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Biomedical subjects

A Ray

Publications and source records attributed to A Ray.

At least 289 records · Page 16Linked to original sources
PubMed1984

Cloning and molecular analysis of the finO region from the antibiotic-resistance plasmid R6-5.

The cloning of the finO region from the antibiotic-resistance plasmid R6-5 is reported. On the basis of DNA deletion analysis and Tn5 transposon insertional mutagenesis of finO+ chimeric plasmids, finO has been located within the coordinates 94.0-94.85 on the R6-5 map. A 32,000-Da polypeptide (32K), which is encoded within 92.75-94.25R6-5, has been identified and shown not to be associated with the FinO phenotype.

Chromosome Mapping↗
PubMed1984

Pyrimidine nucleotide metabolism in cardiac hypertrophy.

Cardiac hypertrophy was induced in rats either by isoprenaline treatment or by experimental abdominal aortic stenosis. In both models, the UTP content increased in the hypertrophying heart, while the ATP level remained depressed. The rate of net synthesis of uracil nucleotides, estimated by phosphate incorporation into alpha-phosphate groups, was largely increased during the first stage of hypertrophy (X 3.6 and 2.6, respectively). At identical stages of hypertrophy, the rate of synthesis of ribosomal RNA, measured after continuous intracardiac infusion of 3H-uridine, was increased by 1.6 and 2.5 times. A comparison of the changes in time course of the levels of UTP and RNA and their turnover suggests that the metabolism of uracil nucleotides and that of ribosomal RNA are closely interrelated. The increase in the rate of synthesis of pyrimidine is interpreted as an adaptational change in nucleotide metabolism in response to the increased requirement of precursors for RNA synthesis. The possible limiting role of pyrimidine nucleotides in the hypertrophic process is discussed.

Adenosine Triphosphate↗
PubMed1984

Role of vagus in the antagonism of ouabain induced arrhythmias in dogs by beta-adrenoceptor antagonists and related drugs.

The effects of propranolol and related drugs were investigated on ouabain-induced ventricular tachycardia (VT) in dogs with intact and ablated vagi. Propranolol and UM-272 completely antagonized the ouabain VT in dogs with intact vagi, whereas timolol was ineffective. Bilateral vagotomy completely abolished the effect of UM-272 and reduced the effect of propranolol. Diphenylhydantoin, however, reversed ouabain VT in dogs with both intact and ablated vagi. It is inferred that the vagus plays a significant role in the arrhythmolytic effect of propranolol and UM-272.

Adrenergic beta-Antagonists↗
PubMed1983

A method for measuring free-nucleotide pool sizes and incorporation of labeled precursors: its application in studying myocardial pyrimidine nucleotides.

A procedure for a rapid and accurate determination of nucleotide pool sizes in heart muscle is described. The method involves an enzymatic cleavage of all nucleotides by phosphodiesterase to nucleoside 5'-monophosphates and an HPLC separation (Partisil 10 SAX) by isocratic or two-step elution. This method permits reproducible measurements of the pools of pyrimidine nucleotides which are particularly small in cardiac tissue. Moreover, this technique may be conveniently applied in studies on the incorporation of labeled precursors into free nucleotides. Experimental evidence is presented showing the accuracy of the method.

Adenosine Monophosphate↗
PubMed1983

Procedure for isolation of neuron- and astrocyte-enriched fractions from chick brain of different ages.

A method for the isolation of neurons and astrocytes from chick brain of different ages is described. In brief, the procedure involves incubation of the gray matter with trypsin, passage of the tissue successively through nylon/stainless steel screens of decreasing pore size, and further separation and purification of cell-enriched fractions by centrifugation on Ficoll discontinuous gradient. Phase-contrast microscopy revealed intact morphology of the cells. The cells were viable by trypan blue exclusion test.

Age Factors↗
PubMed1983

Comparative changes in the 32P labeling of adenine and uracil nucleotides in the hypertrophying rat heart.

The turnover of cardiac adenine and uracil nucleotides was studied in the hypertrophying rat heart by means of the kinetics of incorporation of labeled phosphate into the alpha-phosphate groups of nucleotides. Cardiac hypertrophy was induced either by chronic isoproterenol treatment (5 mg X kg-1 body wt. daily, s.c.) or by abdominal aortic constriction. In both experimental models, although the labeling of alpha-P groups of adenine nucleotides was at first unmodified, the incorporation of [32P]Phosphate into uracil nucleotides was accelerated early and the stimulation maintained for several days. The intramyocardial concentration of UTP and uracil nucleotides rose during the early phase of hypertrophy, while the ATP and adenine nucleotide pools were depleted. All of these alterations were more pronounced in isoproterenol-treated animals than in those with aortic stenosis. In this experimental model (isoproterenol treatment), the hypertrophy develops faster and is accompanied by a larger increase in cardiac RNA concentration. Thus, the increase in the rate of synthesis of uracil nucleotides may be interpreted as an adaptative change of nucleotide metabolism in response to an increased requirement of precursors for RNA synthesis. The possible limiting role of pyrimidine nucleotides in the hypertrophic process is discussed.

