Persius/hicric huggingface dataset:
Bcl-2-associated death promoter
The Bcl-2-associated death promoter (BAD) protein is a pro-apoptotic member of the Bcl-2 gene family which is involved in initiating apoptosis. BAD is a member of the BH3-only family, a subfamily of the Bcl-2 family. It does not contain a C-terminal transmembrane domain for outer mitochondrial membrane and nuclear envelope targeting, unlike most other members of the Bcl-2 family. After activation, it is able to form a heterodimer with anti-apoptotic proteins and prevent them from stopping apoptosis.

# Mechanism of action
Bax/Bak are believed to initiate apoptosis by forming a pore in the mitochondrial outer membrane that allows cytochrome c to escape into the cytoplasm and activate the pro-apoptotic caspase cascade.  The anti-apoptotic Bcl-2 and Bcl-xL proteins inhibit cytochrome c release through the mitochondrial pore and also inhibit activation of the cytoplasmic caspase cascade by cytochrome c.
Dephosphorylated BAD forms a heterodimer with Bcl-2 and Bcl-xL, inactivating them and thus allowing Bax/Bak-triggered apoptosis.  When BAD is phosphorylated by Akt/protein kinase B (triggered by PIP3), it forms the BAD-(14-3-3) protein heterodimer.  This leaves Bcl-2 free to inhibit Bax-triggered apoptosis.  BAD phosphorylation is thus anti-apoptotic, and BAD dephosphorylation (e.g., by Ca2+-stimulated Calcineurin) is pro-apoptotic.  The latter may be involved in neural diseases such as schizophrenia.

# Interactions
Bcl-2-associated death promoter has been shown to interact with:
- BCL2L1,
- BCL2A1,
- BCL2L2,
- Bcl-2,
- MCL1
- S100A10,
- YWHAQ,  and
- YWHAZ.
Beta adrenergic receptor kinase
Beta adrenergic receptor kinase (also referred to as ARK or BARK) is a serine/threonine intracellular kinase.  It is activated by PKA and its target is the beta adrenergic receptor.  It is one method by which the cell will desensitize itself from epinephrine overstimulation.

# Activation
- (steps 1) Upon stimulation of the Beta adrenergic receptor by epinephrine, Gs will be activated.
- (steps 2 and 3) Gs alpha will then stimulate adenyl cyclase to make cAMP.
- (steps 3 through 6) cAMP will then activate cAMP-dependent kinase (PKA), which, among other proteins that it acts on, will phosphorylate serine and threonine residues on ARK.
- (step 7) ARK, itself a serine/threonine kinase, will then phosphorylate serine and threonine residues on the -adrenergic receptor itself.
- (step 8) This will facilitate Beta-arrestin's binding to the receptor.  Additional stimulation by epinephrine will now be unable to activate Gs due to arrestin.
Therefore, ARK is a negative feedback enzyme that will prevent overstimulation of the -adrenergic receptor.

# Other similar systems
In the rhodopsin system, which regulates rod cell function in the retina, rhodopsin kinase will phosphorylate serine and threonine residues on the rhodopsin receptor.  Similarly to the ARK system, the phosphorylated rhodopsin residues will then bind to arrestin, resulting in receptor desensitization.

# Structure

## Protein structure
The structure of ARK1 consists of a protein of 689 amino acids (79.7 kilodaltons) with a protein kinase catalytic domain that bears greatest sequence similarity to protein kinase C and the cyclic adenosine monophosphate (cyclic AMP)-dependent protein kinase.

## Gene structure
The gene spans approximately 23 kilobases and is composed of 21 exons interrupted by 20 introns. Exon sizes range from 52 bases (exon 7) to over 1200 bases (exon 21), intron sizes from 68 bases (intron L) to 10.8 kilobases (intron A). The splice sites for donor and acceptor were in agreement with the canonical GT/AG rule. Functional regions of beta ARK are described with respect to their location within the exon-intron organization of the gene. Primer extension and RNase protection assays suggest a major transcription start site approximately 246 bases upstream of the start ATG. Sequence analysis of the 5'-flanking/promoter region reveals many features characteristic of mammalian housekeeping genes, i.e. the lack of a TATA box, an absent or nonstandard positioned CAAT box, high GC content, and the presence of Sp1-binding sites. The extraordinarily high GC content of the 5'-flanking region (> 80%) helps define this region as a CpG island that may be a principal regulator of beta ARK expression.

