Persius/hicric huggingface dataset:
Leukocoria

# Overview
Leukocoria refers to an abnormal white hue of the retina when viewed through routine medical ophthalmoscopy.

# Diagnosis
Usually, when a light is shone through the iris, the retina appears red to the observer. In leukocoria, the retina abnormally appears white. This may indicate congential cataracts, retrolental fibroplasia, corneal scarring, retinoblastoma, ocular toxocariasis, persistence of the tunica vasculosa lentis (PFV/PHPV), or Coats' disease, Norrie Disease, etc.  Because of the potential life threatening nature of retinoblastoma, that condition is usually considered in the evaluation of leukocoria.

## Physical Examination

### Eyes
The term is also sometimes spelled leukokoria. In British English the usual spelling is leucocoria.
Prevalence

# Overview
Prevalence is a measure of disease frequency which counts the total number of existing cases of disease within a population during a specified period of time. As it is a proportion, prevalence is often expressed in term of a percentage within a population.

# Epidemiologic Usage
- Prevalence rates for specific diseases are calculated from periodic health examination surveys that government agencies conduct. Annual changes in prevalence as reported in this booklet only reflect changes in the population; rates do not change until theres a new survey. Changes in rates can only be evaluated with data from new surveys. 

## Types of Prevalence
- Point prevalence measures the proportion of a population that is diseased at a single point in time. It is viewed as a "snapshot" of disease frequency associated to a specific time period.
- Period prevalence measures the proportion of a population that is diseased during a specified duration of time. Period prevalence differs from point prevalence in that it counts the number of cases that were present at the start of the defined time period and accounts for the number that develop over time. It is viewed more as a serious of snapshots of disease frequency associated to a string of time versus a single time point.
- Lifetime prevalence (LTP) is the number of individuals in a statistical population that at some point in their life (up to the time of assessment) have experienced a "case" (e.g., a disorder), compared to the total number of individuals (i.e. it is expressed as a ratio or percentage). Often, a 12-month prevalence (or some other type of "period prevalence") is used in conjunction with lifetime prevalence. There is also point prevalence, the prevalence of disorder at a more specific (a month or less) point in time. There is also a related figure lifetime morbid risk - the theoretical prevalance at any point in life for anyone, regardless of time of assessment. (example: Synopsis of article on "How Prevalent Is Schizophrenia?" from Public Library of Science)

# Critical Considerations
- Prevalence utilizes two key assumptions:
- The numerator (number of existing cases of disease) accounts for all currently living cases 'regardless of disease onset.
- The denominator (number in total population) accounts for everyone in the population studied. This includes sick, healthy, at-risk and non-at-risk.
- Prevalence, as a value, is a proportional measurement and can only between zero to one or 0-100%.

# Relationship to Incidence
- P/(1-P) = IR - D (where: P is prevalence, IR is incidence rate, and D is duration of time)
Lipotropin
Lipotropin is a hormone produced by the cleavage of pro-opiomelanocortin (POMC).  The anterior pituitary gland produces the pro-hormone POMC, which is then cleaved again to form adrenocorticotropin (ACTH) and -lipotropin (-LPH).

# -Lipotropin
-Lipotropin is a 90-amino acid polypeptide that is the carboxy-terminal fragment of POMC. It was initially reported to stimulate melanocytes to produce melanin. It was also reported to perform lipid-mobilizing functions such as lipolysis and steroidogenesis. However, no subsequent studies have been published that support these early findings and no receptor has been identified for -lipotropin.
-Lipotropin can be cleaved into smaller peptides. In humans, -lipotropin, -MSH, and -endorphin, are all possible fragments of -lipotropin. -Lipotropin is the predominant opioid of the anterior human and rat pituitary gland. It is found in essentially equimolar concentrations to that of corticotropin. Evidence shows that -Lipotropin is metabolized into endorphins that can greatly affect mood and behavior and is thus regarded as a prohormone.

# -Lipotropin
-lipotropin is the amino-terminal peptide fragment of -lipotropin. In humans, it has 56 amino acids. Gamma lipotropin is identical to the first 56 amino acid sequences of -lipotropin. It can be cleaved to -melanocyte stimulating hormone.

