Persius/hicric huggingface dataset:
Defense and stress-responsive element gene transcriptions

# Human genes

# Consensus sequences
Defense and stress-responsive elements (ATTTTCTTCA).

# Hypotheses
- A1BG has no DREs in either promoter.
- A1BG is not transcribed by a DRE.
- DRE does not participate in the transcription of A1BG.

# Samplings
Copying the consensus of the DRE: 5'-ATTTTCTTCA-3' and putting the sequence in "F" finds no locations for this sequence in any A1BG direction as can be found by the computer programs.
For the Basic programs testing consensus sequence 5'-ATTTTCTTCA-3' (starting with SuccessablesDRE.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 5'-ATTTTCTTCA-3', 0.
- negative strand, positive direction, looking for 5'-ATTTTCTTCA-3', 0.
- positive strand, negative direction, looking for 5'-ATTTTCTTCA-3', 0.
- positive strand, positive direction, looking for 5'-ATTTTCTTCA-3', 0.
- complement, negative strand, negative direction, looking for 5'-TAAAAGAAGT-3', 0.
- complement, negative strand, positive direction, looking for 5'-TAAAAGAAGT-3', 0.
- complement, positive strand, negative direction, looking for 5'-TAAAAGAAGT-3', 0.
- complement, positive strand, positive direction, looking for 5'-TAAAAGAAGT-3', 0.
- inverse complement, negative strand, negative direction, looking for 5'-TGAAGAAAAT-3', 0.
- inverse complement, negative strand, positive direction, looking for 5'-TGAAGAAAAT-3', 0.
- inverse complement, positive strand, negative direction, looking for 5'-TGAAGAAAAT-3', 0.
- inverse complement, positive strand, positive direction, looking for 5'-TGAAGAAAAT-3', 0.
- inverse negative strand, negative direction, looking for 5'-ACTTCTTTTA-3', 0.
- inverse negative strand, positive direction, looking for 5'-ACTTCTTTTA-3', 0.
- inverse positive strand, negative direction, looking for 5'-ACTTCTTTTA-3', 0.
- inverse positive strand, positive direction, looking for 5'-ACTTCTTTTA-3', 0.
Differentiating Diabetic ketoacidosis from other diseases

# Overview
Diabetic ketoacidosis (DKA) must be differentiated from other conditions presenting with hyperglycemia, ketosis and metabolic acidosis. The differentials include diabetes mellitus, non-ketotic hyperosmolar state, impaired glucose tolerance, ketotic hypoglycemia, alcoholic ketosis, starvation ketosis, lactic acidosis, salicylic acid ingestion, uremic acidosis and drug-induced acidosis. All these conditions may be differentiated on the basis of history findings, clinical features and laboratory abnormalities.

# Differentiating Diabetic Ketoacidosis From Other Diseases
Diabetic ketoacidosis must be differentiated from other diseases causing the following conditions:
- Hyperglycemia
Diabetes mellitus
Non-ketotic hyperosmolar state
Impaired glucose tolerance
Stress hyperglycemia
- Diabetes mellitus
- Non-ketotic hyperosmolar state
- Impaired glucose tolerance
- Stress hyperglycemia
- Ketosis
Ketotic hypoglycemia
Alcoholic ketosis
Starvation ketosis
- Ketotic hypoglycemia
- Alcoholic ketosis
- Starvation ketosis
- Metabolic acidosis
Lactic acidosis
Salicylic acid ingestion
Uremic acidosis
Drug-induced acidosis
- Lactic acidosis
- Salicylic acid ingestion
- Uremic acidosis
- Drug-induced acidosis

## Differentiating Diabetic Ketoacidosis from Hyperosmolar Hyperglycemia state

## Differential diagnosis of increased anion gap metabolic acidosis
- Causes of increased anion gap metabolic acidosis can be differetiated from each other with the help of following alogrhythm:
Emtricitabine rilpivirine tenofovir indications and usage

