Persius/hicric huggingface dataset:
Neuropeptides B/W receptor 1
Neuropeptides B/W receptor 1, also known as NPBW1 and GPR7, is a human protein encoded by the NPBWR1 gene. As implied by its name, it and related gene NPBW2 (with which it shares 70% nucleotide identity) are transmembranes protein that bind Neuropeptide B (NPB) and Neuropeptide W (NPW), both proteins expressed strongly in parts of the brain that regulate stress and fear including the extended amygdala and stria terminalis. When originally discovered in 1995, these receptors had no known ligands ("orphan receptors") and were called GPR7 and GPR8, but at least three groups in the early 2000s independently identified their endogenous ligands, triggering the name change in 2005.

# Structure
NPBW1 has seven transmembrane domains, which it unsurprisingly shares with NPBWR2, but also a family of somatostatin and opioid receptors, and like these proteins couple to Gi-class G proteins.

# Functions
In rodent models, NPBWR1 is over-expressed in Schwann cells associated with neuropathic pain, suggesting it inhibits inflammatory pain responses. Mice without NPBW1 exhibited a stronger hostile reaction to intruders, suggesting NPBW1 has a role in stress responses. Early studies indicated that NPB and NPW had a complex effect on appetite, but generally led to anorexia. Similarly, male rats lacking NPBWR1 exhibited hyperphagia and adult-onset obesity, though why female rats are unaffected is unknown. Researchers speculated that activating these pathways might decrease obesity, and synthesized a small-molecule ligand that is capable of stimulating both receptors at low concentrations.
Neurotransmitter transporter
Neurotransmitter transporters are proteins that span cellular membranes and that serve to carry neurotransmitters across these membranes and to transport them to specific locations.  There are more than twenty types of neurotransmitter transporters.  The transporters exist in the membranes of neurons and glia.
Vesicular transporters move neurotransmitters into synaptic vesicles, regulating the concentrations of substances within them.  Vesicular transporters rely on a proton gradient created by the hydrolysis of adenosine triphosphate (ATP) in order to carry out their work:  vesicle ATPase hydrolyzes ATP, causing protons to be pumped into the vesicle and creating a proton gradient.   Then the efflux of protons from the vesicle provides the energy to bring the neurotransmitter into the vesicle.
Neurotransmitter transporters frequently use electrochemical gradients that exist across cell membranes to carry out their work.  For example, some transporters use energy obtained by the cotransport of Na+ in order to move glutamate across membranes.
Normally, transporters in the synaptic membrane serve to remove neurotransmitters from the synaptic cleft and prevent their action or bring it to an end.  However, on occasion transporters can work in reverse, transporting neurotransmitters into the synapse, allowing these neurotransmitters to bind to their receptors and exert their effect.  This "nonvesicular release" of neurotransmitters is used by some cells, such as amacrine cells in the retina, as a normal form of neurotransmitter release.

# Types
Specific types of neurotransmitter transporters include the following:
- GABA transporters, including:
GABA transporter type 1 (GAT-1)
GABA transporter type 2 (GAT-2)
GABA transporter type 3 (GAT-3)
Betaine transporter (BGT-1)
Vesicular GABA transporter (VGAT)
- GABA transporter type 1 (GAT-1)
- GABA transporter type 2 (GAT-2)
- GABA transporter type 3 (GAT-3)
- Betaine transporter (BGT-1)
- Vesicular GABA transporter (VGAT)
- Glutamate transporters
- Glutamine transporters
- Glycine transporters, including:
Glycine transporter type 1 (GlyT-1)
Glycine transporter type 2 (GlyT-2)
- Glycine transporter type 1 (GlyT-1)
- Glycine transporter type 2 (GlyT-2)
- Monoamine transporters including:
The dopamine transporter, DAT.
The norepinephrine transporter, NET.
The serotonin transporter, SERT.
- The dopamine transporter, DAT.
- The norepinephrine transporter, NET.
- The serotonin transporter, SERT.
- Vesicular acetylcholine transporters
- Vesicular monoamine transporters