# Interactions
Beta adrenergic receptor kinase has been shown to interact with:
- Beta-gamma complex,
- G protein
- GIT1,
- GNAQ,
- PDE6G,
- PRKCB1  and
- Src.
Bleomycin (patient information)

# IMPORTANT WARNING
Bleomycin can cause severe lung problems. If you experience any of the following symptoms, call your doctor immediately: breathing discomfort, shortness of breath, wheezing, fever, or chills.

# About your treatment
Your doctor has prescribed the drug bleomycin to help treat your illness. The drug is given by injection into a large muscle, a vein, or just under the skin. The drug also can be placed, through a chest tube, into the space surrounding the lungs. Occasionally, small test doses are given to check your reaction before the remainder of the drug is administered.
This medication is used to treat:
- lymphomas
- squamous cell carcinomas
- testicular carcinomas
- malignant pleural effusions
This medication is sometimes prescribed for other uses; ask your doctor or pharmacist for more information.
Bleomycin is an antibiotic that is used only for its cancer-fighting effects; it slows or stops the growth of cancer cells in your body. The length of treatment depends on the types of drugs you are taking, how well your body responds to them, and the type of cancer you have.

# Other uses for this medicine
Bleomycin is also used to treat Kaposi's sarcoma related to acquired immunodeficiency syndrome (AIDS), renal carcinoma, soft tissue sarcomas, otorhinolaryngeal tumors, and mycosis fungoides. Talk to your doctor about the possible risks of using this drug for your condition.

# Precautions
Before taking bleomycin:
- tell your doctor and pharmacist if you are allergic to bleomycin or any other drugs.
- tell your doctor and pharmacist what prescription and nonprescription medications you are taking, especially aspirin, filgrastim (GCSF, Neupogen) or other cytokines (GMCSF, Sargramostim), and vitamins.
- tell your doctor if you have or have ever had kidney or lung disease.
- Women who are pregnant or breast-feeding should tell their doctor before they begin taking this drug. You should not plan to have children while receiving chemotherapy or for a while after treatments. (Talk to your doctor for further details.) Use a reliable method of birth control to prevent pregnancy. Bleomycin may harm the fetus.
- do not have any vaccinations (e.g., measles or flu shots) without talking to your doctor.

# Side effects

## Minor side effects
Side effects from bleomycin are common and include:
- nausea and vomiting
- loss of appetite
- weakness
- darkened and thickened areas of skin
Tell your doctor if the following symptom is severe or lasts for several hours:
- lightheadedness

## Severe side effects
If you experience the following symptom, call your doctor immediately:
- skin reactions such as itching, tenderness, redness, or swelling
If you experience a serious side effect, you or your doctor may send a report to the Food and Drug Administration's (FDA) MedWatch Adverse Event Reporting program online  or by phone .

# In case of emergency/overdose
In case of overdose, call your local poison control center at 1-800-222-1222. If the victim has collapsed or is not breathing, call local emergency services at 911.

# Brand names
- Blenoxane
Brnsted-Lowry acid-base theory
In chemistry, the Brnsted-Lowry acid-base theory or Brnsted-Lowry concept is an acid-base theory describing the reaction mechanism between acids and bases, and was independently proposed by Johannes Nicolaus Brnsted and Thomas Martin Lowry in 1923. In this system, a Brnsted-Lowry acid is defined as any species which has the tendency to lose, or "donate" a hydrogen ion (proton), and a Brnsted-Lowry base as a substance with a tendency to gain or "accept" a hydrogen ion (proton). Thus, other substances such as water molecules can have behaviours not defined in the common definition of an acid or base.
In the reaction between acetic acid and water, acetic acid acts as an acid by donating a proton to water, which acts as a base. The equation given is:
Water can also act as an acid, for instance when it reacts with ammonia. The equation given for this reaction is:
in which H2O donates a proton to NH3. Thus water is amphoteric: able to act as either an acid or a base. These reactions can act in reverse as well as in the forward direction. The reverse of the reaction between acetic acid and water is:
In the reverse reactions H3O+ acts as an acid to donate a proton to CH3COO-, which is acting as a base.
In the forward reaction, CH3COOH acts as an acid to donate a proton, and water as a base to receive it.  H2O and H3O+ are therefore considered one acid-base conjugate pair, and CH3COOH and CH3COO- as another conjugate pair.
CAMP response element modulator
"cAMP-response-element modulator (CREM), a transcription factor responsive to the cAMP signal transduction pathway, drives expression of key testis-specific genes."
"Transcription factors of the cAMP-response-element binding protein (CREB)CREM family target genes with cAMP response elements (CREs) constituted by the palindromic consensus sequence TGACGTCA (Sassone-Corsi et al. 1988)."
"Within the activation domain is the P-(phosphorylation) box containing the target residue for PKA phosphorylation, among other phosphoacceptor sites."
Natriuretic peptide precursor C
Natriuretic peptide precursor C, also known as NPPC, is a protein that in humans is encoded by the NPPC gene. The precursor NPPC protein is cleaved to the 22 amino acid peptide C-type natriuretic peptide (CNP).