# Use in sport
Lipotropin has also, under its alternate name AOD-9604 (Anti-Obesity Drug-9604), been connected with controversies in Australian Rules Football. Allegations have arisen around the use of the drug and its administration to players of the Essendon Football Club as a supplement, including weekly administration to players in the 2012 season.  The matters are currently under investigation due to the relationship between Lipotropin and growth hormones, as noted by club medical staff.
Live birth
For organisms where the embryo develops inside the mother as opposed to an egg, see vivipary.

# Overview
A live birth occurs when a fetus, whatever its gestational age, exits the maternal body and subsequently shows any sign of life, such as voluntary movement, heartbeat, or pulsation of the umbilical cord, for however brief a time and regardless of whether the umbilical cord or placenta are intact.

# Historical Perspective
This definition of the term "live birth" was created by the World Health Organization in 1950 and is chiefly used for public health and statistical purposes. Whether the birth is vaginal or by Caesarean section, and whether the neonate is ultimately viable, is not relevant to this statistical definition. However, the term "live birth" was in common use long before 1950.
In the United States, the term "born alive" is defined by federal statute.
Lofentanil
Lofentanil is an opioid analgesic that is an analogue of fentanyl and was developed in the early 1980s.
Lofentanil is most similar to the highly potent opioid carfentanil (4-carbomethoxyfentanyl). Lofentanil can be described as 3-methylcarfentanil, or 3-methyl-4-carbomethoxyfentanyl. However it is interesting to note that while 3-methylfentanyl is considerably more potent than fentanyl itself, lofentanil is only slightly stronger than carfentanil. This suggests that substitution at both the 3 and 4 positions of the piperidine ring introduces steric hindrance which prevents -opioid affinity from increasing much further. As with other 3-substituted fentanyl derivatives such as ohmefentanyl, the stereoisomerism of lofentanil is very important, with some stereoisomers being much more potent than others.
Lofentanil is very similar to carfentanil in effects, but has a longer duration of action. This makes it unsuitable for most practical applications, with carfentanil being the preferred agent for tranquilizing large animals, and short-acting derivatives such as sufentanil or remifentanil being preferred for medical use in human surgical procedures. The long duration and high lipophilicity of lofentanil has been suggested as an advantage for certain types of analgesia, but the main application for lofentanil at the present time is research into opiate receptors.
Side effects from lofentanil would be predicted to be similar to other potent fentanyl analogues, and would include sedation, euphoria, nausea, and pronounced itching and respiratory depression. Side effects from lofentanil might be particularly problematic given its reportedly long duration of action. Another side effect which is characteristic of fentanyl and its derivatives is their tendency to rapidly induce tolerance, due to their high binding affinity triggering rapid internalization of chronically activated opiate receptors. This might be expected to be a particular problem with lofentanil as it is not only one of the most potent drugs in the series, but also is longer acting than most other fentanyl analogues, meaning that development of tolerance triggered by receptor over-activation is likely to be especially rapid.
Lonidamine

# Overview
Lonidamine is a derivative of indazole-3-carboxylic acid, which for a long time, has been known to inhibit aerobic glycolysis in cancer cells. It seems to enhance aerobic glycolysis in normal cells, but suppress glycolysis in cancer cells. This is most likely through the inhibition of the mitochondrially bound hexokinase. Later studies in Ehrlich ascites tumor cells showed that lonidamine inhibits both respiration and glycolysis leading to a decrease in cellular ATP.
Clinical trials of lonidamine in combination with other anticancer agents for a variety of cancers has begun.  This is due to its proven ability to inhibit energy metabolism in cancer cells, and to enhance the activity of anticancer agents.
Lonidamine has been used in the treatment of brain tumours in combination with radiotherapy and temozolomide. Results showed that a combination of temozolomide and lonidamine at clinically achievable, low plasma concentrations, could inhibit tumour growth, and lonidamine could reduce the dose of temozolomide required for radiosensitization of brain tumours.
A derivative of lonidamine, gamendazole, is in testing as a possible male contraceptive pill.
Lophophine
Lophophine, homomyristicylamine, (or 3-methoxy-4,5-methylendioxyphenethylamine) is an homologue of MMDA.  It is also related to mescaline and Alexander Shulgin suggests it could be a natural component in the peyote cactus because it is the only logical chemical intermediate for the biosynthesis of several of tetrahydroisoquinolines known to be present in the cactus.  Lophophine produces hallucinogenic, psychedelic, and entheogenic effects that are similar to mescaline.