# Indications and Usage
COMPLERA, a combination of two nucleoside analog HIV 1 reverse transcriptase inhibitors (emtricitabine and tenofovir disoproxil fumarate) and one non-nucleoside reverse transcriptase inhibitor (rilpivirine), is indicated for use as a complete regimen for the treatment of HIV-1 infection in adult patients with no antiretroviral treatment history and with HIV-1 RNA less than or equal to 100,000 copies/mL at the start of therapy, and in certain virologically-suppressed (HIV-1 RNA <50 copies/mL) adult patients on a stable antiretroviral regimen at start of therapy in order to replace their current antiretroviral treatment regimen (see below).
The following points should be considered when initiating therapy with COMPLERA in adult patients with no antiretroviral treatment history:
- More rilpivirine-treated subjects with HIV-1 RNA greater than 100,000 copies/mL at the start of therapy experienced virologic failure (HIV-1 RNA 50 copies/mL) compared to rilpivirine-treated subjects with HIV-1 RNA less than or equal to 100,000 copies/mL .
- Regardless of HIV-1 RNA level at the start of therapy, more rilpivirine-treated subjects with CD4+ cell count less than 200 cells/mm3 experienced virologic failure compared to rilpivirine-treated subjects with CD4+ cell count greater than or equal to 200 cells/mm3 .
- The observed virologic failure rate in rilpivirine-treated subjects conferred a higher rate of overall treatment resistance and cross-resistance to the NNRTI class compared to efavirenz .
- More subjects treated with rilpivirine developed tenofovir and lamivudine/emtricitabine associated resistance compared to efavirenz .
The efficacy of COMPLERA was established in patients who were virologically-suppressed (HIV-1 RNA <50 copies/mL) on stable ritonavir-boosted protease inhibitor-containing regimen. The following points should be met when considering replacing the current regimen with COMPLERA in virologically-suppressed adults :
- Patients should have no history of virologic failure.
- Patients should have been stably suppressed (HIV-1 RNA <50 copies/mL) for at least 6 months prior to switching therapy.
- Patients should currently be on their first or second antiretroviral regimen prior to switching therapy.
- Patients should have no current or past history of resistance to any of the three components of COMPLERA.
Additional monitoring of HIV-1 RNA and regimen tolerability is recommended after replacing therapy to assess for potential virologic failure or rebound.
COMPLERA is not recommended for patients less than 18 years of age.
Infective endocarditis prevention resident survival guide
For infective endocarditis resident survival guide click here.

# Overview
Prevention of infective endocarditis can be achieved through the administration of antiobiotic prophylaxis to high risk subjects who are undergoing high risk procedures.  The choice of antibiotic prophylaxis depends on whether the subject can tolerate oral intake or not, as well as on whether patient has allergy to penicillin or not.

# Prevention
Shown below is an algorithm depicting the general prophylactic approaches of infective endocarditis.

## Antibiotic Prophylaxis
Shown below is an algorithm depicting the prophylaxis antibiotic regimens for infective endocarditis.
Familial encephalopathy with neuroserpin inclusion bodies
Familial encephalopathy with neuroserpin inclusion bodies (FENIB) is a progressive disorder of the nervous system that is characterized by a loss of intellectual functioning (dementia) and seizures. At first, affected individuals may have difficulty sustaining attention and concentrating. Their judgment, insight, and memory become impaired as the condition progresses. Over time, they lose the ability to perform the activities of daily living, and most people with this condition eventually require comprehensive care.
The signs and symptoms of familial encephalopathy with neuroserpin inclusion bodies vary in their severity and age of onset. In severe cases, the condition causes seizures and episodes of sudden, involuntary muscle jerking or twitching (myoclonus) in addition to dementia. These signs can appear as early as a person's teens. Less severe cases are characterized by a progressive decline in intellectual functioning beginning in a person's forties or fifties.
Mutations in the SERPINI1 gene cause familial encephalopathy with neuroserpin inclusion bodies. The SERPINI1 gene provides instructions for making a protein called neuroserpin. This protein is found in nerve cells, where it plays a role in the development and function of the nervous system. Neuroserpin helps control the growth of nerve cells and their connections with one another, which suggests that this protein may be important for learning and memory. Mutations in the gene result in the production of an abnormally shaped, unstable version of neuroserpin. Abnormal neuroserpin proteins can attach to one another and form clumps (called neuroserpin inclusion bodies or Collins bodies) within nerve cells. These clumps disrupt the cells' normal functioning and ultimately lead to cell death. Progressive dementia results from this gradual loss of nerve cells in certain parts of the brain. Researchers believe that a buildup of related, potentially toxic substances in nerve cells may also contribute to the signs and symptoms of this condition.
This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In many cases, an affected person has a parent with the condition.
Fluorescent treponemal antibody absorbtion (FTA-ABS) test

