Persius/hicric huggingface dataset:
Guanidinoacetate methyltransferase deficiency
Guanidinoacetate methyltransferase deficiency, also called GAMT deficiency, is an autosomal recessive metabolic disorder that primarily affects the nervous system and muscles. It is the first observed disorder of creatine metabolism.

# Presentation
This disorder usually appears in the first few months of life, when development of new motor and cognitive skills becomes delayed or stops. Eventually, affected children may lose previously acquired skills such as head control or the ability to sit unsupported.

# Diagnosis
People with guanidinoacetate methyltransferase deficiency have a wide spectrum of neurological symptoms. In addition to mental retardation and muscle weakness, some children with this disorder experience seizures. They may also develop autistic behaviors that affect communication and social interaction. Some affected children exhibit certain involuntary movements such as tremors or facial tics.
Guanidinoacetate methyltransferase deficiency is a very rare disorder. Only a few dozen affected individuals have been reported worldwide. Of these, approximately one third are of Portuguese origin.

# Pathophysiology
Mutations in the GAMT gene are associated with guanidinoacetate methyltransferase deficiency. This gene codes for the enzyme guanidinoacetate methyltransferase, which participates in the two-step synthesis of the compound creatine from amino acids glycine, arginine and methionine. Specifically, guanidinoacetate methyltransferase controls the second step of the sequence, in which creatine is produced from another compound called guanidinoacetate.
GAMT gene mutations impair the ability of the guanidinoacetate methyltransferase enzyme to participate in creatine synthesis. Creatine is needed for many tissues in the body to be able to store and use energy properly.  The effects of guanidinoacetate methyltransferase deficiency are most severe in organs and tissues that require large amounts of energy, such as the brain and muscles.
This disorder is inherited in an autosomal recessive pattern, which means the defective gene is located on an autosome, and two copies of the gene - one from each parent - are required to inherit the disorder. The parents both carry one copy of the defective gene, but are usually not affected by the disorder.
IMITREX tablet patient counseling information

# Patient Counseling Information
Advise the patient to read the FDA-approved patient labeling (Patient Information).
Risk of Myocardial Ischemia and/or Infarction, Prinzmetals Angina, Other Vasospasm-Related Events, Arrhythmias, and Cerebrovascular Events: Inform patients that IMITREX Tablets may cause serious cardiovascular side effects such as myocardial infarction or stroke. Although serious cardiovascular events can occur without warning symptoms, patients should be alert for the signs and symptoms of chest pain, shortness of breath, irregular heartbeat, significant rise in blood pressure, weakness, and slurring of speech, and should ask for medical advice if any indicative sign or symptoms are observed. 
Apprise patients of the importance of this follow-up .
Anaphylactic/Anaphylactoid Reactions: Inform patients that anaphylactic/anaphylactoid reactions have occurred in patients receiving IMITREX Tablets. Such reactions can be life threatening or fatal. In general, anaphylactic reactions to drugs are more likely to occur in individuals with a history of sensitivity to multiple allergens .
Concomitant Use With Other Triptans or Ergot Medications: Inform patients that use of IMITREX Tablets within 24 hours of another triptan or an ergot-type medication (including dihydroergotamine or methysergide) is contraindicated .
Serotonin Syndrome: Caution patients about the risk of serotonin syndrome with the use of IMITREX Tablets or other triptans, particularly during combined use with SSRIs, SNRIs, TCAs, and MAO inhibitors .
Medication Overuse Headache: Inform patients that use of acute migraine drugs for 10 or more days per month may lead to an exacerbation of headache and encourage patients to record headache frequency and drug use (e.g., by keeping a headache diary) .
Pregnancy: Inform patients that IMITREX Tablets should not be used during pregnancy unless the potential benefit justifies the potential risk to the fetus .
Nursing Mothers: Advise patients to notify their healthcare provider if they are breastfeeding or plan to breastfeed .
Ability to Perform Complex Tasks: Treatment with IMITREX Tablets may cause somnolence and dizziness; instruct patients to evaluate their ability to perform complex tasks after administration of IMITREX Tablets.
IMITREX is a registered trademark of the GlaxoSmithKline group of companies.
Immune hemolytic anemia (patient information)
For the WikiDoc page for this topic, click here
Synonyms and Keywords: Autoimmune hemolytic anemia, AIHA.

