Persius/hicric huggingface dataset:
Mitral Regurgitation Treatment

# Overview of Treatment of Mitral Regurgitation
- In patients with mitral regurgitation (acute or chronic) with hemodynamic instability, an electrocardiogram should be done to assess for the presence of Myocardial Infarction. In its absence, infective endocarditis should be excluded by drawing blood cultures and ordering an echocardiogram.
- Diuretics should be administered to patients with pulmonary congestion.
- Afterload reduction should be instituted through the use of vasodilators such as ACE inhibitors.
- In the presence of atrial fibrillation, beta blocker, calcium channel blocker or digoxin can be administered to slow the heart rate down and improve left ventricular filling.
- Anti-coagulation therapy should be considered in patients with atrial fibrillation and in patients with prosthetic mitral valve replacement surgery.
- Prophylactic antibiotics prior to a periodontal procedure which involves manipulation of gingival tissue, the periapical region of a tooth, or perforation of oral mucosa is recommended in patients with previous infective endocarditis, patients who have a prosthetic mitral valve implanted and in those with congentital heart disease.
- Based on age of patient, co-morbidities, symptoms and severity of mitral regurgitation, risks and benefits of valve surgery should be considered.
Acute Mitral Regurgitation | Chronic Mitral Regurgitation
Wells score for DVT (modified)

# Overview

# Modified Wells Score for DVT

# Modified Wells Score Calculator for DVT
This handy calculator computes the pre-test probability of deep vein thrombosis (DVT) using modified Wells criteria.
Check all boxes that apply to your patient:
function calcScore(){
var score = 0;
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score += 1;}
if(document.forms.checked == 1){score -= 2;}
document.forms.value = score;
if(score < 2){document.forms.value = "DVT is unlikely (Prevalence of DVT or PE - 6%)";}
if(score >= 2){document.forms.value = "DVT is likely (Prevalence of DVT or PE - 28%)";}

# Interpretation
The interpretation of the score is as follows:
- Score <2: DVT is unlikely (Prevalence of DVT or PE - 6%)
- Score 2: DVT is likely (Prevalence of DVT or PE - 28%)
Mohs scale of mineral hardness
The Mohs scale of mineral hardness characterizes the scratch resistance of various minerals through the ability of a harder material to scratch a softer material. It was created in 1812 by the German mineralogist Friedrich Mohs and is one of several definitions of hardness in materials science.   
Mohs based the scale on ten minerals that are all readily available. As the hardest known naturally occurring substance, diamond is at the top of the scale. The hardness of a material is measured against the scale by finding the hardest material that the given material can scratch, and/or the softest material that can scratch the given material. For example, if some material is scratched by apatite but not by fluorite, its hardness on the Mohs scale would fall between 4 and 5.
The Mohs scale is a purely ordinal scale. For example, corundum (9) is twice as hard as topaz (8), but diamond (10) is almost four times as hard as corundum. The table below shows comparison with absolute hardness measured by a sclerometer.
On the Mohs scale, a pencil lead has a hardness of 1; a fingernail has hardness 2.5; a copper penny, about 3.5; a knife blade, 5.5; window glass, 5.5; steel file, 6.5. Using these ordinary materials of known hardness can be a simple way to approximate the position of a mineral on the scale.
The table below incorporates additional substances that may fall between levels:
Molybdenum cofactor deficiency

# Overview
Molybdenum cofactor deficiency is a rare human disease in which the absence of molybdenum cofactor leads to accumulation of toxic levels of sulphite and neurological damage. Usually this leads to death within months of birth, due to the lack of active sulfite oxidase. Furthermore, a mutational block in molybdenum cofactor biosynthesis causes absence of enyzme activity of xanthine dehydrogenase/oxidase and aldehyde oxidase.

# Pathophysiology
Molybdenum cofactor deficiency is caused by a mutation in the MOCS1 gene of the type A variant. It can also be caused by a mutation in the MOCS2 gene or the GEPH gene.

# Epidemiology and Demographics
As of 2010, there had been approximately 132 reported cases.

# Differentiating Molybdenum cofactor deficiency from other Diseases
It should not be confused with molybdenum deficiency.

