Persius/hicric huggingface dataset:
Melanin-concentrating hormone receptor 1
Melanin-concentrating hormone receptor 1, also known as MCH1, is one of the melanin-concentrating hormone receptors found in all mammals. 
The protein encoded by this gene, a member of the G protein-coupled receptor family 1, is an integral plasma membrane protein which binds melanin-concentrating hormone. The encoded protein can inhibit cAMP accumulation and stimulate intracellular calcium flux, and is probably involved in the neuronal regulation of food consumption. Although structurally similar to somatostatin receptors, this protein does not seem to bind somatostatin.

# Function
MCH1 is thought to have a number of functions including in the regulation of appetite, and in stress, anxiety and depression.

# Selective ligands

## Agonists
- Melanin concentrating hormone (MCH)
- S-36057 - modified MCH 6-13 fragment substituted with 3-iodotyrosine at N-terminus via dioxyoctanoyl linker, used as 125I radioligand for mapping MCH1 in vivo.

## Antagonists
- ATC-0065
- ATC-0175
- GW-803,430
- NGD-4715
- SNAP-7941
- SNAP-94847
- T-226,296
Melanin-concentrating hormone receptor 2
Melanin-concentrating hormone receptor 2 (MCH2) also known as G-protein coupled receptor 145 (GPR145) is a protein that in humans is encoded by the MCHR2 gene.
MCH2 is also found in dogs, ferrets, and some other primates and carnivores, but is not found in mice or rats. This has delayed research into the receptor as a therapeutic target, due to most early pharmaceutical research usually being conducted in small mammals such as mice, rats or rabbits which lack the MCH2 gene and its receptor product.

# Clinical significance
Treatment of human cells expressing MCHR2 with MCH resulted in upregulation of IDH3A, PCK1 and PFKFB4 and the downregulation of INSIG2 and ACOT8.
Methysergide use in specific populations

# Use In Specific Populations

### Pregnancy Category: X
Sansert (methysergide maleate) is contraindicated in pregnancy due to its oxytocic actions.

### Nursing Mothers
There are no specific studies on the use of Sansert (methysergide maleate) in nursing mothers. Ergot alkaloids, in general, appear in mothers milk.
Sansert (methysergide maleate) is a semi-synthetic compound structurally related to ergotamine, and thus it may appear in breast milk. Ergot alkaloids have been reported to cause nausea, vomiting, diarrhea and weakness in the nursing infant and suppression of prolactin secretion and lactation in the mother.
Because of the potential for serious adverse reactions in nursing infants from Sansert (methysergide maleate), a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.

### Pediatric Use
Safety and effectiveness in pediatric patients have not been established.
Metipranolol use in specific populations

# Use in Specific Populations

### Pregnancy
Teratogenic Effects

### Pregnancy Category: C
No drug related effects were reported for the segment II teratology study in fetal rats after administration, during organogenesis, to dams of up to 50 mg/kg/day. Metipranolol ophthalmic solution has been shown to increase fetal resorption, fetal death, and delayed development when administered orally to rabbits at 50 mg/kg/day during organogenesis.
There are no adequate and well-controlled studies in pregnant women. Metipranolol ophthalmic solution should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

### Nursing Mothers
It is not known whether metipranolol ophthalmic solution is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when metipranolol ophthalmic solution is administered in nursing women.

### Pediatric Use
Safety and effectiveness in pediatric patients have not been established.
Geriatric Use
No overall differences in safety or effectiveness have been observed between elderly and younger patients.
Microsomal triglyceride transfer protein
Microsomal triglyceride transfer protein large subunit is a protein that in humans is encoded by the MTTP gene.
MTP encodes the large subunit of the heterodimeric microsomal triglyceride transfer protein. Protein disulfide isomerase (PDI) completes the heterodimeric microsomal triaglyceride transfer protein, which has been shown to play a central role in lipoprotein assembly. Mutations in MTP can cause abetalipoproteinemia.
Apolipoprotein B48 on chylomicra and Apolipoprotein B100 on LDL, IDL, and VLDL are important for MTP binding.

