Persius/hicric huggingface dataset:
Leukotriene C4 synthase
Leukotriene C4 synthase is an enzyme that in humans is encoded by the LTC4S gene.
The protein encoded by this gene, LTC4S (or glutathione S-transferase II) is an enzyme that converts leukotriene A4 and glutathione to create leukotriene C4. This is a member of MAPEG family of transmembrane proteins.  A trimer of Leukotriene C4 synthase is localized on the outer nuclear membrane and endoplasmic reticulum, where it forms a complex with 5-Lipoxygenase-activating protein.  This protein is remotely related to microsomal glutathione S-transferase.

# Function
The MAPEG (Membrane-Associated Proteins in Eicosanoid and Glutathione metabolism) family includes a number of human proteins, several of which are involved the production of leukotrienes. This gene encodes an enzyme that catalyzes the first step in the biosynthesis of cysteinyl leukotrienes, potent biological compounds derived from arachidonic acid. Leukotrienes have been implicated as mediators of anaphylaxis and inflammatory conditions such as human bronchial asthma. This protein localizes to the nuclear envelope and adjacent endoplasmic reticulum.
Levator scapulae muscle

# Overview
The levator scapulae is situated at the back and side of the neck.

# Origin and insertion
It arises by tendinous slips from the transverse processes of the atlas and axis and from the posterior tubercles of the transverse processes of the third and fourth cervical vertebrae.
It is inserted into the vertebral border of the scapula, between the medial angle and the triangular smooth surface at the root of the spine.

# Actions
If the head is fixed, the Levator scapul raises the medial angle of the scapula.
If the shoulder is fixed, the muscle inclines the neck to the corresponding side and rotates it in the same direction.

# Variations
The number of vertebral attachments varies; a slip may extend to the occipital or mastoid, to the Trapezius, Scalene or Serratus anterior, or to the first or second rib.
The muscle may be subdivided into several distinct parts from origin to insertion.
Levator clavicul from the transverse processes of one or two upper cervical vertebr to the outer end of the clavicle corresponds to a muscle of lower animals.
More or less union with the Serratus anterior.

# Nerves
The Levator scapul are supplied by the third and fourth cervical nerves, and frequently by a branch from the dorsal scapular.

# Additional images
- A cervical vertebra
- Side view of a typical cervical vertebra
- Left scapula. Dorsal surface.
- Section of the neck at about the level of the sixth cervical vertebra.
- Muscles of the neck. Lateral view.
- Hypoglossal nerve, cervical plexus, and their branches.
- The right brachial plexus with its short branches, viewed from in front.
Level III trauma center

# Overview
In the United States a Level III trauma center provides Emergency medicine to trauma patients who do not need the services of a Level I or a Level II trauma center.
A Level III trauma center is required to have a certain number of surgeons on call 24 hours a day.
Hospitals are designated as a Level III trauma center by the American College of Surgeons for a period of three years.
Round ligament of liver

# Overview
In anatomy, the round ligament of (the) liver (also commonly known by its Latin name, ligamentum teres - or more specifically ligamentum teres hepatis as the human body has three round ligaments in total) is a degenerative string of tissue that exists in the free edge of the falciform ligament of the liver.
The round ligament represents the remnant of the left fetal umbilical vein. The round ligament therefore only exists in humans (and other animals) that are more than a few months old. Prenatally and for a month or two after birth, the umbilical vein is patent.
The umbilical vein/round ligament inserts around the umbilicus and is an important landmark of the inner surface of the anterior abdominal wall.
Light-gated ion channel

# Overview
Light-gated ion channels are a group of transmembrane proteins that form ion channels; pores which open or close in response to light. Most light-gated ion channels have been synthesized in the laboratory for study, though one naturally occurring example, Channelrhodopsin, is currently known. There are, however, many known photoreceptor proteins, which act in a similar manner to light-gated ion channels but are generally G protein coupled receptors and not actually gated ion channels.

# Synthetic Purpose
Other types of gated ion channels, ligand-gated and voltage-gated, have been synthesized with a light-gated component in an attempt to better understand their nature and properties. By the addition of a light-gated section, the kinetics and mechanisms of operation can be studied in depth. For example, the addition of a light-gated component allows for the introduction of many highly similar ligands to be introduced to the binding site of a ligand-gated ion channel to assist in the determination of the mechanism.
In 1980, the first ion channel to be adapted for study with a light-gated mechanism was the nicotinic acetylcholine receptor. This receptor was well-known at the time, and so was aptly suited to adaptation, and allowed for a study of the kinetics as not allowed before.