# Chemistry
Lophophine is in a class of compounds commonly known as phenethylamines, and the full chemical name is 2-(7-methoxy-1,3-benzodioxol-5-yl)ethanamine.

# Effects
Little is known about the psychopharmacological effects of lophophine, but it does appear to have qualitative and quantitative effects that resemble mescaline.  Shulgin reports in Mescaline: The Chemistry and Pharmacology of its Analogs that lophophine is active at 150-250 mg.  He states at these dosages that the action of this base is quite similar to that of mescaline; there is a peaceful elevation of mood, euphoria, enhancement of visual perception, and the generation of eyes-closed imagery.  At dosages above 300 mg, visual distortions that resemble those of mescaline begin to appear.  He also notes that in contrast to mescaline, little nausea is produced from lophophine ingestion.

# Pharmacology
The mechanism that produces the hallucinogenic and entheogenic effects of lophophine is unknown. Although structure-activity relationships mean that it is likely to be caused by 5-HT2A receptor agonism - similar to other psychedelic drugs such as LSD and Mescaline.

# Dangers
The toxicity of lophophine is not known.

# Legality
Lophophine is unscheduled and unregulated in the United States, however because of its close similarity in structure and effects to MDA and MMDA, possession and sale of lophophine may be subject to prosecution under the Federal Analog Act.
Loracarbef

# Overview
Loracarbef is a synthetic carbacephem antibiotic. Loracarbef has a spectrum of activity similar to that of the second generation cephalosporins. It is an analogue of cefaclor from which the sulfur atom is replaced with a methylene group. Therefore loracarbef has a greater stability in solution and may be stored at room temperature.
Diarrhea is the most common adverse effect. Side effects are more frequently seen with children under the age of twelve. It received FDA approval in 1991. Its use was discontinued in 2006.

# Category
Carbacephem

# Brand Names
LORABID (DISCONTINUED)

# Mechanism of Action
Loracarbef is an oral, synthetic beta-lactam antibiotic of the carbacephem class. Loracarbef, like all beta-lactams and cephalosporins, inhibits penicillin binding proteins, enzymes that create the cross-linkage of the peptidoglycan polymer. This binding leads to interference with the formation and remodeling of the cell wall structure.
Lornoxicam

# Overview
Lornoxicam (INN, or chlortenoxicam; trade name Xefo, among others) is a non-steroidal anti-inflammatory drug (NSAID) of the oxicam class with analgesic (pain relieving), anti-inflammatory and antipyretic (fever reducing) properties. It is available in oral and parenteral formulations.

# Indications
Lornoxicam is used for the treatment of various types of pain, especially resulting from inflammatory diseases of the joints, osteoarthritis, surgery, sciatica, and other inflammations.

# Contraindications
The drug is contraindicated in patients that must not take other NSAIDs, possible reasons including salicylate sensitivity, gastrointestinal bleeding and bleeding disorders, and severe impairment of heart, liver or kidney function. Lornoxicam is not recommended during pregnancy and breastfeeding and is contraindicated during the last third of pregnancy.

# Adverse effects
Lornoxicam has side effects similar to other NSAIDs, most commonly mild ones like gastrointestinal disorders (nausea and diarrhea) and headache. Severe but seldom side effects include bleeding, bronchospasms and the extremely rare StevensJohnson syndrome.

# Interactions
Interactions with other drugs are typical of NSAIDs. Combination with vitamin K antagonists like warfarin increases the risk of bleeding. Combination with ciclosporin can lead to reduced kidney function, and to acute renal failure in rare cases. Lornoxicam can also increase the adverse effects of lithium, methotrexate and digoxin and its derivatives. The effect of diuretics, ACE inhibitors and angiotensin II receptor antagonists can be reduced, but this is only relevant in patients with special risks like heart failure. As with piroxicam, cimetidine can increase plasma levels but is unlikely to cause relevant interactions.
Magaldrate

# Overview
Magaldrate (INN) is a common antacid drug that is used for the treatment of duodenal and gastric ulcers, esophagitis from gastroesophageal reflux.

