Persius/hicric huggingface dataset:
Carbohydrate-responsive element-binding protein
Carbohydrate-responsive element-binding protein (ChREBP) also known as MLX-interacting protein-like (MLXIPL) is a protein that in humans is encoded by the MLXIPL gene.  The protein name derives from the protein's interaction with carbohydrate response element sequences of DNA.

# Function
This gene encodes a basic helix-loop-helix leucine zipper transcription factor of the Myc / Max / Mad superfamily. This protein forms a heterodimeric complex and binds and activates, in a glucose-dependent manner, carbohydrate response element (ChoRE) motifs in the promoters of triglyceride synthesis genes.

# Clinical significance
This gene is deleted in Williams-Beuren syndrome, a multisystem developmental disorder caused by the deletion of contiguous genes at chromosome 7q11.23.

# Interactions
MLXIPL has been shown to interact with MLX.

# Role in glycolysis
ChREBP is translocated to the nucleus and binds to DNA after dephosphorylation of a p-Ser and a p-Thr residue by PP2A, which itself is activated by Xylulose-5-phosphate. Xu5p is produced in the pentose phosphate pathway when levels of Glucose-6-phosphate are high (the cell has ample glucose). In the liver, ChREBP mediates activation of several regulatory enzymes of glycolysis and lipogenesis including L-type pyruvate kinase (L-PK), acetyl CoA carboxylase, and fatty acid synthase.
Chloroquine phosphate dosage and administration

# Dosage And Administration
The dosage of chloroquine phosphate is often expressed in terms of equivalent chloroquine base. Each 250 mg tablet of chloroquine phosphate is equivalent to 150 mg base and each 500 mg tablet of chloroquine phosphate is equivalent to 300 mg base. In infants and children the dosage is preferably calculated by body weight.

## Malaria
Suppression  Adult Dose: 500 mg (= 300 mg base) on exactly the same day of each week.

### Pediatric Dose
The weekly suppressive dosage is 5 mg calculated as base, per kg of body weight, but should not exceed the adult dose regardless of weight.
If circumstances permit, suppressive therapy should begin two weeks prior to exposure. However, failing this in adults, an initial double (loading) dose of 1 g (= 600 mg base), or in children 10 mg base/kg may be taken in two divided doses, six hours apart. The suppressive therapy should be continued for eight weeks after leaving the endemic area.

### For Treatment of Acute Attack
An initial dose of 1 g (= 600 mg base) followed by an additional 500 mg (= 300 mg base) after six to eight hours and a single dose of 500 mg (= 300 mg base) on each of two consecutive days. This represents a total dose of 2.5 g chloroquine phosphate of 1.5 g base in three days.
- The dosage for adults of low body weight and for infants and children should be determined as follows:
- First dose: 10 mg base per kg (but not exceeding a single dose of 600 mg base).
- First dose: 10 mg base per kg (but not exceeding a single dose of 600 mg base).
- Second dose: (6 hours after first dose) 5 mg base per kg (but not exceeding a single dose of 300 mg base).
- Second dose: (6 hours after first dose) 5 mg base per kg (but not exceeding a single dose of 300 mg base).
- Third dose: (24 hours after first dose) 5 mg base per kg.
- Third dose: (24 hours after first dose) 5 mg base per kg.
- Fourth dose: (36 hours after first dose) 5 mg base per kg.
- Fourth dose: (36 hours after first dose) 5 mg base per kg.
For radical cure of vivax and malariae malaria concomitant therapy with an 8-aminoquinoline compound is necessary.

## Extraintestinal Amebiasis
Adults: 1 g (600 mg base) daily for two days, followed by 500 mg (300 mg base) daily for at least two to three weeks. Treatment is usually combined with an effective intestinal amebicide.
====Geriatric Use==== See Precautions, Geriatric Use.
Clindamycin hydrochloride clinical pharmacology

