Persius/hicric huggingface dataset:
Monocarboxylate transporter 8
Monocarboxylate transporter 8 (MCT8) is an active transporter protein that in humans is encoded by the SLC16A2 gene.

# Function
MCT8 actively transports a variety of iodo-thyronines including the thyroid hormones T3 and T4.

# Clinical significance
A genetic disorder (discovered in 2003 and 2004) is caused by mutation in the transporter of thyroid hormone, MCT8, also known as SLC16A2, is believed to be account for a significant fraction of the undiagnosed neurological disorders (usually resulting in hypotonic/floppy infants with delayed milestones). This genetic defect was known as AllanHerndonDudley syndrome (since 1944) without knowing its actual cause. It has been shown mutated in cases of X-linked leukoencephalopathy. Some of the symptoms for this disorder as are follows: normal to slightly elevated TSH, elevated T3 and reduced T4 (ratio of T3/T4 is about double its normal value). Normal looking at birth and for the first few years, hypotonic (floppy), in particular difficulty to hold the head, possibly difficulty to thrive, possibly with delayed myelination (if so, some cases are reported with an MRI pattern similar to PelizaeusMerzbacher disease, known as PMD), possibly with decreased mitochondrial enzyme activities, possibly with fluctuating lactate level. Patients have an alert face, a limited IQ, patients may never talk/walk, 50% need feeding tube, patients have a normal life span. This disease can be ruled out with a simple TSH/T4/T3 thyroid test.

# Model organisms

## Mice
A conditional knockout mouse line, called Slc16a2tm1a(KOMP)Wtsi was generated as part of the International Knockout Mouse Consortium programa high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.
Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Twenty one tests were carried out on mutant mice and three significant abnormalities were observed. Female homozygote mutants had decreased circulating glucose levels. Male hemizygous mutants had an increased susceptibility to bacterial infection. Both sexes had various abnormal plasma chemistry parameters.

## Zebrafish
A knockout zebrafish line was generated in 2014 using the zinc-finger nuclease (ZFN)-mediated targeted gene editing system. Similar to human patients, the zebrafish larvae exhibited neurological and behavioral deficiencies. They demonstrated reduced locomotor activity, altered myelin-related genes and neuron-specific deficiencies in circuit formation.

## Xenopus
Expression of mct8 has been characterised in Xenopus laevis and Xenopus tropicalis.
Multicopy single-stranded DNA
Multicopy single-stranded DNA (msDNA) is a type of extrachromosomal satellite DNA which consists of a single-stranded DNA molecule linked via a phosphodiester bond to a branched RNA molecule. The resultant structure possesses two stem-loop structures, and functions as both a primer and a template for the creation of more msDNA. It is known to encode a type of reverse transcriptase. Its function remains unknown even though many copies are present within cells.
Before the discovery of msDNA in Myxoccocus xanthus, a species of soil-dwelling bacteria, it was thought that the enzymes known as reverse transcriptases (RT) existed only in eukaryotes and viruses. The discovery led to an increase in research of the area, subsequently msDNA was found to exist within certain strains of the bacterium Escherichia coli. Further research discovered similarities between the open reading frames of HIV-encoded reverse transcriptase and msDNA, and was  later tested for reverse transcriptase activity and RNase H activity. It was found that both the RNase H domain and the enzyme reverse transcriptase were required in order for msDNA to replicate.
The discovery of msDNA has led to questions regarding where reverse transcriptase originated, as genes encoding for it have been found in prokaryotes, eukaryotes, and even viruses. After a DNA fragment coding for the production of msDNA in E. coli was discovered, it was suggested that bacteriophages may have been responsible for the introduction of the RT gene into E. coli. These discoveries suggest that reverse transcriptase played a role in the evolution of viruses from bacteria, with one hypothesis stating that with the help of reverse transcriptase, viruses may have arisen as a breakaway msDNA gene which acquired a protein coat.
Mycobacterium austroafricanum
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Mycobacterium austroafricanum
Type strain: strain E9789-SA12441 = ATCC 33464 = CCUG 37667 = CIP 105395 = DSM 44191 = HAMBI 2271 = JCM 6369.
N-Ethyl-3-piperidyl benzilate
N-ethyl-3-piperidyl benzilate (JB-318) is an anticholinergic drug related to the chemical warfare agent 3-Quinuclidinyl benzilate.
N-ethyl-3-piperidyl benzilate is less potent and shorter acting than 3-quinuclidyl benzilate, but like 3-QNB its effects on the central nervous system predominate over peripheral effects. It produces deliriant and hallucinogenic effects similar to those of plants such as datura and may be abused recreationally at low doses, however unpleasant side effects such as dysphoria, nausea and vomiting, dizziness and extreme dry mouth tend to make abuse of these kind of drugs uncommon. Both the N-methyl and N-ethyl analogues of 3-piperidyl benzilate are however Schedule I controlled drugs.
Radiolabelled versions of this drug have been used in scientific research to map the distribution of muscarinic acetylcholine receptors in the brain, however this drug has slightly lower binding affinity than the N-methyl analogue and so is less potent and not so widely used for this application.
Nafcillin sodium how supplied

