Persius/hicric huggingface dataset:
Nonpathogenic intestinal amebae infection overview

# Pathophysiology
Human beings may become infected with nonpathogenic intestinal amebae by swallowing something, such as food or water, or touching something (and then putting fingers in mouth) that was contaminated with stool from an infected person. The parasite can stay in the body for weeks, months, or years. But they never spread from the intestines to other parts of the body.

# Epidemiology and Demographics
The species that are nonpathogenic (Chilomastix mesnili, Endolimax nana, Entamoeba coli, Entamoeba dispar, Entamoeba hartmanni, Entamoeba polecki, Iodamoeba buetschlii) are distributed worldwide. Consequently, infections by these species occur worldwide. Entamoeba polecki in nature is primarily a parasite of pigs and monkeys, and human infection is more prevalent in areas where the people have animal contact.

# Diagnosis

## Laboratory Findings
For diagnosing nonpathogenic intestinal amebae infection, identification of E. coli, E. hartmanni, E. polecki, E. nana, and I. buetschlii is made by observing cysts and/or trophozoites in stool specimens, both concentrated wet mounts and permanent stained smears. They are generally considered nonpathogenic, although they have been found in the stool of patients presenting with diarrhea where no known pathogens were identified.  Their presence in stool can be an indicator of fecal contamination of a food or water source, and does not rule-out the presence of other parasites. Entamoeba gingivalis is also considered nonpathogenic, but is found in about 95% of patients with gum disease and about 50% of patients with healthy gums.

# Treatment
As these six species are generally considered nonpathogenic, there are currently no treatment recommendations for them.
North Thames Regional Cleft Lip and Palate Service
The North Thames Regional Cleft Lip and Palate Service also known as the North Thames Cleft Centre is responsible for treating children and adult patients with clefts of the lip and palate the North Thames region.  This includes North London, Essex and South and West Hertfordshire.
This service is run jointly by the world renouned St Andrews Centre, Broomfield Hospital, Chelmsford and Great Ormond Street Hospital, London.
In 1995, the number of centres in England and Wales offering treatment for clefts was reduced from around fifty to thirteen.  This means the specialist teams at the thirteen centres are now treating more patients with clefts per year and as a result are able to offer a better service to their patients and families.

# Research
The North Thames Cleft Team have been involved in extensive interdisciplinary research and have many ongoing projects.
Pegylated interferon alfa-2a indications and usage

# Indications And Usage

## Chronic hepatitis C
PEGASYS, peginterferon alfa-2a, alone or in combination with COPEGUS, is indicated for the treatment of patients 5 years of age and older with chronic hepatitis C (CHC) virus infection with compensated liver disease and have not been previously treated with interferon alpha. Efficacy has been demonstrated in subjects with compensated liver disease and histological evidence of cirrhosis (Child-Pugh class A) and in adult subjects with clinically stable HIV disease and CD4 count greater than 100 cells/mm3.
Pegasys in combination with Copegus and an approved hepatitis C Virus (HCV) NS3/4A protease inhibitor is indicated in adult patients (18 years of age and older) with HCV genotype 1 infection (see the Package Insert of the specific HCV NS3/4A protease inhibitor for further information).
Pegasys in combination with Copegus is indicated in patients with HCV genotypes other than 1, pediatric patients (5-17 years of age), or in patients with HCV genotype 1 infection where use of an HCV NS3/4A protease inhibitor is not warranted based on tolerability, contraindications or other clinical factors.
The following points should be considered when initiating therapy with PEGASYS and COPEGUS:
Use of PEGASYS monotherapy is not recommended for treatment of CHC unless a patient has a contraindication to or significant intolerance to ribavirin. Combination therapy provides substantially better response rates than monotherapy .
Safety and efficacy have not been demonstrated for treatment longer than 48 weeks.
The safety and efficacy have not been established in liver or other organ transplant recipients .

## Chronic hepatitis B
PEGASYS is indicated for the treatment of adult patients with HBeAg positive and HBeAg negative chronic hepatitis B infection who have compensated liver disease and evidence of viral replication and liver inflammation.
Pituitary-specific positive transcription factor 1
POU domain, class 1, transcription factor 1 (Pit1, growth hormone factor 1), also known as POU1F1, is a transcription factor for growth hormone.