# Function
Natriuretic peptides comprise a family of 3 structurally related molecules: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP), encoded by a gene symbolized NPPC. These peptides possess potent natriuretic, diuretic, and vasodilating activities and are implicated in body fluid homeostasis and blood pressure control.
Unlike ANP and BNP, CNP does not have direct natriuretic activity. This is because CNP is a selective agonist for the B-type natriuretic receptor (NPRB) whereas ANP and BNP are selective for the A-type natriuretic receptor (NPRA). It is synthesized and secreted from the endothelium in response to many stimuli, for example shear stress (like NO) and certain proinflammatory cytokinea.
Carbamoyl phosphate synthase II
Carbamoyl phosphate synthetase II (EC 6.3.5.5) is an enzyme that catalyzes the reactions that produce carbamoyl phosphate in the cytosol (as opposed to type I, which functions in the mitochondria). Its systemic name is hydrogen-carbonate:L-glutamine amido-ligase (ADP-forming, carbamate-phosphorylating).
In pyrimidine biosynthesis, it serves as the rate-limiting enzyme and catalyzes the following reaction:
It is activated by ATP and PRPP and it is inhibited by UMP (Uridine monophosphate, the end product of the pyrimidine synthesis pathway).
Neither CPSI nor CPSII require biotin as a coenzyme, as seen with most carboxylation reactions.
It is one of the three enzyme functions coded by the CAD gene. It is classified under EC 6.3.5.5.

# Nomenclature
Carbamoyl-phosphate synthetase (glutamine-hydrolysing) is also known as:
- hydrogen-carbonate:L-glutamine amido-ligase (ADP-forming, carbamate-phosphorylating)
- carbamyl phosphate synthetase (glutamine)
- glutamine-dependent carbamyl phosphate synthetase
- carbamoyl phosphate synthetase
- CPS
- carbon-dioxide:L-glutamine amido-ligase (ADP-forming, carbamate-phosphorylating)
Cardiac effects of insect bites

# Snake bite
Cardiovascular effects of snake bites (snake venom) as follow;
- Coronary spasm and acute myocardial infarction   
- Hypercoagulability. There are some procoagulants such as arginine esterase in snake venom. Therefore, significant envenomation may result in Disseminated Intravascular Coagulation (DIC)
- Myocarditis 
- Hypovolemic shock: Snake venom has haemorrhagins. Haemorrhagins increase vascular permeability and cause tendency to bleeding. Acute myocardial infarction can occur by profound hypotension and hypovolemic shock secondary to this bleeding tendency effect of snake venom. 

## EKG Examples
Acute Myocardial Infarction Complicating Snake Bite

# Scorpions
Death by scorpion sting, if it occurs, is the result of heart failure or respiratory failure a few hours after the incident. 
The most frequent cardiovascular and pulmonary findings are:   
- Tachypnea
- Tachycardia
- Hypertension
- Arrhythmias
- Hyperkinetic pulmonary edema