# How Supplied
Each nafcillin for injection, USP Pharmacy Bulk Package bottle contains nafcillin sodium equivalent to 10 grams of nafcillin.
Nafcillin for Injection, USP is a sterile, white to yellowish-white powder supplied in Pharmacy Bulk Package bottles as follows:
- Nafcillin for Injection USP, 10 g
- Pharmacy Bulk Package bottles in a Box of 1- NDC 55150-124-99
Store at 20 to 25C (68 to 77F). 
The container closure is not made with natural rubber latex.
Nafcillin sodium microbiology

# Microbiology
Penicillinase-resistant penicillins exert a bactericidal action against penicillin-susceptible microorganisms during the state of active multiplication. All penicillins inhibit the biosynthesis of the bacterial cell wall. The drugs in this class are highly resistant to inactivation by staphylococcal penicillinase and are active against penicillinase producing strains of Staphylococcus aureus. The penicillinase-resistant penicillins are active in vitro against a variety of other bacteria.

## Susceptibility Test Methods
When available, the clinical microbiology laboratory should provide the results of in vitro susceptibility test results for antimicrobial drugs used in local hospitals and practice areas to the physician as periodic reports that describe the susceptibility profile of nosocomial and community-acquired pathogens. These reports should aid the physician in selecting the most effective antimicrobial.

## Dilution Techniques
Quantitative methods are used to determine antimicrobial minimum inhibitory concentrations (MICs). These MICs provide estimates of the susceptibility of bacteria to antimicrobial compounds. The MICs should be determined using a standardized procedure based on dilution method1,2 (broth, agar or microdilution) or equivalent. It has been reported that determination of susceptibility or resistance of a microorganism to all penicillinase-resistant penicillins, including nafcillin, may be deduced by testing microorganisms against either oxacillin or cefoxitin.2 For this reason, routine dilution testing of nafcillin is not advised and susceptibility to nafcillin should be determined by dilution using standardized inoculum and concentrations of oxacillin according to the criteria in table 1.

## Diffusion Techniques
Quantitative methods that require measurement of zone diameters also provide reproducible estimates of the susceptibility of bacteria to antimicrobial compounds. One such standardized procedure2,3 requires the use of standardized inoculum concentrations. It has been reported that determination of susceptibility or resistance of a microorganism to all penicillinase-resistant penicillins, including nafcillin, may be deduced by testing microorganisms against either oxacillin or cefoxitin.2 Disk diffusion results using cefoxitin have been shown to be more reproducible than those obtained with oxacillin,4,5 therefore cefoxitin is the preferred reagent for testing nafcillin susceptibility by diffusion. Reports from the laboratory providing results of the standard single-disk susceptibility test with a 30 microgram cefoxitin disk should be interpreted according to the following criteria in Table 2.
Naratriptan contraindications

