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S Mante

Publications and source records attributed to S Mante.

9 recordsLinked to original sources
PubMed1992

Variation in genomic Alu repeat density as a basis for rapid construction of low resolution physical maps of human chromosomes.

Human DNA restriction fragments containing high numbers of Alu repeat sequences can be preferentially detected in the presence of other human DNA restriction fragments in DNA from human: rodent somatic cell hybrids when the DNA is fragmented with enzymes that cleave mammalian DNA infrequently. This ability to lower the observed human DNA complexity allowed us to develop an approach to order rapidly somatic hybrid cell lines retaining overlapping human genomic domains. The ordering process also generates a relative physical map of the human fragments detected with Alu probe DNA. This process can generate physical mapping information for human genomic domains as large as an entire chromosome (100,000 kb). The strategy is demonstrated by ordering Alu-detected NotI fragments in a panel of mouse: human hybrid cells that span the entire long arm of human chromosome 17.

Chromosome Mapping↗
PubMed1991

The alkylating prazosin analog SZL 49 inactivates both alpha 1A- and alpha 1B-adrenoceptors.

A chemically reactive prazosin analog (SZL 49) has been suggested to be an alpha 1A-selective alkylating agent. We found SZL 49 competed for alpha 1-adrenoceptor binding sites with a similar potency (IC50 1 nM) in tissues enriched in both the alpha 1A (hippocampus) and alpha 1B (liver) subtypes. SZL 49 was very difficult to wash out of membrane preparations. However, pretreatment with a high concentration of SZL 49 (0.1 microM) followed by multiple washings resulted in a similar 40-50% loss of alpha 1-adrenoceptor binding sites in both liver and hippocampus. Pretreatment of hippocampal membranes with both SZL and the alpha 1B-selective alkylating agent chloroethylclonidine, sequentially or in combination, caused only a slightly greater inactivation than did either drug alone. Analysis of WB 4101 inhibition curves showed that pretreatment of hippocampal membranes with SZL 49 did not alter the proportions of alpha 1A- and alpha 1B-adrenoceptor subtypes. These data suggest that SZL 49 does not demonstrate in vitro selectivity for either the alpha 1A- or alpha 1B-receptor subtypes.

Adrenergic alpha-Antagonists↗
PubMed1991

Role of adenosine receptors in caffeine tolerance.

Caffeine is a competitive antagonist at adenosine receptors. Receptor up-regulation during chronic drug treatment has been proposed to be the mechanism of tolerance to the behavioral stimulant effects of caffeine. This study reassessed the role of adenosine receptors in caffeine tolerance. Separate groups of rats were given scheduled access to drinking bottles containing plain tap water or a 0.1% solution of caffeine. Daily drug intake averaged 60-75 mg/kg and resulted in complete tolerance to caffeine-induced stimulation of locomotor activity, which could not be surmounted by increasing the dose of caffeine. 5'-N-ethylcarboxamidoadenosine (0.001-1.0 mg/kg) dose dependently decreased the locomotor activity of caffeine-tolerant rats and their water-treated controls but was 8-fold more potent in the latter group. Caffeine (1.0-10 mg/kg) injected concurrently with 5-N-ethylcarboxamidoadenosine antagonized the decreases in locomotor activity comparably in both groups. Apparent pA2 values for tolerant and control rats also were comparable: 5.05 and 5.11. Thus, the adenosine-antagonist activity of caffeine was undiminished in tolerant rats. The effects of chronic caffeine administration on parameters of adenosine receptor binding and function were measured in cerebral cortex. There were no differences between brain tissue from control and caffeine-treated rats in number and affinity of adenosine binding sites or in receptor-mediated increases (A2 adenosine receptor) and decreases (A1 adenosine receptor) in cAMP accumulation. These results are consistent with theoretical arguments that changes in receptor density should not affect the potency of a competitive antagonist. Experimental evidence and theoretical considerations indicate that up-regulation of adenosine receptors is not the mechanism of tolerance to caffeine-induced stimulation of locomotor activity.

Adenosine↗
PubMed1990

Caffeine inhibits forskolin-stimulated cyclic AMP accumulation in rat brain.

Caffeine potently inhibited forskolin-stimulated cyclic AMP accumulation in slices of rat cerebral cortex. The IC50 for this inhibition was 21 +/- 2.9 microM, and 200 microM caffeine almost completely blocked the forskolin response. Theophylline which is a behavioural stimulant mimicked the effect of caffeine. However, there was only a slight inhibition of the forskolin response by theobromine and IBMX (3-isobutyl-1-methylxanthine), both of which lack behavioral stimulant effects.

1-Methyl-3-isobutylxanthine↗
PubMed1990

Is adenosine involved in inhibition of forskolin-stimulated cyclic AMP accumulation by caffeine in rat brain?

Caffeine potently inhibited forskolin-stimulated cyclic AMP accumulation in slices of rat cerebral cortex, with an IC50 of 21 +/- 3 microM. Because caffeine competitively blocks adenosine receptors, we examined whether the action of forskolin involved endogenous adenosine or whether caffeine was acting through some novel mechanism. Inhibition by caffeine was observed at all forskolin concentrations examined, although the degree of inhibition decreased at higher concentrations of forskolin. The effect of caffeine was not blocked by the presence of a phosphodiesterase inhibitor but was mimicked by several other methylxanthines. The most potent of these was 8-(p-sulfophenyl)-theophylline, which does not readily cross cell membranes, arguing for an extracellular site of action. Addition of either adenosine or the adenosine uptake blocker dipyridamole potentiated the forskolin response, suggesting that forskolin and adenosine act synergistically in increasing cyclic AMP accumulation. The nonxanthine adenosine receptor antagonist CGS 15943 potently blocked cyclic AMP responses to forskolin, adenosine, and combinations. 3-Isobutyl-1-methylxanthine potently blocked the response to adenosine but caused little or no inhibition of the response to forskolin. Adenosine deaminase (ADA) was added to eliminate contributions of endogenous adenosine. ADA inhibited the response to both adenosine and forskolin; however, 200 times as much enzyme was necessary to inhibit the forskolin response. Inhibition of added ADA with 2'deoxycoformycin dramatically increased the concentration of ADA required to inhibit the adenosine response, without altering the concentration required to inhibit the forskolin response. These results suggest that forskolin-stimulated cyclic AMP accumulation may be partially dependent on endogenous adenosine but that the inhibition observed with caffeine is not solely due to blockade of adenosine receptors.

Adenosine↗
PubMed1975

[Muscular involvement in rheumatic pelvispondylitis].

The authors explored a group of patients suffering from rheumatic pelvispondylitis from the point of view of muscular lesions: clinical muscular examination, anatomo-pathological investigation of the muscle (optical microscopy, histochemistry), electromyographic investigation, and determination of certain serum and muscle enzymes. Some muscular anomalies were observed, which were predominant in the muscles of the lumbar grooves, although there were some lesions of the quadriceps muscle, with a myogenous appearance, but without inflammation. The clearest anomalies were neurogenic and were present particularly in the muscles of the lumbar grooves.

Adult↗