Persius/hicric huggingface dataset:
Downstream transcription factor II B recognition element gene transcriptions
The downstream B recognition element designated as the BREd, or dBRE, is an additional core promoter element that occurs downstream of the TATA box and is recognized by general transcription factor II B.

# Consensus sequences
A consensus sequence is 5'-A/G-T-A/G/T-G/T-G/T-G/T-G/T-3' or in the transcription direction on the template strand 3'-A/G-T-A/G/T-G/T-G/T-G/T-G/T-5'.

# Eukaryote genes
Of 140 promoters from the eukaryotic promoter database, "ix percent ...  at least six out of seven bases of the consensus sequence, 18% contain at least five of seven bases and 37% contain at least four of seven".

# Human genes
GeneID: 9555 H2A histone family, member Y (H2AFY) "contains a poor TATA element, but both a consensus Inr and DPE in addition to a six/seven match BREd."

# General transcription factor II Bs
A TFIIB recognition element (BRE) functions to determine the orientation of the TFIIB-TBP-TATA complex that projects the zinc ribbon of TFIIB toward the TSS.
General transcription factor II B can recognize two distinct sequence elements that flank the TATA box. "The selected sequences contain a strong representation of  bases and a striking preference against  (especially between bases -17 and -20)."
"here are ... some weakly conserved features including the TFIIB-Recognition Element (BRE), approximately 5 nucleotides upstream (BREu) and 5 nucleotides downstream (BREd) of the TATA box."
The TFIIB-DNA contact with the BREd takes place via the minor groove, while that with the upstream B recognition element  (BREu) takes place through the major groove.

# Transcription start sites
dBRE is cis-TATA box, between the TATA box and the Inr or transcription start site (TSS) and trans-TSS.

# Hypotheses
- The dBRE is not involved in the transcription of A1BG.
Hepatology, Gallbladder, and Biliary Tract Diseases Project Chapter Priority

# Overview
Start adding content to chapters of the highest priority first (priority 1). Once all chapters of a priority level are successfully completed, move to the chapters of the subsequent priority level.

# Distribution of Chapters by Priority
- The table below shows all the chapters that will be completed, as well as their corresponding priority for completion and their suggested format.
- To avoid duplicated efforts, once you choose a chapter, change the status from "available" to "pending". Once you complete the chapter, change the status from "pending" to "complete".
- Make sure you add your name as the author for the chapter once you start working on a chapter.
- Priority in descending order (1 corresponds to top priority):
Antihypertensive and lipid-lowering treatment to prevent heart attack trial

# Overview
The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) trial compared major outcomes in high risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic.  No significant difference was observed on CHD mortality in the group treated with pravastatin 40 mg daily as compared to the usual care group with well controlled hypertension and moderately elevated LDL. Possible explanations for failure to observe a significant reduction included a modest reduction in total cholesterol, unblinded study with no placebo group and a large crossover of high risk subjects

# Design
Randomized, double-blind, multi-center clinical trial

# Interventions
Control arm:
- Chlorthalidone
Comparators:
- Calcium channel blocker
- ACE inhibitors
- Alpha blocker

# Endpoint
Determine whether occurrence of fatal CHD or nonfatal MI is lower for high-risk hypertensive patients treated with newer
agents (CCB, ACEI, alpha-blocker) compared with a diuretic

# Population
42,418 high-risk hypertensive patients  55 years

# Results
The alpha blocker arm (doxazosin) was dropped early due to futility.
- There were no significant differences among the comparator arms in the primary outcome.
- With respect to stroke ACEi was better than the diuretic or CCB
- With respect to heart Failure ACEi/CCB was better than the diuretic
Cardiac allograft vasculopathy natural history, complications and prognosis

# Overview
CAV is responsible for approximately 40% of deaths in heart transplant recipients. Survival in these patients has improved significantly over the decades, owing primarily to improved diagnostic techniques, and optimal immunosuppression and risk factor modification. The 2013 adult heart transplant registry noted that 5-year survival in both pediatric and adult heart transplant recipients is 69%.