# Function
PIT1 is a pituitary-specific transcription factor responsible for pituitary development and hormone expression in mammals and is a member of the POU family of transcription factors that regulate mammalian development. The POU family is so named because the first 3 members identified were PIT1 and OCT1 (MIM 164175) of mammals, and Unc-86 of C. elegans (Herr et al., 1988). PIT1 contains 2 protein domains, termed POU-specific and POU-homeo, which are both necessary for high affinity DNA binding on genes encoding growth hormone (GH; MIM 139250) and prolactin (PRL; MIM 176760). PIT1 is also important for regulation of the genes encoding prolactin and thyroid-stimulating hormone beta subunit (TSHB; MIM 188540) by thyrotropin-releasing hormone (TRH; MIM 257120) and cyclic AMP.

# Interactions
Pituitary-specific positive transcription factor 1 has been shown to interact with GATA2 and PITX1.
Restrictive cardiomyopathy resident survival guide

# Overview
Restrictive cardiomyopathy is defined as heart-muscle disease with impaired ventricular filling usually due to increased stiffness. The diastolic volume of either or both ventricles is normal or decreased,the systolic function usually remains normal and wall thickness may be normal or increased. The symptoms and signs may consist of right (jugular venous pressure, peripheral edema, and ascites) or left ventricular failure (breathlessness and evidence pulmonary edema).

# Classification

# Causes

## Common Causes
- Idiopathic cardiomyopathy
- Amyloisosis
- Sarcoidosis
- Endomyocardial fibrosis
- Radiation
- Toxic effects of anthracycline

# Complete Diagnostic Approach
A complete diagnostic approach should be carried out after a focused initial rapid evaluation is conducted and following initiation of any urgent intervention.

# Treatment

### Symptomatic therapy
- Loop diuretics (low to medium dose): to relieve venous congestion in the pulmonary and systemic circulation, may cause signs of hypotension and hypoperfusion. Monitor systemic perfusion with physical examination, blood urea nitrogen and serum creatinine concentration
- Calcium channel blockers: may increase diastolic function
- Beta blockers: may have benefit by improving ventricular relaxation
- Angiotensin-converting enzyme inhibitors and/or angiotensin II receptor blockers: may improve diastolic filling
- Digoxin: increases intracellular calcium and therefore should be used with caution
- Treat atrial fibrillation: atrial fibrillation with the removal of the atrial contribution to ventricular filling may worsen existing diastolic dysfunction, patients with atrial fibrillation should be anticoagulated
- Advanced conduction-system disease (i.e. advanced AV-block): Treat by the implantation of a pacemaker
- Malignant ventricular arrhythmias:May require treatment with an automatic implantable defibrillator or an antitachycardia device
- Cardiac transplantation should be performed in eligible patients with intractable heart failure
Tetracycline controlled transcriptional activation
Tetracycline Controlled Transcriptional Activation is a method of inducible expression where transcription is reversibly turned on or off in the presence of the antibiotic tetracycline or one of its derivatives (etc. doxycycline).  In nature, pTet promotes TetR, the repressor, and TetA, the protein that pumps tetracycline antibiotic out of the cell. Two systems named Tet-off and Tet-on are used.

# Tet-off
The Tet-off system for controlling expression of genes of interest in mammalian cells was  developed by Professors Hermann Bujard and Manfred Gossen at the University of Heidelberg   This system makes use of the tetracycline transactivator (tTA) protein created by fusing one protein, TetR(tetracycline repressor), found in Escherichia coli bacteria with another protein, VP16, produced by the Herpes Simplex Virus.  The tTA protein binds on DNA at a 'tet'O operator.  Once bound the 'tet'O operator will activate a promoter coupled to the 'tet'O operator, activating the transcription of nearby gene. Tetracycline derivatives bind tTA and render it incapable of binding to TRE sequences, therefore preventing transactivation of target genes. This expression system is also used in generation of transgenic mice, which conditionally express gene of interest.

