|
Kca4.2
|
|
ILX:0105839
|
3
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
Kca5.1
|
|
ILX:0105840
|
3
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
KChIP
|
|
ILX:0105841
|
3
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
KChIP1
|
|
ILX:0105842
|
3
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
KChIP2
|
|
ILX:0105843
|
3
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
KChIP3
|
|
ILX:0105844
|
3
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
KChIP4
|
|
ILX:0105845
|
3
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
Kearns-Sayer Syndrome
|
A mitochondrial disorder featuring the triad of chronic progressive EXTERNAL OPHTHALMOPLEGIA, cardiomyopathy ( CARDIOMYOPATHIES) with conduction block ( HEART BLOCK), and RETINITIS PIGMENTOSA. Disease onset is in the first or second decade. Elevated CSF protein, sensorineural deafness, seizures, and pyramidal signs may also be present. Ragged-red fibers are found on muscle biopsy.
|
ILX:0105846
|
3
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
Keep-track task
|
A task in which subjects are first shown a set of categories to keep track of for a particular trial (e.g., animals, colors, and countries). They are then presented with words (including words from each category), and must remember the last word that was presented from each of the categories and recall those words at the end of the trial.
|
ILX:0105847
|
4
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
Kennedy Syndrome
|
Kennedy's disease is an inherited motor neuron disease that affects males. It is one of a group of disorders called spinal muscular atrophy (SMA). Onset of the disease is usually between the ages of 20 and 40, although it has been diagnosed in men from their teens to their 70s. Early symptoms include tremor of the outstretched hands, muscle cramps with exertion, and fasciculations (fleeting muscle twitches visible under the skin). Eventually, individuals develop limb weakness which usually begins in the pelvic or shoulder regions. Weakness of the facial and tongue muscles may occur later in the course of the disease and often leads to dysphagia (difficulty in swallowing), dysarthria (slurring of speech), and recurrent aspiration pneumonia. Some individuals develop gynecomastia (excessive enlargement of male breasts) and low sperm count or infertility. Still others develop non-insulin-dependent diabetes mellitus. Kennedy's disease is an x-linked recessive disease, which means the patient's mother carries the defective gene on one of her X chromosomes. Daughters of patients with Kennedy's disease are also carriers and have a 1 in 2 chance of having a son affected with the disease. Parents with concerns about their children may wish to talk to a genetic counselor. (http://www.ninds.nih.gov/disorders/kennedys/kennedys.htm)
|
ILX:0105848
|
4
|
FDI Lab - SciCrunch.org
|
08/24/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
troy sincomb |
|
Kenyon cell
|
A Kenyon cell is an intrinsic neuron of the mushroom body. Its cell body, situated in the cortex above the calyx of the mushroom body, is smaller than those in the surrounding midbrain cortex. Four short fascicles extend from the cell bodies of the Kenyon cells into the calyx. Each fascicle corresponds to axons from a set of cell bodies descended from a single mushroom body neuroblast. These 4 smaller fascicles converge in the calyx where they arborize and form pre- and post-synaptic terminals (Christiansen et al., 2011).They emerge from the calyx as a thick axon bundle referred to as the peduncle that bifurcates to innervate the dorsal and medial lobes of the mushroom body.
|
ILX:0105849
|
3
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
Ketamine
|
A cyclohexanone derivative used for induction of anesthesia. Its mechanism of action is not well understood, but ketamine can block NMDA receptors (receptors, N-methyl-D-aspartate) and may interact with sigma receptors. (PubChem) Pharmacology: Ketamine is a rapid-acting general anesthetic producing an anesthetic state characterized by profound analgesia, normal pharyngeal-laryngeal reflexes, normal or slightly enhanced skeletal muscle tone, cardiovascular and respiratory stimulation, and occasionally a transient and minimal respiratory depression. Ketamine is indicated as the sole anesthetic agent for diagnostic and surgical procedures that do not require skeletal muscle relaxation. The anesthetic state produced by Ketamine has been termed dissociative anesthesia in that it appears to selectively interrupt association pathways of the brain before producing somesthetic sensory blockade. It may selectively depress the thalamoneocortical system before significantly obtunding the more ancient cerebral centers and pathways (reticularactivating and limbic systems). Mechanism of action: Ketamine has several clinically useful properties, including analgesia and less cardiorespiratory depressant effects than other anaesthetic agents, it also causes some stimulation of the cardiocascular system. Ketamine has been reported to produce general as well as local anaesthesia. It interacts with N-methyl-D-aspartate (NMDA) receptors, opioid receptors, monoaminergic receptors, muscarinic receptors and voltage sensitive Ca ion channels. Unlike other general anaesthetic agents, ketamine does not interact with GABA receptors. Drug type: Approved. Small Molecule. Drug category: Analgesics. Anesthetics, Dissociative. Excitatory Amino Acid Antagonists. General Anesthetics
|
ILX:0105850
|
4
|
FDI Lab - SciCrunch.org
|
01/17/2023
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
Ketoconazole
|