# Interactive pathway map
Click on genes, proteins and metabolites below to link to respective articles. 
-  The interactive pathway map can be edited at WikiPathways: "Statin_Pathway_WP430"..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}

# Pharmacology
Drugs that inhibit MTTP prevent the assembly of apo B-containing lipoproteins thus inhibiting the synthesis of chylomicrons and VLDL and leading to decrease in plasma levels of LDL-C.
- Lomitapide (Juxtapid) was approved by the US FDA for adjunctive treatment of homozygous familial hypercholesterolemia.
- Dirlotapide (Slentrol) and mitratapide (Yarvitan) are veterinary drugs for the management of obesity in dogs.
Mitochondrial membrane transport protein
Mitochondrial membrane transport proteins are proteins which exist in the membranes of mitochondria and which serve to transport molecules and other factors such as ions into or out of the organelles.

# Examples
Examples of mitochondrial transport proteins include the following:
- The mitochondrial permeability transition pore, which opens in response to increased mitochondrial calcium (Ca2+) load and oxidative stress
- The mitochondrial calcium uniporter which transports calcium from the cytosol of the cell into the mitochondrial matrix
- The mitochondrial sodium/calcium exchanger, which carries Ca2+ ions out of the matrix in exchange for Na+ ions.  These transport proteins serve to maintain the proper electrical and chemical gradients in mitochondria by keeping ions and other factors in the right balance between the inside and outside of mitochondria.
Myotonia congenita (patient information)
For the WikiDoc page for this topic, click here

# Overview
Myotonia congenita is an inherited condition that affects muscle relaxation. It is congenital, meaning that it is present from birth.

# What are the symptoms of Myotonia congenita?
The hallmark of this condition is the myotonia -- the inability of the muscle to quickly relax after contracting. For example, after a handshake, the person is only very slowly able to open and pull away his hand.
Early symptoms may include:
- Difficulty in swallowing
- Gagging
- Stiff movements that improve when they are repeated
- Shortness of breath or tightening of the chest at the beginning of exercise
Children with myotonia congenita often appear to be muscular and well-developed. The child may not have symptoms of myotonia congenita until age 2 or 3.

# What causes Myotonia congenita?
Myotonia congenita is caused by a change (mutation) to a gene. It is passed down from either one or both parents to the children (inherited).
Myotonia congenita is believed to be caused by a problem in the part of the muscle cells that are needed for muscles to relax. Abnormal repeated electrical discharges occur in the muscles, causing a stiffness called myotonia.

# Who is at highest risk?
People with a family history of myotonia congenita are at risk, as the condition is genetic.

# When to seek urgent medical care?
Call your health care provider if your child has symptoms of myotonia congenita.

# Diagnosis
The doctor may ask if there is a family history of myotonia congenita.
Tests include:
- Muscle biopsy
- Test of the electrical activity in muscles (EMG)

# Treatment options
Treatment for symptoms includes:
- Mexiletine
- Phenytoin
- Procainamide

# Where to find medical care for Myotonia congenita?
Directions to Hospitals Treating Myotonia congenita

# What to expect (Outlook/Prognosis)?
People can do well with this condition. Symptoms only occur when a movement is first started. After a few repetitions, the muscle relaxes and the movement becomes normal. Symptoms may improve later in life.

# Possible complications
- Aspiration pneumonia caused by swallowing difficulties
- Frequent choking, gagging, or difficulty swallowing in an infant
- Abdominal muscle weakness
- Chronic joint problems

# Sources
National Human Genome Research Institute
The National Human Genome Research Institute (NHGRI) is a division of the National Institutes of Health, located in Bethesda, Maryland.
NHGRI began as the National Center for Human Genome Research (NCHGR), which was established in 1989 to carry out the role of the NIH in the International Human Genome Project (HGP). The HGP was developed in collaboration with the United States Department of Energy (DOE) and began in 1990 to map the human genome. In 1993, NCHGR expanded its role on the NIH campus by establishing the Division of Intramural Research (DIR) to apply genome technologies to the study of specific diseases. In 1996, the Center for Inherited Disease Research (CIDR) was also established (co-funded by eight NIH institutes and centers) to study the genetic components of complex disorders.
In 1997 the United States Department of Health and Human Services (DHHS) renamed NCHGR the National Human Genome Research Institute (NHGRI), officially elevating it to the status of research institute - one of 27 institutes and centers that make up the NIH.
Now, with the human genome sequence complete since April 2003, scientists around the world have access to a database that greatly facilitates and accelerates the pace of biomedical research.

