Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some preparations of both native aspartate transcarbamylase from Escherichia coli and catalytic subunit have fewer tight binding sites per oligomer for carbamyl-P than the number of catalytic peptide chains. In contrast, the number of sites for the tight-binding inhibitor N-(phosphonacetyl)-L-aspartate does equal the number of catalytic chains in each case. Binding of the labile carbamyl-P was determined using rapid gel filtration, with conversion to stable carbamyl-L-aspartate during collection. Native enzyme (six catalytic chains) obtained from cells grown under the conditions of J.C. Gerhart and H. Holoubek (J. Biol. Chem. (1967) 242, 2886-2892) has 5.4 tight sites for carbamyl-P at pH 8.0 (KD = 9.9 muM), whereas native enzyme from cells grown with higher concentrations of glucose, uracil, and histidine (to yield more enzyme per unit volume of culture) has only 1.9 tight sites at pH 8.0 (KD = 4.6 muM) and only 2.3 tight sites at pH 7.0 (KD = 2.6 muM). At pH 8.0, catalytic subunit (three catalytic chains) obtained from the former native enzyme has 2.2 tight sites for carbamyl-P (KD = 2.4 muM) and the number of sites is 2.3 in the presence of 35 mM succinate, whereas catalytic subunit obtained from the latter native enzyme has 1.8 tight sites (KD = 3.6 muM) in the absence of succinate and 2.3 tight sites in its presence. The number of tight binding sites is also less than the number of subunit peptide chains in 19F nuclear magnetic resonance experiments performed with catalytic subunit and two fluorinated analogs of carbamyl-P at comparable concentrations of analogs and active sites. A model is proposed in which incomplete removal of formylmethionine from the NH2 termini of the enzyme under conditions of extreme depression affects affinity for ligands.
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PMID:Aspartate transcarbamylase of Escherichia coli. Heterogeneity of binding sites for carbamyl phosphate and fluorinated analogs of carbamyl phosphate. 0 9

The acute electrophysiologic effects of intravenous Tenormine (0.1 mg/kg body weight), a new cardioselective beta-adrenoreceptor blocking drug, were studied in 18 subjects with estimated normal impulse formation and conduction. The most significant (P less than 0.01) effects were sinus cycle lengthening, depression of intranodal conduction and prolongation of AV node refractory periods. Sinus node recovery time, sinoatrial conduction time and atrial refractory periods were only slightly prolonged (P less than 0.05). Intraatrial conduction and infra-His conduction were unchanged. These properties are compared with those of the most commonly employed beta-blocking agents. The clinical implications are discussed.
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PMID:Electrophysiologic properties of intravenous Tenormine in man. 3 20

The electrophysiological effects of anti-arrhythmic drugs in man may be classified in three groups: -- Group I: comprising drugs whose characteristic action is on the AV node (beta blockers, verapamil, digitalis) The nodal conduction time (A-H interval) and refractory periods are increased. -- Group II: comprising drugs acting on the His-Purkinje system, the AV nodal conduction staying unchanged. This group has two sub-groups. Sub-group A: these drugs delay the His-Prukinje conduction (increased H-V interval). Examples are quinidine, procainamide, disopyramide, ajmaline, chloro-acetyl-ajmaline. In addition these drugs usually increase the atrial refractory periods and those of accessory pathways. Sub-group B: the His-Purkinje conduction is unchanged but the refractory periods are modified: lengthened (bretylium tosylate) or shortened (diphenylhydantoin, lignocaine, mexiletine). -- Group III: which includes amiodarone and aprindine whose effects are mixed: on the one hand AV nodal depression, and on the other, alteration of the His-Purkinje conduction manifested by an increased H-V internal (aprindine) or refractory periods (amiodarone). These preparations also increase the refractory periods of accessory AV pathways and amiodarone increase the refractory periods of the atria. This type of classification could help towards a more rational clinical approach to the use of anti-arrhythmic drugs.
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PMID:[Electrophysiological effects of anti-arrhythmia agents in man. Attempt at classification]. 10 85

The influence of the new antiarrhythmic agent Propafenon on cardiac conduction and sinus node function was studied by using His-bundle recordings and atrial stimulation in 14 patients with normal and diseases conduction system. Intravenous administration of Propafenon in therapeutic dose (1-2 mg/kg) produced a significant prolongation of the atrioventricular conduction time. Increase of the A-H interval was observed in 13 of 14 subjects during sinus rhythm. Second degree A-V block (Wenckebach form) during atrial stimulation occurred at lower frequencies after administration of the drug. The impulse propagagion within the His-Purkinje system was depressed significantly (H-V interval in 8, H-S interval in 10 of 14 subjects). Propafenon did not cause any alteration in intraatrial conduction, but depression of the sinus node automaticity was noted. Total reversal of the drug induced prolonged atrioventricular conduction and a decrease of the sinus rate was seen after administration of orciprenaline. Beta-adrenergic receptor blocking and local anaesthetic direct membrane actions are discussed as possible cause of the prolongation of atrioventricular and intraventricular conduction.
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PMID:[Effect of the antiarrhythmic agent propaphenone on cardiac conduction. clinical studies using bundle of his electrography]. 23 45