# CLINICAL PHARMACOLOGY

## Human Pharmacology
Absorption
Serum level studies with a 150 mg oral dose of clindamycin hydrochloride in 24 normal adult volunteers showed that clindamycin was rapidly absorbed after oral administration. An average peak serum level of 2.50 mcg/mL was reached in 45 minutes; serum levels averaged 1.51 mcg/mL at 3 hours and 0.70 mcg/mL at 6 hours. Absorption of an oral dose is virtually complete (90%), and the concomitant administration of food does not appreciably modify the serum concentrations; serum levels have been uniform and predictable from person to person and dose to dose. Serum level studies following multiple doses of CLEOCIN HCl for up to 14 days show no evidence of accumulation or altered metabolism of drug. Doses of up to 2 grams of clindamycin per day for 14 days have been well tolerated by healthy volunteers, except that the incidence of gastrointestinal side effects is greater with the higher doses.
Distribution
Concentrations of clindamycin in the serum increased linearly with increased dose. Serum levels exceed the MIC (minimum inhibitory concentration) for most indicated organisms for at least six hours following administration of the usually recommended doses. Clindamycin is widely distributed in body fluids and tissues (including bones). No significant levels of clindamycin are attained in the cerebrospinal fluid, even in the presence of inflamed meninges.
Excretion
The average biological half-life is 2.4 hours. Approximately 10% of the bioactivity is excreted in the urine and 3.6% in the feces; the remainder is excreted as bioinactive metabolites.

## Special Populations
Renal Impairment
Serum half-life of clindamycin is increased slightly in patients with markedly reduced renal function. Hemodialysis and peritoneal dialysis are not effective in removing clindamycin from the serum.
Use in Elderly
Pharmacokinetic studies in elderly volunteers (6179 years) and younger adults (1839 years) indicate that age alone does not alter clindamycin pharmacokinetics (clearance, elimination half-life, volume of distribution, and area under the serum concentration-time curve) after IV administration of clindamycin phosphate. After oral administration of clindamycin hydrochloride, elimination half-life is increased to approximately 4.0 hours (range 3.45.1 h) in the elderly compared to 3.2 hours (range 2.1  4.2 h) in younger adults. The extent of absorption, however, is not different between age groups and no dosage alteration is necessary for the elderly with normal hepatic function and normal (age-adjusted) renal function.
Clindamycin hydrochloride indications and usage

# INDICATIONS AND USAGE
Clindamycin is indicated in the treatment of serious infections caused by susceptible anaerobic bacteria.
Clindamycin is also indicated in the treatment of serious infections due to susceptible strains of streptococci, pneumococci, and staphylococci. Its use should be reserved for penicillin-allergic patients or other patients for whom, in the judgment of the physician, a penicillin is inappropriate. Because of the risk of colitis, as described in the WARNING box, before selecting clindamycin, the physician should consider the nature of the infection and the suitability of less toxic alternatives (e.g., erythromycin).
Anaerobes: Serious respiratory tract infections such as empyema, anaerobic pneumonitis, and lung abscess; serious skin and soft tissue infections; septicemia; intra-abdominal infections such as peritonitis and intra-abdominal abscess (typically resulting from anaerobic organisms resident in the normal gastrointestinal tract); infections of the female pelvis and genital tract such as endometritis, nongonococcal tubo-ovarian abscess, pelvic cellulitis, and postsurgical vaginal cuff infection.
Streptococci: Serious respiratory tract infections; serious skin and soft tissue infections.
Staphylococci: Serious respiratory tract infections; serious skin and soft tissue infections.
Pneumococci: Serious respiratory tract infections.
Bacteriologic studies should be performed to determine the causative organisms and their susceptibility to clindamycin.
To reduce the development of drug-resistant bacteria and maintain the effectiveness of CLEOCIN HCl and other antibacterial drugs, CLEOCIN HCl should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. When culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy.
Clindamycin palmitate hydrochloride description

# DESCRIPTION
Clindamycin palmitate hydrochloride is a water soluble hydrochloride salt of the ester of clindamycin and palmitic acid. Clindamycin is a semisynthetic antibiotic produced by a 7(S)-chloro-substitution of the 7(R)-hydroxyl group of the parent compound lincomycin.
The structural formula is represented below:
The chemical name for clindamycin palmitate hydrochloride is Methyl 7-chloro-6, 7, 8-trideoxy-6-(1-methyl-trans-4-propyl-L-2-pyrrolidinecarboxamido)-1-thio-L-threo--D-galacto-octopyranoside 2-palmitate monohydrochloride.
Clindamycin palmitate hydrochloride for oral solution, USP (Pediatric) flavored granules contains clindamycin palmitate hydrochloride for reconstitution. The drug powder appears as a white to off-white powder. The reconstituted solution appears as a clear to slightly hazy solution with no significant precipitate.
Each 5 mL contains the equivalent of 75 mg clindamycin. Inactive ingredients: natural cherry flavor, dextrin, ethylparaben, poloxamer 188, simethicone, sucrose.
Colistimethate sodium dosage and administration

# Dosage and Administration
Important: Coly-Mycin M Parenteral is supplied in vials containing colistimethate sodium equivalent to 150 mg colistin base activity per vial.
Reconstitution for Intravenous or Intramuscular Administration
The 150 mg vial should be reconstituted with 2 mL Sterile Water for Injection, USP. The reconstituted solution provides colistimethate sodium at a concentration equivalent to 75 mg/mL colistin base activity.
During reconstitution swirl gently to avoid frothing.
Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit. If these conditions are observed, the product should not be used.