# Natural History
- CAV is a slowly progressive disease of the graft vessels. However it may progress rapidly in some post-transplant patients. For example, about 7% of patients from the Cardiac Transplant Research Database had severe disease that progressed rapidly by the end of 5 years.
- In a few years post-transplant, the disease progresses from clean coronary vasculature to diffusely diseased, obstructive pattern.
- A 5 year prospective study by Tsutsui and colleagues using intravascular ultrasound (IVUS) revealed that most of the intimal thickening in CAV develops during the first year after heart transplantation .
- Late onset of CAV is infrequent. The process of development of CAV is rather slow in those who develop CAV 10 years post-transplant.

# Complications
Most of the complications of CAV are related to myocardial hypoperfusion. These include:
- Graft failure
- Myocardial infarction
- Sudden death
- Congestive heart failure (sometimes in the form of rapidly developing systolic failure)
- Arrhythmias

# Prognosis
- All-cause mortality data from 1982 up to June 2011 shows 1 year survival of 81% and 5 year survival of 69%, with median survival of 10 years for all and 13 years for those surviving until the end of first year. The most recent cohort of patients show unadjusted 1 year survival of 84%.
- The survival curve demonstrates a steep fall in survival in the first 6 months post-transplant. Thereafter, it steadily decreases by 3.5% per year and continues to do so well beyond 15 years. Presence of CAV is the strongest predictor of mortality in patients who survive beyond 1 year post-transplant.
- The ISHLT Registry showed that CAV together with late graft failure was responsible for about 33% of deaths 5 years post-transplant.
- Also the survival of patients with CAV has in fact improved over the last decade.
Recommendation for Duration of DAPT in Patients With ACS Treated With CABG

# 2016 ACC/AHA Guideline Focused Update on Duration of Dual Antiplatelet Therapy in Patients With Coronary Artery Disease

# Duration of DAPT in Patients With ACS Treated With CABG:Recommendation
-  Levine GN, Bates ER, Bittl JA, Brindis RG, Fihn SD, Fleisher LA;  et al. (2016). "2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines". J Thorac Cardiovasc Surg. 152 (5): 12431275. doi:10.1016/j.jtcvs.2016.07.044. PMID 27751237.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link) .mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
Sandbox:Zika virus infection natural history, complications, and prognosis

# Overview

# Natural History
- The symptoms of Zika virus infection usually develop between 3 and 12 days after contraction.
- Zika virus infection symptoms will usually begin with a mild headache. Within 24 hours, they will progress to include a macropapular rash spread across the face, neck, trunk, upper arms, palms, and soles; fever, malaise, and back pain follow shortly.
- Without treatment, Zika virus infection symptoms will usually last from 4-7 days
The rash is expected to begin to fade after the second day.
The fever is expected to break after the third day.
- The rash is expected to begin to fade after the second day.
- The fever is expected to break after the third day.

# Complications
- Complications that can develop from Zika virus infection include congenital anomalies such as:
Microcephaly
Brain lesions
Brainstem dysfunction
Fetal celebral malformations
- Microcephaly
- Brain lesions
- Brainstem dysfunction
- Fetal celebral malformations
- They also include neurological syndromes:
Guillain-Barre syndrome
- Guillain-Barre syndrome

# Prognosis
- The prognosis for Zika virus infection is excellent, with the majority of patients experiencing full recovery within 4-7 days of contraction.
- The presence of congenital or neurological complications caused by Zika virus infection can lead to a worse prognosis.
Elvitegravir cobicistat emtricitabine tenofovir dosage and administration

# Dosage and Administration

## Dosage Information
The recommended dosage of STRIBILD is one tablet taken orally once daily with food .

## Dosage Adjustment in Patients with Renal Impairment
Initiation of STRIBILD in patients with estimated creatinine clearance below 70 mL per minute is not recommended. Because STRIBILD is a fixed-dose combination tablet, STRIBILD should be discontinued if estimated creatinine clearance declines below 50 mL per min during treatment with STRIBILD as dose interval adjustment required for emtricitabine and tenofovir disoproxil fumarate (DF) cannot be achieved .

