X
X
Total 393357 Results
| Label | Description | ILX | Version | Created CID | Modified Time | ||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| Buoyancy | A physical quality inhering in a bearer by virtue of its tendency or ability to rise or float in a fluid medium such as water or air. | ILX:0101496 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Bupivacaine | A widely used local anesthetic agent. (PubChem) Pharmacology: Bupivacaine is a widely used local anesthetic agent. Bupivacaine is often administered by spinal injection prior to total hip arthroplasty. It is also commonly injected into surgical wound sites to reduce pain for up to 20 hours after surgery. In comparison to other local anesthetics it has a long duration of action. It is also the most toxic to the heart when administered in large doses. This problem has led to the use of other long-acting local anaesthetics:ropivacaine and levobupivacaine. Levobupivacaine is a derivative, specifically an enantiomer, of bupivacaine. Systemic absorption of local anesthetics produces effects on the cardiovascular and central nervous systems. At blood concentrations achieved with therapeutic doses, changes in cardiac conduction, excitability, refractoriness, contractility, and peripheral vascular resistance are minimal. However, toxic blood concentrations depress cardiac conduction and excitability, which may lead to atrioventricular block, ventricular arrhythmias and to cardiac arrest, sometimes resulting in fatalities. In addition, myocardial contractility is depressed and peripheral vasodilation occurs, leading to decreased cardiac output and arterial blood pressure. Following systemic absorption, local anesthetics can produce central nervous system stimulation, depression or both. Mechanism of action: Local anesthetics such as bupivacaine block the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse, and by reducing the rate of rise of the action potential. In general, the progression of anesthesia is related to the diameter, myelination and conduction velocity of affected nerve fibers. Clinically, the order of loss of nerve function is as follows: (1) pain, (2) temperature, (3) touch, (4) proprioception, and (5) skeletal muscle tone. The analgesic effects of Bupivicaine are thought to be due to its binding to the prostaglandin E2 receptors, subtype EP1 (PGE2EP1), which inhibits the production of prostaglandins, thereby reducing fever, inflammation, and hyperalgesia. Drug type: Approved. Investigational. Small Molecule. Drug category: Anesthetics, Local | ILX:0101497 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Buprenorphine | A derivative of the opioid alkaloid thebaine that is a more potent and longer lasting analgesic than morphine. It appears to act as a partial agonist at mu and kappa opioid receptors and as an antagonist at delta receptors. The lack of delta-agonist activity has been suggested to account for the observation that buprenorphine tolerance may not develop with chronic use. (PubChem) Pharmacology: Buprenorphine is a synthetic opioid analgesic and thebaine derivative, with a longer duration of action than morphine. Buprenorphine 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, buprenorphine exerts its principal pharmacologic effects on the central nervous system. Its primary actions of therapeutic value are analgesia and sedation. Buprenorphine 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. Buprenorphine depresses the respiratory centers, depresses the cough reflex, and constricts the pupils. Mechanism of action: Buprenorphine's analgesic effect is due to partial agonist activity at mu-opioid receptors. Buprenorphine is also a kappa-opioid receptor antagonist. The partial agonist activity means that opioid receptor antagonists (e.g., an antidote such as naloxone) only partially reverse the effects of buprenorphine. The binding to the mu and kappa receptors results in hyperpolarization and reduced neuronal excitability. Drug type: Approved. Illicit. Investigational. Small Molecule. Drug category: Analgesics, Opioid. Narcotic Antagonists. Narcotics | ILX:0101498 | 5 | scicrunch | 08/24/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | troy sincomb |