The acute electrophysiologic effects of intravenous Bunaphtine 1,5 mg/kg body weight, a new antiarrhythmic drug, were studied in 19 subjects with estimated normal impulse formation and conduction. Significant effects were sinus bradycardia, prolongation of atrial refractory periods, depression of intranodal and infranodal conduction and prolongation of His-Purkinje system refractory periods. These properties are compared with those of amiodarone and quinidine and form the basis for a correct use of Bunaphtine in the management of arrhythmias.
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PMID:Electrophysiologic evaluation of intravenous bunaphtine in man. 30 72

The acute electrophysiological effects of intravenous verapamil (0.15 mg/kg body weight) were studied in 21 subjects with estimated normal impulse formation and conduction. Significant effects were sinus cycle shortening, depression of intranodal conduction and prolongation of AV node refractory periods. Sinus node recovery time, sinoatrial conduction time, atrial refractory periods, infranodal conduction, His--Purkinje system, and bundle branch refractory periods were unchanged. The clinical implications of these properties are discussed.
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PMID:Electrophysiologic evaluation of intravenous verapamil in man. 33 5

Electrophysiological changes produced by intravenous (0.1 mg/kg) metoprolol, a new selective beta 1-blocking agent devoid of intrinsic activity, were studied in 16 subjects with estimated normal impulse formation and conduction. The most important effects were sinus bradycardia, mild increase of sinoatrial conduction time, depression of intranodal conduction, and prolongation of AV node refractory periods. Sinus node recovery time and atrial refractory periods were unmodified. Infranodal conduction and the refractory periods of the His-Purkinje system, as well as of the bundle-branches, were unchanged. These effects are compared with those observed after intravenous propranolol, pindolol, and oxprenolol.
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PMID:Electrophysiological properties of intravenous metoprolol in man. 35 Feb 45

A healthy 18-year-old man was admitted to our unit two hours after a suicidal ingestion of 2 gm of verapamil. There was mild hypotension, depression of the sinus node, atrioventricular dissociation, changes of repolarization, and first-degree intranodal atrioventricular block (the His bundle electrogram revealed an atrio-His [A-H] interval of 155 msec). Twenty-four hours after ingestion, the patient was well, and the electrocardiogram was completely normal. This case gave us a good opporturnity to study the electrocardiologic effects of a huge oral dose of verapamil on a healthy young heart.
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PMID:Acute intoxication with verapamil. 42 59

The ability of low protein diets containing small neutral, dispensable amino acids to induce threonine imbalance has been examined. Diets containing amino acids which compete for threonine transport in vitro (serine, alanine, alpha-amino-n-butyrate) caused depressions of growth and food intake which could be corrected to varying degrees by adding threonine to the diet. Large neutral, indispensable amino acids, moderately inhibitory of threonine transport, also induced the imbalance. Some amino acids that had little or no effect on threonine transport in vitro (acidic amino acids and proline) did not cause growth and food intake depressions. Other non-inhibitory amino acids (arginine and lysine) caused growth depressions which were not satisfactorily corrected by additional threonine alone, but were prevented by supplements of all the indispensable amino acids including threonine. Ornithine which was also not inhibitory of threonine transport was an exception. It induced a moderate growth depression which was corrected by additional threonine. Similar studies showed that histidine or tryptophan imbalance could be induced by feeding diets containing only those large neutral amino acids which compete for histidine or tryptophan transport in vitro. These experiments show that, based on the results of transport competition experiments, it is generally possible to devise amino acid supplements which can induce a dietary imbalance of a given amino acid.
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PMID:Induction of threonine imbalance by dispensable amino acids: relation to competition for amino acid transport into brain. 43 Feb 32

Incubation of the CFs Gly-His-Glyc or CCF with PMNs in the absence of a gradient, resulted in a dose-dependent depression in chemotactic activity when, after washing, the cells were challenged with the CFs in a Boyden chamber. When the cells were preincubated with either CF and suitable concentrations of colchicine, the inhibition of chemotaxis that either of these agents induced when incubated with the cells alone was abolished. Deactivation reappeared when the optimal ratio between colchicine and CF was altered in either direction. Ultramicroscopic studies showed an increase in centriole-associated microtubules following incubation of cells with CFs. This increase was arrested by prior exposure of the cells to colchicine. Colchicine did not alter the specific binding of CCF to human neutrophils, and lumicolchicine had no effect on either chemotaxis or deactivation. Our data suggest that the control of PMN chemotaxis is predicted upon microtubule assembly evoked by cell interaction with a chemotactic gradient. Chemotaxis would be prevented by conditions that inappropriately organize responsive microtubules in either a polymerized or depolymerized configuration.
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PMID:A proposed model for chemotactic deactivation: evidence for microtubule modulation of polymorphonuclear leukocyte chemotaxis. 45 52


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