
Axitinib
Aztreonam
Bicalutamide
Cefadroxil
Cefepime
Cefotaxime sodium
Cefprozil
Ceftazidime
Cladribine
Crizotinib
Desmopressin
Doxorubicin Hydrochloride
Idelalisib
Indinavir
Interferon gamma
Ivacaftor
Lamivudine
Lincomycin Hydrochloride
Meropenem
Niacin
Pralidoxime
Ritonavir
Ruxolitinib
Streptozocin
Vedolizumab
- Amoxicillin
- Anidulafungin
- Artemether and lumefantrin
- Asparaginase Erwinia Chrysanthemi
- Asenapine maleate
- Axitinib
- Aztreonam
- Bicalutamide
- Cefadroxil
- Cefepime
- Cefotaxime sodium
- Cefprozil
- Ceftazidime
- Cladribine
- Crizotinib
- Desmopressin
- Doxorubicin Hydrochloride
- Idelalisib
- Indinavir
- Interferon gamma
- Ivacaftor
- Lamivudine
- Lincomycin Hydrochloride
- Meropenem
- Niacin
- Pralidoxime
- Ritonavir
- Ruxolitinib
- Streptozocin
- Vedolizumab
- Epstein-Barr Virus
- Fatty liver
- Hepatic tumor
- Hypothyroid myopathy
- Infliximab
- Malignant hyperthermia
- Malignancy
- Myocardial Infarction
- Myositis
- Open heart surgery
- Perimyocarditis
- Polymyositis
- Primary biliary cirrhosis
- Progressive myodystrophia
- Pulmonary Embolism
- Renal infarction
- Seizure
- Severe muscle trauma
- Spasms, muscle injuries
- Strong physical work
ATP synthase subunit C
ATPase, subunit C of F0/V0 complex is the main transmembrane subunit of V-type , A-type and F-type ATP synthases.
ATPases (or ATP synthases) are membrane-bound enzyme complexes/ion transporters that combine ATP synthesis and/or hydrolysis with the transport of protons across a membrane. ATPases can harness the energy from a proton gradient, using the flux of ions across the membrane via the ATPase proton channel to drive the synthesis of ATP. Some ATPases work in reverse,
using the energy from the hydrolysis of ATP to create a proton gradient. There are different types of ATPases, which can
differ in function (ATP synthesis and/or hydrolysis), structure (F-, V- and A-ATPases contain rotary motors) and in the type of ions they transport.
- F-ATPases (F1F0-ATPases) in mitochondria, chloroplasts and bacterial plasma membranes are the prime producers of ATP, using the proton gradient generated by oxidative phosphorylation (mitochondria) or photosynthesis (chloroplasts).
- V-ATPases (V1V0-ATPases) are primarily found in eukaryotic vacuoles, catalysing ATP hydrolysis to transport solutes and lower pH in organelles.
- A-ATPases (A1A0-ATPases) are found in Archaea and function like F-ATPases.
- P-ATPases (E1E2-ATPases) are found in bacteria and in eukaryotic plasma membranes and organelles, and function to transport a variety of different ions across membranes.
- E-ATPases are cell-surface enzymes that hydrolyse a range of NTPs, including extracellular ATP.
The F-ATPases (or F1F0-ATPases) and V-ATPases (or V1V0-ATPases) are each composed of two linked complexes: the F1 or V1 complex contains the catalytic core that synthesizes/hydrolyses ATP, and the F0 or V0 complex that forms the membrane-spanning pore. The F- and V-ATPases all contain rotary motors, one that drives proton translocation across the membrane and one that drives ATP synthesis/hydrolysis.
Subunit C (also called subunit 9, or proteolipid in F-ATPases, or the 16 kDa proteolipid in V-ATPases) was found in the F0 or V0 complex of F- and V-ATPases, respectively. In F-ATPases, ten C subunits form an oligomeric ring that makes up the F0 rotor. The flux of protons through the ATPase channel drives the rotation of the C subunit ring, which in turn is coupled to the rotation of the F1 complex gamma subunit rotor due to the permanent binding between the gamma and epsilon subunits of F1 and the C subunit ring of F0. The sequential protonation and deprotonation of Asp61 of subunit C is coupled to the stepwise movement of the rotor.
In V-ATPases, there are three proteolipid subunits (c, c and c) that form part of the proton-conducting pore, each containing a buried glutamic acid residue that is essential for proton transport, and together they form a hexameric ring spanning the membrane.