# Diagnosis

# History and Symptoms
- Early seizures

# Laboratory Findings
- Low blood levels of uric acid
- High levels of sulphite, xanthine, and uric acid in urine

# MRI
The disease produces characteristic MRI images that can aid in diagnosis.

# Treatment
In 2009, Monash Children's Hospital at Southern Health in Melbourne, Australia reported that a patient known as Baby Z became the first person to be successfully treated for molybdenum cofactor deficiency type A. The patient was treated with cPMP, a precursor of the molybdenum cofactor. Baby Z will require daily injections of cyclic pyranopterin monophosphate (cPMP) for the rest of her life.

# Related Chapter
- Sulfite oxidase
Moxifloxacin adverse reactions

# ADVERSE REACTIONS

## Serious and Otherwise Important Adverse Reactions
The following serious and otherwise important adverse reactions are discussed in greater detail in the warnings and precautions section of the label:
Tendinopathy and Tendon Rupture 
QT Prolongation 
Hypersensitivity Reactions 
Other Serious and Sometimes Fatal Reactions 
Central Nervous System Effects 
Clostridium difficile-Associated Diarrhea 
Peripheral Neuropathy that may be irreversible 
Photosensitivity/Phototoxicity 
Development of Drug Resistant Bacteria 

## Clinical Trial Experience
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.
The data described below reflect exposure to AVELOX in 14981 patients in 71 active controlled Phase II- IV clinical trials in different indications . The population studied had a mean age of 50 years (approximately 73% of the population was <65 years of age), 50% were male, 63% were Caucasian, 12% were Asian and 9% were Black. Patients received AVELOX 400 mg once daily PO, IV, or sequentially (IV followed by PO). Treatment duration was usually 6-10 days, and the mean number of days on therapy was 9 days.
Discontinuation of AVELOX due to adverse events occurred in 5.0% of patients overall, 4.1% of patients treated with 400 mg PO, 3.9% with 400 mg IV and 8.2% with sequential therapy 400 mg PO/IV. The most common adverse events leading to discontinuation with the 400 mg PO doses were nausea (0.8%), diarrhea (0.5%), dizziness (0.5%), and vomiting (0.4%). The most common adverse event leading to discontinuation with the 400 mg IV dose was rash (0.5%). The most common adverse events leading to discontinuation with the 400 mg IV/PO sequential dose were diarrhea (0.5%), pyrexia (0.4%).
Adverse reactions occurring in 1% of AVELOX-treated patients and less common adverse reactions, occurring in 0.1 to <1% of AVELOX-treated patients, are shown in Tables 2 and Table 3, respectively. The most common adverse drug reactions (3%) are nausea, diarrhea, headache, and dizziness.
MedDRA Version 12.0

## Laboratory Changes
Changes in laboratory parameters, without regard to drug relationship, which are not listed above and which occurred in  2% of patients and at an incidence greater than in controls included: increases in MCH, neutrophils, WBCs, PT ratio, ionized calcium, chloride, albumin, globulin, bilirubin; decreases in hemoglobin, RBCs, neutrophils, eosinophils, basophils, PT ratio, glucose, pO2, bilirubin, and amylase. It cannot be determined if any of the above laboratory abnormalities were caused by the drug or the underlying condition being treated.

## Postmarketing Experience
Table 4 lists adverse reactions that have been identified during post-approval use of AVELOX. Because these events are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug
Mycobacterium avium silvaticum
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Mycobacterium avium subsp. silvaticum
Type strain: strain 6409 = ATCC 49884 = CCUG 47446 = CIP 103317 = DSM 44175.
Mycobacterium avium subsp. silvaticum Thorel et al. 1990 was previously known as Mycobacterium avium strain wood pigeon.
Mycobacterium chlorophenolicum
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Mycobacterium chlorophenolicum
Type strain: strain PCP-I = ATCC 49826 = CIP 104189 = DSM 43826 = HAMBI 2278 = IEGM 559 = IFO (now NBRC) 15527 = JCM 7439 = NRRL B-16528.
N-Methyl-3-piperidyl benzilate
N-methyl-3-piperidyl benzilate (JB-336) is an anticholinergic drug related to the chemical warfare agent 3-Quinuclidinyl benzilate.
N-methyl-3-piperidyl benzilate is less potent and shorter acting than 3-quinuclidyl benzilate, but like 3-QNB its effects on the central nervous system predominate over peripheral effects. It produces deliriant and hallucinogenic effects similar to those of plants such as datura and may be abused recreationally at low doses, however unpleasant side effects such as dysphoria, nausea and vomiting, dizziness and extreme dry mouth tend to make abuse of these kind of drugs uncommon. Both the N-methyl and N-ethyl analogues of 3-piperidyl benzilate are however Schedule I controlled drugs.
Radiolabelled versions of this drug are used in scientific research to map the distribution of muscarinic acetylcholine receptors in the brain.
N-Methyl-N-isopropyltryptamine
N-Methyl-N-isopropyltryptamine (MIPT) is a psychedelic tryptamine, closely related to DMT, DIPT and Miprocin.