## Dosage
Adults and Pediatric PatientsIntravenous or Intramuscular Administration
The dose of Coly-Mycin M Parenteral should be 2.5 to 5 mg/kg per day of colistin base in 2 to 4 divided doses for patients with normal renal function, depending on the severity of the infection.
In obese individuals, dosage should be based on ideal body weight.
The daily dose and frequency should be reduced for the patients with renal impairment. Suggested modifications of dosage schedule for patients with renal impairment are presented in Table 1.

## Intravenous Administration
- Direct Intermittent AdministrationSlowly inject one-half of the total daily dose over a period of 3 to 5 minutes every 12 hours.
- Continuous InfusionSlowly inject one-half of the total daily dose over 3 to 5 minutes. Add the remaining half of the total daily dose of Coly-Mycin M Parenteral to one of the following:
0.9% NaCI
5% dextrose in 0.9% NaCI
5% dextrose in water
5% dextrose in 0.45% NaCI
5% dextrose in 0.225% NaCI
lactated Ringer's solution
10% invert sugar solution
There are not sufficient data to recommend usage of Coly-Mycin M Parenteral with other drugs or other than the above listed infusion solutions.
Administer the second half of the total daily dose by slow intravenous infusion, starting 1 to 2 hours after the initial dose, over the next 22 to 23 hours. In the presence of impaired renal function, reduce the infusion rate depending on the degree of renal impairment.
The choice of intravenous solution and the volume to be employed are dictated by the requirements of fluid and electrolyte management.
Any final intravenous infusion solution containing colistimethate sodium should be freshly prepared and used for no longer than 24 hours.

## Intramuscular Administration
For intramuscular Injection, administer by deep intramuscular injection into a large muscle mass (such as the gluteal muscles or lateral part of the thigh).
Store reconstituted solution for intramuscular injection in a refrigerator 2 to 8C (36 to 46F) or between 20 to 25C (68 to 77F) and use within 7 days.
Corticobasal degeneration (patient information)
For the WikiDoc page for this topic, click here

# Overview
Corticobasal degeneration is a progressive neurological disorder characterized by nerve cell loss and atrophy (shrinkage) of multiple areas of the brain including the cerebral cortex and the basal ganglia.

# What are the symptoms of Corticobasal degeneration?
- Initial symptoms, which typically begin at or around age 60, may first appear on one side of the body (unilateral), but eventually affect both sides as the disease progresses.
- Symptoms include:
- Poor coordination,
- Akinesia (an absence of movements),
- Rigidity (a resistance to imposed movement),
- Disequilibrium (impaired balance),
- Limb dystonia (abnormal muscle postures).
- Other symptoms:
- Cognitive and visual-spatial impairments,
- Apraxia (loss of the ability to make familiar, purposeful movements),
- Hesitant and halting speech,
- Myoclonus (muscular jerks),
- Dysphagia (difficulty swallowing).

# Treatment options
- There is no treatment available to slow the course of corticobasal degeneration, and the symptoms of the disease are generally resistant to therapy.
- Drugs used to treat Parkinson disease-type symptoms do not produce any significant or sustained improvement.
- Clonazepam may help the myoclonus.
- Occupational, physical, and speech therapy can help in managing disability.

# Diseases with similar symptoms
- Parkinson's disease

# Where to find medical care for Corticobasal degeneration?
Directions to Hospitals Treating Corticobasal degeneration

# What to expect (Outlook/Prognosis)?
- Corticobasal degeneration usually progresses slowly over the course of 6 to 8 years.
- An individual with corticobasal degeneration eventually becomes unable to walk.

# Possible complications
- Death is generally caused by pneumonia
- Other complications of severe debility such as sepsis or pulmonary embolism.

# Source
National Institute of Neurological Disorders and Stroke
Differentiating tonsillitis from other diseases

# Overview
Tonsillitis must be differentiated from other diseases that present with edema and erythema of the tonsils and nasopharynx, lymphadenopathy, fever, dysphonia, and dysphagia.