# Overview
FTA-ABS is a treponemal test for Syphilis. Using antibodies specific for the Treponema pallidum species, such tests are more specific than Non-Treponemal testing such as VDRL.
FTA (Fluorescent Treponemal Antibody) - ABS (Absorption) should always be followed to confirm a positve RPR and/or VDRL test for syphilis. The ABS suffix refers particularly to a processing step used to remove nonspecific antispirochetal antibodies present in normal serum.
This test is not useful for following therapy, because it does not wane with successful treatment of the disease, and will continue to be positive for the life of the patient after primary exposure.

# Related chapters
- Syphilis
- Venereal Disease Research Laboratory Test
- Rapid Plasma Reagent Test
Granulocyte-macrophage colony-stimulating factor receptor
The granulocyte-macrophage colony-stimulating factor receptor also known as CD116 (Cluster of Differentiation 116), is a receptor for granulocyte-macrophage colony-stimulating factor, which stimulates the production of white blood cells. The receptor is normally located on myeloblast, mature neutrophil, but not on any erythroid or megakaryocytic lineage cells.
It is associated with Surfactant metabolism dysfunction type 4.

# Structure
The granulocyte-macrophage colony-stimulating factor receptor is a heterodimer composed of at least two different subunits; an  chain, and a  chain which is also present in the receptors for IL-3 and IL-5. The  subunit contains a binding site for granulocyte macrophage colony-stimulating factor. The  chain is involved in signal transduction. Association of the  and  subunits results in receptor activation.

# Signal transduction
Upon dimerisation of the  and  subunits the  subunit becomes phosphorylated on tyrosine residues by members of the Janus kinase (JAK) family.  This leads to association with a Shc adaptor protein. Then Shc interacts with GRB2/SoS complex which results in activation of more downstream molecules in the pathway.
Granulocyte macrophage colony-stimulating factor receptor
The granulocyte macrophage colony-stimulating factor receptor is a receptor for granulocyte macrophage colony-stimulating factor, which stimulates the production of white blood cells. The receptor is normally located on myeloblast, mature neutrophil, but not on any erythroid or megakaryocytic lineage cells..

# Structure
The granulocyte macrophage colony-stimulating factor receptor is a heterodimer composed of at least two different subunits; an  chain, and a  chain which is also present in the receptors for IL-3 and IL-5. The  subunit contains a binding site for granulocyte macrophage colony-stimulating factor. The  chain is involved in signal transduction. Association of the  and  subunits results in receptor activation.

# Signal transduction
Upon dimerisation of the  and  subunits the  subunit becomes phosphorylated on tyrosine residues by members of the Janus kinase (JAK) family.  This leads to association with a Shc adaptor protein. Then Shc interacts with GRB2/SoS complex which results in activation of more downstream molecules in the pathway.
Haemophilus b conjugate vaccine dosage and administration

# DOSAGE AND ADMINISTRATION

## Reconstitution Instructions
HIBERIX is to be reconstituted only with the accompanying saline diluent. The reconstituted vaccine should be a clear and colorless solution. Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit. If either of these conditions exists, the vaccine should not be administered.
After reconstitution, HIBERIX should be administered promptly or stored refrigerated between 2 and 8C and administered within 24 hours. If the vaccine is not administered promptly, shake the solution vigorously again before injection.

## Dose and Administration
HIBERIX is administered as a single dose (approximately 0.5 mL) by intramuscular injection into the anterolateral aspect of the thigh or deltoid.
Do not administer this product intravenously, intradermally, or subcutaneously.
HIBERIX is to be used as a booster dose in children who have received a primary series with a Haemophilus b Conjugate Vaccine that is licensed for primary immunization .
Myelocytomatosis transcription factor gene transcriptions
L-myc-1 proto-oncogene protein is a protein that in humans is encoded by the MYCL1 gene.
MYCL1 is a bHLH (basic helix-loop-helix) transcription factor implicated in lung cancer.