## Dosage in Patients with Hepatic Impairment
No dosage adjustment of STRIBILD is required in patients with mild (Child-Pugh Class A) or moderate (Child-Pugh Class B) hepatic impairment. No pharmacokinetic or safety data are available regarding the use of STRIBILD in patients with severe hepatic impairment (Child-Pugh Class C). Therefore, STRIBILD is not recommended for use in patients with severe hepatic impairment .

## Testing Prior to Initiation of STRIBILD
Prior to initiation of STRIBILD, patients should be tested for hepatitis B infection  and estimated creatinine clearance, urine glucose and urine protein should be documented in all patients .

## DOSAGE FORMS AND STRENGTHS
Each STRIBILD tablet contains 150 mg of elvitegravir, 150 mg of cobicistat, 200 mg of emtricitabine, and 300 mg of tenofovir disoproxil fumarate (tenofovir DF, equivalent to 245 mg of tenofovir disoproxil).
The tablets are green, capsule-shaped, film-coated, debossed with "GSI" on one side and the number "1" surrounded by a square box (  ) on the other side of the tablet.
Safety, Tolerability and Pharmacokinetics of CSL112 in Healthy Volunteers

# Official Title
An Adaptive, Phase I, Single-Centre, Randomised, Double-blind, Placebo-controlled Single Ascending Dose Study to Investigate the Safety, Tolerability and Pharmacokinetics, of Intravenous CSL112 in Healthy Volunteers

# Objective
- To assess the safety and tolerability of escalating doses of CSL112 after single intravenous infusions in healthy volunteers.
- To measure the pharmacokinetics of CSL112 after single intravenous infusions in healthy volunteers.

# Sponsor
CSL Limited

# Timeline
The previous information was derived from ClinicalTrials.gov on 09/19/2013 using the identification number NCT01129661.

# Study Description
The previous information was derived from ClinicalTrials.gov on 09/19/2013 using the identification number NCT01129661.

# Eligibility Criteria

## Inclusion Criteria
- Healthy males and females aged 18 years to less than 55 years
- Body weigh 45 kg or greater

## Exclusion Criteria
- Evidence of a clinically significant medical condition, disorder or disease
- Evidence of clinically relevant abnormal laboratory test result
- Evidence of history of alcohol or substance abuse

# Outcomes

## Primary Outcomes
- Safety and tolerability as measured by the frequency and intensity of clinical adverse events
Time Frame: Up to 14 days after infusion of CSL112
Designated as safety issue: Yes
- Time Frame: Up to 14 days after infusion of CSL112
- Designated as safety issue: Yes
- Safety and tolerability as measured by clinical laboratory tests and assessments
Time Frame: Up to 14 days after infusion of CSL112
Designated as safety issue: Yes
- Time Frame: Up to 14 days after infusion of CSL112
- Designated as safety issue: Yes
- Pharmacokinetics of CSL112
Time Frame: Up to 10 days after infusion of CSL112
Designated as safety issue: No
- Time Frame: Up to 10 days after infusion of CSL112
- Designated as safety issue: No

## Secondary Outcomes
- Pharmacokinetic and pharmacodynamic measures of lipid, lipoprotein and related exploratory biomarkers
Time Frame: Up to 10 days after infusion of CSL112
Designated as safety issue: No
- Time Frame: Up to 10 days after infusion of CSL112
- Designated as safety issue: No

# Publications

## Results

## Conclusion
Sudden infant death syndrome natural history, complications and prognosis

# Overview
Common complications of SIDS include sudden unexplained death. Depending on the risk factors for recurrence, the prognosis may vary for SIDS. SIDS is typically unexplained death during without any prior symptoms.

