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Biomedical subjects

C M Wang

Publications and source records attributed to C M Wang.

13 recordsLinked to original sources

Alterations of mitogenic responses of mononuclear cells by arsenic in arsenical skin cancers.

We have studied the endemic occurrence of chronic arsenism in a limited area on the southwest coast of Taiwan. The effects of arsenic on the mitogenic responses of mononuclear cells (MNC) derived from patients with arsenical skin cancers in that area were evaluated. The subjects enrolled in this study included patients with 1) Bowen's disease, 2) arsenical skin cancers (basal cell carcinoma and squamous cell carcinoma), 3) non-arsenical skin cancers (basal cell carcinoma and squamous cell carcinoma), 4) nasopharyngeal cancer and 5) healthy controls from endemic and non-endemic areas. Phytohemagglutinin (PHA) stimulated [3H]thymidine incorporation in MNC in all groups except the arsenical skin cancer group. However, when a low concentration of As2O3 (2.5 x 10(-7) M) was added to PHA-stimulated MNC, a tremendous amplification of the uptake of [3H]thymidine was noticed in patients with arsenical skin cancer. In this study, this phenomenon did not occur in cancers not related to arsenic. This result shows that arsenical carcinomas are hyperreactive to its specific etiology--arsenic. Arsenic seems to play a role as a co-stimulant of PHA similar to interleukin-1.

Arsenic

Molecular cloning and mapping of phenol degradation genes from Bacillus stearothermophilus FDTP-3 and their expression in Escherichia coli.

Two genes of the meta pathway of phenol degradation were cloned from a phenol-utilizing strain of Bacillus stearothermophilus and were mapped by subcloning and by use of a Tn5 insertion mutation. They code for phenol hydroxylase and catechol 2,3-dioxygenase, respectively. The gene encoding catechol 2,3-dioxygenase, which is more thermostable than catechol 2,3-dioxygenase encoded by the other gene, shares rather limited homology with that from Pseudomonas putida.

Catechol 2,3-Dioxygenase

Studies on chemical protectors against radiation. XXXV. Effects of radioprotective Chinese traditional medicines on radiation-induced lipid peroxidation in vivo and in vitro.

The fluctuation of lipid peroxidation (LP) in 9 tissues was investigated in mice for 7 d after whole-body X-irradiation with a lethal dose of bone marrow death. LP increased significantly in bone marrow, thymus, spleen and liver following irradiation, and slightly in brain and testis, but not in blood plasma, submaxillary gland or kidney. The effects of 7 radioprotective Chinese traditional medicines (CTMs) and cysteamine (MEA) on the radiation-induced LP in 4 tissues were studied by i.p. injection before or after irradiation and their LP content in tissues was measured 2 d after irradiation. Most CTMs showed significant inhibition of radiation-induced LP in bone marrow and liver, especially when injected prior to irradiation. Some CTMs also showed such inhibition in spleen. MEA only inhibited the increase of LP in liver when injected before irradiation, but enhanced the increase of LP in spleen. None of these radioprotectors including MEA was recognized to inhibit radiation-induced LP in thymus. The in vitro experiments were carried out using mouse liver microsomal suspensions (MS). The MS were prepared from normal (non-irradiated) mice. Each of the 8 radioprotectors was added to MS before or after irradiation and then post-irradiation-incubated at 37 degrees C. All markedly inhibited radiation-induced LP if added before irradiation, but were slightly less effective if added after.

Animals

Effects of bretylium on rat cardiac muscle: the electrophysiological effects and its uptake and binding in normal and immunosympathectomized rat hearts.

Bretylium produced electrophysiological effects on both rat atrium and ventricle in vitro at concentrations ranging from 2 times 10- minus 5 to 10- minus three M. Those effects included lengthening of action potential duration and effective refractory period; increasing effective refractory period/action potential duration; decreasing dv/dt of phase zero of the action potential and suppressing the action potential amplitude and overshoot. These effects, which could serve as a basis for the antiarrhythmic action of bretylium, were observed also in hearts from immunosympathectomized rats confirming a direct effect of this drug on the electrical properties of the cardiac muscle cells. In vivo and in vitro exposure of the myocardium to 14-C-bretylium showed that this drug is concentrated in cardiac ventricle and that this concentrating ability of the heart may be responsible for attaining effective antiarrhythmic concentrations in the myocardium at low plasma concentrations of the drug. Uptake of bretylium by the sympathetic nerves never amounted to more than 15% of the total bretylium binding by the cardiac ventricle and this neuronal uptake became insignificant compared to total bretylium uptake at concentrations greater than 10- minus 6 M. Subcellular distribution of the bretylium bound to the cardiac ventricle from immunosympathectomized rats suggested a binding to plasma membranes. Efflux studies indicate that this binding was tight, although reversible. These results indicate that underlying the antiarrhythmic effects of bretylium is an accumulation of the drug by cardiac muscle cells and a direct effect of the drug on the electrical properties of the cardiac muscle membrane independent of any action on the adrenergic neuron.

Action Potentials