# Clinical significance
Antidepressants act by inhibiting norepinephrine and serotonin reuptake transporters.
Cocaine exerts its effect by acting on the dopamine transporter.
The antiepileptic drug tiagabine prevents the uptake of GABA by acting on the GABA transporter GAT-1.
The expression of GABA transporter GAT-1 is decreased in the axonal cartridges of chandelier neurons in schizophrenia.
Nevirapine drug interactions

# Drug Interactions
Nevirapine is principally metabolized by the liver via the cytochrome P450 isoenzymes, 3A and 2B6. Nevirapine is known to be an inducer of these enzymes. As a result, drugs that are metabolized by these enzyme systems may have lower than expected plasma levels when co-administered with nevirapine.
The results of drug interactions studies with immediate-release VIRAMUNE are expected to also apply to VIRAMUNE XR. The specific pharmacokinetic changes that occur with co-administration of nevirapine and other drugs are listed in Clinical Pharmacology, Table 5. Clinical comments about possible dosage modifications based on established drug interactions are listed in Table 4. The data in Tables 4 and 5 are based on the results of drug interaction studies conducted in HIV-1 seropositive subjects unless otherwise indicated. In addition to established drug interactions, there may be potential pharmacokinetic interactions between nevirapine and other drug classes that are metabolized by the cytochrome P450 system. These potential drug interactions are also listed in Table 4. Although specific drug interaction studies in HIV-1 seropositive subjects have not been conducted for some classes of drugs listed in Table 4, additional clinical monitoring may be warranted when co-administering these drugs.
The in vitro interaction between nevirapine and the antithrombotic agent warfarin is complex. As a result, when giving these drugs concomitantly, plasma warfarin levels may change with the potential for increases in coagulation time. When warfarin is co-administered with nevirapine, anticoagulation levels should be monitored frequently.
Niacin/lovastatin overdosage

# Overdosage
Information on acute overdose with ADVICOR in humans is limited. Until further experience is obtained, no specific treatment of overdose with ADVICOR can be recommended. The patient should be carefully observed and given supportive treatment.

## Niacin
The s.c. LD50 of niacin is 5 g/kg in rats.
The signs and symptoms of an acute overdose of niacin can be anticipated to be those of excessive pharmacologic effect: severe flushing, nausea/vomiting, diarrhea, dyspepsia, dizziness, syncope, hypotension, possibly cardiac arrhythmias and clinical laboratory abnormalities. Insufficient information is available on the potential for the dialyzability of niacin.

## Lovastatin
After oral administration of lovastatin to mice the median lethal dose observed was >15 g/m2.
Five healthy human volunteers have received up to 200 mg of lovastatin as a single dose without clinically significant adverse experiences. A few cases of accidental overdose have been reported; no patients had any specific symptoms, and all patients recovered without sequelae. The maximum dose taken was 5 to 6 g. The dialyzability of lovastatin and its metabolites in man is not known at present.
Peripheral ossifying fibroma
Synonyms and keywords: Ossifying fibroma

# Overview
Peripheral ossifying fibroma is an oral pathologic condition that appears in the mouth as an overgrowth of gingival tissue due to irritation or trauma.  Because of its overwhelming incidence on the gingiva, the condition is associated with two other diseases, though not because they occur together.  Instead, the three are associated with each other because they appear frequently on gingiva and they also begin with the letter "p": pyogenic granuloma and peripheral giant cell granuloma.  Some researchers believe peripheral ossifying fibromas to be related to pyogenic fibromas and, in some instances, are the result of a pyogenic granuloma which has undergone fibrosis and calcification.
The color of peripheral ossifying fibromas ranges from red to pink, and is frequently ulcerated.  It can be sessile or pedunculated with the size usually being less than 2 cm. Weeks or months may pass by before it seen and diagnosed.
There is a gender difference with 66% of the disease occurring in females.  The prevalence of peripheral ossifying fibromas is highest around 10 - 19 years of age.  It appears only on the gingiva, more often on the maxilla rather than the mandible, and is frequently found in the area around incisors and canines.  The adjacent teeth are usually not affected.
Peripheral ossifying fibromas appear microscopically as a combination of a mineralized product and fibrous proliferation.  The mineralized portion may be bone, cementum-like, or dystrophic calcifications.  Additionally, highly developed bone or cementum is more likely to be present when the peripheral ossifying fibroma has existed for a longer period of time.
Treatment usually involves surgical removal of the lesion down to the bone.  If there are any adjacent teeth, they are cleaned thoroughly to remove any possible source of irritation.  Recurrence is around 16%.
Nucleolar protein, member A1
H/ACA ribonucleoprotein complex subunit 1 is a protein that in humans is encoded by the GAR1 gene.

