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Total 422235 Results
| Label | Description | ILX | Version | Created CID | Modified Time | ||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| Postrhinal cortex of rodent of Burwell et al 1995 | Cortical region lying caudal to the perirhinal cortex in the rat. It encompasses the caudal levels of area 35 and the caudal portion of area 36 (ectorhinal cortex). It is bordered medially by agranular retrosplenial cortex and ventrally by the entorhinal cortex (with the exception of the caudomedial portion). The authors note that the ventral portion of the postrhinal cortex in rat may by homologous with the parahippocampal cortex in the monkey. | ILX:0109163 | 6 | FDI Lab - SciCrunch.org | 06/23/2020 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Postsubiculum | Division of subicular cortex characterized by projections from the anterodorsal thalamic nucleus and to a lesser extent the anteroventral nucleus, bordered ventrally and laterally by the presubiculum and dorsally and medially by the retrosplenial granular a cortex.. The border is characterized by an abrupt change in the cyto- and chemoarchitecture | ILX:0109164 | 8 | FDI Lab - SciCrunch.org | 01/17/2023 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Postsubiculum of ABA 2009 | ILX:0109165 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex | |
| Postsynaptic Congenital Myasthenic Syndrome | ILX:0109166 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex | |
| Postsynaptic inhibition | The hyperpolarization of a postsynaptic cell, reducing the likelihood of or preventing an action potential in the postsynaptic cell | ILX:0109167 | 5 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Postvaccinal Myelitis | A form of Transverse Myelitis induced by a vaccine-induced infection.(MeSH). | ILX:0109168 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Potassium Channel | Cell membrane glycoproteins that are selectively permeable to potassium ions. At least eight major groups of K channels exist and they are made up of dozens of different subunits (MSH). | ILX:0109169 | 4 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Potassium Chloride | A white crystal or crystalline powder used as an electrolyte replenisher, in the treatment of hypokalemia, in buffer solutions, and in fertilizers and explosives. Pharmacology: The potassium ion is in the principle intracellular cation of most body tissues. Potassium ions participate in a number of essential physiological processes including the maintenance of intracellular tonicity, the transmission of nerve impulses, the contraction of cardiac, skeletal and smooth muscle, and the maintenance of normal renal function. The intracellular concentration of potassium is approximately 150 to 160 mEq per liter. The normal adult plasma concentration is 3.5 to 5 mEq per liter. An active ion transport system maintains this gradient across the plasma membrane. Potassium is a normal dietary constituent and under steady-state conditions the amount of potassium absorbed from the gastrointestinal tract is equal to the amount excreted in the urine. The usual dietary intake of potassium is 50 to 100 mEq per day. Potassium depletion will occur whenever the rate of potassium loss through renal excretion and/or loss from the gastrointestinal tract exceeds the rate of potassium intake. Such depletion usually develops as a consequence of therapy with diuretics, primarily or secondary hyperaldosteronism, diabetic ketoacidosis, or inadequate replacement of potassium in patients on prolonged parenteral nutrition. Depletion can develop rapidly with severe diarrhea, especially if associated with vomiting. Potassium depletion due to these causes is usually accompanied by concomitant loss of chloride and is manifested by hypokalemia and metabolic alkalosis. Potassium depletion may produce weakness, fatigue, disturbances of cardiac rhythm (primarily ectopic beats), prominent U-waves in the electrocardiogram, and, in advanced cases, flaccid paralysis and/or impaired ability to concentrate urine. If potassium depletion associated with metabolic alkalosis cannot be managed by correcting the fundamental cause of the deficiency, e.g., where the patient requires long-term diuretic therapy, supplemental potassium in the form of high potassium food or potassium chloride may be able to restore normal potassium levels. In rare circumstances (e.g., patients with renal tubular acidosis) potassium depletion may be associated with metabolic acidosis and hyperchloremia. In such patients, potassium replacement should be accomplished with potassium salts other than the chloride, such as potassium bicarbonate, potassium citrate, potassium acetate, or potassium gluconate. Mechanism of action: Supplemental potassium in the form of high potassium food or potassium chloride may be able to restore normal potassium levels. Drug type: Approved. Small Molecule. Withdrawn. Drug category: | ILX:0109170 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Potassium current | Contributes to neuronal resting "leak"conductance. Helps determine resting membrane potential. | ILX:0109171 | 4 | FDI Lab - SciCrunch.org | 08/24/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | troy sincomb |
