Persius/hicric huggingface dataset:
Mothers against decapentaplegic homolog 6
SMAD family member 6, also known as SMAD6, is a protein that in humans is encoded by the SMAD6 gene.
SMAD6 is a protein that, as its name describes, is a homolog of the Drosophila gene "mothers against decapentaplegic". It belongs to the SMAD family of proteins, which belong to the  TGF superfamily of modulators. Like many other TGF family members SMAD6 is involved in cell signalling. It acts as a regulator of TGF family (such as bone morphogenetic proteins) activity by competing with SMAD4 and preventing the transcription of SMAD4's gene products. There are two known isoforms of this protein.

# Nomenclature
The SMAD proteins are homologs of both the drosophila protein, mothers against decapentaplegic (MAD) and the C. elegans protein SMA. The name is a combination of the two. During Drosophila research, it was found that a mutation in the gene MAD in the mother repressed the gene decapentaplegic in the embryo. The phrase "Mothers against" was added as a humorous take-off on organizations opposing various issues e.g., Mothers Against Drunk Driving, or MADD; and based on a tradition of such unusual naming within the gene research community.

# Disease associations
Heterozygous, damaging mutations in SMAD6 are the most frequent genetic cause of non-syndromic craniosynostosis identified to date. 

# Interactions
Mothers against decapentaplegic homolog 6 has been shown to interact with:
- HOXC8,
- MAP3K7,
- Mothers against decapentaplegic homolog 7,
- PIAS4,  and
- STRAP.
Mothers against decapentaplegic homolog 9
Mothers against decapentaplegic homolog 9 also known as SMAD9, SMAD8, and MADH6 is a protein that in humans is enocoded by the SMAD9 gene.
SMAD9, as its name describes, is a homolog of the Drosophila gene: "Mothers against decapentaplegic". It belongs to the SMAD family of proteins, which belong to the  TGF superfamily of modulators. Like many other TGF family members, SMAD9 is involved in cell signalling. When a bone morphogenetic protein binds to a receptor (BMP type 1 receptor kinase) it causes SMAD9 to interact with SMAD anchor for receptor activation (SARA).The binding of ligands causes the phosphorylation of the SMAD9 protein and the dissociation from SARA and the association with SMAD4. It is subsequently transferred to the nucleus where it forms complexes with other proteins and acts as a transcription factor. SMAD9 is a receptor regulated SMAD (R-SMAD) and is activated by bone morphogenetic protein type 1 receptor kinase. There are two isoforms of the protein.  Confusingly, it is also sometimes referred to as SMAD8 in the literature.

# Nomenclature
The SMAD proteins are homologs of both the drosophila protein, mothers against decapentaplegic (MAD) and the C. elegans protein SMA. The name is a combination of the two. During Drosophila research, it was found that a mutation in the gene, MAD, in the mother, repressed the gene, decapentaplegic, in the embryo. The phrase "Mothers against" was added since mothers often form organizations opposing various issues e.g. Mothers Against Drunk Driving or (MADD); and based on a tradition of such unusual naming within the gene research community.
N-ethylmaleimide sensitive fusion protein
N-ethylmaleimide-sensitive factor, also known as NSF or N-ethylmaleimide sensitive fusion proteins, is an enzyme which in humans is encoded by the NSF gene.

# Function
NSF is a homohexameric AAA ATPase involved in membrane fusion. NSF is ubiquitously found in the cytoplasm of eukaryotic cells. It is a central component of the cellular machinery in the transfer of membrane vesicles from one membrane compartment to another. During this process, SNARE proteins on two joining membranes (usually a vesicle and a target membrane such as the plasma membrane) form a tight complex. This aids fusion of the vesicle with the target membrane. It has been proposed that the role of NSF is to undo these SNARE complexes once membrane fusion has occurred, using the hydrolysis of ATP as an energy source, allowing the dissociated SNAREs to be recycled for reuse in further rounds of membrane fusion.  This proposal remains controversial, however.  Recent work indicates that the ATPase function of NSF does not function in recycling of vesicles but rather functions in the act of fusing vesicles with the plasma membrane.