# Subfamilies
- ATPase, V0 complex, proteolipid subunit C, InterPro: IPR000245
- ATPase, F0 complex, subunit C InterPro: IPR000454

# Human proteins containing this domain
ATP5G1;    ATP5G2;    ATP5G3;    ATP6V0B;   ATP6V0C;
Abrupt closure case 10

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the mid LAD.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the mid LAD depicting abrupt closure.
Shown below is a post-intervention angiogram without any occlusion in the LAD after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 11

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the proximal part of obtuse marginal branch of the left circumflex artery.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the proximal part of obtuse marginal branch of the left circumflex artery depicting abrupt closure.
Shown below is a post-intervention angiogram without any occlusion in the obtuse marginal branch of the left circumflex artery after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 12

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the proximal part of SVG (saphenous vein graft) to the LAD.

## Intervention
Shown below is an angiogram with ongoing intervention on the significant lesion described above.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the proximal part of SVG (saphenous vein graft) to the LAD depicting abrupt closure.
Shown below is a post-intervention angiogram without any occlusion in the SVG (saphenous vein graft) to the LAD after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 13

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the mid LAD.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the mid LAD depicting abrupt closure.
Shown below is a post-intervention angiogram without any occlusion in the LAD after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 14

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the distal part of SVG (saphenous vein graft) to the LAD.

## Intervention
Shown below is an angiogram with ongoing intervention on the significant lesion described above.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the distal part of SVG (saphenous vein graft) to the LAD depicting abrupt closure.
Abrupt closure case 15

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the mid LAD.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the mid LAD depicting abrupt closure.
Shown below is a post-intervention angiogram without any occlusion in the LAD after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 16

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the mid LAD.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the mid LAD depicting abrupt closure.
Shown below is a post-intervention angiogram without any occlusion in the LAD after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 17

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the mid LAD.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the mid LAD depicting abrupt closure.
Shown below is a post-intervention angiogram without any occlusion in the LAD after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 18

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the mid left circumflex artery.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the mid left circumflex artery depicting abrupt closure.
Shown below is a post-intervention angiogram without any occlusion in the left circumflex artery after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 19

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the mid LAD.

## Intervention
Shown below is an angiogram with ongoing intervention on the significant lesion described above.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the mid LAD depicting abrupt closure.
Shown below is an angiogram with ongoing re-intervention on the occlusion described above.
Shown below is a post-intervention angiogram without any occlusion in the LAD after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 20

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the mid median ramus.

## Intervention
Shown below is an angiogram with ongoing intervention on the significant lesion described above with occlusion at the mid median ramus depicting abrupt closure.

## Post-intervention
Shown below is a post-intervention angiogram without any occlusion in the median ramus after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 21

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the mid LAD.

## Intervention
Shown below is an angiogram with ongoing intervention on the significant lesion described above with occlusion at the mid LAD depicting abrupt closure.
Shown below is an angiogram with ongoing intervention on the occlusion in the mid LAD.

## Post-intervention
Shown below is a post-intervention angiogram without any occlusion in the LAD after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 22

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the mid RCA. The small circle indicates the presence of thrombus in the proximal RCA.

## Intervention
Shown below is an angiogram with ongoing intervention on the significant lesion described above.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the mid RCA depicting abrupt closure.
Shown below is a post-intervention angiogram without any occlusion in the RCA after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 23

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the proximal LAD.

## Intervention
Shown below is an angiogram with ongoing intervention on the significant lesion described above with occlusion at the proximal LAD depicting abrupt closure.
Shown below is an angiogram with ongoing intervention on the occlusion described above.

## Post-intervention
Shown below is a post-intervention angiogram without any occlusion in the LAD after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 24

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the proximal part of diagonal branch of the LAD.

## Intervention
Shown below is an angiogram with ongoing intervention on the significant lesion described above.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the proximal part of diagonal branch of the LAD depicting abrupt closure.
Shown below is an angiogram with ongoing intervention on the occlusion described above.
Shown below is a post-intervention angiogram without any occlusion in the diagonal branch of the LAD after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 25

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the obtuse marginal branch of LCX.