# Mechanism
Light-gated ion channels function in a similar manner to other gated ion channels. When exposed to a certain stimulus, a conformational change occurs in the transmembrane proteins, which constitute the pore. This conformational change then opens or closes the ion channel, allowing for the flow of ions according to their electrochemical gradient. In the specific case of light-gated ion channels, the transmembrane proteins are usually coupled with a molecule that acts as a photoswitch. Retinal is a good example of a molecular photoswitch and is found in the naturally-occurring Channelrhodopsins. The photoswitch absorbs a specific photon and changes its conformation, which in-turn, changes the conformation of the transmembrane proteins opening or closing the pore through which ions flow.

# Examples
Examples of light-gated ion channels occur in both natural and synthetic environments. These include:

## Naturally Occurring
- Channelrhodopsins were the first discovered family of light-gated ion channels.
Channelrhodopsin-1 
Channelrhodopsin-2
- Channelrhodopsin-1
- Channelrhodopsin-2

## Synthetically Adapted
- nicotinic acetylcholine receptor was the first ion channel to be synthetically adapted with a light-gated mechanism.
- Many other, fully-synthetic, light-gated channels have produced as well.

# See Also
Channelrhodopsin
Ion channels
Voltage-gated ion channel
Ligand-gated ion channel
Photoreceptor protein
Lincomycin how supplied

# HOW SUPPLIED
LINCOCIN Sterile Solution is available in the following strength and package sizes:
300 mg 
2 mL Vials  NDC 0009-0555-01
10 mL Vials  NDC 0009-0555-02
Each mL of LINCOCIN Sterile Solution contains lincomycin hydrochloride equivalent to lincomycin 300 mg; also benzyl alcohol, 9.45 mg added as preservative.
Store at controlled room temperature 20 to 25C (68 to 77F)
Lincomycin microbiology

# Microbiology
Lincomycin has been shown to be active against most strains of the following organisms both in vitro and in clinical infections: (seeINDICATIONS AND USAGE).
Staphylococcus aureus (penicillinase- and non-penicillinase producing strains)
Streptococcus pneumoniae
The following in vitro data are available; but their clinical significance is unknown.
Lincomycin has been shown to be active in vitro against the following microorganisms; however, the safety and efficacy of LINCOCIN in treating clinical infections due to these organisms have not been established in adequate and well controlled trials.
Aerobic gram-positive cocci:
Streptococcus pyogenes 
Viridans group streptococci
Aerobic gram-positive bacilli:
Corynebacterium diphtheriae
Anaerobic gram-positive non-sporeforming bacilli:
Propionibacterium acnes
Anaerobic gram-positive sporeforming bacilli:
Clostridium tetani
Clostridium perfringens
This drug is not active against most strains of Enterococcus faecalis nor against Neisseria gonorrhoeae, Neisseria meningitidis, Haemophilus influenzae or other gram-negative organisms or yeasts.
Cross resistance has been demonstrated between clindamycin and lincomycin. Some cross resistance witherythromycin including a phenomenon known as dissociated cross resistance ormacrolide effect has been reported.
Studies indicate that lincomycin does not share antigenicity with penicillin compounds.
Lipinski's Rule of Five
Lipinski's Rule of Five is a rule of thumb to evaluate druglikeness, or determine if a chemical compound with a certain pharmacological or biological activity has properties that would make it a likely orally active drug in humans. The rule was formulated by Christopher A. Lipinski in 1997, based on the observation that most medication drugs are relatively small and lipophilic molecules.
The rule describes molecular properties important for a drug's pharmacokinetics in the human body, including their absorption, distribution, metabolism, and excretion ("ADME"). However, the rule does not predict if a compound is pharmacologically active.
The rule is important for drug development where a pharmacologically active lead structure is optimized step-wise for increased activity and selectivity, as well as drug-like properties as described by Lipinski's rule. The modification of the molecular structure often leads to drugs with higher molecular weight, more rings, more rotatable bonds, and a higher lipophilicity.

# The rule
Lipinski's Rule of Five states that, in general, an orally active drug has:
- Not more than 5 hydrogen bond donors (OH and NH groups)
- Not more than 10 hydrogen bond acceptors (notably N and O)
- A molecular weight under 500 g/mol
- A partition coefficient log P less than 5
Note that all numbers are multiples of five, which is the origin of the rule's name.