# Function
This gene is a member of the H/ACA snoRNPs (small nucleolar ribonucleoproteins) gene family. snoRNPs are involved in various aspects of rRNA processing and modification and have been classified into two families: C/D and H/ACA. The H/ACA snoRNPs also include the DKC1, NOLA2 and NOLA3 proteins. These four H/ACA snoRNP proteins localize to the dense fibrillar components of nucleoli and to coiled (Cajal) bodies in the nucleus. Both 18S rRNA production and rRNA pseudouridylation are impaired if any one of the four proteins is depleted. These four H/ACA snoRNP proteins are also components of the telomerase complex. The encoded protein of this gene contains two glycine- and arginine-rich domains and is related to Saccharomyces cerevisiae Gar1p. Two splice variants have been found for this gene.

# Interactions
Nucleolar protein, member A1 has been shown to interact with SMN1.
Nucleotide sugars metabolism
Nucleotide sugars are a group of biochemicals that act as donors for sugar residues in the glycosylation reactions that produce polysaccharides in metabolism. They are substrates for glycosyltransferases. Various forms of these molecules exist, with GDP often being used in eukaryotes for the donation of disaccharides, such as GDP-mannose, and UDP for monosaccharides such as UDP-glucose and UDP-galactose. The nucleotide sugars are also intermediates in nucleotide sugar interconversions that produce some of the activated sugars needed for glycosylation reactions.
Nucleotide sugar metabolism is particularly well-studies in bacterial pathogens, such as E. coli and Mycobacterium tuberculosis, since these molecules are required for the synthesis of glycoconjugates on the surfaces of these organisms. These glycoconjugates are virulence factors and components of the bacterial cell wall. These pathways are also studied in plants, but here the enzymes involved are less well understood.
Since most glycosylation takes place in the endoplasmic reticulum and golgi apparatus, there are a large family of nucleotide sugar transporters that allow nucleotide sugars to move from the cytoplasm, where they are produced, into the organelles where they are consumed.
Ogechukwu Hannah Nnabude, MD

# Ogechukwu Hannah Nnabude, MD
Ogechukwu Hannah Nnabude, MD Medical Graduate, Windsor University School of Medicine
Contact: hannahnnabude@yahoo.com

# Current Position at WikiDoc
- Research Fellow

# Professional Background
Ogechukwu Hannah Nnabude, MD is currently a clinical extern at Texas Medical Center. She has previously been a Chief Editor for CMDA Publications.

# Education
- Medical Degree (MD): Windsor University School of Medicine, St Kitts.
- Bachelors in Human Anatomy: Bingham University

# Brief Biography
Hannah is passionate about volunteer work, research, dermatology and reaching the medically underserved. She is currently a Clinical Extern at Texas Medical Center.
Although she completed majority of her rotations at Joseph N. France General Hospital, Hannah had the opportunity to rotate at the University Hospitals Coventry and Warwickshire NHS Trust, United Kingdom Cardiology Department. She has several medical and educational certifications.

