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Biomedical subjects

R Tseng

Publications and source records attributed to R Tseng.

14 recordsLinked to original sources
PubMed1999

Pore structure and adsorption performance of the activated carbons prepared from plum kernels.

According to iodine number, amount of methylene blue adsorption, the BET specific surface area, and the yield, the conditions for preparing activated carbons as adsorbents from plum kernels were optimized. The activation temperature and time tested were in the ranges 750-900 degrees C and 1-4 h, respectively. Adsorption isotherms of two commercial dyes and phenol from water on such activated carbons were measured at 30 degrees C. It was shown that the optimal activation temperature and time depended on the molar mass of the solutes, and all equilibrium isotherms could be fitted by the Langmuir equation. The experimental results indicated that the prepared activated carbons were economically promising for adsorption removal of dyes and phenol, in contrast to other commercial adsorbents.

Adsorption↗
PubMed1996

Lego asthma.

Explore the source record for details and available documents.

Asthma↗
PubMed1991

Lead, cadmium, arsenic, and mercury levels in maternal and fetal cord blood.

In this study the levels of lead, arsenic, cadmium and mercury were measured by the method of graphite-furnace atomic absorption spectrophotometry in paired maternal and fetal cord blood (n = 168) collected from three cities in Taiwan, (Kaohsiung, Taipei and Keelung). The mean values of those heavy metals were within normal limits. There was no difference in levels by maternal parity or fetal sex. The mean value for the level of lead in maternal blood was 64.8 micrograms/L, and 40.9 micrograms/L for the umbilical-cord blood; comparing the three locations by ANOVA analysis, there was no difference in maternal or fetal blood levels. Mean maternal As concentrations (6.8 +/- 0.58 micrograms/L) and umbilical cord blood levels (7.9 +/- 0.67 micrograms/L) were within reference levels. The mean Cd concentrations in maternal blood were (1.30 micrograms/L) significantly higher than that of the umbilical-cord blood concentrations (0.78 micrograms/L). The maternal Cd concentrations (1.62 micrograms/L) of Kaohsiung were significantly higher than that (1.24 micrograms/L) of Taipei. The fetal Cd concentrations of Kaohsiung (1.04 micrograms/L) were also significantly higher than those (0.7 micrograms/L, 0.6 micrograms/L) of Taipei and Keelung. The mean umbilical-cord blood Hg concentration (28.8 micrograms/L) was higher than that (19.4 micrograms/L) of maternal blood. The maternal Hg concentrations of Taipei were significantly higher than those of Keelung. The fetal Hg concentrations (28.8 micrograms/L) of Taipei were also marginally higher than that of Keelung and Kaohsiung.

Arsenic↗
PubMed1989

Effecting change in multicultural health promotion: a systems approach.

Given the context of a rapidly changing demography and an evolving health care system, the project described in this article was designed to address the system-wide need for changes in allied health service delivery to minority populations. A multidisciplinary, multicultural, and participative model was adopted to initiate attitudinal and behavioral changes among three groups: faculty from three allied health departments, students preparing for careers in these three professions, and community health care practitioners. This paper briefly describes the major objectives, activities, and outcomes of the project as well as insight into the factors and dynamics that affected its immediate and long-range success. The idea that significant and lasting change requires strategies that incorporate the interactive dynamics of individuals and groups of the inclusive health care system was supported in the outcomes of the project.

Attitude to Health↗
PubMed1981

Distinct regulations by calcium of cyclic GMP levels and catecholamine secretion in isolated bovine adrenal chromaffin cells.

