Persius/hicric huggingface dataset:
Sandbox: Ventricular Arrhythmias ACC -2017

# 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death

## General Evaluation of Patients With Documented or Suspected Ventricular Arrhythmias

## History and Physical Examination

## Noninvasive Evaluation

## 12-lead ECG and Exercise Testing

## Acute Management of Specific Ventricular Arrhythmia

# Ongoing Management of Ventricular Arrhythmia (VA) and Sudden Cardiac Death (SCD) Risk Related to Specific Disease States

## Secondary Prevention of SCD in Patients With Ischemic Heart Disease

## Coronary Artery Spasm

## Primary Prevention of SCD in Patients With Ischemic Heart Disease

## Treatment and Prevention of Recurrent VA in Patients With Ischemic Heart Disease

## Nonischemic Cardiomyopathy (NICM)

## Secondary Prevention of SCD in Patients With NICM

## Primary Prevention of SCD in Patients With NICM

## Treatment of Recurrent VA in Patients With NICM

## Arrhythmogenic Right Ventricular Cardiomyopathy

## Hypertrophic Cardiomyopathy

## Myocarditis

## Cardiac Sarcoidosis

## Heart Failure (HR)

## Left Ventricular Assist Device (LVAD)

## Implantable Cardioverter Defibrillator (ICD) Use After Heart Transplantation

## Neuromuscular Disorders

## Cardiac Channelopathies

## Specific Cardiac Channelopathy Syndromes

## Catecholaminergic Polymorphic Ventricular Tachycardia

## Brugada Syndrome

## Early Repolarization J-wave Syndrome

## Short QT Syndrome

## Ventricular Arrhythmia in the Structurally Normal Heart

## Outflow Tract and Atrioventricular Annular Ventricular Arrhythmia (VA)

## Papillary Muscle Ventricular Arrhythmia (VA)

## Interfascicular Reentrant Ventricular Tachycardia (VT) (Belhassen Tachycardia)

## Idiopathic Polymorphic (Ventricular Tachycardia) VT/ Ventricular Fibrillation (VF)

## Premature Ventricular Complexes (PVC)-Induced Cardiomyopathy

## Pregnancy

## Older Patients With Comorbidities

## Medication-Induced Arrhythmias

## Adult Congenital Heart Disease

## Defibrillators Other than Transvenous Implantable Cardioverter Defibrillators (ICDs)

## Wearable Cardioverter-Defibrillator

## Special Considerations for Catheter Ablation

## Postmortem Evaluation of Sudden Cardiac Death (SCD)

## Terminal Care

## Shared Decision-Making
Sandbox: spontaneous bacterial peritonitis

# Overview
Spontaneous bacterial peritonitis(SBP) is an advanced clinical expression of a pathological bacterial translocation as it develops from normal inhabitant gut bacteria through breakage of immune barriers.

# Pathogenesis

## Bacterial Translocation
It is defined as the translocation of either bacteria or bacterial products such as lipopolysacharides (LPS), bacterial DNA, peptidoglycans, muramyl-dipeptides from gut into mesenteric lymph nodes.
Physiological: It is the normal bacterial translocation in healthy individuals due to lack of pro-inflammatory responses against commensal bacteria. Physiological translocation is crucial for the development of host immunity response.
Pathological: It is developed due to abnormal increase in physiological translocation in both rate and degree by breaking the normal immunological barriers.
Barriers that limit pathological transmission:
- Interstinal lumen and it's secretory components such as inner and outer mucus layer, antimicrobial peptides: This is the primary barrier that limit direct contact between the intestinal bacteria and the epithelial cell surface
- Epithelial barrier with the gut-associated lymphatic tissue (GALT) and autonomic nervous system: This is a mechanical barrier with local immunological response elements (e.g., TNF and other pro-inflammatory cytokines) that  rapidly detects and kill the pathogen that manage to penetrate
- Systemic immune system: This includes hematogenous (portal venous) and lymphatic (ductus thoracicus) route of delivery that acts as a third immune barrier to prevent or minimize the pathogen to disseminate systemically from local immune system such as lymph nodes.