# SNARE hypothesis
Because  neuronal function depends on the release of neurotransmitters at a synapse  a process in which synaptic vesicles fuse with the presynaptic membrane  NSF is a key synaptic component. Thus, conditional temperature-sensitive mutations in the Drosophila melanogaster gene for NSF lead to a comatose behaviour at the restrictive temperature (and hence the gene is called comatose), presumably because neuronal functions are blocked. In Dictyostelium discoideum amoebae, similar mutations lead to a cessation of cell movement at the restrictive temperature, indicating a role for intracellular membrane transport in migration. Another neuronal role for NSF is indicated by its direct binding to the GluR2 subunit of AMPA type glutamate receptors (which detect the neurotransmitter glutamate). This gives NSF a putative role in delivery and expression of AMPA receptors at the synapse.
NSF was discovered by James Rothman and colleagues in 1987 while at Stanford University; they identified NSF after observing that a cytoplasmic factor, required for membrane fusions, was inactivated by treatment with N-ethylmaleimide. This assay enabled them to purify NSF.

# Interactions
N-ethylmaleimide sensitive fusion protein has been shown to interact with NAPA.
National Heart, Lung, and Blood Institute
The National Heart, Lung, and Blood Institute (or NHLBI) is a division of the National Institutes of Health, located in Bethesda, Maryland. It is tasked with allocating about $2.7 billion in United States tax revenue per year (fiscal year 2004 estimate), to advancing the understanding of: development and progression of disease, diagnosis of disease, treatment of disease, disease prevention, reduction of health care disparities within the American population, and advancing the effectiveness of the U.S. medical system.

# Mission statement
NHLBI is best described by the mission statement, which reads as follows:
The National Heart, Lung, and Blood Institute (NHLBI) provides leadership for a national program in diseases of the heart, blood vessels, lung, and blood; blood resources; and sleep disorders. Since October 1997, the NHLBI has also had administrative responsibility for the NIH Woman's Health Initiative.

# Operation
The Institute plans, conducts, fosters, and supports an integrated and coordinated program of basic research, clinical investigations and trials, observational studies, and demonstration and education projects. Research is related to the causes, prevention, diagnosis, and treatment of heart, blood vessel, lung, and blood diseases; and sleep disorders. The NHLBI plans and directs research in development and evaluation of interventions and devices related to prevention, treatment, and rehabilitation of patients suffering from such diseases and disorders. It also supports research on clinical use of blood and all aspects of the management of blood resources. Research is conducted in the NHLBI's own laboratories and by scientific institutions and individuals supported by research grants and contracts.
For health professionals and the public, the NHLBI conducts educational activities, including development and dissemination of materials in the above areas, with an emphasis on prevention.
The NHLBI supports research training and career development of new and established researchers in fundamental sciences and clinical disciplines to enable them to conduct basic and clinical research related to heart, blood vessel, lung, and blood diseases, sleep disorders, and blood resources through individual and institutional research training awards and career development awards.
The NHLBI coordinates relevant activities in the above areas, including the related causes of stroke, with other research institutes and federal health programs. Relationships are maintained with institutions and professional associations, and with international, national, state, and local officials as well as voluntary agencies and organizations working in the above areas.
Nonspecific ST-segment and T-wave changes
Synonyms and keywords: NSSTW changes

# Overview
Non specific ST T wave changes refer to changes in the T waves (such as inversion or flattening) and ST segments (such as ST depression) on the electrocardiogram that due not follow an anatomic distribution and are not diagnostic of any one condition.

# Causes of Non Specific ST Segment and T Wave Changes 
- Adrenal insufficiency
- Anxiety
- Central nervous system diseases
- Congestive heart failure
- Digoxin
- Electrolyte disturbances
- Gallbladder disease
- Heart failure
- Hyperkalemia
- Hyperventilation (in 70% of patients after 30 to 60 seconds)
- Hypokalemia
- Hypopituitarism
- Hypothyroidism
- Ischemic heart disease
- Left ventricular hypertrophy (LVH)
- Mitral valve prolapse (MVP)
- Orthostatic changes (3 to 23%), most prominent in the inferior leads
- Pacemaker
- Pancreatitis
- Pheochromocytoma
- Postprandial T-waves changes
- Pulmonary embolism
- Pericarditis
- Right ventricular hypertrophy (RVH)
- Truncal vagotomy
PCI equipment: guiding catheter selection

# Overview
Diagnostic catheters used for coronary arteriography are usually constructed from polyethylene or polyurethane with a fine wire braid within the wall to allow advancement and directional control (torquability) and to prevent kinking. The outer diameter size of the catheters ranges from 4 to 8F, but 5 and 6F catheters are used most commonly for diagnostic arteriography.