Broad spectrum antifungal agent used for long periods at high doses, especially in immunosuppressed patients. (PubChem) Pharmacology: Ketoconazole, like clotrimazole, fluconazole, itraconazole, and miconazole, is an imidazole antifungal agent. Mechanism of action: Ketoconazole interacts with 14- demethylase, a cytochrome P-450 enzyme necessary for the conversion of lanosterol to ergosterol. This results in inhibition of ergosterol synthesis and increased fungal cellular permeability. Other mechanisms may involve the inhibition of endogenous respiration, interaction with membrane phospholipids, inhibition of yeast transformation to mycelial forms, inhibition of purine uptake, and impairment of triglyceride and/or phospholipid biosynthesis. Ketoconazole can also inhibit the synthesis of thromboxane and sterols such as aldosterone, cortisol, and testosterone. Drug type: Approved. Investigational. Small Molecule. Drug category: Antifungal Agents. Antifungals
|
ILX:0105851
|
3
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
Ketoprofen
|
An ibuprofen-type anti-inflammatory analgesic and antipyretic. It is used in the treatment of rheumatoid arthritis and osteoarthritis. (PubChem) Pharmacology: Ketoprofen is a nonsteroidal antiinflammatory drug (NSAID) with analgesic and antipyretic properties. Ketoprofen has pharmacologic actions similar to those of other prototypical NSAIDs, that is thought to be associated with the inhibition of prostaglandin synthesis. Ketoprofen is used to treat rheumatoid arthritis, osteoarthritis, dysmenorrhea, and to alleviate moderate pain. Mechanism of action: Ketoprofen is a nonsteroidal anti-inflammatory drug with analgesic and antipyretic properties. Its antiinflammatory effects are believed to be due to inhibition of both cylooxygenase-1 (COX-1) and cylooxygenase-2 (COX-2) which leads to the inhibition of prostaglandin synthesis, and leukotriene synthesis, to have antibrady-kinin activity, as well as to have lysosomal membrane-stabilizing action. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation. Drug type: Approved. Small Molecule. Drug category: Anti-Inflammatory Agents, Non-Steroidal. Cyclooxygenase Inhibitors
|
ILX:0105852
|
4
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
Ketorolac
|
A pyrrolizine carboxylic acid derivative structurally related to indomethacin. It is an NSAID and is used principally for its analgesic activity. (From Martindale The Extra Pharmacopoeia, 31st ed) Pharmacology: Ketorolac, an antiinflammatory agent with analgesic and antipyretic properties, is used to treat osteoarthritis and control acute pain. It is a peripherally acting analgesic. The biological activity of ketorolac tromethamine is associated with the S-form. Ketorolac tromethamine possesses no sedative or anxiolytic properties. Mechanism of action: Ketorolac is a nonsteroidal anti-inflammatory drug (NSAID) chemically related to indomethacin and tolmetin. Ketorolac tromethamine is a racemic mixture of (-)S- and (+)R-enantiomeric forms, with the S-form having analgesic activity. Its antiinflammatory effects are believed to be due to inhibition of both cylooxygenase-1 (COX-1) and cylooxygenase-2 (COX-2) which leads to the inhibition of prostaglandin synthesis leading to decreased formation of precursors of prostaglandins and thromboxanes from arachidonic acid. The resultant reduction in prostaglandin synthesis and activity may be at least partially responsible for many of the adverse, as well as the therapeutic, effects of these medications. Analgesia is probably produced via a peripheral action in which blockade of pain impulse generation results from decreased prostaglandin activity. However, inhibition of the synthesis or actions of other substances that sensitize pain receptors to mechanical or chemical stimulation may also contribute to the analgesic effect. In terms of the ophthalmic applications of ketorolac - ocular administration of ketorolac reduces prostaglandin E2 levels in aqueous humor, secondary to inhibition of prostaglandin biosynthesis. Drug type: Approved. Small Molecule. Drug category: Anti-Inflammatory Agents, Non-Steroidal. Cyclooxygenase Inhibitors
|
ILX:0105853
|
3
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
Ketotifen
|
A cycloheptathiophene blocker of histamine H1 receptors and release of inflammatory mediators. It has been proposed for the treatment of asthma, rhinitis, skin allergies, and anaphylaxis. (PubChem) Pharmacology: Ketotifen is a fast acting non-competitive histamine antagonist. It inhibits the release of mediators from mast cells. It is a non-bronchodilator antiasthmatic drug (when taken orally). Mechanism of action: Ketotifen is a relatively selective, non-competitive histamine antagonist (H1-receptor) and mast cell stabilizer. Ketotifen inhibits the release of mediators from mast cells involved in hypersensitivity reactions. Decreased chemotaxis and activation of eosinophils has also been demonstrated. Ketotifen also inhibits cAMP phosphodiesterase. Properties of ketotifen which may contribute to its antiallergic activity and its ability to affect the underlying pathology of asthma include inhibition of the development of airway hyper-reactivity associated with activation of platelets by PAF (Platelet Activating Factor), inhibition of PAF-induced accumulation of eosinophils and platelets in the airways, suppression of the priming of eosinophils by human recombinant cytokines and antagonism of bronchoconstriction due to leukotrienes. Ketotifen inhibits of the release of allergic mediators such as histamine, leukotrienes C4 and D4(SRS-A) and PAF. Drug type: Approved. Small Molecule. Drug category: Anti-Allergic Agents. Antipruritics. Histamine H1 Antagonists
|
ILX:0105854
|
3
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
KIF3A
|
|
ILX:0105855
|
4
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
Kinase
|
|
ILX:0105856
|
2
|
FDI Lab - SciCrunch.org
|
01/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
Kindling
|
long-lasting epileptogenic changes induced by daily sub threshold electrical brain stimulation; used as an induced model for epilepsy (adapted from Mammalian Phenotype Ontology)
|
ILX:0105857
|
3
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |
|
Kinesthetic system function
|
|
ILX:0105858
|
3
|
FDI Lab - SciCrunch.org
|
06/18/2018
|
FDI Lab - SciCrunch.org |
term |
12/08/2016 |
0 |
NeuroLex |
NeuroLex |