# Improvements
To evaluate druglikeness better, the rules have spawned many extensions, for example one from a 1999 paper by Ghose et al.:
- Partition coefficient log P in -0.4 to +5.6 range
- Molar refractivity from 40 to 130
- Molecular weight from 160 to 480
- Number of heavy atoms from 20 to 70
Over the past decade Lipinski's profiling tool for druglikeness has led to further investigations by scientists to extend profiling tools to lead-like properties of compounds in the hope that a better starting point in early discovery can save time and cost.
Rajab-Spranger syndrome
Synonyms and keywords: Lipodystrophy-mental retardation-deafness

# Overview
Rajab-Spranger syndrome is characterized by the association of generalized congenital lipodystrophy,  in early childhood, intellectual deficit, and skeletal manifestations

# Pathophysiology

## Genetics
The syndrome has been described in three patients from two families of the same ethnic origin. The parents of two of the patients were consanguineous, suggesting autosomal recessive inheritance.

# Differentiating from other diseases
Rajab-Spranger syndrome differs from
- SHORT syndrome by the absence of Rieger anomaly and joint hyperlaxity
- Cockayne syndrome through normal DNA repair after UV exposure
- A/C laminopathy through the absence of mutations in the lamin A/C gene.

# Natural History, Complications, Prognosis
The functional prognosis of these patients depends on their intellectual development. Bone fractures must be diagnosed early and treated. This disease is not life-threatening in the first decades of life.

# Diagnosis

## Symptoms
- Progressive sensorineural deafness
- Fractures

## Physical examination

### Neurologic
- Mental retardation - decreased intellectual capacity

## Imaging

### X-ray
- Slender, undermineralized tubular bones
- Delayed skeletal maturation
- Late-onset dense metaphyseal striations.
List of benzodiazepines
The various benzodiazepines and their respective trade-names, half-lives, and primary uses are listed in the following table.

# Atypical benzodiazepine receptor ligands
*Not all trade names are listed.  Click on drug name to see a more comprehensive list.
The duration of apparent action is usually considerably less than the half-life. With most benzodiazepines, noticeable effects usually wear off within a few hours. Nevertheless, as long as the drug is present it will exert subtle effects within the body. These effects may become apparent during continued use or may appear as withdrawal symptoms when dosage is reduced or the drug is stopped.
*Equivalent doses are based on clinical experience but may vary between individuals.
Litmus test (chemistry)
Litmus is a water-soluble mixture of different dyes extracted from lichens, specially Roccella tinctoria.  The mixture has CAS number 1393-92-6. It is often absorbed on to filter paper.  The resulting piece of paper or solution with water becomes a pH indicator (one of the oldest), used to test materials for acidity.  Blue litmus paper turns red under acidic conditions and red litmus paper turns blue under basic (i.e. alkaline) conditions, the color change occurring over the pH range 4.5-8.3 (at 25C). Neutral litmus paper is purple in color.  The mixture contains 10 to 15 different dyes (Erythrolein (or Erythrolitmin), Azolitmin, Spaniolitmin, Leucoorcein and Leucazolitmin). Pure Azolitmin does show nearly the same effect as litmus.

# History
Litmus was used the first time about 1300 AD by Spanish alchemist Arnaldus de Villa Nova. From 16th century on the blue dye was extracted from some lichens especially in the Netherlands.

# Natural sources
Litmus can be found in different species of lichens. Formerly, the dyes would be extracted from such species as Roccella tinctoria (South America), Roccella fuciformis (Angola and Madagascar), Roccella pygmaea (Algeria), Roccella phycopsis, Lecanora tartarea (Norway, Sweden), Variolaria dealbata, Ochrolechia parella, Parmotrema tinctorum and Parmelia. Currently, the main sources are Roccella montagnei (Mozambique) and Dendrographa leucophoea (California).