# Natural History, Complications, and Prognosis

## Natural History
- The symptoms of sudden infant death syndrome (SIDS) usually develop in between one month and one year of age in the United States.
- SIDS is typically unexplained death during without any prior symptoms.

## Complications
- Common complications of sudden infant death syndrome (SIDS) include:
Women whose infants die from sudden infant death syndrome (SIDS) are highly likely to have complications in their following pregnancies with the following:
Placenta previa
Abruptio placenta
Premature rupture of membranes
- Women whose infants die from sudden infant death syndrome (SIDS) are highly likely to have complications in their following pregnancies with the following:
Placenta previa
Abruptio placenta
Premature rupture of membranes
- Placenta previa
- Abruptio placenta
- Premature rupture of membranes

## Prognosis
- Depending on the risk factors for recurrence, the prognosis may vary for SIDS, which include apparent life-threatening events (ALTE).
- History of multiple events preceding the hospital admission, and infections that are viral in nature also play a important role in determining the prognosis in SIDS victims.
The EKG in the patient treated with encainide, flecainide and propafenone

# Electrocardiographic Findings
- Prolong the PR and the QRS
- Propafenone may also slow the sinus rate due to its -blocking effects

# Additional resources
- ECGpedia: Course for interpretation of ECG
- The whole ECG - A basic ECG primer
- 12-lead ECG library
- Simulation tool to demonstrate and study the relation between the electric activity of the heart and the ECG
- ECG information from Children's Hospital Heart Center, Seattle
- ECG Challenge from the ACC D2B Initiative
- National Heart, Lung, and Blood Institute, Diseases and Conditions Index
- A history of electrocardiography
- EKG Interpretations in infants and children
Alpha-1,3-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase A
Alpha-1,3-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase A is a type II membrane protein and an enzyme  particularly a glycosyltransferase  that, in addition to the related isoenzyme B (MGAT4B), takes part in the transfer of N-acetylglucosamine (GlcNAc) to the core mannose residues of N-linked glycans in Golgi apparatus. Therefore, it is essential for the formation of tri- and tetra-antennary sugar chains. Furthermore, it is involved in glucose transport by mediating SLC2A2/GLUT2 glycosylation with controlling cell-surface expression of SLC2A2 in pancreatic beta cells  and, as it is suggested, in regulating the availability of serum glycoproteins, oncogenesis, and differentiation.

# Cloning and expression
In humans the enzyme is encoded by the MGAT4A gene. The related cDNA was first isolated by Yoshida and others. Equipped with three potential N-glycosylation sites and a length of 535 amino acids the structure of the MGAT4A gene product is similar to other known Golgi glycosyltransferases. The amino acid sequence of humans and of bovines are identical to 95%. Up to now MGAT4A was found in all human tissues and cell lines tested, whether they are normal tissues or cancer cell lines. The expression levels of MGAT4A relative to one another are similar among all tissues, but the expression levels of the correlating mRNA are quite different: Of the normal tissues, spleen, thymus, peripheral blood leukocyte, lymph node, prostate, pancreas, and small intestine showed the highest mRNA level; of the cancer cell lines the promyelocytic leukemia cell line HL-60 and the lymphoblastic leukemia cell line MOLT-4 exhibited the highest expression.