## Mechanism of pathological bacterial translocation
Breaking these immune barriers can progress physiological BT into pathological BT.
Sexual dysfunction resident survival guide
Synonyms and keywords: Approach to sexual dysfunction, Approach to dyspareunia

# Overview
Sexual dysfunction is defined as recurrent and persistent issues with sexual response, desire, experience of pain or achieving orgasm. Sexual dysfunction often causes distress to the partners in a relationship. Sexual dysfunction conditions are broadly classified into disorders of sexual desire, arousal, orgasm and pain disorders. Treatment often includes identifying the underlying cause and treatment along with counselling and supportive care.

# Causes

## Disorders of sexual desire
- Psychological disorders or stress
- Advanced age
- Menopause
- Emotional distress
- Medications such as antidepressants, anxiolytics, antihypertensives

## Disorders of sexual arousal
- Trauma
- Chronic disorders such as diabetes, multiple sclerosis
- Neuropathy
- Stroke
- Previous genital surgery

## Disorders of orgasm
- History of sexual or emotional abuse
- Medication such as antihypertensives, anxiolytics
- Previous trauma or surgery

## Disorders of sexual pain
- Endometriosis
- Pelvic inflammatory disease
- Decreased vaginal lubrication
- Sexually transmitted infections
- Vaginismus

# Diagnosis
Shown below is an algorithm summarizing the diagnosis of Sexual dysfunction according the the Journal of Sexual Medicine 2017 Opinion paper on The Diagnosis/Classification of sexual arousal concerns in women and the American College of Obstetricians and Gynecologists' Committee Practice Bulletin Summary on Sexual Dysfunction. 

# Treatment
Shown below is an algorithm summarizing the treatment of sexual dysfunction.

# Do's
- Encourage patients to discuss sexual health with their primary care provider or obgyn.
- Referral to a psychiatrist may be needed to alleviate patient distress.
- Pelvic floor rehabilitation must be done in patients with dyspareunia.
- Encourage non coital behaviours such as massages to improve communication and understanding between partners.
- Education about sexually transmitted infections must be done to all patients.
- Early identification and treatment can help prevent PID and associated cervical motion tenderness, dyspareunia and even subsequent infertility.

# Don'ts
- Don't forget to do an endocrine/hormonal evaluation in patients with sexual dysfunction.
- Oral contraceptive use can cause vaginal dryness which leads to sexual dysfunction. Don't treat patients without taking a proper and thorough drug history.
- Do not do counselling on patients alone, both involved partners must be encouraged to undergo sex education and counselling.
- Do not proceed to genital examination without properly explaining to the patient about the procedure to be done. Some patients might have severe discomfort due to vaginismus or prior trauma.
Shoot specific element gene transcriptions

# Human genes

# Consensus sequences
Shoot specific elements (GATAatGATG).

# SHOOT samplings
Copying the apparent consensus sequence for Shoot  (GATAATGATG) and putting it in "F" finds none located between ZSCAN22 and A1BG or between ZNF497 and A1BG as can be found by the computer programs.
For the Basic programs testing consensus sequence GATAATGATG (starting with SuccessablesSHOOT.bas) written to compare nucleotide sequences with the sequences on either the template strand (-), or coding strand (+), of the DNA, in the negative direction (-), or the positive direction (+), the programs are, are looking for, and found:
- negative strand, negative direction, looking for GATAATGATG, 0.
- positive strand, negative direction, looking for GATAATGATG, 0.
- positive strand, positive direction, looking for GATAATGATG, 0.
- negative strand, positive direction, looking for GATAATGATG, 0.
- complement, negative strand, negative direction, looking for CTATTACTAC, 0.
- complement, positive strand, negative direction, looking for CTATTACTAC, 0.
- complement, positive strand, positive direction, looking for CTATTACTAC, 0.
- complement, negative strand, positive direction, looking for CTATTACTAC, 0.
- inverse complement, negative strand, negative direction, looking for CATCATTATC, 0.
- inverse complement, positive strand, negative direction, looking for CATCATTATC, 0.
- inverse complement, positive strand, positive direction, looking for CATCATTATC, 0.
- inverse complement, negative strand, positive direction, looking for CATCATTATC, 0.
- inverse negative strand, negative direction, looking for GTAGTAATAG, 0.
- inverse positive strand, negative direction, looking for GTAGTAATAG, 0.
- inverse positive strand, positive direction, looking for GTAGTAATAG, 0.
- inverse negative strand, positive direction, looking for GTAGTAATAG, 0.

