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Biomedical subjects

J L Fox

Publications and source records attributed to J L Fox.

At least 91 records · Page 5Linked to original sources
PubMed1997

Oestradiol release from self-setting apatitic bone cement responsive to plasma-calcium level in ovariectomized rats, and its physicochemical mechanism.

The effect of plasma calcium levels on the release of oestradiol from a self-setting apatite bone cement containing 0.5% oestradiol was investigated in ovariectomized rats. The profiles of in-vitro release from the cements in simulated body fluid containing 0, 5 or 10 mg calcium per 100 mL indicated that the rate of release of oestradiol decreased with increasing calcium concentration in the dissolution media. After subcutaneous implantation of oestradiol-loaded cement in healthy and vitamin D-deficient rats, oestradiol release in diseased rats with low plasma calcium levels was significantly higher than that in healthy rats. These results suggest that in-vitro release of oestradiol from apatite bone cement was dependent on the calcium concentration in the buffer and that the in-vivo release of oestradiol from apatite bone cement was dependent on plasma calcium levels.

Animals↗
PubMed1996

Stability of ceftazidime sodium and teicoplanin sodium in a peritoneal dialysis solution.

The stability of ceftazidime sodium and teicoplanin sodium separately and in combination in a peritoneal dialysis (PD) solution was studied. PD solutions containing ceftazidime 100 micrograms/mL (as the sodium salt), teicoplanin 25 micrograms/mL (as the sodium salt), or ceftazidime 100 micrograms/mL plus teicoplanin 24 micrograms/mL were prepared in triplicate for each of two conditions: condition A, storage at 25 degrees C (room temperature) for 24 hours, then at 37 degrees C for eight hours; and condition B, storage for seven days at 4 degrees C, followed by 16 hours at 25 degrees C and 8 hours at 37 degrees C. The dialysis solution used was Dianeal PD-2 with 1.5% dextrose. Samples were removed at intervals and analyzed by stability-indicating high-performance liquid chromatography. Under condition A, ceftazidime sodium alone was stable for 24 hours at 25 degrees C but only 2 hours when then heated to 37 degrees C. Under condition B, ceftazidime sodium alone was stable throughout the observation period. Teicoplanin sodium alone was stable throughout the observation periods under both conditions. In combination, the drugs were stable if initially refrigerated and then brought to room temperature one week later, but were unstable when initially stored at 25 degrees C. No visual changes were noted, and pH did not vary substantially. Ceftazidime 100 micrograms/mL (as the sodium salt) and teicoplanin 25 micrograms/mL (as the sodium salt) combined in a PD solution were unstable when first kept at 25 degrees C before storage at 37 degrees C. The drugs in the combination remained stable when the solution was kept at 4 degrees C before storage at 37 degrees C.

Anti-Bacterial Agents↗
PubMed1996

The anxiolytic serotonin 5-HT1A receptor agonists buspirone, ipsapirone and gepirone are inhibitors of tyrosine hydroxylation in rat striatum.

The anxiolytics buspirone (BUS), ipsapirone (IPSAP) and gepirone (GEP) were investigated as 5-HT1A receptor-mediated inhibitors of tyrosine hydroxylation (TH) in a synaptosome-rich preparation of rat striatum. BUS, IPSAP and GEP were moderately potent inhibitors of TH with EC50 values of 48.4 microM, 50 microM and 836 microM, respectively. By comparison, 8-OH-DPAT, a 5-HT1A receptor selective agonist, has been previously shown to be more potent with an EC50 value of 7.0 microM. Each of these agents demonstrated full agonist activity at the striatal 5-HT1A receptors regulating TH. The inhibitory effects of each agent were attenuated by prior exposure to the 5-HT1A antagonist NAN-190, (10 microM) (P < 0.05), but not by the dopamine D2 antagonist (-)-sulpiride (10 microM). The potencies of 8-OH-DPAT, BUS, IPSAP and GEP were correlated with their reported affinities for the 5-HT1A receptor (P < 0.01) but not the dopamine D2 receptor. These results support the hypothesis that BUS, IPSAP and GEP inhibit TH through activation of a striatal 5-HT1A heteroreceptor on dopamine nerve terminals.

Animals↗