X
X
Total 393357 Results
| Label | Description | ILX | Version | Created CID | Modified Time | ||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| Alcohol drug abuse and mental health administration | ADAMHA is now transferred to the newly-organized SAMSHA.http://www.samhsa.gov/grants/ | ILX:0100443 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Alcohol Withdrawal Delirium | An acute organic mental disorder induced by cessation or reduction in chronic alcohol consumption. Clinical characteristics include CONFUSION; DELUSIONS; vivid HALLUCINATIONS; TREMOR; agitation; insomnia; and signs of autonomic hyperactivity (e.g., elevated blood pressure and heart rate, dilated pupils, and diaphoresis). This condition may occasionally be fatal. It was formerly called delirium tremens (MeSH). | ILX:0100444 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Alcohol-nonpreferring rat | An inbred rat developed at Indiana University for low-alcohol-preferring behavior through bidirectional selective breeding of Wistar rats. These have low voluntary oral consumption of alcohol which results in low blood alcohol. The NP line of rat, as it is referred to, show a preference ratio of less than 0.5:1 for an EtOH solution over water. These rat lines also demonstrate distinct physiological and behavioral phenotypes in response to alcohol. RGD ID | ILX:0100445 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Alcohol-preferring rat | An inbred rat developed at Indiana University for high-alcohol-preferring behavior through bidirectional selective breeding of Wistar rats. These have high voluntary oral consumption of alcohol which leads to high blood alcohol. The P line of rat, as it is referred to, prefers an EtOH solution over water at least at 2:1 ratio. These rat lines also demonstrate distinct physiological and behavioral phenotypes in response to alcohol. RDG ID | ILX:0100446 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Alcohol-Related Addiction | ILX:0100447 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| Alcohol-Related Disorder | Disorder related to or resulting from abuse or mis-use of alcohol (MeSH). | ILX:0100448 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Alcohol-Related Withdrawal | ILX:0100449 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| Alcoholic Intoxication | An acute brain syndrome which results from the excessive ingestion of ETHANOL or ALCOHOLIC BEVERAGES (MeSH). | ILX:0100450 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Alcoholic Psychosis | A group of mental disorders associated with organic brain damage and caused by poisoning from alcohol (MeSH). | ILX:0100451 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Alcoholism | A primary, chronic disease with genetic, psychosocial, and environmental factors influencing its development and manifestations. The disease is often progressive and fatal. It is characterized by impaired control over drinking, preoccupation with the drug alcohol, use of alcohol despite adverse consequences, and distortions in thinking, most notably denial. Each of these symptoms may be continuous or periodic (MeSH). | ILX:0100452 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Aldesleukin | Proleukin, a lymphokine, is produced by recombinant DNA technology using a genetically engineered E. coli strain containing an analog of the human interleukin-2 gene. Genetic engineering techniques were used to modify the human IL-2 gene, and the resulting expression clone encodes a modified human interleukin-2. This recombinant form differs from native interleukin-2 in the following ways:a) proleukin is not glycosylated because it is derived from E. coli ; b) the molecule has no N-terminal alanine; the codon for this amino acid was deleted during the genetic engineering procedure; c) the molecule has serine substituted for cysteine at amino acid position 125. Pharmacology: Used to treat renal cell carcinoma, proleukin induces the enhancement of lymphocyte mitogenesis and stimulation of long-term growth of human interleukin-2 dependent cell lines, the enhancement of lymphocyte cytotoxicity, the induction of killer cell (lymphokine-activated (LAK) and natural (NK)) activity; and the induction of interferon-gamma production. IL-2 is normally produced by the body, secreted by T cells, and stimulates growth and differentiation of T cell response. It can be used in immunotherapy to treat cancer. It enhances the ability of the immune system to kill tumor cells and may interfere with blood flow to the tumor. Mechanism of action: Proleukin binds to the IL-2 receptor which leads to heterodimerization of the cytoplasmic domains of the IL-2R beta and gamma(c) chains, activation of the tyrosine kinase Jak3, and phosphorylation of tyrosine residues on the IL-2R beta chain. These events led to the creation of an activated receptor complex, to which various cytoplasmic signaling molecules are recruited and become substrates for regulatory enzymes (especially tyrosine kinases) that are associated with the receptor. These events stimulate growth and differentiation of T cells. Drug type: Approved. Biotech. Investigational. Drug category: Antineoplastic Agents | ILX:0100453 