# Tet-on
The Tet-on system works in the opposite fashion.  In that system the rtTA protein is only capable of binding the operator when bound by doxycycline.  Thus the introduction of doxycyline to the system initiates the transcription of the genetic product.  The tet-on system is sometimes preferred for the faster responsiveness.
Tet system has advantages over Cre, FRT and ER (estrogen receptor) conditional gene expression systems. In Cre and FRT systems, activation of knockout of the gene is irreversible once recombination is accomplished, while in Tet and ER systems it is reversible. Tet system has very tight control on expression, while ER system is somewhat leaky. However, Tet system, which depends on transcription and subsequent translation of target gene, is not as fast acting as ER system, which stabilizes the already expressed target protein upon hormone administration.
Valganciclovir hydrochloride indications and usage

# Indications and Usage

## Adult Patients
Treatment of Cytomegalovirus (CMV) Retinitis: Valcyte tablets are indicated for the treatment of CMV retinitis in patients with acquired immunodeficiency syndrome (AIDS) .
Prevention of CMV Disease: Valcyte tablets are indicated for the prevention of CMV disease in kidney, heart, or kidney-pancreas transplant patients at high risk (Donor CMV seropositive/Recipient CMV seronegative ) .

## Pediatric Patients
Prevention of CMV Disease: Valcyte for oral solution and tablets are indicated for the prevention of CMV disease in kidney or heart transplant patients (4 months to 16 years of age) at high risk .

## Limitations of Use
Valcyte is not indicated for use in either adult or pediatric liver transplant patients .
The safety and efficacy of Valcyte have not been established for:
- Prevention of CMV disease in solid organ transplants other than those indicated .
- Prevention of CMV disease in pediatric solid organ transplant patients < 4 months of age .
- Treatment of congenital CMV disease
Viewed 330,000 times daily, 120 million times/year
Note Alexa and Compete.com and other traffic tracking sites do not account for the volume through our unique squid architecture.
Squid is a high-performance proxy server that can also be used as a HTTP  accelerator for the webserver. Explained in layman terms, Squid will store a copy of the pages served by webserver and the next time the same page is requested, Squid will serve the copy. This process is called "caching" and it removes the need for the webserver to regenerate that same page again, resulting in a tremendous performance boost for the webserver.  "Hitcounters" and traffic tracking sites do not take into account the "hits" on the various squids.
Since MediaWiki websites are generated entirely dynamically, there is a substantial performance gain in running Squid as a HTTP accelerator for your webserver. In fact, sites like Wikipedia use several Squid caches to enhance their performance.
Because of this performance gain, MediaWiki has been designed to integrate closely with Squid. For example, MediaWiki will notify Squid when a page should be purged from the cache in order to be regenerated.
Viewed 400,000 times daily, 150 million times/year
Note Alexa and Compete.com and other traffic tracking sites do not account for the volume through our unique squid architecture.
Squid is a high-performance proxy server that can also be used as a HTTP  accelerator for the webserver. Explained in layman terms, Squid will store a copy of the pages served by webserver and the next time the same page is requested, Squid will serve the copy. This process is called "caching" and it removes the need for the webserver to regenerate that same page again, resulting in a tremendous performance boost for the webserver.  "Hitcounters" and traffic tracking sites do not take into account the "hits" on the various squids.
Since MediaWiki websites are generated entirely dynamically, there is a substantial performance gain in running Squid as a HTTP accelerator for your webserver. In fact, sites like Wikipedia use several Squid caches to enhance their performance.
Because of this performance gain, MediaWiki has been designed to integrate closely with Squid. For example, MediaWiki will notify Squid when a page should be purged from the cache in order to be regenerated.
Below you will find a screenshot of statistics from our Amazon right scale server verifying the fact that the site was recently viewed 5,671,148 times in 2 weeks:
3-hydroxyacyl-coenzyme A dehydrogenase deficiency
3-hydroxyacyl-coenzyme A dehydrogenase deficiency (HADH deficiency) is a rare condition that prevents the body from converting certain fats to energy, particularly during fasting. Normally, through a process called fatty acid oxidation, several enzymes work in a step-wise fashion to metabolize fats and convert them to energy. People with 3-hydroxyacyl-coenzyme A dehydrogenase deficiency have inadequate levels of an enzyme required for a step that metabolizes groups of fats called medium-chain fatty acids and short-chain fatty acids; for this reason this disorder is sometimes called medium- and short-chain 3-hydroxyacyl-coenzyme A dehydrogenase (M/SCHAD) deficiency.
Typically, initial signs and symptoms of this disorder occur during infancy or early childhood and can include poor appetite, vomiting, diarrhea, lethargy, hypoglycemia, hypotonia, liver problems, and abnormally high levels of hyperinsulinism. Insulin controls the amount of sugar that moves from the blood into cells for conversion to energy. Individuals with 3-hydroxyacyl-coenzyme A dehydrogenase deficiency are also at risk for complications such as seizures, life-threatening heart and breathing problems, coma, and sudden unexpected death.
Problems related to 3-hydroxyacyl-coenzyme A dehydrogenase deficiency can be triggered by periods of fasting or by illnesses such as viral infections. This disorder is sometimes mistaken for Reye syndrome, a severe disorder that may develop in children while they appear to be recovering from viral infections such as chicken pox or flu. Most cases of Reye syndrome are associated with the use of aspirin during these viral infections.
Mutations in the HADH gene lead to inadequate levels of an enzyme called 3-hydroxyacyl-coenzyme A dehydrogenase. Medium-chain and short-chain fatty acids cannot be metabolized and processed properly without sufficient levels of this enzyme. As a result, these fatty acids are not converted to energy, which can lead to characteristic features of this disorder, such as lethargy and hypoglycemia. Medium-chain and short-chain fatty acids or partially metabolized fatty acids may build up in tissues and damage the liver, heart, and muscles, causing more serious complications.
This condition is inherited in an autosomal recessive pattern, which means two copies of the gene in each cell are altered. Most often, the parents of an individual with an autosomal recessive disorder each carry one copy of the altered gene but do not show signs and symptoms of the disorder.
Blood cholesterol LDL and non-HDL treatment goals