# Overview
Immune hemolytic anemia is a condition in which there is a reduced blood cell count due to the premature destruction of red blood cells by the immune system.

# What are the symptoms of Immune hemolytic anemia?
- Dark urine
- Fatigue
- Pale (pallor) or yellow (jaundice) skin color
- Rapid heart rate
- Shortness of breath

# What causes Immune hemolytic anemia?
- Immune hemolytic anemia occurs when antibodies form against the body's own red blood cells. The antibodies destroy the blood cells because the immune system mistakenly recognizes these blood cells as foreign material within the body.
- The antibodies may be caused by:
- Complication of another disease
- Past blood transfusions
- Pregnancy (if the baby's blood type is different from the mother's)
- Reaction to certain medications
- Reaction to certain infections
- Secondary immune hemolytic anemia: If the cause of antibody formation is a disease or medication.
- Idiopathic autoimmune hemolytic anemia: accounts for one-half of all immune hemolytic anemias.

# Who is at highest risk?
Risk factors are related to the causes.

# When to seek urgent medical care?
Call your health care provider if you have unexplained fatigue or chest pain, or signs of infection.

# Diagnosis
- Absolute reticulocyte count
- Direct or indirect Coombs' test
- Hemoglobin in the urine
- LDH (level of this enzyme rises as a result of tissue damage)
- Red blood cell count (RBC), hemoglobin, and hematocrit
- Serum bilirubin levels
- Serum free hemoglobin
- Serum haptoglobin

# Treatment options
- Treatment with a steroid medication such as prednisone is usually the first therapy tried.
- If a steroid medication does not improve the condition, removal of the spleen (splenectomy) may be considered. Treatments with drugs that suppress the immune system (immunosuppressants) may also be given if you do not respond to steroids.
- Blood transfusions, if needed for severe anemia, are given with caution because the blood may not be compatible and it may cause further hemolysis.

# Where to find medical care for Immune hemolytic anemia?
Directions to Hospitals Treating Immune hemolytic anemia

# Prevention
Screening for antibodies in donated blood and in the recipient may prevent hemolytic anemia related to blood transfusions.

# What to expect (Outlook/Prognosis)?
- The disease may start quickly and be very serious, or it may remain mild and not need specific treatment.
- In most people, steroids or splenectomy can control anemia.
- In others, treatment can usually partially control the anemia.

# Possible complications
- Severe anemia rarely leads to death.
- Severe infection may occur as a complication of treatment with steroids, other medications that suppress the immune system, or splenectomy, because these treatments impair the body's ability to fight infection.
List of chemical compounds with unusual names
Chemical nomenclature, replete as it is with compounds with complex names, is a repository for some very peculiar and sometimes startling names. A browse through the Physical Constants of Organic Compounds in the CRC Handbook of Chemistry and Physics (a fundamental resource) will reveal not just the whimsical work of chemists, but the sometimes peculiar compound names that occur as the consequence of simple juxtaposition. Some names derive legitimately from their chemical makeup, from the geographic region where they may be found, the plant or animal species from which they are isolated or the name of the discoverer.
Some are given intentionally unusual trivial names based on their structure, a notable property or at the whim of those who first isolate them. However many trivial names predate formal naming conventions. Trivial names can also be ambiguous or carry different meanings in different industries, geographic regions and languages.
Godley noted that "Trivial names having the status of INN or ISO are carefully tailor-made for their field of use and are internationally accepted". In his preface to Chemical Nomenclature, Thurlow wrote that "Chemical names do not have to be deadly serious". A classic website in existence since 1997  and maintained at the University of Bristol lists a selection of molecules with silly or unusual names strictly for entertainment. These so-called silly or funny trivial names (of course depending on culture) can also serve an educational purpose. In an article in the Journal of Chemical Education Dennis Ryan argues that students of organic nomenclature (considered a dry and boring subject) may actually take an interest in it when tasked with the job of converting funny-sounding chemical trivial names to their proper systematic names. 
The collection listed below presents a sample of trivial names and gives an idea how chemists are inspired when they coin a brand new name for a chemical compound outside of systematic naming. It also includes some examples of systematic names and acronyms that accidentally resemble English words.
National Center for Biotechnology Information