# Guiding Catheter Selection

## Judkins Catheters
The left Judkins catheter has been developed to allow entry into the left coronary ostium from the femoral approach with minimal catheter manipulation. A preformed left Judkins catheter can also be used from the left brachial or radial artery, but a catheter with 0.5 cm less curvature than required for the femoral approach is generally better suited for coronary cannulation. The right Judkins catheter is shaped to permit entry into the right coronary artery (RCA) with a small amount of rotational (clockwise) catheter manipulation from any vascular approach.
Selection of Judkins catheter shape is based on the body habitus of the patient and size of the aortic root. The left coronary artery (LCA) is easily engaged with the Judkins left 4.0 catheter from the femoral approach in most patients, whereas patients with a dilated ascending aorta (e.g., in the setting of congenital aortic stenosis and post- stenotic dilation) may require the use of a Judkins left 5.0 or 6.0 catheter.
Patients with large ascending aortic aneurysms may require arteriography with heat-modified catheters to achieve Judkins left 7.0 to 10.0 shapes. Use of a Judkins shape that is too small for the ascending aorta often leads to folding of the catheter within the aortic root. The best technique for removing a folded Judkins left catheter from the body involves withdrawing the folded catheter into the descending aorta and advancing a guidewire anterograde in the contralateral common iliac artery. On withdrawal of the catheter and guidewire together, the catheter straightens and can be removed safely from the body without disrupting the arterial access site.

## Amplatz Catheters
Amplatz catheters can be used for the femoral or brachial approach to coronary arteriography. The Amplatz catheters are an excellent alternative in cases in which the Judkins catheter is not appropriately shaped to enter the coronary arteries. The Amplatz L-1 or L-2 catheter may be used for coronary angiography from the right brachial or radial approach. A modified right Amplatz catheter (AR-1 or AR-2) can be used for engagement of a horizontal or upward takeoff RCA or SVG.

## Other Catheters
Other catheters used for coronary arteriography include the left IMA catheter with an angulated tip that allows engagement of the IMA or an upward takeoff RCA. Catheter shapes that permit engagement of SVGs include the multipurpose catheter, right Judkins, modified right Amplatz, and hockey stick catheters. Specially designed catheters for engagement of the coronary arteries from the radial artery have also been developed.
Pentamidine Isethionate adverse reactions

# Adverse Reactions
CAUTION: Fatalities due to severe hypotension, hypoglycemia, acute pancreatitis and cardiac arrhythmias have been reported in patients treated with pentamidine isethionate, both by the IM and IV routes.  Nephrotoxic events (increased creatinine, impaired renal function, azotemia, and renal failure) are common with the parenteral administration of pentamidine isethionate.  The administration of the drug should, therefore, be limited to the patients in whom Pneumocystis carinii has been demonstrated.
The most frequently reported spontaneous adverse events (1 to 30%) reported in clinical trials, regardless of their relation to pentamidine isethionate therapy were as follows (n=424):
Adverse events with a frequency of less than 1% incidence were as follows (No causal relationship to treatment has been established for these adverse events):
Body as a whole:
- Allergic reaction (i.e. urticaria, itching, rash), anaphylaxis, arthralgia, chills, extrapulmonary pneumocystosis, headache, night sweats, and Stevens-Johnson syndrome.
- Cardiovascular:
Abnormal ST segment of electrocardiogram, cardiac arrhythmias, cerebrovascular accident, hypertension, palpitations, phlebitis, syncope, tachycardia, vasodilatation, vasculitis and ventricular tachycardia.
- Gastrointestinal:
Abdominal pain, diarrhea, dry mouth, dyspepsia, hematochezia, hypersalivation, melena, pancreatitis, splenomegaly, and vomiting.
- Hematological:
Defibrination, eosinophilia, neutropenia, pancytopenia, and prolonged clotting time.
- Hepatic:
Hepatic dysfunction, hepatitis and hepatomegaly
- Metabolic:
Hyperglycemia, hyperkalemia, hypocalcemia, and hypomagnesemia.
- Neurological:
Anxiety, confusion, depression, dizziness, drowsiness, emotional lability, hypesthesia, insomnia, memory loss, neuropathy, nervousness, neuralgia, paranoia, paresthesia, peripheral neuropathy, seizure, tremors, unsteady gait, and vertigo.
- Respiratory system:
Asthma, bronchitis, bronchospasm, chest congestion, chest tightness, coryza, cyanosis, eosinophilic or interstitial pneumonitis, gagging, hemoptysis, hyperventilation, laryngitis, laryngospasm, non-specific lung disorder, nasal congestion, pleuritis, pneumothorax, rales, rhinitis, shortness of breath, and tachypnea.
- Skin:
Desquamation, dry and breaking hair, dry skin, erythema, dermatitis, pruritus, rash, and urticaria.
- Special senses:
Blepharitis, blurred vision, conjunctivitis, contact lens discomfort, eye pain or discomfort, loss of hearing, loss of taste, and loss of smell.
- Urogenital:
Flank pain, hematuria, incontinence, nephritis, renal dysfunction and renal failure.
From post-marketing clinical experience with pentamidine isethionate, the following adverse events have been reported: cough, diabetes mellitus/ketoacidosis, dyspnea, infiltration (extravasationsee WARNINGS), and torsades de pointes.
Perioral dermatitis (patient information)
For the WikiDoc page for this topic, click here