# Research
- The Effect of Monosodium Glutamate on the Visual Cortex of Wistar Rats
Otosclerosis pathophysiology

# Pathophysiology
The pathophysiology of otosclerosis is complex.  The key lesions of otosclerosis are multifocal areas of sclerosis within the endochondral temporal bone.  These lesions share some characteristics with Pagets Disease, but they are not thought to be otherwise related.  Histopathologic studies have all been done on cadaveric temporal bones, so only inferences can be made about progression of the disease histologically.  This being said, it seems that the lesions go through an active spongiotic / hypervascular phase before developing into sclerotic phase lesions.  There have been many genes and proteins identified that, when mutated, may lead to these lesions.  Also there is mounting evidence thatmeasles virus is present within the otosclerotic foci, implicating an infectious etiology (this has also been noted in Pagets Disease).
CHL in otosclerosis is caused by two main sites of involvement of the sclerotic (or scar-like) lesions.  The best understood mechanism is fixation of the stapes footplate to the oval window of the cochlea.  This greatly impairs movement of the stapes and therefore transmission of sound into the inner ear (ossicular coupling).  Additionally the cochleas round window can also become sclerotic, and in a similar way impair movement of sound pressure waves through the inner ear (acoustic coupling).
SNHL in otosclerosis is controversial.  Over the past century, leading otologists and neurotologic researchers have argued whether the finding of SNHL late in the course of otosclerosis is due to otosclerosis or simply to typical presbycusis.  There are certainly a few well documented instances of sclerotic lesions directly obliterating sensory structures within the cochlea and spiral ligament, which have been photographed and reported post-mortem.  Other supporting data includes a consistent loss of cochlear hair cells in patients with otosclerosis; these cells being the chief sensory organs of sound reception.  A suggested mechanism for this is the release of hydrolytic enzymes into the inner ear structures by the spongiotic lesions.

## Genetics
The disease can be considered to be heritable, but its penetrance and the degree of expression is so highly variable that it may be difficult to detect an inheritance pattern.  Most of the implicated genes are transmitted in an autosomal dominant fashion.
Oxacillin sodium description

# Description
Oxacillin for Injection, USP is a semisynthetic penicillin antibiotic derived from 6-amino-penicillanic acid. It is the sodium salt in a parenteral dosage form. Each vial of Oxacillin for Injection, USP contains oxacillin sodium monohydrate equivalent to 1 gram or 2 grams of oxacillin. The sodium content is 57.30 mg  per gram oxacillin. The product is buffered with 20 mg sterile disodium hydrogen phosphate per gram oxacillin.
Oxacillin for Injection, USP is a sterile, white to off-white powder supplied in vials.
Oxacillin sodium, C19H18N3NaO5S H2O molecular weight 441.43, is designated as 4-Thia-1-azabicyclo heptane-2-carboxylic acid, 3,3-dimethyl-6- amino]-7-oxo-, monosodium salt, monohydrate,  and has the following structural formula:
Palivizumab clinical studies

# Clinical Studies
The safety and efficacy of Synagis were assessed in two randomized, double-blind, placebo-controlled trials of prophylaxis against RSV infection in children at high risk of an RSV-related hospitalization. Trial 1 was conducted during a single RSV season and studied a total of 1502 children less than or equal to 24 months of age with BPD or infants with premature birth (less than or equal to 35 weeks gestation) who were less than or equal to 6 months of age at study entry. Trial 2 was conducted over four consecutive seasons among a total of 1287 children less than or equal to 24 months of age with hemodynamically significant congenital heart disease. In both trials participants received 15 mg per kg Synagis or an equivalent volume of placebo via intramuscular injection monthly for five injections and were followed for 150 days from randomization. In Trial 1, 99% of all subjects completed the study and 93% completed all five injections. In Trial 2, 96% of all subjects completed the study and 92% completed all five injections. The incidence of RSV hospitalization is shown in Table 1. The results were shown to be statistically significant using Fishers exact test.
In Trial 1, the reduction of RSV hospitalization was observed both in children with BPD (34/266  placebo versus 39/496  Synagis) and in premature infants without BPD (19/234  placebo versus 9/506  Synagis). In Trial 2, reductions were observed in acyanotic (36/305  placebo versus 15/300  Synagis) and cyanotic children (27/343  placebo versus 19/339  Synagis).
The clinical studies do not suggest that RSV infection was less severe among children hospitalized with RSV infection who received Synagis for RSV prophylaxis compared to those who received placebo.
Palmar branch of ulnar nerve
The palmar branch of the ulnar nerve arises about 5 cm above the wrist from where the ulnar nerve splits into palmar and dorsal branches.
The palmar branch represents the continuation of the ulnar nerve as it crosses the flexor retinaculum of the hand on the lateral side of the pisiform bone, medial to and a little behind the ulnar artery.
It ends by dividing into a superficial and a deep branch.