# Acknowledgements
The content on this page was first contributed by: Henry A. Hoff.
Status epilepticus resident survival guide

# Overview
Status epilepticus is defined as continuous clinical and/or electroencephalographic seizure persisting longer than 5 minutes or the occurrence of two or more episodes of seizures within one hour without returning to the baseline level of consciousness between the seizures.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. Status epilepticus is a life threatening condition by itself because it results in serious immediate and long term morbidity and mortality if the convulsive seize is not terminated by 30 minutes; therefore, treatment is required urgently.

## Common Causes
- Alcoholism
- Brain abscess
- Brain trauma
- Cardiac arrest
- Cerebrovascular disorders
- CNS tumor
- Drug toxicity
- Electrolytes abnormalities
- Encephalitis
- Hypertensive encephalopathy
- Hypoglycemia
- Hypoxia
- Low antiepileptic drug levels in patients with epilepsy
- Meningitis
- Sepsis
- Stroke
- Uremia
- Withdrawal from opioids, benzodiazepine, barbiturates or alcohol

# Management
Shown below is an algorithm summarizing the approach to status epilepticus.  The goal of the treatment is to stop the seizure as soon as possible; therefore, begin the general measures and administer the antiepileptic medications (AED) SIMULTANEOUSLY.

# Do's
- Make sure to secure airway and maintain blood pressure within normal ranges, then administer anticonvulsants and then proceed to complete the diagnostic workup.
- Consult neurology and anesthesiology.
- In the case of seizures lasting more than 5 minutes, it is beneficial do begin pre-hospital treatment with rectal diazepam (15-20 mg) among adults and children known to have frequent seizure episodes.  IV lorazepam (2 mg, may repeat one) or IV diazepam (5 mg, may repeat once) can be started by well-trained teams of paramedics during the pre-hospital care of patients with seizures lasting more than 5 minutes.
- The initial treatment with IV benzodiazepines ( lorazepam, midazolam or diazepam) may be repeated once 10 minutes following the first administered dose.
- Buccal midazolam (10 mg) or rectal diazepam (15-20 mg) can be used if IV access could not be established to administer IV benzodiazepine.

# Dont's
- Don't delay the initiation of treatment during the initial diagnostic evaluation.
Sulfamethoxazole dosage and administration

# Dosage and Administration
BACTRIM is contraindicated in pediatric patients less than 2 months of age.
Urinary Tract Infections and Shigellosis in Adults and Pediatric Patients, and Acute Otitis Media in Children:
Adults: The usual adult dosage in the treatment of urinary tract infections is 1 BACTRIM DS (double strength) tablet or 2 BACTRIM tablets every 12 hours for 10 to 14 days. An identical daily dosage is used for 5 days in the treatment of shigellosis.
Children: The recommended dose for children with urinary tract infections or acute otitis media is 40 mg/kg sulfamethoxazole and 8 mg/kg trimethoprim per 24 hours, given in two divided doses every 12 hours for 10 days. An identical daily dosage is used for 5 days in the treatment of shigellosis. The following table is a guideline for the attainment of this dosage:
Acute Exacerbations of Chronic Bronchitis in Adults:
The usual adult dosage in the treatment of acute exacerbations of chronic bronchitis is 1 BACTRIM DS (double strength) tablet or 2 BACTRIM tablets every 12 hours for 14 days.
Pneumocystis Jiroveci Pneumonia:
Treatment: Adults and Children:
The recommended dosage for treatment of patients with documented Pneumocystis jiroveci pneumonia is 75 to 100 mg/kg sulfamethoxazole and 15 to 20 mg/kg trimethoprim per 24 hours given in equally divided doses every 6 hours for 14 to 21 days.11 The following table is a guideline for the upper limit of this dosage:
For the lower limit dose (75 mg/kg sulfamethoxazole and 15 mg/kg trimethoprim per 24 hours) administer 75% of the dose in the above table.
Prophylaxis:
Adults:
The recommended dosage for prophylaxis in adults is 1 BACTRIM DS (double strength) tablet daily.12
Children:
For children, the recommended dose is 750 mg/m2/day sulfamethoxazole with 150 mg/m2/day trimethoprim given orally in equally divided doses twice a day, on 3 consecutive days per week. The total daily dose should not exceed 1600 mg sulfamethoxazole and 320 mg trimethoprim.13 The following table is a guideline for the attainment of this dosage in children:
Traveler's Diarrhea in Adults:
For the treatment of traveler's diarrhea, the usual adult dosage is 1 BACTRIM DS (double strength) tablet or 2 BACTRIM tablets every 12 hours for 5 days.
Superficial palmar branch of radial artery
The superficial palmar branch of the radial artery arises from the radial artery, just where this vessel is about to wind around the lateral side of the wrist.
Running forward, it passes through, occasionally over, the thenar muscles, which it supplies, and sometimes anastomoses with the terminal portion of the ulnar artery, completing the superficial palmar arch.
This vessel varies considerably in size: usually it is very small, and ends in the muscles of the thumb; sometimes it is as large as the continuation of the radial artery itself.
United States National Library of Medicine