# Human genes
Gene ID: 4609 is MYC proto-oncogene, bHLH transcription factor: "This gene is a proto-oncogene and encodes a nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. The encoded protein forms a heterodimer with the related transcription factor MAX. This complex binds to the E box DNA consensus sequence and regulates the transcription of specific target genes."

# Interactions
MYCL1 has been shown to interact with MAX.

# Consensus sequences

# Samplings
Otosclerosis natural history, complications and prognosis
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# Complications
- Complete deafness
- Funny taste in the mouth
- Infection, dizziness, pain, or a blood clot in the ear after surgery
- Nerve damage

# Prognosis
Otosclerosis gets worse without treatment. Surgery may restore at least some of your hearing. Pain and dizziness from the surgery usually go away within a few weeks.
To reduce the risk of complications after surgery:
- Do not blow your nose for 2 -3 weeks after surgery.
- Avoid people with respiratory or other infections.
- Avoid bending, lifting, or straining, which may cause dizziness.
- Avoid loud noises or sudden pressure changes, such as scuba diving, flying, or driving in the mountains until you have healed.
- If surgery does not work, you may have total hearing loss. Treatment then involves developing skills to cope with deafness, and using hearing aids to transmit sounds from the non-hearing ear to the good ear.
Rifampin isoniazid pyrazinamide dosage and administration

# Dosage and Administration
RIFATER is recommended in the initial phase of short-course therapy which is usually continued for 2 months. The Advisory Council for the Elimination of Tuberculosis, the American Thoracic Society, and the Centers for Disease Control and Prevention recommend that either streptomycin or ethambutol be added as a fourth drug in a regimen containing isoniazid (INH), rifampin and pyrazinamide for initial treatment of tuberculosis unless the likelihood of INH or rifampin resistance is very low. The need for a fourth drug should be reassessed when the results of susceptibility testing are known. If community rates of INH resistance are currently less than 4%, an initial treatment regimen with less than four drugs may be considered.
Following the initial phase, treatment should be continued with rifampin and isoniazid (e.g., RIFAMATE) for at least 4 months. Treatment should be continued for longer if the patient is still sputum or culture positive, if resistant organisms are present, or if the patient is HIV positive.
Concomitant administration of pyridoxine (B6) is recommended in the malnourished, in those predisposed to neuropathy (e.g., alcoholics and diabetics), and in adolescents.
See Clinical Pharmacology, General, for dosing information in patients with renal failure.

## Adults
Patients should be given the following single daily dose of RIFATER either 1 hour before or 2 hours after a meal with a full glass of water.
Patients weighing 44 kg  4 tablets
Patients weighing between 4554 kg  5 tablets
Patients weighing 55 kg  6 tablets

## Pediatric Patients
The ratio of the drugs in RIFATER may not be appropriate in pediatric patients under the age of 15 (e.g., higher mg/kg doses of isoniazid are usually given in pediatric patients than adults).
The heart in progressive systemic sclerosis (scleroderma)
Assistant Editor-In-Chief: Brian Blank

# Overview
Severe complications from Progressive Systemic Scleroderma (Scleroderma) can include:
- Untreated high blood pressure that strains the heart
- enlargement of the heart, which leads to heart failure
- pericardial effusion
- arrhythmias (both atrial and ventricular)
- conduction system defects
- valvular abnormalities
- myocardial ischaemia
- myocardial hypertrophy
It's generally thought cardiac disease is a major cause of death from scleroderma, or that it often contributes to death, though cardiac disease is only reported in about 10 percent of cases.  Conduction abnormalities, myocardial and pericardial disease disease may also be common.  Some have suggested a 'cardiac Raynaud's phenomenon' exists, but exactly how myocardial involvement develops in scleroderma is unclear.
An angiography-based study of 172 patients has suggested patients who may have obstructive epicardial disease associated with scleroderma should be treated the same as patients without scleroderma.