# Available forms
Magaldrate is available in the form of oral suspension or tablets.

# Pharmacology
Magaldrate is a hydroxymagnesium aluminate complex that is converted rapidly in gastric acid to Mg(OH)2 and Al(OH)3, which are absorbed poorly and thus provide a sustained antacid effect.

# Interactions and adverse reactions
Magaldrate may negatively influence drugs like tetracyclines, benzodiazepines, and indomethacin. High doses or prolonged usage may lead to an increment of defecation and a reduction in feces consistence. In some cases it can alter the functionality of the gastrointestinal tract, occasionally provoking constipation or diarrhea.

# Brand names
The drug is sold with the following brand names: Digecid Plus (Beximco Pharma, Bangladesh), Marlox Plus (Incepta pharma Bangladesh), Gastid (SK+F, Bangladesh), Novelta (Bangladesh), Gadral (Italy); Magaltop (Italy); Magralibi (Italy); Mylanta (Australia); Riopan (Argentina, Austria, Brazil, Egypt, Germany, Italy, Mexico, Belgium, Switzerland, Greece).
Loxoprofen
Loxoprofen (INN) is a non-steroidal anti-inflammatory drug in the propionic acid derivatives group, which also includes ibuprofen and naproxen among others. It is marketed in Brazil, Mexico and Japan by Sankyo as its sodium salt, loxoprofen sodium, under the trade name Loxonin, and in Argentina as Oxeno. It is available in these countries for oral administration, and a transdermal preparation was approved for sale in Japan on January 2006.

# Pharmacokinetics
Loxoprofen is a prodrug. It is quickly converted to its active trans-alcohol metabolite following oral administration, and reaches its peak plasma concentration within 30 to 50 minutes.

# Mechanism of action
As most NSAIDs, loxoprofen is a non-selective cyclooxygenase inhibitor, and works by reducing the synthesis of prostaglandins from arachidonic acid.

# Interactions
Loxoprofen should not be administered concomitantly with second-generation quinolone antibiotics such as ciprofloxacin and norfloxacin, as it increases their inhibition of GABA and this may cause seizures.
It may also increase the plasma concentration of warfarin, methotrexate, sulfonylurea derivatives and lithium salts, so care should be taken when loxoprofen is administered to patients taking any of these drugs.
M2 protein
The M2 protein is a proton-selective ion channel protein, integral in the viral envelope of the influenza A virus. The channel itself is a homotetramer (consists of four identical M2 units), where the units are helixes stabilized by two disulfide bonds. It is activated by low pH.

# Structure
The M2 protein unit consists of three protein domains: the 24 amino acids on the N-terminal end, exposed to the outside environment, the 19 hydrophobic aminoacids on the transmembrane region, and the 54 aminoacids on the C-terminal end, oriented towards the inside of the viral particle.

# Function
The M2 protein has an important role in the life cycle of the influenza A virus. It is located in the viral envelope. It enables hydrogen ions to enter the viral particle (virion) from the endosome, thus lowering pH of the inside of the virus, which causes dissociation of the viral matrix protein M1 from the ribonucleoprotein RNP. This is a crucial step in uncoating of the virus and exposing its content to the cytoplasm of the host cell.

# Inhibition and resistance
The function of the M2 channel can be inhibited by antiviral drugs amantadine and rimantadine, which then blocks the virus from taking over the host cell. The molecule of the drug binds to the transmembrane region, sterically blocking the channel. This stops the protons from entering the virion, which then does not disintegrate.
However, the M2 gene is susceptible to mutations. When one of five aminoacids in the transmembrane region gets suitably substituted, the virus gains resistance to the existing M2 inhibitors. As the mutations are relatively frequent, presence of the selection factors (eg. using amantadine for treatment of sick poultry) can lead to emergence of a resistant strain.
MAX (gene)
MAX (also known as myc-associated factor X) is a gene that in humans encodes the MAX transcription factor.

# Function
The protein product of MAX contains the basic helix-loop-helix and leucine zipper motifs. It is therefore included in the bHLHZ family of transcription factors. It is able to form homodimers with other MAX proteins and heterodimers with other transcription factors, including Mad, Mxl1 and Myc. The homodimers and heterodimers compete for a common DNA target site (the E-box) in a gene promoter zone. Rearrangement of dimers (e.g., Mad:Max, Max:Myc) provides a system of transcriptional regulation with greater diversity of gene targets. Max must dimerise in order to be biologically active.
Transcriptionally active hetero- and homodimers involving Max can promote cell proliferation as well as apoptosis.