# Important Events in NHGRI History
- October 1, 1988 - The Office for Human Genome Research is created within the Office of the Director, National Institutes of Health (NIH). Also, NIH and the Department of Energy (DOE) sign a memorandum of understanding to "coordinate research and technical activities related to the human genome."
- April 11, 1996 - Human DNA sequencing begins with pilot studies at six universities in the United States.
- March 1999 - Large-scale sequencing of the human genome begins.
- April 2003 - The National Human Genome Research Institute (NHGRI) celebrates the completion of the human genome sequence, the 50th anniversary of the description of the DNA double helix and the publication of the vision document for the future of genomics research.
- May 4, 2007-The National Human Genome Research Institute (NHGRI) and the National Cancer Institute (NCI), have teamed with Group Health Cooperative in Seattle and Henry Ford Health System in Detroit to launch the Multiplex Initiative, a study to investigate the interest level of healthy, young adults in receiving genetic testing for eight common conditions.
Neurogenic locus notch homolog protein 4
Neurogenic locus notch homolog 4 also known as notch 4 is a protein that in humans is encoded by the NOTCH4 gene located on chromosome 6.

# Gene
An alternative splice variant of the NOTCH4 gene has been described, but its biological significance has not been determined.

# Structure
The neurogenic locus notch homolog 4 protein is a member of the Notch family. Members of this type 1 transmembrane protein family share structural characteristics. These include an extracellular domain consisting of multiple epidermal growth factor-like (EGF) repeats, and an intracellular domain that consists of multiple, but different, domain types.

# Function
Notch protein family members play a role in a variety of developmental processes by controlling cell fate decisions. The Notch signaling pathway is an evolutionarily conserved intercellular signaling pathway that regulates interactions between physically adjacent cells
In Drosophilia, notch interacts with its cell-bound ligands (delta and serrate), and establishes an intercellular signaling pathway that then plays a key role in development. Homologues of the notch-ligands have also been identified in humans, but precise interactions between these ligands and the human notch homologues remain to be determined. The notch protein is cleaved in the trans-Golgi network, and then presented on the cell surface as a heterodimer. The protein functions as a receptor for membrane bound ligands, and may play a role in vascular, renal, and hepatic development.

# Clinical significance
Mutations in the notch4 gene may be associated with susceptibility to schizophrenia in a small portion of cases.
Niacin/Simvastatin indications and usage

# Indications and Usage
Therapy with lipid-altering agents should be only one component of multiple risk factor intervention in individuals at significantly increased risk for atherosclerotic vascular disease due to hypercholesterolemia. Drug therapy is indicated as an adjunct to diet when the response to a diet restricted in saturated fat and cholesterol and other nonpharmacologic measures alone has been inadequate.

## Patients with hypercholesterolemia Requiring Modifications of Lipid Profiles

### SIMCOR
SIMCOR is indicated to reduce Total-C, LDL-C, Apo B, non-HDL-C, TG, or to increase HDL-C in patients with primary hypercholesterolemia and mixed dyslipidemia when treatment with simvastatin monotherapy or Niacin extended-release monotherapy is considered inadequate.
SIMCOR is indicated to reduce TG in patients with hypertriglyceridemia when treatment with simvastatin monotherapy or Niacin extended-release monotherapy is considered inadequate.