# Overview
The United States National Library of Medicine (NLM), operated by the United States federal government, is the world's largest medical library. The collections of the National Library of Medicine include more than seven million books, journals, technical reports, manuscripts, microfilms, photographs, and images on medicine and related sciences, including some of the world's oldest and rarest works.
Since 1879, the NLM has published the Index Medicus, a monthly guide to articles in nearly five thousand selected journals. The last issue of Index Medicus was printed in December 2004, but this information is offered in the freely accessible PubMed amongst the more than fifteen million MEDLINE journal article references and abstracts going back to the 1960s and 1.5 million references going back to the 1950s.
The NLM also runs the National Center for Biotechnology Information (NCBI) which houses biological databases freely accessible over the Internet through the Entrez search engine and PubMed.
The Toxicology and Environmental Health Program (TEHIP)], established at the NLM in 1967, is charged with developing computer databases compiled from the medical literature and from the files of governmental and nongovernmental organizations. TEHIP has implemented several information systems for chemical emergency response and public education, such as the Toxicology Data Network (TOXNET), Tox Town, Wireless Information System for Emergency Responders (WISER), ToxMystery,and the Household Products Database. These resources are accessible without charge on the Web.
The Extramural Programs Division provides grants to support research in medical information science and to support planning and development of computer and communications systems in medical institutions. Research and publications in the history of medicine and the life sciences are also supported.

# History
The precursor of the NLM, established in 1836, was the Library of the Surgeon General's Office, a part of the office of the U.S. Army Surgeon General. The Armed Forces Institute of Pathology and its Medical Museum were founded in 1862 as the Army Medical Museum. Throughout their history the Army Medical Library and the Army Medical Museum often shared quarters. From 1866 to 1887, they were housed in Ford's Theatre after production there was stopped after the assassination of President Abraham Lincoln.
In 1956, the Library collection was transferred from the control of the U.S. Department of Defense to the Public Health Service of the Department of Health, Education and Welfare and renamed the National Library of Medicine. The Library moved to its current quarters in Bethesda, Maryland, on the campus of the National Institutes of Health in 1962.
Upper respiratory tract infection overview

# Overview
Upper respiratory tract infection is the illness caused by an acute infection which involves the upper respiratory tract: nose, sinuses, pharynx or larynx. In the United States, this represents approximately one billion acute upper respiratory illnesses annually.

# Causes
15% of acute pharyngitis cases may be caused by bacteria, commonly Group A Strep ("Strep Throat"). Generally, patients with "Strep Throat" start with a sore throat as their first symptom, and they usually do not have a runny nose, cough, or sneezing.

# Epidemiology and Demographics
Upper respiratory tract infection  is the illness caused by an acute infection which involves the upper respiratory tract. In the United States, this represents approximately one billion acute upper respiratory illnesses annually.

# Risk Factors
Any individual can be afflicted with the common cold, but children, geriatric patients, and people with a decreased immune system are affected more commonly.
Valproic acid capsule/solution description

# Description
Depakene (valproic acid) is a carboxylic acid designated as 2-propylpentanoic acid. It is also known as dipropylacetic acid. Valproic acid has the following structure:
Valproic acid (pKa 4.8) has a molecular weight of 144 and occurs as a colorless liquid with a characteristic odor. It is slightly soluble in water (1.3 mg/mL) and very soluble in organic solvents.
Depakene capsules and syrup are antiepileptics for oral administration. Each soft elastic capsule contains 250 mg valproic acid. The syrup contains the equivalent of 250 mg valproic acid per 5 mL as the sodium salt.