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Aldrin | Organic Compound;Pesticide;Organochloride; Aldrin is a chlorinated hydrocarbon used as an insecticide. Once in the insect, aldrin is oxidized into dieldrin, a neurotoxin. Due to the toxicity and ability of bioaccumulate of dieldrin, the use of aldrin is now banned in most parts of the world. | ILX:0100454 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Alefacept | Immunosuppressive dimeric fusion protein that consists of the extracellular CD2-binding portion of the human leukocyte function antigen-3 (LFA-3) linked to the Fc (hinge, CH2 and CH3 domains) portion of human IgG1. Produced by CHO cells, mW is 91.4 kD. Pharmacology: Interferes with lymphocyte activation by specifically binding to the lymphocyte antigen, CD2, and inhibiting LFA-3/CD2 interaction. Activation of T lymphocytes involving the interaction between LFA-3 on antigen-presenting cells and CD2 on T lymphocytes plays a role in the pathophysiology of chronic plaque psoriasis. Also causes a reduction in subsets of CD2+ T lymphocytes as well as CD4+ and CD8+ T lymphocytes. Mechanism of action: Inhibits T-lymphocyte activation and production by binding to the CD2 lymphocyte antigen. Drug type: Approved. Biotech. Investigational. Drug category: Immunomodulatory Agents. Immunosuppressive Agents | ILX:0100455 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Alemtuzumab | Humanized monoclonal antibody specific to lymphocyte antigens. It is a recombinant DNA-derived humanized monoclonal antibody (Campath-1H) that is directed against the 21-28 kD cell surface glycoprotein,CD52. The Campath-1H antibody is an IgG1 kappa with human variable framework and constant regions, and complementarity-determining regions from a murine (rat) monoclonal antibody (Campath-1G). Campath is produced in mammalian cell (Chinese hamster ovary) suspension culture in a medium containing neomycin. Pharmacology: Campath is used to treat leukemia by exploiting antibody mediated lysis of CD52 presenting cells. The CD52 antigen is a cell surface protein found on essentially all B and T lymphocytes, a majority of monocytes, macrophages and most granulocytes. The CD52 antigen is not present on erythrocytes or hematopoetic stem cells. In leukemia there is an excess of B and T cells, so Campath permits selective reduction of lymphocyte populations. Mechanism of action: Campath binds to the CD52 antigen present on most B and T lymphocytes. This binding leads to antibody-dependent lysis of leukemic cells. Drug type: Approved. Biotech. Investigational. Drug category: Antineoplastic Agents | ILX:0100456 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Alendronate | A nonhormonal medication for the treatment of postmenopausal osteoporosis in women. This drug builds healthy bone, restoring some of the bone loss as a result of osteoporosis. (PubChem) Pharmacology: Alendronate, a second-generation bisphosphonate is the first member of a group of drugs which strengthens bone. Alendronate is used to reduce hypercalcemia in tumor-induced bone disease, to treat corticosteroid-induced osteoporosis and Paget's disease, and to prevent osteoporosis in postmenopausal women. Mechanism of action: The action of Alendronate on bone tissue is based partly on its affinity for hydroxyapatite, which is part of the mineral matrix of bone. Alendronate also targets farnesyl pyrophosphate (FPP) synthase. Nitrogen-containing bisphosphonates (such as pamidronate, alendronate, risedronate, ibandronate and zoledronate) appear to act as analogues of isoprenoid diphosphate lipids, thereby inhibiting FPP synthase, an enzyme in the mevalonate pathway. Inhibition of this enzyme in osteoclasts prevents the biosynthesis of isoprenoid lipids (FPP and GGPP) that are essential for the post-translational farnesylation and geranylgeranylation of small GTPase signalling proteins. This activity inhibits osteoclast activity and reduces bone resorption and turnover. In postmenopausal women, it reduces the elevated rate of bone turnover, leading to, on average, a net gain in bone mass. Drug type: Approved. Small Molecule. Drug category: Antihypocalcemic Agents. Antiresorptives. Bisphosphonates. Bone Density Conservation Agents | ILX:0100457 | 5 | scicrunch | 08/24/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | troy sincomb |
| Alexander Disease | A rare inherited disorder of myelin formation. Alexander disease is a progressive leukoencephalopathy whose hallmark is the widespread accumulation of cytoplasmic inclusions called Rosenthal fibers. The fibers contain GLIAL FIBRILLARY ACIDIC PROTEIN in association with ALPHA-CRYSTALLIN B CHAIN. Rosenthal fibers are found predominantly in ASTROCYTES located in the subependymal, subpial, and periventricular areas of the BRAIN (MeSH). | ILX:0100458 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Alfentanil | A short-acting opioid anesthetic and analgesic derivative of fentanyl. It produces an early peak analgesic effect and fast recovery of consciousness. Alfentanil is effective as an anesthetic during surgery, for supplementation of analgesia during surgical procedures, and as an analgesic for critically ill patients. (PubChem) Pharmacology: Alfentanil is a synthetic opioid