# Chemistry
MIPT base, unlike many other tryptamines in their freebase form, does not decompose rapidly in the presence of light in oxygen.

# Dosage
10-25 mg is usually taken orally, with effects lasting 4-6 hours.

# Effects
MIPT is said to emphasize psychedelic/entheogenic effects over sensory/hallucinogenic activity.  Users report strong mental effects, but few perceptual alterations.

# Legality
MiPT is unscheduled and unregulated in the United States, however its close similarity in structure and effects to DMT and DET could potentially subject possession and sale of MIPT to prosecution under the Federal Analog Act. This seems to be the tact the federal government is taking in the wake of the DEA's Operation Web Tryp. A series of Court Cases in the US involving the prosecution of several online vendors in ongoing as of 2004.
National Brain Research Centre
National Brain Research Centre is a neuroscience research institute, situated in Manesar, Gurgaon, Haryana-India. It is an autonomous institute and a deemed university, under Department of Biotechnology (DBT), India.Dr. Vijayalaxmi Ravindranath is the founder director of NBRC and also holds the distinguishing place of being the first women from Ministry of Science and Technology, India to head a national lab.NBRC was formally inagurated on December 16, 2003 by his excellency Dr. A.P.J. Abdul Kalam, former President of India..Cellular and Molecular Neuroscience, Systems Neuroscience, Theoretical and Computational Neuroscience are some of the sub-fields of neuroscience being researched here.The institute has collaborations with RIKEN-Japan,IMH-USA, Pavlov Institute-Russia, INSERM-France.NBRC-INSERM are jointly setting up an associated laboratory called "PROTECT" which is an acronym for "Promoting Research Oriented Towards Early Central nervous sysTem ".Template:5

# References:
-  Dbt_Institutions
-  Inside the Mastermind- Hindustan Times
-  The Lancet Neurology, February 2004, Vol 3, Page 77
-  Welcome to Department of Science and Technology, Govt. of India ::
Neomycin clinical pharmacology

# Clinical Pharmacology
Neomycin sulfate is poorly absorbed from the gastrointestinal tract. The small absorbed fraction is rapidly distributed in the tissues and is excreted by the kidney in keeping with the degree of kidney function. The unabsorbed portion of the drug (approximately 97 percent) is eliminated unchanged in the feces.
Growth of most intestinal bacteria is rapidly suppressed following oral administration of neomycin sulfate, with the suppression persisting for 48 to 72 hours. Nonpathogenic yeasts and occasionally resistant strains of Enterobacter aerogenes (formerly Aerobacter aerogenes) replace the intestinal bacteria.
As with other aminoglycosides, the amount of systemically absorbed neomycin transferred to the tissues increases cumulatively with each repeated dose administered until a steady state is achieved. The kidney functions as the primary excretory path as well as the tissue binding site with the highest concentration found in renal cortex. With repeated dosings, progressive accumulation also occurs in the inner ear. Release of tissue bound neomycin occurs slowly over a period of several weeks after dosing has been discontinued.
Protein binding studies have shown that the degree of aminoglycoside protein binding is low and, depending upon the methods used for testing, this may be between 0 and 30 percent.
Netherlands Forensic Institute
The Netherlands Forensic Institute, (Dutch Nederlands Forensisch Instituut)  is the national forensics institute of the Netherlands, located in the Ypenburg quarter of The Hague.
It is an autonomous division of the Dutch Ministry of Justice and resorts under the Directorate-General for Law Enforcement.