# Additional images
- Diagram of segmental distribution of the cutaneous nerves of the right upper extremity. Anterior view.
Papillary muscle dysfunction

# Overview
Related Key Words and Synonyms:

# Epidemiology and Demographics

# Pathophysiology & Etiology
Left ventricular papillary muscles are perfused by the terminal portion of the coronary vascular bed, therefore, they are particularly vulnerable to ischemia, and any disturbance in coronary perfusion may result in papillary muscle dysfunction.
The posterior papillary muscle (supplied by the posterior descending branch of the right coronary artery) more frequently becomes ischemic and infarcted than the anterolateral papillary muscle (supplied by diagonal branches of the left anterior descending coronary artery and/or by the left circumflex artery).

## Burch classification
Burch et al first proposed that papillary muscle dysfunction could be due to either mitral valve prolapse or incomplete mitral valve closure
- Papillary muscle ischemia.
- Left ventricular dilatation.
- Non ischemic papillary muscle atrophy.
- Congenital abnormalities of papillary muscles or tendons.
- Endocardial diseases (endocarditis, fibroelastosis).
- Expansion or hypertrophic cardiomyopathy.
- Papillary muscle contraction coordination abnormalities.
- Papillary muscle or tendon rupture.

# Natural History

# Diagnosis

## Differential Diagnosis

## History and Symptoms
Palpitations, shortness of breath and cough.

## Physical Examination
- Acute onset of hypotension is present.

### Heart
- Hyperactive precordium is present
- Loud mid-to-late systolic or holosystolic murmur is present

### Lungs
- Pulmonary edema may also be present

## Laboratory Findings

### Electrocardiogram
Left atrial enlargement or non specific ST segment and T wave changes may occur.

### Chest X Ray
Left atrial enlargement may be present

### Echocardiography and Doppler Ultrasound
- Two dimensional electrocardiograph may show changes in thickness of papillary muscle, an increase in leaflet flexibility, ventricular dilatation and tendon rupture if there is any.
- Doppler US may detect mitral regurgitating flow 

# Treatment

## Pharmacotherapy

### Acute Pharmacotherapies

### Chronic Pharmacotherapies

## Surgery and Device Based Therapy

### Indications for Surgery
Parathyroid hormone receptor
There are two known parathyroid hormone receptors in mammals termed PTH1R and PTH2R. These receptors bind parathyroid hormone and are members of the  GPCR family of transmembrane proteins.
- parathyroid hormone 1 receptor (PTH1R) is the classical PTH receptor, is expressed in high levels in bone and kidney and regulates calcium ion homeostasis through activation of adenylate cyclase and phospholipase C.
- parathyroid hormone 2 receptor (PTH2R) is expressed primarily in the central nervous system, pancreas, testis, and placenta.
Paroxysmal AV Block Etiology

# Overview
Intrinsic conduction/ structural defects particularly those located in this intra His Bundle (intrinsic paroxysmal AV block), low adenosine levels (idiopathic  paroxysmal AV block) and increase vagal tone/vagal surge (extrinsic vagal paroxysmal AV block) are the major causes of paroxysmal AV block. However, several reversible causes need to be ruled out before coming to a diagnosis.

# Etiology
- Intrinsic conduction/ structural defects particularly those located in this intra His Bundle (intrinsic paroxysmal AV block), low adenosine levels (idiopathic paroxysmal AV block) and increase vagal tone/vagal surge (extrinsic paroxysmal AV block) are the major causes of paroxysmal AV block.
- However, some studies have shown an association of AV nodal blocking agents (beta blockers, calcium channel blockers),   degenerative valvular heart disease, degeneration of the conduction system (the His bundle in particular), acute coronary syndromes (inferior /anterior wall myocardial infarction in particular) and paroxysmal AV block.
- Less common causes that have been cited are Lev- Lenegre disease, aneurysmal membranous septum, rheumatic heart disease, mitral valvulitis, sarcoidosis, h/o surgery and infective endocarditis with abscess formation.
- A study of 20 patients conducted by Zabarski et al found that ischemic heart disease, dilated cardiomyopathy, carotid sinus hypersensitivity, chronic AV blocker consumption and aortic valve replacement were associated paroxysmal AV block.

# 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: Etiology of AV Block