# Overview
The National Center for Biotechnology Information (NCBI) is part of the  United States National Library of Medicine (NLM), a branch of the National Institutes of Health.  The NCBI is located in Bethesda, Maryland and was founded in 1988. The NCBI houses genome sequencing data in GenBank and an index of biomedical research articles in PubMed Central and PubMed, as well as other information relevant to biotechnology. All these databases are available online through the Entrez search engine.
The NCBI is directed by David Lipman, one of the original authors of the BLAST sequence alignment program and a widely respected figure in Bioinformatics. He also leads an intramural research program, including groups led by Stephen Altschul (another BLAST co-author), David Landsman, and Eugene Koonin (a prolific author on comparative genomics).

# GenBank
The NCBI has had responsibility for making available the GenBank DNA sequence database since 1992. GenBank coordinates with individual laboratories and other sequence databases such as those of the European Molecular Biology Laboratory (EMBL) and the DNA Database of Japan (DDBJ).
Since 1992, NCBI has grown to provide other databases in addition to GenBank. NCBI provides Online Mendelian Inheritance in Man, the Molecular Modeling Database (3D protein structures), the Unique Human Gene Sequence Collection, a Gene Map of the Human genome, a Taxonomy Browser, and coordinates with the National Cancer Institute to provide the Cancer Genome Anatomy Project. The NCBI assigns a unique identifier (Taxonomy ID number) to each species of organism.
The NCBI has software tools that are available by WWW browsing or by FTP. For example, BLAST is a sequence similarity searching program. BLAST can do sequence comparisons against the GenBank DNA database in less than 15 seconds.

# NCBI Bookshelf
The NCBI Bookshelf is a collection of freely available, on-line versions of selected biomedical books. As of March 2006, the Bookshelf had 55 titles covering aspects of molecular biology, biochemistry, cell biology, genetics, microbiology, a couple of disease states from a molecular and cellular point of view, research methods, and virology. Some of the books are online versions of previously published books, while others, such as Coffee Break (book), are written and edited by NCBI staff.  The Bookshelf is a complement to the Entrez PubMed repository of peer-reviewed publication abstracts in that Bookshelf contents provide established perspectives on evolving areas of study and a context in which many disparate individual pieces of reported research can be organized.
Non-rapid eye movement sleep arousal disorder
Synonyms and keywords: NREM sleep arousal disorder

# Overview
Non-rapid eye movement sleep arousal disorder is characterized by incomplete arousal from the first third of a sleep cycle associated with either sleepwalking or sleep terrors.

# Differential Diagnosis
- Alcohol-induced blackouts
- Breathing-related sleep disorders
- Dissociative amnesia, with dissociative fugue
- Sleep-related seizures
- Malingering or other voluntary behavior occurring during wakefulness
- Medication-induced complex behaviors
- REM sleep behavior disorder
- Night eating syndrome
- Nightmare disorder
- Panic disorder
- Parasomnia overlap syndrome

# Epidemiology and Demographics

## Prevalence
- Among children, the prevalence of non-rapid eye movement sleep arousal disorders is 10,000 to 30,000 per 100,000 (10% to 30%).
- Among adults, the lifetime prevalence of non-rapid eye movement  sleep arousal disorder is 29,200 (29.2%) among adults.

# Risk Factors
- Sedative use
- Sleep deprivation
- Sleep-wake schedule disruptions
- Fatigue
- Physical or emotional stress

# Prognosis
Poor prognostic factors include:
- Emotional stress
- Males during adulthood
- Fatigue
- Females during childhood
- Physical stress
- Sleep-wake schedule disruptions

# Diagnostic Criteria

## DSM-V Diagnostic Criteria for Non-Rapid Eye Movement Sleep Arousal Disorder
Naratriptan how supplied storage and handling