# Animal studies
It has been proposed that the MGAT4A isoenzyme acts as a toggle for developing of type 2 diabetes. Mice that lack MGAT4A are hyperglycemic and hypoinsulinemic and have impaired glucose tolerance. Moreover, MGAT4A normally protects mice from developing diabetes but is suppressed by high-fat diet. If this mechanism also operates in human islets, MGAT4A may represent a link between type 2 diabetes and high-fat diet.
Arrhythmogenic right ventricular cardiomyopathy resident survival guide

# Overview
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic disease characterized by myocyte loss and fibro-fatty tissue replacement of the right ventricular myocardium. This puts patients into risk of life-threatening ventricular arrhythmias and slowly progressive ventricular dysfunction. The diagnostic is challenging. Diagnosis of ARVC relays on a scoring system, with major or minor criteria on the Revised Task Force Criteria. Pharmacologic treatment of arrhythmias, catheter ablation of ventricular tachycardia, and ICD are main goals of the treatment.

# Classification

## Stages of disease
- Concealed phase: Subclinical asymptomatic phase
- Overt electrical disorder: Palpitations, syncope and typically with symptomatic ventricular arrhythmias of RV
- RV failure: Progressive loss of RV myocardium due to fibro-fatty replacement impairs RV function, pump failure
- Biventricular failure: Involvement of the interventricular septum and LV causing congestive heart failure (HF)

## Patterns of expression
- Classic ARVC:Increased RV to LV volume ratio, more severe involvement of the RV, negative anterior T waves and ventricular arrhythmias with LBBB morphology
- Left-dominant arrhythmogenic cardiomyopathy (LDAC):Predominantly involves the LV, LV wall motion abnormalities, chamber dilation, systolic impairment, and late gadolinium enhancement (LGE), ventricular arrhythmias of right bundle branch block (RBBB) morphology, (infero)-lateral T-wave inversion
- Biventricular arrhythmogenic:Early and parallel involvement of the RV and LV, biventricular dilation and systolic impairment, ventricular arrhythmias of both RBBB and LBBB configuration may occur, ratio of RV to LV volume remains close to 1

# Causes
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic disease.

# FIRE: Focused Initial Rapid Evaluation
A Focused Initial Rapid Evaluation (FIRE) should be performed to identify patients in need of immediate intervention. The diagnosis of ARVC is currently based on the presence of major and minor standardised Task Force Criteria. Diagnosis is established when two major, one major plus two minor, or four minor criteria from different groups are fulfilled.
  Global and/or regional dysfunction and structural alterations: 
Major
Minor
  Tissue characterisation of wall 
Major
  Repolarisation abnormalities 
Minor
  Depolarisation/conduction abnormalities 
Major
Minor
  Arrhythmias 
Major
Minor
  Family history 
Major
Minor

# 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
  Prevention of sudden death:
  Patients with heart failure: Diuretics, angiotensin-converting-enzyme inhibitors and digitalis, and anticoagulants
  Patients with refractory congestive heart failure or untreatable ventricular arrhythmias:Heart transplantation as final therapeutic option
  Restriction of physical exercise for all patients
Progressive encephalopathy with edema, hypsarrhythmia and optic atrophy
Synonyms and keywords: Infantile cerebello optic atrophy ; PEHO syndrome 

# Overview
PEHO (Progressive encephalopathy with Edema, Hypsarrhythmia and Optic atrophy) syndrome is a rare neurodegenerative disorder belonging to the group of infantile progressive encephalopathies.

# Epidemiology
The incidence in Finland has been estimated at 1 in 78 000, but a few patients have been described from other countries including (The Netherlands, Spain France).

# Diagnosis

## Symptoms
Onset occurs during the first few weeks or months of life with
- Poor feeding
- Drowsiness
- Abnormal movements

## Physical Examination

### Head
- Microcephaly
- Facial dysmorphism (including a 'Pear-shaped' face with a narrow forehead and full cheeks, receding chin, epicanthic folds, an open mouth with a curved upper lip, protruding ear lobes and a short nose with anteverted nostrils)

### Eyes
- Visual loss
- Abnormal eye movements
- Optic atrophy also occur during infancy

### Extremeties
- Edema
- Tapered fingers

### Neurologic
- Infantile spasms
- Hypsarrhythmia
- Seizures
- Psychomotor development
- Intellectual deficit
- Hypotonia