## Intervention
Shown below is an angiogram with ongoing intervention on the significant lesion described above with occlusion in the obtuse marginal branch of LCX depicting abrupt closure.
Shown below is an angiogram with ongoing intervention on the occlusion in the obtuse marginal branch of LCX.

## Post-intervention
Shown below is a post-intervention angiogram without any occlusion in the obtuse marginal branch of LCX after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 26

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant diffuse in-stent lesion in the SVG to LAD.

## Intervention
Shown below is an angiogram with ongoing intervention on the significant lesion described above.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the proximal part of SVG to LAD depicting abrupt closure.
Abrupt closure case 27

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the proximal left circumflex artery.

## Intervention
Shown below is an angiogram with ongoing intervention on the significant lesion described above along with occlusion at the proximal LCX depicting abrupt closure.

## Post-intervention
Shown below is a post-intervention angiogram without any occlusion in the left circumflex artery after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 28

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with narrowing of the lumen in the proximal part of obtuse marginal branch of left circumflex artery.

## Intervention
Shown below is an angiogram with ongoing intervention on the narrowing described above.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the proximal part of obtuse marginal branch depicting abrupt closure.
Shown below is a post-intervention angiogram without any occlusion in the obtuse marginal branch of left circumflex artery after transient occlusion as seen above, which indicates transient abrupt closure.
Abrupt closure case 29

# Abrupt Closure

## Pre-intervention
Shown below is a pre-intervention angiogram with significant lesion in the mid SVG to LAD.

## Intervention
Shown below is an angiogram with ongoing intervention on the significant lesion described above.

## Post-intervention
Shown below is a post-intervention angiogram with occlusion at the mid SVG depicting abrupt closure.
Shown below is a post-intervention angiogram without any occlusion in the SVG to LAD after transient occlusion as seen above, which indicates transient abrupt closure.
Decreased bowel sounds

# Overview
- Sensitivity and specificity of the auscultation of bowel sounds are quite low.
- Decreased bowel sounds can range from hunger pains to an impending abdominal catastrophe.
- One must ascultate for a mininum of five minutes before declaring an absence of bowel sounds. 

# Differential Diagnosis

## Common Causes
- Intestinal obstruction
- Adynamic ileus
- Intestinal ischemia
- Peritonitis
- Acute appendicitis
- Hypokalemia
- Opiates

## Causes by Organ System

## Causes in Alphabetical Order

# Diagnosis

## History and Symptoms
- Complete history including:
Characterization of pain
Ascultate before palpation
- Characterization of pain
- Ascultate before palpation

## Physical Examination
- Complete physical exam including rectal exam

## Appearance of the Patient
- Abdominal guarding, rebound, tenderness and appear very ill (patients with peritonitis)

## Laboratory Findings
- Complete blood count (CBC)
- Liver function tests (LFTs)
- Glucose
- Amylase
- Blood urea nitrogen (BUN) / creatinine
- Calcium
- Lipase
- Urinalysis

## Electrolyte and Biomarker Studies
- Electrolytes

## MRI and CT
- CT scan (abdominal) may be indicated

## Echocardiography or Ultrasound
- Ultrasound may be indicated for gynecologic concerns

# Treatment
- Treatment should not be based solely on bowel sounds
- Treatment specific to underlying etiology
- For those patients with ileus, bowel rest and IV hydration
- Ambulation is suggested
- Correct electrolytes
- Discontinue use of constipating drugs
- Nasogastric decompression

## Acute Pharmacotherapies
- Prokinetic drugs (ileus)

## Surgery and Device Based Therapy
- In patients with peritonitis, surgical entervention is usually required
Absent pulmonary valve
Synonyms and Related Keywords: Absent pulmonary valve syndrome, APVS, Congenital absence of the pulmonary valve, Pulmonary valve agenesis
Absent pulmonary valve is a rare congenital heart defect. This anomaly is a combination of poorly formed pulmonary valve tissue and significant pulmonary valve insufficiency. This may cause pulmonary artery dilatation. Massive dilatation of pulmonary arteries may lead to extrinsic compression of bronchial airway.   
Possible associated abnormalities include;
- Abnormal tricuspid valve
- Atrial septal defect
- Double outlet right ventricle
- Ductus arteriosis
- Endocardial cushion defect
- Marfan's syndrome
- Tricuspid atresia
- Ventricular septal defect

# Diagnosis
Symptoms can vary depending on associated defects, and may include:
- Cough
- Cyanosis
- Respiratory infections
- Tachypnea
- Wheezing

## Diagnostic Tests
- Electrocardiogram
- Chest x-ray
- Echocardiogram
- Computed tomography of the heart
- Magnetic resonance imaging (MRI) of the heart

# Treatment
Infants who have respiratory symptoms should have surgery as soon as possible. Others without symptoms should have surgery within the first 3-6 months of life.