# Overview
Perioral dermatitis is a skin disorder characterized by tiny red bumps (papules) around the mouth.

# What are the symptoms of Perioral dermatitis?
Perioral dermatitis is usually characterized by an uncomfortable burning sensation around the mouth. Itching is not a common symptom.
In most cases, bumps (papules) and fluid- or pus-filled bumps (vesicopustules) are seen around the mouth. Rarely, a similar rash may appear around the eyes, nose, or forehead. The rash appears very similar to acne.
Usually, patients are most concerned with the cosmetic appearance of the bumps.

# What causes Perioral dermatitis?
While its exact cause is unknown, it may appear after skin creams containing steroids are applied to the face to treat other conditions.

# Who is at highest risk?
Perioral dermatitis most commonly affects young women. However, it sometimes affects men, too.

# Diagnosis
Your health care provider will likely diagnose perioral dermatitis based upon the appearance of your skin. A test for bacteria may sometimes be needed to eliminate the possibility of infection.

# When to seek urgent medical care?
Call your health care provider if you notice persistent red bumps around your mouth.

# Treatment options
Generally, skin creams containing steroids should not be used to treat perioral dermatitis. Your health care provider may choose to treat the bumps with other topical (applied directly to the skin) medications, such as metronidazole, erythromycin, benzoyl peroxide, tacrolimus, clindamycin, or pimecrolimus.
In more severe cases, oral antibiotics (such as tetracycline, doxycycline, minocycline, or erythromycin) may be required.

# Where to find medical care for Perioral dermatitis?
Directions to Hospitals Treating Perioral dermatitis

# What to expect (Outlook/Prognosis)?
Perioral dermatitis is a difficult condition to treat effectively. It often requires several months of treatment.
It is not unusual for the bumps to return, particularly if skin creams containing steroids are reapplied to the face.

# Prevention of Perioral dermatitis
Avoid using skin creams containing steroids on your face, unless specifically directed by your dermatologist.

# Sources
Pineocytoma epidemiology and demographics

# Overview

# Epidemiology and Demographics

## Incidence
- The incidence/prevalence of  is approximately  per 100,000 individuals worldwide.
- In , the incidence/prevalence of  was estimated to be  cases per 100,000 individuals worldwide.

## Prevalence
- The incidence/prevalence of  is approximately  per 100,000 individuals worldwide.
- In , the incidence/prevalence of  was estimated to be  cases per 100,000 individuals worldwide.
- The prevalence of  is estimated to be  cases annually.

## Case-fatality rate/Mortality rate
- In , the incidence of  is approximately  per 100,000 individuals with a case-fatality rate/mortality rate of %.
- The case-fatality rate/mortality rate of  is approximately .

## Age
- Patients of all age groups may develop .
- The incidence of  increases with age; the median age at diagnosis is  years.
-  commonly affects individuals younger than/older than  years of age.
-  is usually first diagnosed among .
-  commonly affects .

## Race
- There is no racial predilection to .
-  usually affects individuals of the  race.  individuals are less likely to develop .

## Gender
-  affects men and women equally.
-  are more commonly affected by  than . The  to  ratio is approximately  to 1.