# How Supplied
Naratriptan tablets, USP are available as follows:
1 mg, white colored D shaped, film-coated tablets debossed with SZ on one side and 247 on other side
NDC 0781-5526-37 in unit-of-use pack of 9 tablets (1 blister card containing 9 tablets in 1 carton)
2.5 mg, green colored D shaped, film-coated tablets debossed with SZ on one side and 248 on other side
NDC 0781-5527-37 in unit-of-use pack of 9 tablets (1 blister card containing 9 tablets in 1 carton)

### Storage
Store at 20 to 25C (68 to 77F) .
Nasal septum branch of superior labial artery

# Overview
- The blood supply of the mucosa of the nasal septum is derived mainly from the maxillary artery.
- The sphenopalatine artery, a branch of the maxillary, supplies most of the blood of the nasal mucosa.
- It enters by the sphenopalatine foramen and sends branches to the posterior regions of the lateral wall and to the nasal septum.
- The greater palatine artery, also a branch of the maxillary, passes through the incisive foramen to supply the nasal septum.
- The anterior and posterior ethmoidal arteries, branches of the ophthalmic artery, supply the anterosuperior part of the mucosa of the lateral wall of the nasal cavity and nasal septum.
- Three branches of the facial artery (superior labial, ascending palatine, and lateral nasal) also supply the anterior parts of the nasal mucosa.
Nicotinic acid adenine dinucleotide phosphate
Nicotinic acid adenine dinucleotide phosphate popularly known as NAADP+ is a nucleotide very similar to NADP differing only in that instead of the nicotinamide there is a niacin moiety. But this small change makes a lot of difference in their cellular function. NAADP is one of the most potent Calcium signaling messenger causing release of calcium from intracellular stores.

# Metabolism
Bifunctional ectoenzymes of the CD38 family synthesize NAADP+ from NADP+ (by exchange of nicotinamide for niacin under acidic conditions) and the same enzymes are also capable to hydrolyzing them.

# Transport
The two paralogous enzymes- transmembrane CD38 and GPI anchored CD157, that produce NAADP (and cADPR) in humans both have their active synthesis site in the ectodomain. Though this may involve vesicular synthesis but it has been shown that it is produced at the extracellular sites, and also can act when produced by a different cell or added artificially from outside. So the NAADP has to enter the cell either by diffusion or by transport. Considering the fact that the substrate of NAADP synthesis (NADP) itself is very sparse in the extracellular medium, a purse diffusion based mechanism has been suspected to be less likely than a transporter mediated path. This is compatible with recent data which indicate a carrier mediated transport partially blockable by dipyridamole and cold temperature.

# Mechanism of action
The real target of NAADP which causes the calcium release is still not clear. There has been some report on a ligand gated calcium release channel present in different distribution compared to both Ryanodine receptors and IP3 receptors. This receptor may be present on both endoplasmic reticulum/nuclear membrane compartments as well as some acidified compartments like lysosome and some secretory vesicles. Some report also suggest that NAADP may act on Ryanodine receptor as well.
An unique feature of NAADP action is its desensitization on prolonged action even when at subthreshold concentration. This is supposed to be a part of calcium memory of cellular calcium signaling pathways.
PCI in The Patient With Resistance to Aspirin

# This Page is Under Construction

# Overview
The treatment for antiplatelet drug resistance is not well defined. Detailed patient evaluation and correcting possible clinical causes and factors may be the initial therapeutic steps. Careful drug choose to reduce possible interactions, optimizing blood glucose and cholesterol levels are also beneficial.
Administration of higher doses of Aspirin is evaluated and currently not an actual therapeutic strategy for the lack of evidence demonstrating improvement in clinical outcomes. Increasing the dose of aspirin has been suggested as a measure to overcome aspirin resistance but it is possible that increased doses of aspirin may overcome aspirin resistance in vitro in an individual patient. Higher doses of aspirin may also increase bleeding events.  