# Differentiating Tonsillitis from other Diseases
Tonsillitis must be differentiated from other diseases that present with edema and erythema of the tonsils and nasopharynx, lymphadenopathy, fever, dysphonia, and dysphagia.
- Mononucleosis
- Retropharyngeal abscess
- Epstein Barr virus
- Herpes simplex virus pharyngitis
- Epiglottitis
- Croup
- Peritonsillar abscess
- Diphtheria
- HIV
The table below outlines the differences between tonsillitis and other respiratory tract infections.
Elvitegravir cobicistat emtricitabine tenofovir

# Overview
Elvitegravir/cobicistat/emtricitabine/tenofovir (brand name Stribild), also known as the Quad pill, is a fixed dose combination drug for the treatment of HIV/AIDS.  Elvitegravir, emtricitabine and tenofovir directly suppress viral reproduction. Cobicistat increases the effectiveness of the combination by inhibiting liver enzymes that metabolize the other components. Stribild gained approval by U.S. Food and Drug Administration on August 27, 2012 for use in adult patients starting HIV treatment for the first time as part of the fixed dose combination.

# Category
Antiretroviral

# US Brand Names
STRIBILD

# FDA Package Insert
Description

# Mechanism of Action
- Elvitegravir: Elvitegravir inhibits the strand transfer activity of HIV-1 integrase (integrase strand transfer inhibitor; INSTI), an HIV-1 encoded enzyme that is required for viral replication. Inhibition of integrase prevents the integration of HIV-1 DNA into host genomic DNA, blocking the formation of the HIV-1 provirus and propagation of the viral infection. Elvitegravir does not inhibit human topoisomerases I or II.
- Cobicistat: Cobicistat is a selective, mechanism-based inhibitor of cytochromes P450 of the CYP3A subfamily. Inhibition of CYP3A-mediated metabolism by cobicistat enhances the systemic exposure of CYP3A substrates, such as elvitegravir, where bioavailability is limited and half-life is shortened by CYP3A-dependent metabolism.
- Emtricitabine: Emtricitabine, a synthetic nucleoside analog of cytidine, is phosphorylated by cellular enzymes to form emtricitabine 5'-triphosphate. Emtricitabine 5'-triphosphate inhibits the activity of the HIV-1 RT by competing with the natural substrate deoxycytidine 5'-triphosphate and by being incorporated into nascent viral DNA which results in chain termination. Emtricitabine 5'-triphosphate is a weak inhibitor of mammalian DNA polymerases , , , and mitochondrial DNA polymerase .
- Tenofovir DF: Tenofovir DF is an acyclic nucleoside phosphonate diester analog of adenosine monophosphate. Tenofovir DF requires initial diester hydrolysis for conversion to tenofovir and subsequent phosphorylations by cellular enzymes to form tenofovir diphosphate. Tenofovir diphosphate inhibits the activity of HIV-1 RT by competing with the natural substrate deoxyadenosine 5'-triphosphate and, after incorporation into DNA, by DNA chain termination. Tenofovir diphosphate is a weak inhibitor of mammalian DNA polymerases , , and mitochondrial DNA polymerase .
Emtricitabine rilpivirine tenofovir description

