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J Nathanson

Publications and source records attributed to J Nathanson.

7 recordsLinked to original sources
PubMed1995

Detection and quantitation of the glucuronoxylomannan-like polysaccharide antigen from clinical and nonclinical isolates of Trichosporon beigelii and implications for pathogenicity.

Sera from patients with systemic infections caused by the opportunistic fungus Trichosporon beigelii have been shown to cross-react with anticryptococcal antibodies. We quantitatively compared the amounts of antigen produced and examined the expression of O-acetyl epitopes from 35 strains of T. beigelii isolated from deep and superficial infections. By counterimmunoelectrophoresis, 10 of 10 isolates from deep infections were positive for polysaccharide, compared with 7 of 13 isolates from superficial infections (P = 0.02). All 23 strains tested were positive for polysaccharide when screened by immunodot. By enzyme immunoassay, the cross-reactive antigen produced by deep isolates (n = 9) had a mean titer of 1:5,500. In contrast, superficial isolates (n = 22) produced significantly less antigen than the deep isolates (P < 0.001), with a mean titer of 1:700. Isolates from environmental sources (n = 3) were similar to the superficial isolates, with a mean titer of 1:600. The mean concentrations +/- standard errors of cross-reactive polysaccharide released by deep isolates and superficial isolates were 3.09 +/- 0.44 and 1.74 +/- 0.30 micrograms/ml, respectively, when measured by rocket immunoelectrophoresis (P = 0.02). O-Acetyl epitopes were detected on polysaccharide from 8 of 9 strains of T. beigelii isolated from deep sources, while only 2 of 12 superficial isolates expressed detectable O-acetyl epitopes (P = 0.01). Thus, while all isolates of T. beigelii tested were capable of producing glucuronoxylomannan-like cross-reactive antigen, pathogenic isolates produced significantly more antigen than superficial or environmental isolates. Furthermore, significantly more pathogenic isolates than superficial or environmental isolates expressed antigen that was O acetylated.

Acetylation↗
PubMed1988

Adenylate cyclase activation is not sufficient to stimulate somatostatin release from dispersed cerebral cortical and diencephalic cells in glia-free cultures.

Under conditions in which vasoactive intestinal peptide (VIP) induces somatostatin release from cortical and diencephalic neuronal cultures, VIP causes large increases in intracellular cyclic AMP. Both the release of somatostatin and the increase in cyclic AMP elicited by VIP require exogenous calcium, can be blocked by cobalt ion, and can be qualitatively mimicked by depolarizating concentrations of exogenous potassium ion. Direct activation of adenylate cyclase by forskolin causes large increases in cyclic AMP content but does not induce somatostatin release. In the absence of VIP, the calcium ionophore, ionomycin, and the phorbol ester, phorbol 12-myristate-13-acetate, also stimulate somatostatin release. These results indicate that VIP-stimulation of cyclic AMP formation and VIP-stimulation of somatostatin release are calcium-dependent and that the two phenomena are dissociatable. Cyclic AMP formation is not a necessary condition for VIP-induced somatostatin release. Nucleotide formation may be a sufficient condition for release or, possibly in association with calcium influx, it may be an event unrelated to the release process.

1-Methyl-3-isobutylxanthine↗
PubMed1986

[Effect of forskolin and VIP on the release of somatostatin and the cAMP content of cultured rat diencephalon neurons].

Forskolin, a direct activator of adenylate cyclase, stimulates somatostatin release in dispersed fetal diencephalic cells in culture (10 j). It was found that concentrations ranging from 10(-8) M to 10(-4) M increase the release of somatostatin in a dose-dependent manner, as well as the formation of intracellular cyclic AMP. Furthermore, VIP (10(-6) M) which produces a significant (p less than 0.03) elevation of SRIF release at 30 min of incubation, also induces a prompt increase of intracellular cyclic AMP (10 min). These results suggest that VIP could stimulate the somatostatin release through a cyclic AMP-dependent mechanism.

Animals↗
PubMed1978

Lead blockade of norepinephrine-induced inhibition of cerebellar Purkinje neurons.

Biochemical studies showing that lead (Pb++) inhibits cerebellar adenylate cyclase (IC50 = 2 micrometer) prompted us to test the effects of this cation on the depression of spontaneous discharge of Purkinje (P) cells produced by iontophoresis of norepinephrine (NE). Previous studies have suggested that the effects of NE on P cell discharge may be mediated by activation of a NE-sensitive adenylate cyclase. Iontophoresis of Pb++ in situ, and in cerebellar transplants in oculo, reliably antagonized NE responses in over 80% of the P cells studied in both preparations. Blockade was readily seen at iontophoretic currents of 5 to 10 nA. Superfusion of PB++ (5--10 micrometer) into the anterior eye chamber also antagonized NE responses in P neurons of the transplant. Spontaneous discharge rate was either unaffected or slightly elevated at Pb++ levels that almost completely blocked NE. Barium, a heavy metal which does not inhibit adenylate cyclase in vitro, did not block NE effects. Stimulation of parallel fibers or iontophoresis of acetylcholine excited P cells. No antagonism was seen, however, between Pb++ and these acetylcholine or parallel fiber excitations. These results raise the possibility that blockade of brain catecholamine receptors may partially underlie the central nervous system toxicity seen with lead administration.

Animals↗