### Limitations of use
No incremental benefit of SIMCOR on cardiovascular morbidity and mortality over and above that demonstrated for simvastatin monotherapy and Niacin monotherapy has been established.
Niacin extended-release, one of the components of SIMCOR, at doses of 1,500  2,000 mg/day, in combination with simvastatin, did not reduce the incidence of cardiovascular events more than simvastatin in a randomized controlled trial of patients with cardiovascular disease and mean baseline LDL-C levels of 74 mg per deciliter.
Nitrofurantoin dosage and administration

# Dosage and Administration
Macrobid capsules should be taken with food.
Adults and Pediatric Patients Over 12 Years: One 100 mg capsule every 12 hours for seven days.
HOW SUPPLIED
Macrobid is available as 100 mg opaque black and yellow capsules imprinted (Band) Macrobid (Band) on one half and 52427-285 on the other.
NDC 52427-285-01  bottle of 100
Storage and Handling
Store at controlled room temperature (59 to 86F or 15 to 30C).
Meets USP Dissolution Test 2
Pancreatic neuroendocrine tumor overview

# Overview
Pancreatic neuroendocrine tumors (PanNETs, PETs, or PNETs), often referred to as "islet cell tumors", or "pancreatic endocrine tumors" are neuroendocrine neoplasms that arise from cells of the endocrine (hormonal) and nervous system within the pancreas.
PanNETs are a type of neuroendocrine tumor, representing about one third of gastroenteropancreatic neuroendocrine tumors (GEP-NETs). Many PanNETs are benign, while some are malignant. Aggressive PanNET tumors have traditionally been termed "islet cell carcinoma".
PanNETs are quite distinct from the usual form of pancreatic cancer, the majority of which are adenocarcinomas, which arises in the exocrine pancreas. Only 1 or 2% of clinically significant pancreas neoplasms are PanNETs.
Paroxysmal AV Block physical examination

# Overview
There are no specific physical examination findings seen in patients with paroxysmal AV block.

# Physical Examination
There are no specific physical examination findings seen in patients with paroxysmal AV block.

## Appearance of the Patient
- Patients with paroxysmal AV block may appear to be altered as paroxysmal AV block commonly presents with syncope/presyncope.

## Vital Signs
- Tachycardia with regular pulse or irregular pulse
- Bradycardia with regular pulse or irregular pulse.

## Skin
- Skin examination of patients with paroxysmal AV Block is usually normal.

## HEENT
- HEENT examination of patients with paroxysmal AV Block is usually normal

## Neck
- Neck examination of patients with paroxysmal AV Block  is usually normal.
- Jugular venous distension (rule out)
- Carotid bruits may be auscultated unilaterally/bilaterally using the bell/diaphragm of the otoscope (rule out).

## Lungs
- Pulmonary examination of patients with paroxysmal AV block is usually normal.

## Heart
- Heave / thrill (rule out)
- Friction rub (rule out)
- S1 (rule out)
- S2 (rule out)
- S3 (rule out)
- S4 (rule out)
- Gallops (rule out)
- A high/low grade early/late systolic murmur / diastolic murmur best heard at the base/apex/(specific valve region) may be heard using the bell/diaphgram of the stethoscope (rule out).

## Abdomen
- Abdominal examination of patients with paroxysmal AV block is usually normal.

## Back
- Back examination of patients with paroxysmal AV block is usually normal.

## Genitourinary
- Genitourinary examination of patients with paroxysmal AV block is usually normal.

## Neuromuscular
- Patient is usually oriented to persons, place, and time.
- Altered mental status (rule out)

## Extremities
- Extremities examination of patients with paroxysmal AV block is usually normal.
Pegylated interferon alfa-2a description