# Contraindications
Naratriptan tablets should not be given to patients with history, symptoms, or signs of ischemic cardiac, cerebrovascular, or peripheral vascular syndromes. In addition, patients with other significant underlying cardiovascular diseases should not receive naratriptan tablets. Ischemic cardiac syndromes include, but are not limited to, angina pectoris of any type (e.g., stable angina of effort, vasospastic forms of angina such as the Prinzmetal variant), all forms of myocardial infarction, and silent myocardial ischemia.
Cerebrovascular syndromes include, but are not limited to, strokes of any type as well as transient ischemic attacks. Peripheral vascular disease includes, but is not limited to, ischemic bowel disease (see WARNINGS).
Because naratriptan tablets may increase blood pressure, they should not be given to patients with uncontrolled hypertension (see WARNINGS).
Naratriptan tablets are contraindicated in patients with severe renal impairment (creatinine clearance, <15 mL/min) (see CLINICAL PHARMACOLOGY and DOSAGE AND ADMINISTRATION).
Naratriptan tablets are contraindicated in patients with severe hepatic impairment (Child-Pugh grade C) (see CLINICAL PHARMACOLOGY and DOSAGE AND ADMINISTRATION).
Naratriptan tablets should not be administered to patients with hemiplegic or basilar migraine.
Naratriptan tablets should not be used within 24 hours of treatment with another 5-HT1 agonist, an ergotamine-containing or ergot-type medication like dihydroergotamine or methysergide.
Naratriptan tablets are contraindicated in patients with hypersensitivity to naratriptan or any of the components.
Naratriptan drug interactions

# Drug Interactions
Cases of life-threatening serotonin syndrome have been reported during combined use of SSRIs or SNRIs and triptans (see WARNINGS).
Ergot-containing drugs have been reported to cause prolonged vasospastic reactions. Because there is a theoretical basis that these effects may be additive, use of ergotamine-containing or ergot-type medications (like dihydroergotamine or methysergide) and naratriptan within 24 hours is contraindicated (see CONTRAINDICATIONS).
The administration of naratriptan with other 5-HT1 agonists has not been evaluated in migraine patients. Because their vasospastic effects may be additive, coadministration of naratriptan and other 5-HT1 agonists within 24 hours of each other is not recommended (see CONTRAINDICATIONS).
Naratriptan tablets are not known to interfere with commonly employed clinical laboratory tests.
Necrolytic migratory erythema
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# Overview
Necrolytic migratory erythema (NME) is a classical symptom observed in patients with glucagonoma and is present in 80% of cases. Associated NME is characterized by the spread of erythematous blisters and swelling across areas subject to greater friction and pressure, including the lower abdomen, buttocks, perineum, and groin.

# Diagnosis

## Symptoms
It consists of serpiginous (slow progressing) erythematous plaques. Where the migratory edge has an "eroded" appearance.  It usually starts in the Perineum.
Weight loss, anemia , mild diabetes, diarrhea and glossitis are associated. Liver metastasis is often present.

# Differentiating necrolytic migratory erythema from Other Diseases
- Necrolytic migratory erythema has to be differentiated from Reactive gyrate erythematous eruptions, such as:
Erythema annulare centrifugum (EAC)
Erythema gyratum repens (EGR)
- Erythema annulare centrifugum (EAC)
- Erythema gyratum repens (EGR)
- Reactive (figurate or gyrate) erythemas that are associated with malignancy include:
Neuropsychological assessment
Neuropsychological assessment was traditionally carried out to assess the extent of impairment to a particular skill and to attempt to locate an area of the brain which may have been damaged after brain injury or neurological illness.  With the advent of neuroimaging techniques, location of space-occupying lesions can now be accurately determined so the focus has now moved onto the measurement of cognition and behaviour, including examining the effects of any brain injury or neuropathological process that a person may have experienced.  A core part of neuropsychological assessment is the administration of neuropsychological tests for the formal assessment of cognitive functioning.  Aspects of cognitive functioning that are assessed typically include orientation, new-learning/memory, intelligence, language, visuoperception, and executive-functioning. However, clinical neuropsychological assessment is more than this and also focuses on a person's psychological, personal, interpersonal and wider contextual circumstances.
Assessment may be carried for a variety of reasons, such as:
- Clinical evaluation, to understand the pattern of cognitive strengths as well as any difficulties a person may have, and to aid decision making for use in a medical or rehabilitation environment.
- Scientific investigation, to examine an hypothesis about the structure and function of cognition to be tested, or to provide information that allows experimental testing to be seen in context of a wider cognitive profile.
- Medico-legal assessment, to be used in a court of law as evidence in a legal claim or criminal investigation.
Miller outlined three broad goals of neuropsychological assessment.  Firstly, diagnosis, to determine the nature of the underlying problem.  Secondly, to understand the nature of any brain injury or resulting cognitive problem (see neurocognitive deficit) and its impact on the individual, as a means of devising a rehabilitation programme or offering advice as to an individual's ability to carry out a certain tasks (for example, fitness to drive, or returning to work).  And lastly, assessments may be undertaken to measure change in functioning over time, such as to determine the consequences of a surgical procedure or the impact of a rehabilitation programme over time.
Neutrophil cytosolic factor 1
Neutrophil cytosol factor 1, also known as p47phox, is a protein that in humans is encoded by the NCF1 gene.