# Uses
The main use is to test whether a solution is acidic or alkaline.  Wet litmus paper can also be used to test water-soluble gases; the gas dissolves in the water and the resulting solution colors the litmus paper.
Other reactions can cause a color-change to litmus paper; for instance, chlorine gas turns blue litmus paper white  the litmus paper is bleached. This reaction is irreversible and therefore here the litmus is not acting as an indicator.
To find out if a substance is neutral, a blue and red sheet of litmus paper is needed. When the substance is placed on it, the color should remain the same or turn purple for both.
Long QT syndrome causes

# Overview
Long QT syndrome is a congenital disease resulting from abnormalities in the ion channels of the heart.  Long QT syndrome should be differentiated from secondary QT prolongation.  There are multiple causes of secondary QT prolongation that are distinct from long QT syndrome such as drugs (anti-arrhythmic drugs, anti-psychotic drugs), electrolyte disturbances  (hyperkalaemia, hypocalcaemia, hypoglycaemia, hypokalaemia, and hypomagnesemia), neurologic events such as subarachnoid hemorrhage, and anorexia nervosa.

# Causes of QT Prolongation

## Common Causes

### Drugs
Drug induced QT prolongation is usually a result of treatment by anti-arrhythmic drugs  or a number of other drugs that have been reported to cause this problem (e.g. cisapride).  Some anti-psychotic drugs, such as Haloperidol and Ziprasidone, have a prolonged QT interval as a rare side effect. Genetic mutations may make one more susceptible to drug induced QT prolongation.

### Long QT Syndrome
Genetic abnormalities cause the Long QT Syndrome.

### Electrolyte Disturbances
Electrolyte disturbances such as hyperkalaemia, hypocalcaemia, hypoglycaemia, hypokalaemia, and hypomagnesemia can cause QT prolongation.

### Neurologic Events
Subarachnoid hemorrhage and other intracranial events can cause QT prolongation.  Widely slayed cerebral T waves are often seen as well.

### Anorexia Nervosa
Anorexia nervosa and starvation can cause QT prolongation.

## Causes by Organ System

## Causes in Alphabetical Order
Lucey-Driscoll syndrome

# Overview
Lucey-Driscoll syndrome is an autosomal recessive metabolic disorder affecting enzymes involved in bilirubin metabolism.  It is one of several disorders classified as a transient familial neonatal unconjugated hyperbilirubinemia.

# Historical Perspective

# Classification

# Pathophysiology

# Causes
The common cause is congenital, but it can also be caused by maternal steroids passed on through breast milk to the newborn. It is different from breast milk jaundice (breast-fed infants have higher bilirubin levels than formula-fed ones).

# Differentiating Lucey-Driscoll syndrome from Other Diseases

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis

## Natural History

## Complications

## Prognosis

# Diagnosis

# Genetics
File:Autorecessive.svg
A defect in the UGT1A1-gene, also linked to Crigler-Najjar syndrome and Gilbert's syndrome, is responsible for the congenital form of Lucey-Driscoll syndrome.

## Diagnostic Criteria

## History and Symptoms

## Physical Examination

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Surgery

## Prevention
Pulmonary consolidation

# Overview
A pulmonary consolidation is a region of (normally compressible) lung tissue that has filled with liquid, a condition marked by induration (swelling or hardening of normally soft tissue) of a normally aerated lung. It is considered a radiologic sign. Consolidation occurs through accumulation of inflammatory cellular exudate in the alveoli and adjoining ducts. Simply, it is defined as alveolar space that contains liquid instead of gas. The liquid can be pulmonary edema, inflammatory exudate, pus, inhaled water, or blood (from bronchial tree or hemorrhage from a pulmonary artery). It must be present to diagnose pneumonia: the signs of lobar pneumonia are characteristic and clinically referred to as consolidation.

# Signs
Signs that consolidation may have occurred include:
- Expansion of the thorax on inspiration is reduced on the affected side
- Vocal fremitus is increased on the side with consolidation
- Percussion is dull in affected area
- Breath sounds are bronchial
- Possible medium, late, or pan-inspiratory crackles
- Vocal resonance is increased. Here, the patient's voice (or whisper, as in whispered pectoriloquy) can be heard more clearly when there is consolidation, as opposed to in the healthy lung where speech sounds muffled.
- A pleural rub may be present.
- A lower expected Pa02 than calculated in the alveolar gas equation

# Radiology
- Typically, an area of white lung is seen on a standard X-ray. Consolidated tissue is more radio-opaque than normally aerated lung parenchyma, so that it is clearly demonstrable in radiography and on CT scans. Consolidation is often a middle-to-late stage feature/complication in pulmonary infections.
Mycobacterium fortuitum
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Mycobacterium fortuitum