analgesic. Alfentanil interacts predominately with the opioid mu-receptor. These mu-binding sites are discretely distributed in the human brain, spinal cord, and other tissues. In clinical settings, alfentanil exerts its principal pharmacologic effects on the central nervous system. Its primary actions of therapeutic value are analgesia and sedation. Alfentanil may increase the patient's tolerance for pain and decrease the perception of suffering, although the presence of the pain itself may still be recognized. In addition to analgesia, alterations in mood, euphoria and dysphoria, and drowsiness commonly occur. Alfentanil depresses the respiratory centers, depresses the cough reflex, and constricts the pupils. Mechanism of action: Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Alfentanil's analgesic activity is, most likely, due to its conversion to morphine. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability. Drug type: Approved. Illicit. Small Molecule. Drug category: Analgesics. Analgesics, Opioid. Anesthetics. Anesthetics, Intravenous. Narcotics. Opiate Agonists | ILX:0100459 | 5 | scicrunch | 08/24/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | troy sincomb |
| Alfuzosin | Alfuzosin (INN, provided as the hydrochloride salt) is an alpha-adrenergic blocker used to treat benign prostatic hyperplasia (BPH). It works by relaxing the muscles in the prostate and bladder neck, making it easier to urinate. (Wikipedia) Pharmacology: Alfuzosin is an alpha-adrenergic blocking agent used to treat hypertension and benign prostatic hyperplasia. Accordingly, alfuzosin is a selective inhibitor of the alpha1 subtype of alpha adrenergic receptors. In the human prostate, alfuzosin antagonizes phenylephrine (alpha1 agonist)-induced contractions, in vitro, and binds with high affinity to the alpha1c adrenoceptor, which is thought to be the predominant functional type in the prostate. Studies in normal human subjects have shown that alfuzosin competitively antagonized the pressor effects of phenylephrine (an alpha1 agonist) and the systolic pressor effect of norepinephrine. The antihypertensive effect of alfuzosin results from a decrease in systemic vascular resistance and the parent compound alfuzosin is primarily responsible for the antihypertensive activity. Mechanism of action: Alfuzosin acts by inhibiting the postsynaptic alpha(1)-adrenoceptors on vascular smooth muscle. This inhibits the vasoconstrictor effect of circulating and locally released catecholamines (epinephrine and norepinephrine), resulting in peripheral vasodilation. Drug type: Approved. Investigational. Small Molecule. Drug category: Adrenergic alpha-Antagonists. Antihypertensive Agents | ILX:0100460 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Alglucerase | Human Beta-glucocerebrosidase or Beta-D-glucosyl-N-acylsphingosine glucohydrolase E.C. 3.2.1.45. 497 residue protein with N-linked carbohydrates, MW | ILX:0100461 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Alglucosidase alfa | Alglucosidase alfa consists of the human enzyme acid a-glucosidase (GAA), encoded by the most predominant of nine observed haplotypes of this gene. Alglucosidase alfa is produced by recombinant DNA technology in a Chinese hamster ovary cell line. Alglucosidase alfa degrades glycogen by catalyzing the hydrolysis of a-1,4- and a-1,6- glycosidic linkages of lysosomal glycogen. Pharmacology: Pompe disease (glycogen storage disease type II, GSD II, glycogenosis type II, acid maltase deficiency) is an inherited disorder of glycogen metabolism caused by the absence or marked deficiency of the lysosomal enzyme GAA. In the infantile-onset form, Pompe disease results in intralysosomal accumulation of glycogen in various tissues, particularly cardiac and skeletal muscles, and hepatic tissues, leading to the development of cardiomyopathy, progressive muscle weakness, and impairment of respiratory function. In the juvenile- and adult-onset forms, intralysosomal accumulation of glycogen is limited primarily to skeletal muscle, resulting in progressive muscle weakness. Death in all forms is usually related to respiratory failure. Alglucosidase alfa provides an exogenous source of GAA. Binding to mannose-6-phosphate receptors on the cell surface has been shown to occur via carbohydrate groups on the GAA molecule, after which it is internalized and transported into lysosomes, where it undergoes proteolytic cleavage that results in increased enzymatic activity. It then exerts enzymatic activity in cleaving glycogen. Mechanism of action: Alglucosidase alfa is designed to act as an exogenous source of GAA, acting to correct GAA deficiency that is the hallmark of Pompe disease. Alglucosidase alfa binds to mannose-6-phosphate receptors on the cell surface via carbohydrate groups on the GAA molecule, after which it is internalized and transported into lysosomes, where it undergoes proteolytic cleavage that results in increased enzymatic activity. It then exerts enzymatic activity in cleaving glycogen. Drug type: Approved. Biotech. Drug category: Enzyme Replacement Agents | ILX:0100462 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
About
Base community for the SciCrunch.org infrastructure
Contact Us
X