# Function
The protein encoded by this gene is a 47 kDa cytosolic subunit of neutrophil NADPH oxidase. This oxidase is a multicomponent enzyme that is activated to produce superoxide anion. Mutations in this gene have been associated with chronic granulomatous disease.
Genetic variability in the NCF1 gene has been found to be related to a higher chance of getting autoimmune diseases such as Sjogren's syndrome, rheumatoid arthritis and lupus erythematosus.

## p47 is vital to the activation of NADPH oxidase. P47 becomes heavily phosphorylated

# Interactions
Neutrophil cytosolic factor 1 has been shown to interact with:
- Moesin,
- Neutrophil cytosolic factor 4, and
- RELA.
Neutrophil cytosolic factor 4
Neutrophil cytosol factor 4 is a protein that in humans is encoded by the NCF4 gene.

# Function
The protein encoded by this gene is a cytosolic regulatory component of the superoxide-producing phagocyte NADPH-oxidase, a multicomponent enzyme system important for host defense. This protein is preferentially expressed in cells of myeloid lineage. It interacts primarily with neutrophil cytosolic factor 2 (NCF2/p67-phox) to form a complex with neutrophil cytosolic factor 1 (NCF1/p47-phox), which further interacts with the small G protein RAC1 and translocates to the membrane upon cell stimulation. This complex then activates flavocytochrome b, the membrane-integrated catalytic core of the enzyme system. The PX domain of this protein can bind phospholipid products of the PI(3) kinase, which suggests its role in PI(3) kinase-mediated signaling events. The phosphorylation of this protein was found to negatively regulate the enzyme activity. Alternatively spliced transcript variants encoding distinct isoforms have been observed.

# Clinical significance
GWAS studies showed that Crohn's disease patient with certain SNPs in NCF4 are more susceptible to get Crohn's disease.  Crohn's patient with rs4821544 variants showed a decreased reactive oxygen species after stimulation with GM-CSF which is a proinflammtory cytokine.

# Interactions
Neutrophil cytosolic factor 4 has been shown to interact with Ku70, Neutrophil cytosolic factor 1 and Moesin.
Niacin/lovastatin description