## Region
- The majority of  cases are reported in .
-  is a common/rare disease that tends to affect  and .

## Developed Countries

## Developing Countries

# Epidemiology

## Prevalence
- Pineocytoma constitutes approximately 45% of the pineal parenchymal tumors.
- Pineocytoma constitutes approximately 0.4 - 1% of the intracranial neoplasms.

## Age
- Pineocytoma is a rare disease that tends to affect all age groups, most commonly in the second decade of life.
Pneumocystis jirovecii pneumonia overview

# Overview
Pneumocystis pneumonia (PCP) is a form of pneumonia caused by the yeast-like fungal Pneumocystis jirovecii (Jirovecii is pronounced "yee row vet zee eye"). The causal agent was originally described as a protozoan and spelled P. jiroveci and prior to then was classified as a form of Pneumocystis carinii, a name still in common usage. These names are discussed below. As a result, Pneumocystis pneumonia (PCP) has also been known as Pneumocystis jiroveci pneumonia and as Pneumocystis carinii pneumonia, as is also explained below.
It is relatively rare in people with normal immune systems but common among people with 
weakened immune systems, such as premature or severely malnourished children, the elderly, and especially AIDS patients, in whom it is most commonly observed today. PCP can also develop in patients who are taking immunosuppressant medications (e.g. patients who have undergone solid organ transplantation) and in patients who have undergone bone marrow transplantation.
The organism is distributed worldwide.
Polymyxin B sulfate clinical pharmacology

# Clinical Pharmacology
A wide range of antibacterial action is provided by the overlapping spectra of neomycin, polymyxin B sulfate, and gramicidin.
Neomycin is bactericidal for many gram-positive and gram-negative organisms. It is an aminoglycoside antibiotic which inhibits protein synthesis by binding with ribosomal RNA and causing misreading of the bacterial genetic code.
Polymyxin B is bactericidal for a variety of gram-negative organisms. It increases the permeability of the bacterial cell membrane by interacting with the phospholipid components of the membrane.
Gramicidin is bactericidal for a variety of gram-positive organisms. It increases the permeability of the bacterial cell membrane to inorganic cations by forming a network of channels through the normal lipid bilayer of the membrane.
Neomycin sulfate, polymyxin B sulfate, and gramicidin together are considered active against the following microorganisms: Staphylococcus aureus, streptococci, including Streptococcus pneumoniae, Escherichia coli, Haemophilus influenzae, Klebsiella/Enterobacter  species, Neisseria species, and Pseudomonas aeruginosa. The product does not provide adequate coverage against Serratia marcescens.
Pyroglutamylated RFamide peptide receptor
Pyroglutamylated RFamide peptide receptor also known as orexigenic neuropeptide QRFP receptor or G-protein coupled receptor 103 (GPR103) is a protein that in humans is encoded by the QRFPR gene.

# Function
G protein-coupled receptors (GPCRs, or GPRs) contain 7 transmembrane domains and transduce extracellular signals through heterotrimeric G proteins.
A 26-amino acid RF-amide peptide, P518 functions as a high-affinity ligand of GPR103. Both GPR103 and P518 precursor mRNA exhibited highest expression in brain. The 43-amino acid QRFP peptide, a longer form of the P518 peptide is necessary to exhibit full agonistic activity with GPR103. Intravenous administration QRFP caused release of aldosterone, suggesting that QRFP and GPR103 regulate adrenal function.
Quinine Sulfate dosage and administration

# Dosage And Administration

## Treatment of Uncomplicated P. falciparum Malaria
For treatment of uncomplicated P. falciparum malaria in adults: Orally, 648 mg (two capsules) every 8 hours for 7 days.
QUALAQUIN should be taken with food to minimize gastric upset .

## Renal Impairment
In patients with acute uncomplicated malaria and severe chronic renal impairment, the following dosage regimen is recommended: one loading dose of 648 mg QUALAQUIN followed 12 hours later by maintenance doses of 324 mg every 12 hours.
The effects of mild and moderate renal impairment on the safety and pharmacokinetics of quinine sulfate are not known .

## Hepatic Impairment
Adjustment of the recommended dose is not required in mild (Child-Pugh A) or moderate (Child-Pugh B) hepatic impairment, but patients should be monitored closely for adverse effects of quinine. Quinine should not be administered in patients with severe (Child-Pugh C) hepatic impairment .