The effects of various calcium-dependent secretagogues on cyclic GMP levels and catecholamine (CA) secretion were measured in a preparation of bovine adrenal chromaffin cells. The secretory effect of acetylcholine (ACh; 8--10 fold stimulation) was mimicked by nicotine but not muscarine. Three--five fold stimulations of cyclic GMP levels were also obtained with ACh and muscarine but not nicotine. High concentration of K+, and the ionophore A23187, also elevated cyclic GMP levels. However, secretion produced by veratridine, ouabain, and the ionophore X537A was not accompanied by any rise in cyclic GMP levels. Removal of extracellular calcium significantly decreased both basal levels of CA secretion and of cyclic GMP and completely abolished their stimulation by ACh. The half-maximal effects of calcium on the cholinergic stimulations of cyclic GMP levels and of CA secretion were observed at 0.2 and 2.5 mM, respectively. Substitution of Ca2+ by Sr2+ was more effective in maintaining the cyclic GMP response than the secretory response. The calcium channel blockers Co2+, Mg2+ and Ni2+ inhibited the cholinergic stimulation of cyclic GMP more than that of CA release. On the other hand, the organic calcium channel blockers, verapamil and methoxyverapamil (D--600) were more effective antagonists of the secretory response. These data indicate that the cholinergic stimulations of CA secretion and of cyclic GMP levels in bovine adrenal chromaffin cells are regulated by calcium via two distinct mechanisms.

Adrenal Glands↗
PubMed1981

Studies on the inhibitory action of opiate compounds in isolated bovine adrenal chromaffin cells: noninvolvement of stereospecific opiate binding sites.

In isolated bovine adrenal chromaffin cells, beta-endorphin, dynorphin, and levorphanol caused a dose-dependent inhibition of catecholamine (CA) secretion elicited by acetylcholine (ACh), with an ID50 of 50, 1.3, and 4.3 microM, respectively. The inhibition by the opiate compounds was specific for the release evoked by ACh and nicotinic drugs and was noncompetitive with ACh. Stereospecific binding sites for the opiate agonist [3H]etorphine were found in homogenates of bovine adrenal medulla (KD = 0.59 nM). beta-Endorphin, dynorphin, levorphanol, and naloxone were potent inhibitors of the binding of [3H]etorphine with an ID50 of 12, 0.4, 5.2, and 6.2 nM, respectively. However, [3,5-I2Tyr1]-beta-endorphin, [3,5-I2Tyr1]-dynorphin, and dextrorphan, three opiate compounds with no or little activity in the guinea pig ileum assay, were relatively ineffective in inhibiting the binding of [3H]etorphine (ID50 700, 600, and 10,000 nM, respectively). On the other hand, these three compounds were equipotent with beta-endorphin, dynorphin, and levorphanol, respectively, in inhibiting the ACh-evoked release of CA from the adrenal chromaffin cells (ID50 of 10, 1.5, and 6 microM, respectively). Inhibition of CA release was also obtained with naloxone (ID50 = 14) microM) and naltrexone (ID50 greater than 10(-4) M), two classical antagonists of opiate receptors, and this effect was additive to that of beta-endorphin. These data indicate that the opiate modulation of CA release from adrenal chromaffin cells is not related to the stimulation of the high affinity stereospecific opiate binding sites of the adrenal medulla. The physiological function of these sites remains to be determined.

Acetylcholine↗
PubMed1978

Systemic administration of beta-endorphin: potent hypotensive effect involving a serotonergic pathway.

In normal adult rats anesthetized with urethane, intravenous injections of beta-endorphin (30--150 micrograms kg-1) induced a transient fall of blood pressure followed by a small hypertension and a prolonged hypotension. Prior administration of naloxone completely blocked these effects, whereas naloxone, given 1 hr after beta-endorphin, did not reverse the prolonged depressor phase of the opioid peptide. The effects of beta-endorphin on the arterial blood pressure were greatly reduced in animals pretreated with p-chlorophenylalanine, a specific depletor of serotonin. Moreover, in rats pretreated with potent serotonin antagonists such as cyproheptadine, mianserin, and metergoline, beta-endorphin did not produce a significant hypotension. Furthermore, the depressor effect of beta-endorphin was potentiated by fluoxetine, a specific serotonin uptake inhibitor. These observations suggest the participation of a serotonergic pathway in the action of beta-endorphin on the arterial blood pressure.

Blood Pressure↗