| Bupropion | A unicyclic, aminoketone antidepressant. The mechanism of its therapeutic actions is not well understood, but it does appear to block dopamine uptake. The hydrochloride is available as an aid to smoking cessation treatment. (PubChem) Pharmacology: Bupropion, an antidepressant of the aminoketone class and a non-nicotine aid to smoking cessation, is chemically unrelated to tricyclic, tetracyclic, selective serotonin re-uptake inhibitor, or other known antidepressant agents. Compared to classical tricyclic antidepressants, Bupropion is a relatively weak inhibitor of the neuronal uptake of norepinephrine, serotonin, and dopamine. In addition, Bupropion does not inhibit monoamine oxidase. Bupropion produces dose-related central nervous system (CNS) stimulant effects in animals, as evidenced by increased locomotor activity, increased rates of responding in various schedule-controlled operant behavior tasks, and, at high doses, induction of mild stereotyped behavior. Mechanism of action: Bupropion selectively inhibits the neuronal reuptake of dopamine, norepinephrine, and serotonin; actions on dopaminergic systems are more significant than imipramine or amitriptyline whereas the blockade of norepinephrine and serotonin reuptake at the neuronal membrane is weaker for bupropion than for tricyclic antidepressants. The increase in norepinephrine may attenuate nicotine withdrawal symptoms and the increase in dopamine at neuronal sites may reduce nicotine cravings and the urge to smoke. Bupropion exhibits moderate anticholinergic effects. Drug type: Approved. Small Molecule. Drug category: Antidepressive Agents. Antidepressive Agents, Second-Generation. Dopamine Uptake Inhibitors | ILX:0101499 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Burned In Annotation | Indicates whether or not image contains sufficient burned in annotation to identify the patient and date the image was acquired. | ILX:0101500 | 4 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Burst firing pattern | is an extremely diverse general phenomenon of the activation patterns of neurons in the central nervous system and spinal cord where periods of rapid spiking are followed by quiescent, silent, periods. Bursting is thought to be important in the operation of robust central pattern generators, the transmission of neural codes, and some neuropathologies such as epilepsy. | ILX:0101501 | 5 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Burwell Witter and Amaral (1995) cortical parcellation scheme | ILX:0101502 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| Buspirone | An anxiolytic agent and a serotonin receptor agonist belonging to the azaspirodecanedione class of compounds. Its structure is unrelated to those of the benzodiazepines, but it has an efficacy comparable to diazepam. (PubChem) Pharmacology: Buspirone is used in the treatment of generalized anxiety where it has advantages over other antianxiety drugs because it does not cause sedation (drowsiness) and does not cause tolerance or physical dependence. Buspirone differs from typical benzodiazepine anxiolytics in that it does not exert anticonvulsant or muscle relaxant effects. It also lacks the prominent sedative effect that is associated with more typical anxiolytics. in vitro preclinical studies have shown that buspirone has a high affinity for serotonin (5-HT1A) receptors. Buspirone has no significant affinity for benzodiazepine receptors and does not affect GABA binding in vitro or in vivo when tested in preclinical models. Buspirone has moderate affinity for brain D2-dopamine receptors. Some studies do suggest that buspirone may have indirect effects on other neurotransmitter systems. Mechanism of action: Buspirone binds to 5-HT type 1A serotonin receptors on presynaptic neurons in the dorsal raphe and on postsynaptic neurons in the hippocampus, thus inhibiting the firing rate of 5-HT-containing neurons in the dorsal raphe. Buspirone also binds at dopamine type 2 (DA2) receptors, blocking presynaptic dopamine receptors. Buspirone increases firing in the locus ceruleus, an area of brain where norepinephrine cell bodies are found in high concentration. The net result of buspirone actions is that serotonergic activity is suppressed while noradrenergic and dopaminergic cell firing is enhanced. Drug type: Approved. Investigational. Small Molecule. Drug category: Anti-anxiety Agents. Anxiolytics sedatives and hypnotics. Serotonin Agonists | ILX:0101503 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Busulfan | An alkylating agent having a selective immunosuppressive effect on bone marrow. It has been used in the palliative treatment of chronic myeloid leukemia (myeloid leukemia, chronic), but although symptomatic relief is provided, no permanent remission is brought about. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), busulfan is listed as a known carcinogen. (PubChem) Pharmacology: Busulfan is an antineoplastic in the class of alkylating agents and is used to treat various forms of cancer. Alkylating agents are so named because of their ability to add alkyl groups to many electronegative groups under conditions present in cells. They stop tumor growth by cross-linking guanine bases in DNA double-helix strands - directly attacking DNA. This makes the strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no longer divide. In addition, these drugs add methyl or other alkyl groups onto molecules where they do not belong which in turn inhibits their correct utilization by base pairing and causes a miscoding of DNA. Alkylating agents are cell cycle-nonspecific. Alkylating agents work by three different mechanisms all of which achieve the same end result - disruption of DNA function and cell death. Mechanism of action: Alkylating agents work by three different mechanisms: 1) attachment of alkyl groups to DNA bases, resulting in the DNA being fragmented by repair enzymes in their attempts to replace the alkylated bases, preventing DNA synthesis and RNA transcription from the affected DNA, 2) DNA damage via the formation of cross-links (bonds between atoms in the DNA) which prevents DNA from being separated for synthesis or transcription, and 3) the induction of mispairing of the nucleotides leading to mutations. Drug type: Approved. Investigational. Small Molecule. Drug category: Alkylating Agents. Antineoplastic Agents. Antineoplastic Agents, Alkylating. Immunosuppressive Agents. Myeloablative Agonists | ILX:0101504 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Butabarbital | Butabarbital (trade name Butisol) is a prescription barbiturate sleep aid. Butabarbital has a particularly fast onset of effects and short duration of action compared to other barbiturates, which makes it useful for certain applications such as treating severe insomnia and relieving anxiety before surgical procedures; however it is also relatively dangerous particularly when combined with alcohol, and so is now rarely used, although it is still prescribed in some Eastern European and South American countries. Its short duration of action gives butabarbital a high abuse potential, comparable to secobarbital. (Wikipedia) Pharmacology: Butabarbital, a barbiturate, is used for the treatment of short term insomnia. It belongs to a group of medicines called central nervous system (CNS) depressants that induce drowsiness and relieve tension or nervousness. Little analgesia is conferred by barbiturates; their use in the presence of pain may result in excitation. Mechanism of action: Butabarbital binds at a distinct binding site associated with a Cl- ionopore at the GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged. All of these effects are associated with marked decreases in GABA-sensitive neuronal calcium conductance (gCa). The net result of barbiturate action is acute potentiation of inhibitory GABAergic tone. Barbiturates also act through potent (if less well characterized) and direct inhibition of excitatory AMPA-type glutamate receptors, resulting in a profound suppression of glutamatergic neurotransmission. Drug type: Approved. Illicit. Small Molecule. Drug category: Anti-anxiety Agents. Barbiturates. Hypnotics and Sedatives | ILX:0101505 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Butalbital | Butalbital, 5-allyl-5-isobutylbarbituric acid, is a barbiturate with an intermediate duration of action. It has the same chemical formula as talbutal but a different structure. Butalbital is often combined with other medications, such as acetaminophen or aspirin, and is commonly prescribed for the treatment of pain and headache. (Wikipedia) Pharmacology: Butalbital is a short to intermediate-acting barbiturate. Barbiturates act as nonselective depressants of the central nervous system (CNS), capable of producing all levels of CNS mood alteration from excitation to mild sedation, hypnosis, and deep coma. In sufficiently high therapeutic doses, barbiturates induce anesthesia. Mechanism of action: Butalbital binds at a distinct binding site associated with a Cl- ionopore at the GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged. Drug type: Approved. Illicit. Small Molecule. Drug category: Analgesics | ILX:0101506 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Butane | An alkane that has formula C4H10. | ILX:0101507 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Butenafine | Butenafine hydrochloride is a synthetic benzylamine antifungal agent. Butenafine works by inhibiting the synthesis of ergosterol by inhibiting squalene epoxidase, an enzyme responsible for the creation of sterols needed in fungal cell membranes. Pharmacology: Butenafine is an antifungal agent that acts by