| Potassium(+) | An elemental potassium that has formula K. An essential element in the functioning of the nervous system. Potassium concentrations inside the resting neuron are higher than those outside the cell. The preponderance of resting channels in glial cells are permeable only to K+. | ILX:0109172 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Power | A physical quality inhering in an object by virtue of the rate of doing work. | ILX:0109173 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Practolol | A beta-adrenergic antagonist that has been used in the emergency treatment of cardiac arrhythmias. (PubChem) Pharmacology: Practolol is a beta-adrenergic receptor antagonist that has been used in the emergency treatment of cardiac arrhythmias. Mechanism of action: Like other beta-adrenergic antagonists, practolol competes with adrenergic neurotransmitters such as catecholamines for binding at sympathetic receptor sites. Like propranolol and timolol, practolol binds at beta(1)-adrenergic receptors in the heart and vascular smooth muscle, inhibiting the effects of the catecholamines epinephrine and norepinephrine and decreasing heart rate, cardiac output, and systolic and diastolic blood pressure. Drug type: Approved. Small Molecule. Drug category: Adrenergic beta-Antagonists. Anti-Arrhythmia Agents | ILX:0109174 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Pralidoxime | Pralidoxime is an antidote to organophosphate pesticides and chemicals. Organophosphates bind to the esteratic site of acetylcholinesterase, which results initially in reversible inactivation of the enzyme. If given within 24 hours,after organophosphate exposure, pralidoxime reactivates the enzyme cholinesterase by cleaving the phosphate-ester bond formed between the organophosphate and acetylcholinesterase. Pharmacology: Pralidoxime is to reactivate cholinesterase (mainly outside of the central nervous system) which has been inactivated by phosphorylation due to an organophosphate pesticide or related compound. The destruction of accumulated acetylcholine can then proceed, and neuromuscular junctions will again function normally. Pralidoxime also slows the process of "aging" of phosphorylated cholinesterase to a nonreactivatable form, and detoxifies certain organophosphates by direct chemical reaction. The drug has its most critical effect in relieving paralysis of the muscles of respiration. Because pralidoxime is less effective in relieving depression of the respiratory center, atropine is always required concomitantly to block the effect of accumulated acetylcholine at this site. Pralidoxime relieves muscarinic signs and symptoms, salivation, bronchospasm, etc., but this action is relatively unimportant since atropine is adequate for this purpose. Mechanism of action: Pralidoxime is an antidote to organophosphate pesticides and chemicals. Organophosphates bind to the esteratic site of acetylcholinesterase, which results initially in reversible inactivation of the enzyme. If given within 24 hours,after organophosphate exposure, pralidoxime reactivates the enzyme cholinesterase by cleaving the phosphate-ester bond formed between the organophosphate and acetylcholinesterase. Drug type: Approved. Small Molecule. Drug category: Antidotes. Cholinesterase Reactivators | ILX:0109175 | 4 | FDI Lab - SciCrunch.org | 08/24/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | troy sincomb |
| Pramipexole | Pramipexole (INN, trade names Mirapex and Sifrol) is a medication indicated for treating Parkinson's disease and restless legs syndrome (RLS). It is also sometimes used off-label as a treatment for cluster headache or to counteract the problems with low libido experienced by some users of SSRI antidepressant drugs. Pramipexole has shown robust effects on pilot studies in bipolar disorder. Pramipexole is classified as a non-ergoline dopamine agonist. Pharmacology: Pramipexole is a nonergot dopamine agonist with high relative in vitro specificity and full intrinsic activity at the D2 subfamily of dopamine receptors, binding with higher affinity to D3 than to D2 or D4 receptor subtypes. The relevance of D3 receptor binding in Parkinson's disease is unknown. The precise mechanism of action of Pramipexole as a treatment for Parkinson's disease is unknown, although it is believed to be related to its ability to stimulate dopamine receptors in the striatum. This conclusion is supported by electrophysiologic studies in animals that have demonstrated that Pramipexole influences striatal neuronal firing rates via activation of dopamine receptors in the striatum and the substantia nigra, the site of neurons that send projections to the striatum. Mechanism of action: The precise mechanism of action of Pramipexole as a treatment for Parkinson's disease is unknown, although it is believed to be related to its ability to stimulate dopamine receptors in the striatum. Drug type: Approved. Investigational. Small Molecule. Drug category: Antidyskinetics. Antioxidants. Antiparkinson Agents. Dopamine Agonists. Free Radical Scavengers | ILX:0109176 | 4 | FDI Lab - SciCrunch.org | 08/24/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | troy sincomb |
| Pramlintide | Pramlintide is a relatively new adjunct treatment for diabetes (both type 1 and 2), developed by Amylin Pharmaceuticals. It is derived from amylin, a hormone that is released into the bloodstream, in a similar pattern as insulin, after a meal. Like insulin, amylin is deficient in individuals with diabetes. Pharmacology: Pramlintide is a relatively new adjunct treatment for diabetes (both type 1 and 2), developed by Amylin Pharmaceuticals. It is derived from amylin, a hormone that is released into the bloodstream, in a similar pattern as insulin, after a meal. Like insulin, amylin is deficient in individuals with diabetes. It is provided as an acetate salt. Mechanism of action: Pramlintide is an amlyinomimetic, a functional analog of the naturally occurring pancreatic hormone amylin. Amylin has activity in a number of gastrointestinal and glucodynamic systems, and by mimicking its activity, Pramlintide acts to improve