# Description
COMPLERA is a fixed-dose combination tablet containing emtricitabine, rilpivirine hydrochloride, and tenofovir DF. EMTRIVA is the brand name for emtricitabine, a synthetic nucleoside analog of cytidine. Edurant is the brand name for rilpivirine, a non-nucleoside reverse transcriptase inhibitor. VIREAD is the brand name for tenofovir DF, which is converted in vivo to tenofovir, an acyclic nucleoside phosphonate (nucleotide) analog of adenosine 5-monophosphate. VIREAD and EMTRIVA are the components of TRUVADA.
COMPLERA tablets are for oral administration. Each tablet contains 200 mg of emtricitabine, 27.5 mg of rilpivirine hydrochloride (equivalent to 25 mg of rilpivirine), and 300 mg of tenofovir DF (equivalent to 245 mg of tenofovir disoproxil) as active ingredients. The tablets include the following inactive ingredients: pregelatinized starch, lactose monohydrate, microcrystalline cellulose, croscarmellose sodium, magnesium stearate, povidone, polysorbate 20. The tablets are film-coated with a coating material containing polyethylene glycol, hypromellose, lactose monohydrate, triacetin, titanium dioxide, iron oxide red, FD&C Blue #2 aluminum lake, FD&C Yellow #6 aluminum lake.
Emtricitabine: The chemical name of emtricitabine is 5-fluoro-1-cytosine. Emtricitabine is the () enantiomer of a thio analog of cytidine, which differs from other cytidine analogs in that it has a fluorine in the 5-position.
It has a molecular formula of C8H10FN3O3S and a molecular weight of 247.24. It has the following structural formula:
Emtricitabine is a white to off-white crystalline powder with a solubility of approximately 112 mg per mL in water at 25 C.
Rilpivirine: Rilpivirine is available as the hydrochloride salt. The chemical name for rilpivirine hydrochloride is 4--2,6-dimethylphenyl]amino]-2-pyrimidinyl]amino]benzonitrile monohydrochloride. Its molecular formula is C22H18N6 - HCl and its molecular weight is 402.88. Rilpivirine hydrochloride has the following structural formula:
Rilpivirine hydrochloride is a white to almost white powder. Rilpivirine hydrochloride is practically insoluble in water over a wide pH range.
Tenofovir Disoproxil Fumarate: Tenofovir DF is a fumaric acid salt of the bis-isopropoxycarbonyloxymethyl ester derivative of tenofovir. The chemical name of tenofovir DF is 9-- methoxy]phosphinyl]methoxy]propyl]adenine fumarate (1:1). It has a molecular formula of C19H30N5O10P - C4H4O4 and a molecular weight of 635.52. It has the following structural formula:
Tenofovir DF is a white to off-white crystalline powder with a solubility of 13.4 mg per mL in water at 25 C. All dosages are expressed in terms of tenofovir DF except where otherwise noted.
Excimer laser-assisted nonocclusive anastomosis
Excimer laser assisted nonocclusive anastomosis (ELANA) is a technique in vascular surgery and neurosurgery to create a bypass without interrupting blood supply in the recipient blood vessels.
The ELANA technique is a subtle modification of existing methods to establish a connection between blood vessels (anastomosis) to create a bypass in or to the brain. The only real differences involve how the recipient artery is opened. In conventional techniques the recipient artery is temporarily interrupted (occluded with clips) and opened using microscissors or scalpel while in the ELANA technique blood flow is not interrupted and the opening (arteriotomy) is created with radiation from a 308nm Excimer Laser delivered through a catheter inserted in the vessel that will become the bypass while blood continues to flow through the artery that receives the bypass. This subtle difference, however, is very important for the safety of the procedure and eliminates the risk of ischemia to the regions supplied by the artery receiving the bypass. The technique is most valuable in neurosurgery, as brain cells are particularly sensitive to the lack of blood supply (ischemia) that would be caused by traditional methods of bypass creation. The bypasses created with the help of the ELANA can be to  one of the major arteries in the brain (extracranial to intracranial EC-IC bypass) or between two arteries in the brain (intracranial to intracranial).
Surgeons are creating such a bypass mainly as a step in the treatment of patients with unclippable and uncoilable giant aneurysms or tumors at the skull base or to treat patients at risk of stroke who can not be treated otherwise.
The ELANA technique has been extensively described in medical literature. It was developed in 1993 by Cornelis A.F. Tulleken, professor of neurosurgery at the University Medical Center Utrecht, the Netherlands, to find a way to treat patients with a bypass to a major cerebral artery without the risk of cerebral ischemia during the procedure. The surgery of some patients has been reported upon in the media e.g., in The New York Times in December 2006.
Familial Atherosclerosis Treatment Study (FATS)

# Official Title
Familial Atherosclerosis Treatment Study

# Objective
The objective of this study is to compare the effects of two intensive lipid altering therapies in men with familial combined hyperlipidemia as assessed by arteriography.

# Sponsor
National Heart, Lung, and Blood Institute (NHLBI)

# Timeline
The previous information was derived from ClinicalTrials.gov on 08/18/2014 using the identification number NCT00000512.

# Study Description
The previous information was derived from ClinicalTrials.gov on 09/19/2013 using the identification number NCT00000512.

# Eligibility Criteria

## Inclusion Criteria
- Men
- Age 62 or younger
- Elevated apolipoprotein B levels
- Coronary atherosclerosis
- Family history of coronary heart disease

## Exclusion Criteria
- Diabetes
- Severe hypertension
- Cancer
- Liver disease
- Thyroid disease
- Kidney disease

# Outcomes

## Primary Outcomes
Change in the mean severity of proximal stenosis

# Publications

## Conclusion
Both the intensive lipid lowering therapies were equally effective. Both reduced the frequency of progression of coronary lesions (21% and 25% versus 46% in the control group), increased the frequency of regression (32% and 39% versus 11%), and reduced the incidence of cardiovascular events in men with coronary artery disease who were at high risk for cardiovascular events.