inhibiting squalene epoxidase, thus blocking the biosynthesis of ergosterol, an essential component of fungal cell membranes. It is mainly active against dermatophytes and has superior fungicidal activity against this group of fungi when compared to that of terbinafine, naftifine, tolnaftate, clotrimazole, and bifonazole. It is active also against Candida albicans and this activity is superior to that of terbinafine and naftifine. Butenafine also generates low MICs for Cryptococcus neoformans and Aspergillus spp. as well. Mechanism of action: Like allylamines, butenafine inhibits ergosterol biosynthesis by blocking squalene epoxidation. As ergosterol is an essential component of the fungal cell membrane, inhibition of its synthesis results in increased cellular permeability causing leakage of cellular contents. Drug type: Approved. Small Molecule. Drug category: Antifungal Agents | ILX:0101508 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Butoconazole | Butoconazole is an imidazole antifungal used in gynecology. Pharmacology: Butoconazole is an imidazole derivative that has fungicidal activity in vitro against Candida spp. and has been demonstrated to be clinically effective against vaginal infections due to Candida albicans. Candida albicans has been identified as the predominant species responsible for vulvovaginal candidasis. Mechanism of action: The exact mechanism of the antifungal action of butoconazole is unknown, however, it is presumed to function as other imidazole derivatives via inhibition of steroid synthesis. Imidazoles generally inhibit the conversion of lanosterol to ergosterol via the inhibition of the enzyme cytochrome P450 14-demethylase, resulting in a change in fungal cell membrane lipid composition. This structural change alters cell permeability and, ultimately, results in the osmotic disruption or growth inhibition of the fungal cell. Drug type: Approved. Small Molecule. Drug category: Antifungal Agents | ILX:0101509 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Butorphanol | A synthetic morphinan analgesic with narcotic antagonist action. It is used in the management of severe pain. (PubChem) Pharmacology: Butorphanol is a synthetic opioid agonist-antagonist analgesic with a pharmacological and therapeutic profile that has been well established since its launch as a parenteral formulation in 1978. The introduction of a transnasal formulation of butorphanol represents a new and noninvasive presentation of an analgesic for moderate to severe pain. This route of administration bypasses the gastrointestinal tract, and this is an advantage for a drug such as butorphanol that undergoes significant first-pass metabolism after oral administration. The onset of action and systemic bioavailability of butorphanol following transnasal delivery are similar to those after parenteral administration. Butorphanol blocks pain impulses at specific sites in the brain and spinal cord. Mechanism of action: Butorphanol is a mixed agonist-antagonist with low intrinsic activity at receptors of the -opioid type (morphine-like). It is also an agonist at -opioid receptors. Its interactions with these receptors in the central nervous system apparently mediate most of its pharmacologic effects, including analgesia. Drug type: Approved. Illicit. Small Molecule. Drug category: Analgesics, Opioid. Antitussive Agents. Narcotic Antagonists. Narcotics | ILX:0101510 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| Butyrylcholinesterase | Human butyrylcholinesterase protein (602 aa, 68 kD), a serine esterase, is encoded by the human butyrylcholinesterase (BCHE) gene. This protein, a homotetramer, is present in most cells (except erythrocytes) and catalyzes the hydrolysis of acylcholines to yield a choline and a carboxylate anion. Reduced serum activity of the BCHE protein causes hypocholinesterasemia, a condition resulting in sensitivity to the muscle relaxant suxamethonium, which is commonly used in association with surgical anesthesia. (Definition from NCI Thesaurus and concept from MSH.) | ILX:0101511 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| BXD | ILX:0101512 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| BXH | ILX:0101513 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex | |
| C bouton | Synaptic bouton found in spinal cord on the soma and proximal dendrites of motor neurons | ILX:0101514 | 5 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
| C-C Chemokine | ILX:0101515 | 3 | scicrunch | 06/18/2018 | scicrunch | term | 12/08/2016 | 0 | NeuroLex | NeuroLex |
About
Base community for the SciCrunch.org infrastructure
Contact Us
X