# Overview
No recommendations are made for or against specific LDL-C or non-HDL-C goals for the 
primary prevention or secondary prevention of atherosclerotic cardiovascular disease (ASCVD), given the lack of evidence on the titration of cholesterol-lowering therapy to specific goals.

# 2018 AHA ACC Guideline on the Management of Blood Cholesterol. Primary Prevention

## Implementation

# 2013 ACC AHA guideline on the treatment of blood cholesterol LDL and non-HDL treatment goals
There are few trials that were designed to define the optimal goals for LDL-C or non-HDL-C by titrating cholesterol-lowering therapy. In AIM-HIGH, the additional reduction in non-HDLC levels with niacin therapy did not further reduce ASCVD risk in individuals treated to LDLC levels of 40 to 80 mg/dL. Therefore, no recommendations are made for or against specific LDLC or non-HDLC goals for the primary or secondary prevention of ASCVD due to the lack of evidence on titration of drug therapy to specific goals.
Amphotericin B liposomal warnings and precautions

# Warnings
Anaphylaxis has been reported with amphotericin B deoxycholate and other amphotericin B-containing drugs, including AmBisome. If a severe anaphylactic reaction occurs, the infusion should be immediately discontinued and the patient should not receive further infusions of AmBisome.

# Precautions
General
As with any amphotericin B-containing product the drug should be administered by medically trained personnel. During the initial dosing period, patients should be under close clinical observation. AmBisome has been shown to be significantly less toxic than amphotericin B deoxycholate; however, adverse events may still occur.
Laboratory Tests
Patient management should include laboratory evaluation of renal, hepatic and hematopoietic function, and serum electrolytes (particularly magnesium and potassium).
Bannayan-Riley-Ruvalcaba syndrome pathophysiology

# Overview
Bannayan-Riley-Ruvalcaba syndrome (BRRS) is transmitted in autosomal dominant pattern. It is understood that Bannayan-Riley-Ruvalcaba syndrome (BRRS) is the result caused gene mutations. PTEN track backs to 10q23 which encodes and plays a significant role

# Pathophysiology

## Genetics

## Pathogenesis
- Bannayan-Riley-Ruvalcaba syndrome (BRRS) is transmitted in autosomal dominant pattern, but sporadic cases have been reported.
- The disease belongs to a family of hamartomatous polyposis syndromes, which also includes Peutz-Jeghers syndrome, juvenile polyposis and Cowden syndrome.
- It is understood that Bannayan-Riley-Ruvalcaba syndrome (BRRS) is the result caused by  the following gene mutations:
Germline phosphatase and
Tensin homolog (PTEN) mutations.
- Germline phosphatase and
- Tensin homolog (PTEN) mutations.
- Patients who have Bannayan-Riley-Ruvalcaba syndrome (BRRS), have a positive association with PTEN mutations in 55 to 60 % of cases.
- PTEN track backs to 10q23 which encodes and plays a significant role in the following:
Phosphatidylinositol 3,4,5-triphosphate, a phospholipid in the phosphatidylinositol 3-kinase pathway/Akt pathway
Effects G1 cell cycle arrest and apoptosis
Cellular proliferation and
Migration
- Phosphatidylinositol 3,4,5-triphosphate, a phospholipid in the phosphatidylinositol 3-kinase pathway/Akt pathway
- Effects G1 cell cycle arrest and apoptosis
- Cellular proliferation and
- Migration
Beckwith-Wiedemann syndrome (patient information)
For the WikiDoc page for this topic, click here

# Overview
Beckwith-Wiedemann syndrome is a congenital (present from birth) growth disorder that causes large body size, large organs, and other symptoms.