# Complications
- Atelectasis
- Brain abscess
- Pneumonia
- Right-sided heart failure
- Stroke
Acanthamoeba keratitis
Acanthamoeba keratitis is a rare disease where amoebae invade the cornea of the eye.

# Causes
In the United States, it is nearly always associated with contact lens use, as Acanthamoeba can survive in the space between the lens and the eye. For this reason, contact lenses must be properly disinfected before wearing, and should be removed when swimming or surfing.
However, elsewhere in the world, many cases of Acanthamoeba present in non-contact lens wearers.

# Diagnosis
To detect Acanthamoeba on a contact lens in a laboratory, a sheep blood agar plate with a layer (a lawn) of E. coli is made. Part of the contact lens is placed on the agar plate. If Acanthamoeba are present, they will ingest the bacteria, leaving a clear patch on the plate around the area of the lens. Polymerase chain reaction can also be used to confirm a diagnosis of Acanthamoeba keratitis, especially when contact lenses are not involved. Acanthameoba is also characterized by a brawny edema and hazy view into the interior AC. Late stages of the disease also produces a ring shaped corneal ulcer.

# Presentation
Signs and symptoms include severe pain, severe keratitis (similar to stromal herpetic disease), corneal perineuritis, ring ulcer (although this is late in the disease process)

# Treatment
One treatment used is PHMB.
Propamidine isethionate has also shown some effectiveness.
Another possible agent is chlorhexidine.
Keratoplasty may sometimes be required.
A combined regimen of propamidine, miconazole nitrate, and neomycin has also been suggested.
Acidophile (organisms)
Acidophilic organisms are those that thrive under highly acidic conditions (usually at pH 2.0 or below) .  These organisms can be found in different branches of the tree of life, including Archaea, Bacteria, and Fungus. A partial list of these organisms will include:
- Sulfolobales, an order in the Crenarchaeota branch of Archaea
- Thermoplasmatales, an order in the Euryarchaeota branch of Archaea
- Acidianus brierleyi, A. infernus, facultatively anaerobic thermoacidophilic archaebacteria
- Metallosphaera sedula, thermoacidophilic
- Acidobacteriuma phylum of the Bacteria
- Acidithiobacillales, an order of Proteobacteria
- Thiobacillus ferrooxidans, T. thiooxidans, T. prosperus, T. acidophilus, T. organovorus, T. cuprinus
- Acetobacter aceti, a bacterium that produces acetic acid (vinegar) from the oxidation of ethanol.

# Mechanisms of adaptation to acidic environments
Most acidophilic organism have evolved extremely efficient mechanisms to pump protons out of the intracellular space in order to keep the cytoplasm at or near neutral pH.  Therefore, intracellular proteins do not need to develop acid stability through evolution.  However, other acidophiles, such as Acetobacter aceti, have an acidified cytoplasm which forces nearly all proteins in the genome to evolve acid stability.  For this reason, Acetobacter aceti has become a valuable resource for understanding the mechanisms by which proteins can attain acid stability.
Studies of proteins adapted to low pH have revealed a few general mechanisms by which proteins can achieve acid stability.  In most acid stable proteins (such as pepsin and the soxF protein from Sulfolobus acidocaldarius), there is an overabundance of acidic residues which minimizes low pH destabilization induced by a buildup of positive charge.  Other mechanisms include minimization of solvent accessibility of acidic residues or binding of metal cofactors.  In a specialized case of acid stability, the NAPase protein from Nocardiopsis alba was shown to have relocated acid-sensitive salt bridges to regions that play an important role in the unfolding process.  In this case of kinetic acid stability, protein longevity is accomplished across a wide range of pH.