# Description
Gram-positive, nonmotile and acid-fast rods (1-3m x 0.2-0.4m). Sometimes long rods with occasional beaded or swollen cells having non-acid-fast ovoid bodies at one end.
Colony characteristics
- Smooth hemispheric colonies, usually off-white or cream colored colonies.  May be butyrous, waxy, multilobate and even rosette clustered (dilute inocula).
- On Malachite green containing media, such as Lowenstein-Jensen media, colonies can absorb the green dye.
Physiology
- Rapid growth on Lowenstein-Jensen media within 2-4 days.
- No growth at 45C, but grows on MacConkey agar
Differential characteristics
- Differentiation from M. fortuitum subsp. acetamidolyticum by its ability to utilise L-glutamate and its inability to utilise acetamide as simultaneous nitrogen and carbon source. Both subspecies share an identical 5'-16S rDNA sequence. However, the ITS sequences are different.

# Pathogenesis
- Different types of sporadic infections: pulmonary disease, local abscesses.
- Postoperative sternal wound infections, endocarditis, meningitis, and osteomyelitis.
- Has produced postoperative infections after breast augmentation surgury.
- Biosafety level 2

# Type Strain
- Found world wide in soil, dust, rivers, lakes and tap water.
- First isolated from a 25-year old patient (syringe abscess) in Rio de Janeiro.
- Also isolated from lymph glands of cattle and systemic or nodular infection of frogs.
Strain ATCC 6841 = CCUG 20994 = CIP 104534 = DSM 46621 = IFO (now NBRC) 13159 = JCM 6387 = NCTC 10394.
Subsequently, this species has been divided into subspecies 
M. fortuitum subsp. acetamidolyticum
Mean corpuscular volume
The mean corpuscular volume, or MCV, is a measure of the average red blood cell volume (i.e. size) that is reported as part of a standard complete blood count.
In patients with anemia, it is the MCV measurement that allows classification as either a microcytic anemia (MCV below normal range) or macrocytic anemia (MCV above normal range).
It can be calculated (in litres) by dividing the hematocrit by the red blood cell count (number of red blood cells per litre). The result is typically reported in femtolitres.
If the MCV was determined by automated equipment, the result can be compared to RBC morphology on a peripheral blood smear. Any deviation would be indicative of either faulty equipment or technician error.
The normal range is typically 80-96 fL. In presence of hemolytic anaemia, presence of reticulocytes can increase MCV. In pernicious anemia (macrocytic), MCV can range up to 150 femtolitres. An enlarged MCV is also associated with alcoholism (as are an elevated GGT and a ratio of AST:ALT of 2:1). Vitamin B12 deficiency has also been associated with macrocytic anemia (high MCV numbers). The most common causes of microcytic anemia are iron deficiency (due to inadequate dietary intake, gastrointestinal blood loss, or menstrual blood loss), thalassemia, or  chronic disease. A low MCV number in a patient with a positive stool guaiac test (bloody stool) is highly suggestive of GI cancer. In iron deficiency anemia (microcytic anemia), it can be as low as 60 to 70 femtolitres. In cases of thalassemia, the MCV may be low even though the patient is not iron deficient.
MR Surgical Indications
Indications for surgery for chronic mitral regurgitation include signs of left ventricular dysfunction.
These include an ejection fraction of less than 60 percent and a left ventricular end systolic dimension (LVESD) of greater than 45 mm.
Factors influencing the timing of surgery for MR include
symptoms, LV EF, LV end-systolic dimension, atrial fibrillation,
and pulmonary hypertension. In most situations, MV repair is the operation of choice for those patients with suitable MV anatomy. Operation is indicated for most patients with severe MR and any symptoms. Operation is also indicated in asymptomatic patients who demonstrate mild to moderate LV dysfunction (EF 0.30 to
0.60 and end-systolic dimension 40 to 55 mm). The patient with
severe LV dysfunction (EF less than 0.30 and/or end-systolic
dimension greater than 55 mm) poses a higher risk but may
undergo surgery if chordal preservation is likely.
There is controversy regarding the timing of surgery in the asymptomatic patient with severe MR and normal LV function. If MV repair can be performed with a high degree of success and the operative risk is low, it is reasonable to proceed with
surgery to prevent irreversible LV dysfunction from occurring.
However, this early operation should only be performed at centers in which there is a high likelihood of successful MV repair because of their demonstrated expertise in this area.