# What are the symptoms of Beckwith-Wiedemann syndrome?
- Abdominal wall defect: umbilical hernia or omphalocele
- Creases in ear lobes
- Enlargement of organs and tissues
- External ear (pinna) abnormalities and low-set ears
- Large size for a newborn (large for gestational age)
- Large, prominent eyes
- Large tongue, sometimes protruding
- Lethargy
- Low blood sugar (hypoglycemia)
- Mild microcephaly
- Poor feeding
- Separated abdominal muscles (diastasis recti)
- Seizures
- Undescended testicles (cryptorchidism)

# What are the causes of Beckwith-Wiedemann syndrome?
- The cause of Beckwith-Wiedemann syndrome is unknown, but it may be genetic.
- Most cases are associated with a defect in chromosome 11.

# Diagnosis
- Blood tests for low blood sugar and other abnormalities
- Chromosomal studies for abnormalities in chromosome 11
- MRI or CT scan of the abdomen
- Ultrasound of the abdomen
- X-ray of the abdomen
- X-ray of the long bones

# When to seek urgent medical care?
If you have a child with Beckwith-Wiedemann syndrome and worrisome symptoms develop, call your pediatrician immediately.

# Treatment options
- Infants with low blood sugar may be treated fluids given through a vein ( intravenous solutions).
- Defects in the abdominal wall may need to be repaired. The child must be watched closely for the development of tumors.

# Where to find medical care for Beckwith-Wiedemann syndrome?
Directions to Hospitals Treating Beckwith-Wiedemann syndrome

# Prevention of Beckwith-Wiedemann syndrome
- There is no known prevention for Beckwith-Wiedemann syndrome.
- Genetic counseling may be of value for families who would like to have additional children.

# What to expect (Outlook/Prognosis)?
- Children with Beckwith-Wiedemann syndrome who survive infancy do well, although no long-term follow-up information is available.
- Mental development appears to be normal to very slightly decreased. Swelling of the tongue can cause problems with feeding and sleeping.

# Possible complications
- Development of tumors
- Feeding problems
- Hypoglycemia
- Respiratory difficulties from obstruction due to large tongue
- Seizures

# Sources
Carbon monoxide poisoning resident survival guide

# Overview
Carbon monoxide (CO) is a colorless, odorless, tasteless, non-irritating gas, that is toxic to humans at concentrations more than 100ppm.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. Death can occur from almost all causes of CO poisoning and depends on CO levels in blood.
- Fire

## Common Causes
- Boats, motor vehicles
- Charcoal grills, propane stoves, charcoal briquettes
- Gas powered generators
- Electrical cable fires
- Immediately after hurricanes and other natural calamities
- Poorly functioning heating systems
- Power washers & other gas powered tools 

# Management
Shown below is an algorithm summarizing the approach to Acute carbon monoxide poisoning

# Do's
- Assess for all possible high risk factors & treat with hyperbaric O2 therapy
- Use hyperbaric therapy for pregnant women irrespective of level of CO poisoning.
- Use 100% O2 therapy atleast till pt. is symptom free (4-5 hrs minimum).
- Give atleast 1 hyperbaric treatment to severe cases.
- Warn all pts. of delayed neurological complications.
- Do perform chest X-ray in all severe poisoning cases, also consider doing EKG, troponins & even CT & MRI in these cases.
- Schedule follow up visit in 2 weeks.
- Isolate pt. from the source of poisoning.
- Several pts. with mild symptoms may be safely discharged from emergency, once symptom free.

# Dont's
- Do not rely solely on COHb levels as they are not very reliable, co-relate with clinical symptoms.
- Do not use normal pulse oximetery, it is not useful in this case.
- Do not forget to perform pregnancy test on all women in child bearing age group.
- Do not forget to isolate pt. from the source of poisoning.