glycemic control through modulation of the rate of gastric emptying, prevention of post-prandial rise in glucagon levels, and by increasing sensations of satiety, thereby reducing caloric intake and potentiating weight loss. There appears to be at least three distinct receptor complexes that bind with high affinity to amylin. All three complexes contain the calcitonin receptor at the core, plus one of three Receptor activity-modifying proteins, RAMP1, RAMP2, or RAMP3. Drug type: Approved. Biotech. Investigational. Drug category: | ILX:0109177 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Pranlukast | Pranlukast is a cysteinyl leukotriene receptor-1 antagonist. It antagonizes or reduces bronchospasm caused, principally in asthmatics, by an allergic reaction to accidentally or inadvertently encountered allergens. Pharmacology: Pranlukast is a cysteinyl leukotriene receptor-1 antagonist. Mechanism of action: Pranlukast selectively antagonizes leukotriene D4 (LTD4) at the cysteinyl leukotriene receptor, CysLT1, in the human airway. Pranlukast inhibits the actions of LTD4 at the CysLT1 receptor, preventing airway edema, smooth muscle contraction, and enhanced secretion of thick, viscous mucus. Drug type: Approved. Small Molecule. Drug category: Anti-Asthmatic Agents. Leukotriene Antagonists | ILX:0109178 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Pravastatin | An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (hydroxymethylglutaryl COA reductases). (PubChem) Pharmacology: Pravastatin, an antilipemic agent, is used to treat primary hypercholesterolemia. Unlike lovastatin and simvastatin, pravastatin is relatively hydrophilic and does not require hydrolysis for activation. Mechanism of action: Like lovastatin and simvastatin, pravastatin inhibits hydroxymethylglutaryl-CoA (HMG-CoA) reductase. As HMG-CoA is necessary for the intracellular synthesis of cholesterol, its inhibition results in increased clearance of circulating LDL. Pravastatin also inhibits hepatic synthesis of VLDL, the precursor for LDL, reducing circulating cholesterol and LDL cholesterol. Drug type: Approved. Small Molecule. Drug category: Anticholesteremic Agents. HMG-CoA Reductase Inhibitors. Hydroxymethylglutaryl-CoA Reductase Inhibitors | ILX:0109179 | 3 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
| Praziquantel | An anthelmintic used in most schistosome and many cestode infestations. (PubChem) Pharmacology: Praziquantel is an anthelmintic used in most schistosome and many cestode infestations. Praziquantel effects the permeability of the cell membrane resulting in the contraction of schistosomes. The drug further causes vacuolization and disintegration of the schistosome tegument. The effect is more marked on adult worms compared to young worms. An increased calcium influx may play an important role. Secondary effects are inhibition of glucose uptake, lowering of glycogen levels and stimulation of lactate release. The action of praziquantel is limited very specifically to trematodes and cestodes; nematodes (including filariae) are not affected. Mechanism of action: Praziquantel works by causing severe spasms and paralysis of the worms' muscles. This paralysis is accompanied - and probably caused - by a rapid Ca 2+ influx inside the schistosome. Morphological alterations are another early effect of praziquantel. These morphological alterations are accompanied by an increased exposure of schistosome antigens at the parasite surface. The worms are then either completely destroyed in the intestine or passed in the stool. An interesting quirk of praziquantel is that it is relatively ineffective against juvenile schistosomes. While initially effective, effectiveness against schistosomes decreases until it reaches a minimum at 3-4 weeks. Effectiveness then increases again until it is once again fully effective at 6-7 weeks. Glutathione S-transferase (GST), an essential detoxification enzyme in parasitic helminths, is a major vaccine target and a drug target against schistosomiasis. Drug type: Approved. Small Molecule. Drug category: Anthelmintics | ILX:0109180 | 4 | FDI Lab - SciCrunch.org | 08/24/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | troy sincomb |
| Prazosin | A selective adrenergic alpha-1 antagonist used in the treatment of heart failure, hypertension, pheochromocytoma, Raynaud's syndrome, prostatic hypertrophy, and urinary retention. (PubChem) Pharmacology: Prazosin is an alpha-adrenergic blocking agent used to treat hypertension and benign prostatic hyperplasia. Accordingly, Prazosin is a selective inhibitor of the alpha1 subtype of alpha adrenergic receptors. In the human prostate, Prazosin 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 Prazosin competitively antagonized the pressor effects of phenylephrine (an alpha1 agonist) and the systolic pressor effect of norepinephrine. The antihypertensive effect of Prazosin results from a decrease in systemic vascular resistance and the parent compound Prazosin is primarily responsible for the antihypertensive activity. Mechanism of action: Prazosin 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. Small Molecule. Drug category: Adrenergic alpha-Antagonists. Alpha-adrenergic Blocking Agents. Antihypertensive Agents | ILX:0109181 | 4 | FDI Lab - SciCrunch.org | 08/24/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | troy sincomb |
| Pre-Medication | Medication to be administered at the beginning of the Scheduled Procedure Step, e.g. Nuclear Medicine radiopharmaceutical. | ILX:0109182 | 4 | FDI Lab - SciCrunch.org | 06/18/2018 | FDI Lab - SciCrunch.org | term | 12/09/2016 | 0 | NeuroLex | NeuroLex |
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