## EKG Examples
Cardiovascular Manifestations of Scorpion Sting
Carpal tunnel syndrome overview
Carpal tunnel syndrome (CTS) or Median Neuropathy at the Wrist is a medical condition in which the median nerve is compressed at the wrist, leading to pain, paresthesias, and muscle weakness in the forearm and hand. A form of compressive neuropathy, CTS is more common in women than it is in men, and, though it can occur at any age, has a peak incidence around age 42. The lifetime risk for CTS is around 10% of the adult population.. 
Most cases of CTS are idiopathic, without known cause. Repetitive activities are often blamed for the development of CTS, along with several other possible causes. However, the correlation is often unclear. 
It is a multi-faceted problem and can therefore be challenging to treat. Still, there is a multitude of possible treatments, e.g. treating any possible underlying disease or condition, immobilizing braces, physiotherapy, medication, prioritizing hand activities and ergonomics. Ultimately, carpal tunnel release surgery may be required. Outcomes are generally good.
The condition was first noted in the medical literature in the early 1900s.
Cefotetan clinical pharmacology
High plasma levels of cefotetan are attained after intravenous and intramuscular administration of single doses to normal volunteers.
The plasma elimination half-life of cefotetan is 3 to 4.6 hours after either intravenous or intramuscular administration.
Repeated administration of CEFOTAN does not result in
accumulation of the drug in normal subjects.
Cefotetan is 88% plasma protein bound.
No active metabolites of cefotetan have been detected; however, small amounts (less than 7%) of cefotetan in plasma and urine may be converted to its tautomer, which has antimicrobial activity similar to the parent drug.
In normal patients, from 51% to 81% of an administered dose of CEFOTAN is excreted unchanged by the kidneys over a 24 hour period, which results in high and prolonged urinary concentrations. Following intravenous doses of 1 gram and 2 grams, urinary concentrations are highest during the first hour and reach concentrations of approximately 1700 and 3500 g/mL respectively.
In volunteers with reduced renal function, the plasma half-life of cefotetan is prolonged. The mean terminal half-life increases with declining renal function, from approximately 4 hours in volunteers with normal renal function to about 10 hours in those with moderate renal impairment. There is a linear correlation between the systemic clearance of cefotetan and creatinine clearance. When renal function is impaired, a reduced dosing schedule based on creatinine clearance must be used. (see DOSAGE AND ADMINISTRATION).
In pharmacokinetics studies of eight elderly patients (greater than 65 years) with normal renal function and six healthy volunteers (aged 25 to 28 years), mean ( 1sd) Total Body Clearance (1.8(0.1) L/h vs. 1.8 (0.3) L/h) and mean Volume of Distribution (10.4(1.2) L vs. 10.3 (1.6)L) were similar following administration of a one gram intravenous bolus dose.
Therapeutic levels of cefotetan are achieved in many body tissues and fluids including:
Cefoxitin clinical pharmacology

# CLINICAL PHARMACOLOGY

## Clinical Pharmacology
Following an intravenous dose of 1 gram, serum concentrations were 110 mcg/mL at 5 minutes, declining to less than 1 mcg/mL at 4 hours. The half-life after an intravenous dose is 41 to 59 minutes. Approximately 85 percent of cefoxitin is excreted unchanged by the kidneys over a 6-hour period, resulting in high urinary concentrations. Probenecid slows tubular excretion and produces higher serum levels and increases the duration of measurable serum concentrations.
Cefoxitin passes into pleural and joint fluids and is detectable in antibacterial concentrations in bile.
In a pubished study of geriatric patients ranging in age from 64 to 88 years with normal renal function for their age (creatinine clearance ranging from 31.5 to 174.0 mL/min), the half-life for cefoxitin ranged from 51 to 90 minutes, resulting in higher plasma concentrations than in younger adults. These changes were attributed to decreased renal function associated with the aging process.
Cefprozil indications and usage
Cefprozil is indicated for the treatment of patients with mild to moderate infections caused by susceptible strains of the designated microorganisms in the conditions listed below:

# Upper Respiratory Tract
Pharyngitis/Tonsillitis
caused by Streptococcus pyogenes.
NOTE: The usual drug of choice in the treatment and prevention of streptococcal infections, including the prophylaxis of rheumatic fever, is penicillin given by the intramuscular route. Cefprozil is generally effective in the eradication of Streptococcus pyogenes from the nasopharynx; however, substantial data establishing the efficacy of cefprozil in the subsequent prevention of rheumatic fever are not available at present.
Otitis Media
caused by Streptococcus pneumoniae, Haemophilus influenzae (including -lactamase-producing strains), and Moraxella (Branhamella) catarrhalis(including -lactamase-producing strains). (See CLINICAL STUDIES.)
NOTE: In the treatment of otitis media due to -lactamase-producing organisms, cefprozil had bacteriologic eradication rates somewhat lower than those observed with a product containing a specific -lactamase inhibitor. In considering the use of ceprozil, lower overall eradication rates should be balanced against the susceptibility patterns of the common microbes in a given geographic area and the increased potential for toxicity with products containing -lactamase inhibitors.
Acute Sinusitis
caused by Streptococcus pneumoniae, Haemophilus influenzae (including -lactamase-producing strains), and Moraxella (Branhamella) catarrhalis(including -lactamase-producing strains).

# Lower Respiratory Tract
Secondary Bacterial Infection of Acute Bronchitis and Acute Bacterial Exacerbation of Chronic Bronchitis
caused by Streptococcus pneumoniae, Haemophilus influenza (including -lactamase-producing strains), and Moraxella (Branhamella) catarrhalis(including -lactamase-producing strains).

# Skin and Skin Structure
Uncomplicated Skin and Skin-Structure Infections
caused by Staphylococcus aureus (including penicillinase-producing strains) and Streptococcus pyogenes. Abscesses usually require surgical drainage.
To reduce the development of drug-resistant bacteria and maintain the effectiveness of cefprozil and other antibacterial drugs, cefprozil 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.
Cefuroxime detailed information
Cefuroxime is a second-generation cephalosporin antibiotic that has been widely available in the USA since 1977. It is also available under the brand name Ceftin. Glaxo Smith Kline sells the antibiotic in Australia (and other countries, such as Israel) under the name Zinnat (R), with the Australian pharmaceutical code of R 47621. In Poland it is produced by the Polish firm Bioton S.A. under the name Biofuroksym.
According to the package insert supplied with Zinnat, Cefuroxime is manufactured as tablets as well as a sodium salt, the latter designed for medical injection.

## Indications
As for the cephalosporins, although as a second-generation it is less susceptible to Beta-lactamase and so may have greater activity against Haemophilus influenzae, Neisseria gonorrhoeae and Lyme disease.

# Side effects
Cefuroxime is generally well tolerated and side effects are usually transient. Cefuroxime if taken with food is both better absorbed and less likely to cause its commonest upsets of diarrhea, nausea, vomiting and abdominal pain.
Although there is a widely quoted cross-allergy risk of 10% between cephalosporins and penicillin, an article in the Journal of Family Practice (February 2006) has shown no increased risk for cross-allergy for cefuroxime and several other 2nd generation or later cephalosporins.
Cephalexin detailed information
Cefalexin (INN) (Template:PronEng) or cephalexin (USAN) is a first-generation cephalosporin antibiotic. It is an orally administered agent with a similar antimicrobial spectrum to the intravenous agents cefalotin and cefazolin. It is commonly marketed under the trade name Keflex (Lilly) or Sporidex (Ranbaxy).

# Clinical use

## Indications
Cefalexin is used to treat urinary tract infections, respiratory tract infections (including sinusitis, otitis media, pharyngitis, tonsillitis and pneumonia, bronchitis), skin and soft tissue infections.
Although it is not generally considered first-line treatment for any indication, it is a useful alternative to penicillins in patients with penicillin hypersensitivity. There is, however, cross-reactivity in 10% of patients with hypersensitivity to penicillins and carbapenems.

## Formulations
Cefalexin is commonly marketed as tablets(250 mg and 500 mg), capsules, and powder for oral suspension (125 mg and 250 mg).
It is marketed by generic pharmaceutical manufacturers under a wide range of brand names, including: Apo-Cephalex, Biocef, Cefanox, Ceporex, Cephabos, Cilex, Ialex, Ibilex, Kefexin, Keflet, Keflex, Keforal, Keftab, Keftal, Lopilexin, Novo-Lexin, Ospexin, Zephalexin, Panixine Disperdose and Sporidex.
A version of Keflex 750 mg capsules is marketed for twice-daily dosage, to improve patients' compliance. However, it is not a sustained release formulation, and since it is more expensive than the older strengths, some physicians prescribe three 250 mg capsules to be taken twice daily, as a cheaper alternative.