# History
On July 30 1945 the government decided to install a  Justice Laboratory. Three years later, November 4, 1948, the laboratory became a department on its own in the Ministry of Justice.
In 1951 a similar institute was founded: Gerechtelijk Geneeskundig Laboratorium (Judicial Medical Laboratory), which was later renamed Laboratorium voor Gerechtelijke Pathologie Laboratory for Judicial Pathology.
Pathologist Dr. Jan Zeldenrust was the first CEO of this laboratory.
November 1, 1999 both laboratories integrated to Nederlands Forensisch Instituut (The Netherlands Forensic Institute).
The laboratory was based in Rijswijk until October 2004, when it moved to the Ypenburg quarter of The Hague.
Neuromuscular junction disease

# Overview
Neuromuscular junction disease is a medical condition where the normal conduction through the neuromuscular junction fails to function correctly.

# Autoimmune
In diseases such as myasthenia gravis, the EPP fails to effectively activate the muscle fiber due to an autoimmune reaction against acetylcholine receptors, resulting in muscle weakness and fatigue. 
Myasthenia gravis is caused most commonly by auto-antibodies against the acetylcholine receptor.
It has recently been realized that a second category of gravis is due to auto-antibodies against MuSK.
A different condition, Lambert-Eaton myasthenic syndrome, is usually associated with presynaptic antibodies to the voltage-dependent calcium channel.
It is possible for these conditions to coexist.

# Toxins
Various toxins, such as botulinum toxin prevent the release of acetylcholine, resulting in muscle paralysis.
Niacin/Simvastatin description

# Description
SIMCOR tablets contain niacin extended-release (NIASPAN) and simvastatin in combination. Simvastatin, an inhibitor of HMG-CoA reductase, and niacin are both lipid-altering agents.

## Niacin Extended-Release
Niacin is nicotinic acid, or 3-pyridinecarboxylic acid. Niacin is a white, nonhygroscopic crystalline powder that is very soluble in water, boiling ethanol, and propylene glycol. It is insoluble in ethyl ether. The empirical formula of niacin is C6H5NO2 and its molecular weight is 123.11. Niacin has the following structural formula:

## Simvastatin
Simvastatin is butanoic acid, 2,2-dimethyl-,1,2,3,7,8,8a-hexahydro-3-7-dimethyl-8--1-naphthalenyl ester, ]. Simvastatin is a white to off-white, nonhygroscopic, crystalline powder that is practically insoluble in water and freely soluble in chloroform, methanol, and ethanol. The empirical formula of simvastatin is C25H38O5 and its molecular weight is 418.57. Simvastatin has the following structural formula:
SIMCOR is available for oral administration as tablets containing 500 mg of niacin extended-release (NIASPAN) and 20 mg simvastatin (SIMCOR 500/20 mg), 500 mg of niacin extended-release (NIASPAN) and 40 mg simvastatin (SIMCOR 500/40 mg), 750 mg of niacin extended-release (NIASPAN) and 20 mg simvastatin (SIMCOR 750/20 mg), 1000 mg of niacin extended-release (NIASPAN) and 20 mg simvastatin (SIMCOR 1000/20 mg) and 1000 mg of niacin extended-release (NIASPAN) and 40 mg simvastatin (SIMCOR 1000/40 mg). Each tablet contains the following inactive ingredients: hypromellose, povidone, stearic acid, polyethylene glycol, butylated hydroxyanisole, FD&C Blue #2, lactose monohydrate, titanium dioxide, triacetin. SIMCOR 500/20 mg, SIMCOR 750/20 mg, and SIMCOR 1000/20 mg also contain iron oxide.
Nitazoxanide adverse reactions