### Inactive Ingredients
250 mg capsules: corn oil, FD&C Yellow No. 6, gelatin, glycerin, iron oxide, methylparaben, propylparaben, and titanium dioxide.
Oral Solution: FD&C Red No. 40, glycerin, methylparaben, propylparaben, sorbitol, sucrose, water, and natural and artificial flavors.
WNT1-inducible-signaling pathway protein 1
WNT1-inducible-signaling pathway protein 1 (WISP-1), also known as  CCN4, is a matricellular protein that in humans is encoded by the WISP1 gene.

# Structure
WISP-1 is highly homologous to CYR61 (CCN1) and CTGF (CCN2), and is a member of the CCN family of secreted, extracellular matrix (ECM)-associated signaling proteins (CCN intercellular signaling protein). The CCN family of proteins shares a common molecular protein structure, characterized by an N-terminal secretory signal peptide followed by four distinct domains with homologies to insulin-like growth factor binding protein (IGFBP), von Willebrand type C repeats (vWC), thrombospondin type 1 repeat (TSR), and a cysteine knot motif within the C-terminal (CT) domain. This family of proteins regulates diverse cellular functions, including cell adhesion, migration, proliferation, differentiation, and survival.

# Role in bone development
WISP-1 promotes mesenchymal cell proliferation and osteoblastic differentiation, and represses chondrocytic differentiation. WISP-1 binds BMP2 and enhances BMP2 function in osteogenesis. These activities may be modulated by its direct binding to decorin and biglycan, two members of a family of small leucine-rich proteoglycans present in the extracellular matrix of connective tissue.

# Clinical significance
WISP-1 attenuates p53-mediated apoptosis in response to DNA damage through activation of the Akt kinase, and inhibits TNF-induced cell death in cardiomyocytes. Recombinant WISP-1 enhances ECM deposition in human fibroblasts, suggesting that it might play a role in matrix remodeling in vivo. WISP-1 is upregulated in human patients with idiopathic pulmonary fibrosis and in a mouse model of bleomycin-induced lung fibrosis. Orotracheal application of WISP-1 neutralizing antibodies to the lung ameliorates bleomycin-induced lung fibrosis, raising the possibility that WISP-1 might be a potential target for anti-fibrotic therapy.
Expression of WISP-1 promotes tumor growth, and high WISP-1 expression correlates with advanced tumors of the brain, breast, colon, and lung. WISP-1 appears to inhibit metastasis although expression of a WISP-1 splicing variant lacking the VWC domain appears to enhance the invasive characteristic of gastric carcinoma cells.
WNT1-inducible-signaling pathway protein 2
WNT1-inducible-signaling pathway protein 2, or WISP-2 (also named CCN5) is a matricellular protein that in humans is encoded by the WISP2 gene.

# Function
The CCN family of proteins regulates diverse cellular functions, including cell adhesion, migration, proliferation, differentiation.

# Structure
WISP-2 is a member of the CCN family (CCN intercellular signaling protein) of secreted, extracellular matrix (ECM)-associated signaling matricellular proteins. The CCN acronym is derived from the first three members of the family identified, namely CYR61 (CCN1), CTGF (connective tissue growth factor, or CCN2), and NOV. These proteins, together with WISP1/CCN4, WISP2 (CCN5, this gene), and WISP3 (CCN6) comprise the six-member CCN family in vertebrates. CCN proteins characteristically contain an N-terminal secretory signal peptide followed by four structurally distinct domains with homologies to insulin-like growth factor binding protein (IGFBP), von Willebrand type C repeats (vWC), thrombospondin type 1 repeat (TSR), and a cysteine knot motif within the C-terminal (CT) domain. However, WISP-2 is unique among this family of proteins by lacking precisely the CT domain.

# Clinical significance
WISP-2 (CCN5) inhibits the proliferation of vascular smooth muscle cells, human uterine myometrial cells, and leiomyoma cells. Ectopic expression of WISP-2 also inhibits the motility and invasiveness of breast carcinoma cells. WISP-2 also inhibits cardiac hypertrophy and fibrosis, an effect that appears linked to the absence of the CT domain.