# Pathology
Images courtesy of Professor Peter Anderson DVM PhD and published with permission  PEIR, University of Alabama at Birmingham, Department of Pathology
The Living Textbook Of Interventional Cardiology: Authors
Please add your name to the list of authors once you have contributed a chapter or edited a chapter!

# Creator & Editor-In-Chief of The Living Textbook of Cardiology:
C. Michael Gibson, M.S., M.D.; Beth Israel Deaconess Medical Center, Boston MA, Harvard Medical School.
Jeffrey J. Popma, M.D.; St. Elizabeth's Medical Center, Boston MA, Tufts Medical School
Peter Zimetbaum, M.D.; Beth Israel Deaconess Medical Center, Boston MA, Harvard Medical School
Alena Goldman, M.D.; Beth Israel Deaconess Medical Center, Boston MA, Harvard Medical School
Marc A. Silver, MD; Clinical Professor and Chairman,Department of Medicine, Director, Heart Failure Institute 
Medical Director, Heart Transplant and Mechanical Assist Programs, Advocate Christ Medical Center in Oak Lawn, Illinois
Eli V. Gelfand, M.D.; Beth Israel Deaconess Medical Center, Boston MA, Harvard Medical School

# Authors (In Alphabetical Order)
Alexandra Almonacid, M.D.; Editor-In-Chief WikiDoc News International, Harvard Medical School
Eli V. Gelfand, M.D.; Beth Israel Deaconess Center (Boston, MA), Harvard Medical School
William J. Gibson; Massachusetts Institute of Technology 
Claudia P. Hochberg, M.D. Interventional Cardiology Fellow, Beth Israel Deaconess Medical Center (Boston, MA),Harvard Medical School
Alexander M. Morss, M.D.;  Cardiology Fellow, Beth Israel Deaconess Medical Center (Boston, MA),Harvard Medical School
Michael C. Nguyen, M.B.B.S., FRACP, Interventional Cardiology Fellow, Beth Israel Deaconess Medical Center (Boston, MA),Harvard Medical School
Jan M. Pattanayak, M.D.; Interventional Cardiology Fellow, Beth Israel Deaconess Medical Center (Boston, MA),Harvard Medical School
Joanna J. Wykrzykowska, M.D.: Interventional cardiology fellow, Beth Israel Deaconess Medical Center (Boston, MA), Harvard Medical School
Xin Yang, MA(Cantab), MB BChir, MRCP(Lond); Cardiology Fellow, Beth Israel Deaconess Medical Center (Boston, MA),Harvard Medical School
The Walid-Robinson Opioid-Dependence (WROD) Questionnaire
A questionnaire designed based on the WHO and DSM-IV-TR clinical guidelines for a definite diagnosis of dependence that require three or more of six characteristic features being experienced or exhibited:
- (1) Do you desire to continue taking your opioid medication?
- (2) Do you now experience lengthy periods of use or binge patterns of use?
- (3) Do you have tremors and use substances to relieve withdrawal symptoms?
- (4) Are you able to take more drug without easing the pain?
- (5) Do you neglect food, hygiene or health care?
- (6) Are you willing to continue use the drug despite knowledge of problems caused, or exacerbated by it?
Ubiquitin A-52 residue ribosomal protein fusion product 1
60S ribosomal protein L40 (RPL40)  is a protein that in humans is encoded by the UBA52 gene.

# Function
Ubiquitin is a highly conserved nuclear and cytoplasmic protein that has a major role in targeting cellular proteins for degradation by the 26S proteosome. It is also involved in the maintenance of chromatin structure, the regulation of gene expression, and the stress response. Ubiquitin is synthesized as a precursor protein consisting of either polyubiquitin chains or a single ubiquitin moiety fused to an unrelated protein. This gene encodes a fusion protein consisting of ubiquitin at the N-terminus and ribosomal protein L40 at the C-terminus, a C-terminal extension protein (CEP). Multiple processed pseudogenes derived from this gene are present in the genome.

# Clinical significance
The cell's ribosomal protein eL40 (rpL40), a part of the large 60S subunit. rpL40 is used by certain RNA viruses to translate messenger RNAs (mRNAs) into proteins while few host mRNAs require rpL40.   Hence targeting this protein may provide a means to combat viral infections with minimum side effects to the host.