# Interactions
The protein product of Max has been shown to interact with:
- Myc,
- MNT,
- MSH2,
- MXD1,
- MXI1,
- MYCL1,
- N-Myc,
- SPAG9,
- TEAD1, and
- Transformation/transcription domain-associated protein.

# Clinical relevance
This gene has been shown mutated in cases of hereditary pheochromocytoma. More recently the Max gene becomes mutated and becomes inactivated in small cell lung cancer (SCLC). This is mutually exclusive with alterations at Myc and BRG1, the latter coding for an ATPase of the SWI/SNF complex. It was demonstrated that the BRG1 product regulates the expression of Max through direct recruitment to the Max promoter region, and that depletion of BRG1 strongly hinders cell growth, specifically in Max-deficient cells, suggesting that the two together cause synthetic lethality. Furthermore, Max required BRG1 to activate neuroendocrine transcriptional programs and to up-regulate Myc targets, such as glycolytic-related genes.
MEGA Trial

# Objective
To assess whether evidence for treatment  of hypercholesterolemia with statins derived from western populations can be extrapolated to the Japanese population.

# Methods
Primary prevention of cardiovascular disease with pravastatin in Japan (MEGA Study) was a prospective, randomized, open-labelled, blinded study which enrolled 8214 Japanese men and postmenopausal women aged 40 to 70 years and with a serum total cholesterol concentration of 220 to 270 mg/dL. All the patients were randomly assigned to receive either diet therapy alone or diet therapy plus pravastatin 10 to 20 mg daily and followed-up for a mean period of 5.3 years.

# Results
The following results were obtained at the end of follow-up period:
- Mean total cholesterol was reduced by 2.1% and 11.5% in the patients treated with diet alone and diet plus pravastatin respectively.
- Similarly mean LDL-C reduced by 3.2% and 18.0%.
- Significantly lower CAD in patients treated with diet plus pravastatin than in those treated with diet alone.

# Conclusion
Treatment with a low dose of pravastatin reduces the risk of CAD in Japan by much the same amount as higher doses have shown in Europe and the USA.
MLX (gene)
Max-like protein X is a protein that in humans is encoded by the MLX gene.

# Function
The product of this gene belongs to the family of basic helix-loop-helix leucine zipper (bHLH-Zip) transcription factors. These factors form heterodimers with Mad proteins and play a role in proliferation, determination and differentiation. This gene product may act to diversify Mad family function by its restricted association with a subset of the Mad family of transcriptional repressors, namely Mad1 and Mad4. Alternatively spliced transcript variants encoding different isoforms have been identified for this gene.

# Interactions
MLX (gene) has been shown to interact with MNT, MXD1 and MLXIPL.
MN1 (gene)
MN1 is a gene found on human chromosome 22, with gene map locus 22q12.3-qter.  Its official full name is meningioma (disrupted in balanced translocation) 1 because it is disrupted by a balanced translocation (4;22) in a meningioma.

# Function
MN1 is a transcription coregulator that enhances or represses RAR/RXR-mediated gene transcription through interaction with RAC3 and p300.  MN1 also acts as a coactivator of the vitamin D receptor.

# Clinical significance
Its inactivation may be part of the cause of certain meningiomas. A potential link to leukemia including acute myeloid leukemia has also been described.
MNT (gene)
MNT (Max's Next Tango) is a Max-binding protein that is encoded by the MNT gene 

# Function
The Myc/Max/Mad network comprises a group of transcription factors that co-interact to regulate gene-specific transcriptional activation or repression. This gene encodes a protein member of the Myc/Max/Mad network. This protein has a basic-Helix-Loop-Helix-zipper domain (bHLHzip) with which it binds the canonical DNA sequence CANNTG, known as the E box, following heterodimerization with Max proteins. This protein is a transcriptional repressor and an antagonist of Myc-dependent transcriptional activation and cell growth. This protein represses transcription by binding to DNA and recruiting Sin3 corepressor proteins through its N-terminal Sin3-interaction domain 

# Interactions
MNT (gene) has been shown to interact with MLX, SIN3A and MAX.