### Clinical Trial Data
CAPRIE study (Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events)
Although, whether clopidogrel therapy is superior to aspirin in aspirin resistant patients is currently unknown, CAPRIE study investigators reported significant superiority of clopidogrel monotherapy over aspirin monotherapy. This beneficial effect was more frequently observed in high risk patients.
In fact, aspirin resistance is more frequent finding in high risk patients, such as diabetics and patients with diffuse atherosclerotic disease or acute coronary syndromes.  This group or patients also have increased risk of recurrent ischemic events     
ASCET trial (ASpirin non-responsiveness and Clopidogrel Endpoint Trial)
ISAR-REACT study (Intracoronary Stenting and Antithrombotic Regimen - Rapid Early Action for Coronary Treatment) data suggest that in patients at low to intermediate risk who undergo elective PCI after pretreatment with a high loading dose of clopidogrel, the use of a GP IIb/IIIa inhibitor, although more potent, is associated with no clinically measurable benefit within the first 30 days. In contrast, high-risk patients should receive triple antiplatelet therapy.
A low to medium risk patients study suggests that aspirin and clopidogrel may be insufficient in aspirin non responsive patients and resulted in quite similar results of ISAR-REACT. 
Both study results indicate that there is a gap between applied medication and requirements for optimal antiplatelet treatment.
Most interventional cardiologists give aspirin, clopidogrel, and heparin alone before PCI, however, up to 25% of these patients are aspirin non responsive.
- RESISTOR trial (Research Evaluation to Study Individuals who Show Thromboxane Or P2Y12 Receptor Resistance)
Pelvic organ prolapse resident survival guide
Synonyms and keywords:

# Overview
This section provides a short and straight to the point overview of the disease or symptom.  The first sentence of the overview must contain the name of the disease.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions that may result in death or permanent disability within 24 hours if left untreated.
- Life threatening cause 1
- Life threatening cause 2
- Life threatening cause 3

## Common Causes
- Common cause 1
- Common cause 2
- Common cause 3
- Common cause 4
- Common cause 5

# Diagnosis
Shown below is an algorithm summarizing the diagnosis of ] according the the  guidelines.

# Treatment
Shown below is an algorithm summarizing the treatment of ] according the the  guidelines.

# Do's
- The content in this section is in bullet points.

# Don'ts
- The content in this section is in bullet points.
Penicillin G benzathine clinical pharmacology

# Clinical Pharmacology
Penicillin G benzathine has an extremely low solubility and, thus, the drug is slowly released from intramuscular injection sites. The drug is hydrolyzed to penicillin G.  This combination of hydrolysis and slow absorption results in blood serum levels much lower but much more prolonged than other parenteral penicillins.
Intramuscular administration of 300,000 units of penicillin G benzathine in adults results in blood levels of 0.03 to 0.05 units per mL, which are maintained for 4 to 5 days.  Similar blood levels may persist for 10 days following administration of 600,000 units and for 14 days following administration of 1,200,000 units.  Blood concentrations of 0.003 units per mL may still be detectable 4 weeks following administration of 1,200,000 units.
Approximately 60% of penicillin G is bound to serum protein. The drug is distributed throughout the body tissues in widely varying amounts.  Highest levels are found in the kidneys with lesser amounts in the liver, skin, and intestines. Penicillin G penetrates into all other tissues and the spinal fluid to a lesser degree. With normal kidney function, the drug is excreted rapidly by tubular excretion.  In neonates and young infants and in individuals with impaired kidney function, excretion is considerably delayed.
Penicillin G benzathine indications and usage

# Indications and Usage
To reduce the development of drug-resistant bacteria and maintain the effectiveness of Bicillin L-A and other antibacterial drugs, Bicillin L-A should be used only to treat or prevent infections that are proven or strongly suspected to be caused by bacteria. When culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy.
Intramuscular penicillin G benzathine is indicated in the treatment of infections due to penicillin-G-sensitive microorganisms that are susceptible to the low and very prolonged serum levels common to this particular dosage form. Therapy should be guided by bacteriological studies (including sensitivity tests) and by clinical response.
The following infections will usually respond to adequate dosage of intramuscular penicillin G benzathine:
Mild-to-moderate infections of the upper-respiratory tract due to susceptible streptococci.
Venereal infectionsSyphilis, yaws, bejel, and pinta.
Medical Conditions in which Penicillin G Benzathine Therapy is indicated as Prophylaxis:
Rheumatic fever and/or choreaProphylaxis with penicillin G benzathine has proven effective in preventing recurrence of these conditions. It has also been used as follow-up prophylactic therapy for rheumatic heart disease and acute glomerulonephritis.