# Description
ADVICOR (niacin extended-release and lovastatin) is intended to facilitate the daily administration of its individual components, Niaspan and lovastatin, when used together for the intended patient population (see INDICATIONS AND USAGE and DOSAGE AND ADMINISTRATION).
ADVICOR contains niacin extended-release and lovastatin in combination. Lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, and niacin are both lipid-altering agents.
Niacin is nicotinic acid, or 3-pyridinecarboxylic acid. Niacin is a white, nonhygroscopic crystalline powder that is very soluble in water, boiling ethanol and propylene glycol. It is insoluble in ethyl ether. The empirical formula of niacin is C6H5NO2 and its molecular weight is 123.11. Niacin has the following structural formula:
Lovastatin is ]-1,2,3, 7,8,8a-hexahydro-3,7-dimethyl-8--1-naphthalenyl 2-methylbutanoate. Lovastatin is a white, nonhygroscopic crystalline powder that is insoluble in water and sparingly soluble in ethanol, methanol, and acetonitrile. The empirical formula of lovastatin is C24H36O5 and its molecular weight is 404.55. Lovastatin has the following structural formula:
ADVICOR tablets contain the labeled amount of niacin and lovastatin and have the following inactive ingredients: hypromellose, povidone, stearic acid, polyethylene glycol, titanium dioxide, polysorbate 80.
The individual tablet strengths (expressed in terms of mg niacin/mg lovastatin) contain the following coloring agents:
ADVICOR 500 mg/20 mg - Iron Oxide Yellow, Iron Oxide Red.
ADVICOR 750 mg/20 mg - FD&C Yellow #6/Sunset Yellow FCF Aluminum Lake.
ADVICOR 1000 mg/20 mg - Iron Oxide Red, Iron Oxide Yellow, Iron Oxide Black.
ADVICOR 1000 mg/40 mg - Iron Oxide Red.
Niemann-Pick disease overview
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# Overview
Niemann-Pick disease (NPD) is a group of autosomal recessive disorders that are classified into two broad types. Types A and B NPD are lysosomal storage diseases due to sphingomyelinase deficiency. Type C NPD results from defective intracellular trafficking of cholesterol. Both types are featured by deposition of lipids such as cholesterol, sphingomyelin, and bisphosphonate in various organs.
Types A and B are charachterized by an early age of onset and progressive CNS disease in type A. Type A typically has onset in the first 6 months, with rapidly progressive CNS deterioration, spasticity, failure to thrive, and massive hepatosplenomegaly. In contrast, type B has a later, more variable onset and progression of hepatosplenomegaly, with eventual development of cirrhosis and hepatic replacement by foam cells. Affected patients develop progressive pulmonary disease with dyspnea, hypoxemia, and a reticular infiltrative pattern on chest x-ray.
The diagnosis is established by markedly decreased (110% of normal) sphingomyelinase activity in nucleated cells. There is no specific treatment for Niemann-Pick disease. The efficacy of hepatic or bone marrow transplantation has not been proven yet.  Clinical trials using enzyme therapy are expected in the near future.

# Historical Perspective

# Classification

# Pathophysiology

# Causes

# Differentiating Niemann-Pick disease from Other Diseases

# Epidemiology and Demographics

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis

## Natural History

## Complications

## Prognosis

# Diagnosis

## Diagnostic Criteria

## History and Symptoms

## Physical Examination

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Surgery

## Prevention
No-reflow phenomenon overview

# Overview
Many definitions have been given to this phenomenon based on individual's area of specialty, but the definition that unites all fields was by Kloner et al in 1974 who described the condition as the inability to adequately perfuse myocardium after temporary occlusion
-f an epicardial coronary artery without evidence of persistent mechanical obstruction, thus implying ongoing myocardial ischaemia.  When defined angiographically, it is an acute reduction in coronary flow (TIMI grade 0-1) in the absence of dissection, thrombus, spasm, or high-grade residual stenosis at the original target lesion.  In other words, it is the failure of blood to reperfuse an ischemic area after the physical obstruction has been removed or bypassed.  It has been clearly shown that a complete restoration of epicardial blood flow (TIMI Flow Grade 3) does not correlate with a better myocardial perfusion in achieving better clinical outcomes.  Therefore, over the years, attention has shifted towards methods to evaluate myocardial perfusion.  A lesser degree of obstruction to coronary blood flow (TIMI grade 2) is sometimes referred to as slow flow.  No-reflow is the decline in TIMI flow from TIMI flow 3 or 2 to TIMI flow 1 or 0, which occurs >5 mm distal to the lesion.  No-reflow is an important predictor of mortality after PCI .

# Historical Perspective
This phenomenon was first described by Krug et al  during induced myocardial infarction in dog subjects in 1966, but the term 'no-reflow' was first used by Majno and colleagues in 1967 when they observed that brains of rabbits exposed to prolonged ischemia suffered significant changes in the microvasculature which impeded blood flow to the brain cells.