Adenine Nucleotides↗
PubMed1983

The effect of calcium on the hepatic glucocorticoid receptor.

The unbound glucocorticoid receptor of rat hepatic cytosol was very unstable at 25 degrees C. This receptor instability was increased by the addition of 1-10 mM Ca2+ such that the unbound glucocorticoid receptor was completely inactivated within 30 min at 25 degrees C in the presence of 5 mM Ca2+. Interestingly, Ca2+ inactivation was blocked approximately 80% by simultaneous addition of either 10 mM molybdate or 10 mM molybdate plus 5 mM dithiothreitol. Ten millimolar leupeptin or 10 mM alpha 2-macroglobulin did not inhibit Ca2+ inactivation of the receptor. In fact, leupeptin alone slightly inactivated the receptor. Prior treatment of cytosol with 10 mM molybdate plus 5 mM DTT at 25 degrees C for 30 min offered a complete protection against the subsequent addition of 5 mM Ca2+. The effects of Ca2+ were found to be irreversible since addition of molybdate or molybdate plus dithiothreitol after 5 mM Ca2+ treatment (20 min for 25 degrees C) did not reactivate partially inactivated receptors but did stabilize the remaining receptor binding at the time of molybdate or molybdate plus dithiothreitol addition. Addition of 1-5 mM Ca2+ to preformed [3H]-dexamethasone--receptor complexes slightly inhibited steroid--receptor complex transformation into a nuclear binding form at 25 degrees C. In addition, 10 mM Ca2+ altered the agarose gel filtration profile of the complex. Control cytosol or cytosol treated with 10 mM EDTA or 10 mM leupeptin showed three distinct macromolecular bound radioactivity peaks having Stokes radii of 65, 40 and 20 A. On the other hand, Ca2+-treated cytosol showed a single large aggregated component which was excluded in the void volume of the column. Trypsin (0.5 microgram/ml) generated a small steroid--receptor fragment of 20 A when added alone, but interestingly when added with 10 mM Ca2+ the [3H]-dexamethasone--receptor complex eluted in the agarose gel exclusion volume. These results show that Ca2+ has a profound effect on rat hepatic glucocorticoid receptors and that molybdate can block Ca2+-dependent receptor inactivation.

Animals↗
PubMed1983

Cloning and polypeptide analysis of the leading region in F plasmid DNA transfer.

A segment of the F plasmid DNA, located between the origin of transfer and the primary F replication region, is the first to enter the recipient cell during conjugation. PstI, SalI, and SmaI restriction endonuclease sites have been mapped within this leading region in conjugational DNA transfer and chimeric plasmids carrying overlapping fragments of the region have been constructed. Analyses of polypeptides of Mr 27,800, 23,100, 14,400, and 11,000 to be encoded by sequences within the leading region.

Chromosome Mapping↗
PubMed1983

Possible interrelationship between the biogenic amines involved in the modulation of footshock aggression in rats.

Dopamine, 5-hydroxytryptamine and 4-methylhistamine facilitated whereas noradrenaline and 2-pyridylethylamine inhibited footshock aggression (FSA) in rats. Dopamine increased FSA in cyproheptadine and cimetidine but not in pimozide pretreated animals; 5-hydroxytryptamine potentiated FSA in cimetidine and pimozide but not in cyproheptadine pretreated rats; 4-methylhistamine facilitated FSA in pimozide and cyproheptadine but not in cimetidine pretreated groups. Also 2-pyridylethylamine inhibited FSA in phenoxybenzamine but not mepyramine pretreated animals. These effects were not significantly different from those seen with dopamine, 5-hydroxytryptamine, 4-methylhistamine and 2-pyridylethylamine, alone, respectively on FSA. It is inferred that each of the neurotransmitters involved in the modulation of footshock aggression acts through an independent mechanism which is not under the regulatory control of the other.

Aggression↗
PubMed1981

Effect of histaminergic drugs on footshock-induced aggressive behaviour in rats.

Histamine and 2-pyridylethylamine decreased and 4-methylhistamine increased footshock-induced aggression after their intracerebroventricular administration to rats. Mepyramine and cimetidine had no effect on the fighting response but blocked the effects of the respective agonists. Histamine when given after mepyramine increased and after cimetidine decreased the fighting score, this decrease being more than that with histamine alone. It is inferred that central H1-receptors are inhibitory and H2-receptors facilitatory in footshock aggression and that this is independent of catecholaminergic mechanisms.

Aggression↗