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Biomedical subjects

A M Feldman

Publications and source records attributed to A M Feldman.

136 records · Page 8Linked to original sources
PubMed1979

Effect of cholera toxin and prostaglandins on the rat choroid plexus in vitro.

The present study was performed to measure the effects of cholera toxin (CT) and prostaglandins (PG) on choroid plexus cyclic AMP accumulation. Choroid plexuses, isolated from Sprague-Dawley rats, were incubated in Krebs-Ringer bicarbonate buffer containing either CT (10 microgram/ml), heat inactivated CT, prostaglandins, or appropriate controls. After a minimum incubation period of 60 min with CT, cyclic AMP accumulation (pmol/mg protein) in treated incubates (58.10 +/- 6.43, n = 6) was 4 times that in controls (14.-5 +/- 1.4, n = 6). This large increase was only seen when theophylline (10 mM) was in the incubation mixture 3--10 min prior to the end of the incubation period. The increase in cyclic AMP accumulation was dose responsive and was irreversible after 5 min of incubation. Of the 5 prostaglandins studied, only PGE2 resulted in an increase in cyclic AMP accumulation. Cyclic AMP levels were 29.64 +/- 2.5 in controls and 57.57 +/- 3.5 in plexus which had been incubated with PGE2 (20 microgram/ml) for 1 min, and this increase was dose responsive.

Adenylyl Cyclases↗
PubMed1979

Measurement of the hydrostatic pressures of the cochlear compartments.

A micropressure transducer (sensitive 0.1 cm H2O) utilizing a manual servo nulling system and a micropipette (tip diameter 12-20 micron) was designed in order to measure endolymphatic and perilymphatic hydrostatic pressures in the inner ear of the guinea pig. Perilymphatic pressures were measured through the round window membrane in animals in which the ossicular structures had been removed and in those in which the middle ear structures were intact. Endolymphatic pressures were measured after removal of the middle ear structures. There was a significant (p less than 0.001) difference between perilymphatic pressures in the presence (4.7 +/- 0.36 cm H2O) and absence (2.43 +/- 0.22 cm H2O) of the middle ear structures. The endolymphatic pressure was 0.00 cm H2O when measured through the basilar membrane after disruption of the scala tympani, and was 3.34 +/- 0.57 when monitored through the spiral ligament and stria vascularis. In order to verify the accuracy of these measurements, we monitored pressures in animals whose perilymphatic pressures were artificially maintained by an external source. Recoveries were always 95-100% of the artificially applied pressure. The injection of purified cholera toxin into the scala media through the basilar membrane resulted in a significant (p less than 0.001) increase in endolymphatic pressure.

Animals↗
PubMed1977

Cerebrospinal fluid production: stimulation by cholera toxin.

Large increases in the production of cerebrospinal fluid have been observed after the intraventricular administration of cholera toxin. Because cholera toxin stimulates adenylate cyclase, the data suggest that adenosine 3',5'-monophosphate plays a role in cerebrospinal fluid production.

Adenylyl Cyclases↗
PubMed1977

Effects of methotrexate on proliferation of human keratinocytes in vitro.

Normal human keratinocytes, propagated as epithelial outgrowths in vitro, were exposed to different concentrations of methotrexate (MTX) for different periods of time. After a 1-hr exposure, DNA synthesis was inhibited in a reversible manner. No change in the mitotic index was observed. After a 6-hr exposure, both DNA synthesis and mitosis were inhibited, again in a reversible fashion. Prolonged exposure (24 hr) resulted in irreversible mitotic inhibition even when followed by recovery periods of 168 hr. The effective concentrations of MTX in vitro were similar to those described previously in vivo.

Culture Techniques↗
PubMed1976

Effects of cholera toxin on cochlear endolymph production: model for endolymphatic hydrops.

To evaluate a possible role for adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] and adenosine 3':5'-cyclic monophosphate in the secretion of endolymph, we studied the effect of an intra-scala media injection of purified cholera toxin (an adenylate cyclase stimulant) on cochlear endolymph volume, endolymphatic potential, and endolymphatic Na and K concentrations.

Adenylyl Cyclases↗
PubMed1975

The effect of 3,3',5-triiodo-L-thyronine on the renal handling of citrate.

The effects of a 500 mug injection of T3 on the renal handling of citrate by the albino rat was studied by measuring citrate synthase activity, NADP-isocitrate dehydrogenase activity, and plasma, kidney, and urine citrate concentrations 12, 18, 24, 36, and 48 hr after injection. Kidney citrate synthase activity of the T3-injected rats was significantly lower than the controls in the 24- and 36-hr treatment groups, while NADP-IDH activity was significantly lowered only in the 36-hr treatment group. The injection of T3 resulted in hypercitricemia in the 12-, 18-, and 48-hr experimental animals while there was no significant change in citrate between the control values and treated values in the 24- and 36-hr experiments. There was no significant change in renal citrate levels in any of the treatment groups and hypercitrauria was not observed. The results of the present study suggest that T3 can control citrate utilization by increasing the levels of circulating citrate and then increasing the utilization of citrate by the kidney. This is facilitated by a decrease in NADP-IDH activity resulting in a decrease in biosynthesis and a decrease in citrate synthase activity resulting in a decrease in FFA metabolism. It is proposed that this system functions in providing fuel (citrate) for the increased Krebs cycle flux occurring in hyperthyroidism.

Animals↗
PubMedDate not supplied

Adenosine inhibits lipopolysaccharide-induced cardiac expression of tumor necrosis factor-alpha.

Tumor necrosis factor-alpha (TNF-alpha) is elevated in the failing heart. Very little is known about regulation of TNF-alpha in cardiomyocytes. TNF-alpha expression by macrophages is diminished by adenosine. Therefore, we hypothesized that a similar mechanism might occur in the heart. Neonatal rat myocytes were stimulated with lipopolysaccharide (LPS), and TNF-alpha was measured by ELISA. In the absence of LPS, myocytes did not release TNF-alpha in the medium. After exposure to LPS, TNF-alpha increased to 70.1+/-3.5 pg/mL at 6 hours. Immunofluorescent staining confirmed that TNF-alpha was expressed in myocytes. Adenosine decreased TNF-alpha in a dose-dependent manner (1 to 100 micromol/L, 37% to 65% decrease, P<.01). Adenosine also decreased TNF-alpha in cell homogenates by 78% (P<.0001). The effect of adenosine could be replicated by the A2 agonist PD-125944 (DPMA), by cAMP agonists 8-bromo-cAMP, forskolin, and Ro 20-1724, but not by A1 and A3 agonists. Conversely, the effect of adenosine could be suppressed by the adenylate cyclase inhibitor MDL-12,330. Adenosine also inhibited TNF-alpha in adult rat ventricular myocytes (-60%, P<.005) and rat papillary muscles (-55%, P<.05). In neonatal myocytes, adenosine normalized LPS-induced calcium changes and improved LPS-induced negative inotropic (P<.01) and negative lusitropic (P<.01) effects. Our results demonstrate that adenosine can significantly diminish TNF-alpha levels in the heart. The effect appears to be mediated by the A2 receptor and transduced through a G protein-adenylyl cyclase pathway. These results may explain some cardioprotective effects of adenosine and provide a novel pharmacological intervention in congestive heart failure.

Adenosine↗