# Description
PEGASYS, peginterferon alfa-2a, is a covalent conjugate of recombinant alfa-2a interferon (approximate molecular weight  20,000 daltons) with a single branched bis-monomethoxy polyethylene glycol (PEG) chain (approximate MW 40,000 daltons). The PEG moiety is linked at a single site to the interferon alfa moiety via a stable amide bond to lysine. Peginterferon alfa-2a has an approximate molecular weight of 60,000 daltons. Interferon alfa-2a is produced using recombinant DNA technology in which a cloned human leukocyte interferon gene is inserted into and expressed in Escherichia coli.
PEGASYS is a sterile, preservative-free, colorless to light yellow injectable solution administered subcutaneously.
Each vial of 180 mcg/mL peginterferon alfa-2a (expressed as the amount of interferon alfa-2a) also contains acetic acid (0.05 mg), benzyl alcohol (10 mg), polysorbate 80 (0.05 mg), sodium acetate trihydrate (2.62 mg), and sodium chloride (8 mg) at pH 6  0.5.
Each prefilled syringe of 180 mcg/0.5 mL peginterferon alfa-2a (expressed as the amount of interferon alfa-2a) also contains acetic acid (0.0231 mg), benzyl alcohol (5 mg), polysorbate 80 (0.025 mg), sodium acetate trihydrate (1.3085 mg), and sodium chloride (4 mg) at pH 6  0.5.
Each Autoinjector containing 180 mcg/0.5 mL peginteferon alfa-2a (expressed as the amount of interferon alfa-2a), also contains acetic acid (0.0231 mg), benzyl alcohol (5 mg), polysorbate 80 (0.025 mg), sodium acetate trihydrate (1.3085 mg), and sodium chloride (4 mg) at pH 6  0.5.
Each Autoinjector containing 135 mcg/0.5 mL peginteferon alfa-2a (expressed as the amount of interferon alfa-2a), also contains acetic acid (0.0231 mg), benzyl alcohol (5 mg), polysorbate 80 (0.025 mg), sodium acetate trihydrate (1.3085 mg), and sodium chloride (4 mg) at pH 6  0.5.
Because the autoinjectors are designed to deliver the full content, autoinjectors should only be used for patients who need the full dose (180 or 135 mcg). If the required dose is not available in an autoinjector, prefilled syringes, or vials should be used to administer the required dose. The autoinjector is for subcutaneous administration only.
Penicillin V potassium adverse reactions

# Adverse Reactions
Although the incidence of reactions to oral penicillins has been reported with much less frequency than following parenteral therapy, it should be remembered that all degrees of hypersensitivity, including fatal anaphylaxis, have been reported with oral penicillin.
The most common reactions to oral penicillin are nausea, vomiting, epigastric distress, diarrhea, and black hairy tongue. The hypersensitivity reactions reported are skin eruptions (maculopapular to exfoliative dermatitis), urticaria and other serum-sicknesslike reactions, laryngeal edema, and anaphylaxis.
Fever and eosinophilia may frequently be the only reaction observed. Hemolytic anemia, leukopenia, thrombocytopenia, neuropathy, and nephropathy are infrequent reactions and usually associated with high doses of parenteral penicillin.
Periodic table (electron configurations)
- Grayed out electron numbers indicate subshells that are filled to their maximum.
- Configurations of elements with light gray background are uncertain or not available.
Configurations that are unavailable are guessed to be similar to the element directly above on the Periodic Table.
- The bracketed noble gas symbols on the left represent the inner configurations that are the same in each period. Written out these are:
- Note the non-linear shell ordering, which comes about is due to the different energies of smaller and larger shells.
Phosphoribosylaminoimidazole carboxylase
Phosphoribosylaminoimidazole carboxylase (or AIR carboxylase) is an enzyme involved in nucleotide biosynthesis and in particular in purine biosynthesis. It catalyzes the conversion of 5'-phosphoribosyl-5-aminoimidazole ("AIR") into 5'-phosphoribosyl-4-carboxy-5-aminoimidazole ("CAIR") as described in the reaction:

# In plants and fungi
Phosphoribosylaminoimidazole carboxylase is a fusion protein in plants and fungi, but consists of two non-interacting proteins in bacteria, PurK and PurE.
The crystal structure of PurE indicates a unique quaternary structure that confirms the octameric nature of the enzyme.

# In Escherichia coli
In the bacterium Escherichia coli the reaction is catalyzed in two steps carried out by two separate enzymes, PurK and PurE.
PurK, N5-carboxyaminoimidazole ribonucleotide synthetase, catalyzes the conversion of 5-aminoimidazole ribonucleotide ("AIR"), ATP, and bicarbonate to N5-carboxyaminoimidazole ribonucleotide ("N5-CAIR"), ADP, and Pi.
PurE, N5-carboxyaminoimidazole ribonucleotide mutase, converts N5-CAIR to CAIR, the sixth step of de novo purine biosynthesis. In the presence of high concentrations of bicarbonate, PurE is reported able to convert AIR to CAIR directly and without ATP. Some members of this family contain two copies of this domain.