# Adverse Reactions
Alinia Tablets: In controlled and uncontrolled clinical studies of 1,657 HIV-uninfected patients age 12 years and older who received various dosage regimens of Alinia Tablets, the most common adverse events reported regardless of causality assessment were: abdominal pain (6.6%), diarrhea (4.2%), headache (3.1%) and nausea (3.0%). In placebo-controlled clinical trials using the recommended dose, the rates of occurrence of these events did not differ significantly from those of the placebo. In placebo-controlled trials of HIV-uninfected patients age 12 years and older who received Alinia Tablets for the treatment of diarrhea caused by Giardia lamblia or Cryptosporidium parvum, less than 1% of patients discontinued therapy because of an adverse event.
Adverse events occurring in less than 1% of the patients age 12 years and older participating in clinical trials of Alinia Tablets are listed below:
Body as a Whole: asthenia, fever, pain, allergic reaction, pelvic pain, back pain, chills, chills and fever, flu syndrome.
Nervous System: dizziness, somnolence, insomnia, tremor, hypesthesia.
Digestive System: vomiting, dyspepsia, anorexia, flatulence, constipation, dry mouth, thirst.
Urogenital System: discolored urine, dysuria, amenorrhea, metrorrhagia, kidney pain, edema labia.
Metabolic & Nutrition: increased SGPT.
Hemic & Lymphatic Systems: anemia, leukocytosis.
Skin: rash, pruritus.
Special Senses: eye discoloration, ear ache.
Respiratory System: epistaxis, lung disease, pharyngitis.
Cardiovascular System: tachycardia, syncope, hypertension.
Muscular System: myalgia, leg cramps, spontaneous bone fracture.
Alinia for Oral Suspension: In controlled and uncontrolled clinical studies of 613 HIV-uninfected pediatric patients who received Alinia for Oral Suspension, the most frequent adverse events reported regardless of causality assessment were: abdominal pain (7.8%), diarrhea (2.1%), vomiting (1.1%) and headache (1.1%). These were typically mild and transient in nature. In placebo-controlled clinical trials, the rates of occurrence of these events did not differ significantly from those of the placebo. None of the 613 pediatric patients discontinued therapy because of adverse events.
Adverse events occurring in less than 1% of the pediatric patients participating in clinical trials of Alinia for Oral Suspension are listed below:
Digestive System: nausea, anorexia, flatulence, appetite increase, enlarged salivary glands.
Body as a Whole: fever, infection, malaise.
Metabolic & Nutrition: increased creatinine, increased SGPT.
Skin: pruritus, sweat.
Special Senses: eye discoloration (pale yellow).
Respiratory System: rhinitis.
Nervous System: dizziness.
Urogenital System: discolored urine.
The adverse events seen in adult patients treated with Alinia for Oral Suspension were similar to those observed in adult patients treated with Alinia Tablets.
Nocturia (patient information)
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# Overview
Excessive urination at night is a condition in which you wake up several times during the night to urinate. Waking up several times a night to urinate is called nocturia.

# Considerations
- Normally, urine decreases in amount and become more concentrated at night. That means, most people can sleep 6 to 8 hours without having to urinate.
- But, persons with nocturia get up more than once during the night to urinate. Because of this, those who have excessive urination at night often have disrupted sleep cycles.

# What causes Nocturia?
- Benign prostatic hyperplasia
- Certain drugs including diuretics, demeclocycline, lithium, methoxyflurane, phenytoin, and propoxyphene
- Chronic or recurrent urinary tract infection
- Chronic renal failure
- Congestive heart failure
- Cystitis
- Diabetes
- Drinking too much fluid before bedtime, particularly coffee, caffeinated beverages, or alcohol
- High blood calcium level
- Obstructive sleep apnea and other sleeping disorders

# When to seek urgent medical care?
Make an appointment with your health care provider if:
- Excessive nighttime urination continues over several days, and is not explained by medications or increase of fluids before bedtime
- You are bothered by the number of times you must urinate during the night

# Diagnosis
- Your health care provider will perform a physical examination and ask questions about your nighttime urination, such as:
- When did it start?
- How many times does this occur each night?
- Has there been a change in the volume of urine produced?
- Do you ever have "accidents" or bed wetting?
- How much urine is voided each time?
- What makes the problem worse? Better?
- How much fluid do you drink before bedtime? Have you tried restricting fluids before bedtime?
- What other symptoms are also present? Do you have increased thirst, pain or burning on urination, fever, abdominal pain, or back pain?
- What medications are you taking?
- How much caffeine do you consume each day?
- Have you had any bladder infections in the past?
- Do you have a family history of diabetes?
- Does nighttime urination interfere with adequate sleep and rest?
- Do you drink alcoholic beverages and, if so, how much each day?
- Have you changed your diet recently?
- Diagnostic tests that may be performed include:
- Blood urea nitrogen
- Serum creatinine or creatinine clearance
- Fluid deprivation
- Osmolality
- Serum electrolytes
- Blood sugar (glucose)
- Urinalysis
- Urine concentration
- Urine culture

# Treatment options
- Keep a diary of how much fluid you drink, how often you urinate, and urine output.
- Record your body weight at the same times and on the same scale daily.
- Treatment depends on the cause. If excessive nighttime urination is due to diuretic medications, you may be told to take your medication earlier in the day.

# Where to find medical care for Nocturia?
Directions to Hospitals Treating Nocturia

# Source