Biomedical subjects
Publications and source records attributed to T C Zhou.
On the basis of introducing the structures and relations of evolution in milk protein genes, the factors involved in gene expression including cis-acting elements, trans-acting factors as well as induction of hormones were discussed. Finally the applicable prospect of mammary gland as a bioreactor was estimated.
Using an earthworm (Eisenia foetida) dorsal muscle preparation, it was shown that tetrahydroberberine (THB, 10(-7)-10(-4) mol/L) did not affect both GABA and ACh receptors. DA receptor antagonist haloperidol (HAL) also exerted no effect. Owing to the blocking action of isonicotinyl hydrazine (INH) and thiosemicarbazide (TSC) on biosynthesis of GABA, and of picrotoxin (PT) and bicuculline (Bic) on the GABA-BZ receptor complex mediated transmission, all these agents could induce convulsion in mice. This action could be antagonized by amino- oxyacetic acid (AOAA) and benzodiazepine (BZ), but not by DA receptor antagonists THB and HAL. All the above observations indicate that the GABA inhibition is not involved in the central action of THB.
It was known that epidermal growth factor (EGF) plays an important role in the regulation of reproduction. The present study was undertaken to investigate the effect of EGF on the proliferation and differentiation of cultured rat granulosa cells. The results showed that EGF inhibited the 3H-TdR incorporation into DNA of granulosa cells, while the progesterone production was increased due to enhanced 3 beta-HSD activity. Radioreceptor assay (RRA) suggested that there were specific receptors for EGF on the granulosa cell with a Kd of 1.83 +/- 0.30 x 10(-8) mol/L and a Bmax of 1.75 +/- 0.29 x 10(4) sites/cell. Using method of immunohistochemistry, no EGF-like immunoreactivity was found in the granulosa cells at different age or different estrous cycle, but in the theca folliculi, interstitium and corpus luteum. These results suggest that EGF can regulate the growth and differentiation of the granulosa cells in the course of maturation of the folliculi and granulosa cells.
Three anti-EGF receptor MoAbs were used in these studies. Administration of MoAbs 3 and 176 inhibited tumor formation in nude mice by CNE-2, a poorly differentiated nasopharyngeal carcinoma cell line and A431, an epidermoid carcinoma cell line. When the same MoAbs were used in treatment against HeLa, a cervical carcinoma, tumor growth was not affected. The number of EGF receptors and apparent dissociation constants for 125I-EGF on CNE-2 and A431 was 1.3 x 10(5)/cell (Kd 7.7 x 10(-8) mol/L) and 1.4 x 10(6)/cell (Kd 2.4 x 10(-9) mol/L), respectively. Both MoAbs 3 and 176, capable of competing with EGF for receptor binding, showed significant tumor growth inhibition. MoAb 101 was incapable of blocking the binding of EGF to its receptor, and not as effective as MoAbs 3 and 176 in tumor growth inhibition. Our observation is that the MoAb anti-EGF receptor is cytostatic rather than cytocidal, in vitro against CNE-2 and A431.
Monoclonal antibodies (MoAbs) were developed against epidermal growth factor (EGF) receptor on the human epidermoid carcinoma cell line A431. The A431 antigen recognized by the MoAbs has an apparent molecular weight of approximately 170,000, with the same molecular weight as the CNE-2 cell line (poorly differentiated nasopharyngeal carcinoma). Administration of anti-EGF receptor MoAbs inhibited tumor formation, caused by the CNE-2 and A431 cell lines, in athymic mice. When the same MoAbs were used in therapy against Tca8113 (a human tongue carcinoma) and HeLa cells (a human cervical carcinoma), tumor growth was not affected. The number of EGF receptors and the apparent dissociation constants for 125I-EGF on CNE-2 and A431 were 1.3 x 10(5)/cell (Kd 7.7 x 10(-8) M) and 1.4 x 10(6)/cell (Kd 2.4 x 10(-9) M), respectively. Three anti-EGF receptor MoAbs were used in these studies. MoAbs 3 and 176, capable of competing with EGF for receptor binding, showed significant tumor growth inhibition. MoAb 101 was incapable of blocking the binding of EGF to its receptor and was not as effective as MoAbs 3 and 176 in tumor growth inhibition. Our observation is that in vitro, MoAb anti-EGF receptor is cytostatic, rather than cytocidal, against CNE-2 and A431.
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In our experiments the isolated rat adrenal glomerulosa cells displayed peripheral-type benzodiazepine receptors, which could bind to [3H] PK11195 with an apparent equilibrium dissociation constant (KD) of 9.4 +/- 2.8 nmol/L and a maximal binding capacity (Bmax) of 5.6 +/- 1.8 pmol/10(6) cells. The effects of five ligands: PK11195, Ro5-4846, flunitrazepam, diazepam and clonazepam on aldosterone secretion responses of isolated glomerulosa cells to angiotensin II or extracellular potassium ions were observed. The logarithm of EO50 for these ligands as stimulators was well correlated with the logarithm of their Ki value for [3H] PK11195 binding, suggesting that the stimulative effects might be mediated by the benzodiazepine receptor in isolated glomerulosa cells.
The GABA receptor agonists GABA (400 micrograms icv) and muscimol (1 microgram icv) induced hypotension in urethane-anesthetized rats, while the GABA receptor antagonist bicuculline (2 micrograms icv) elicited hypertension. An endogenous GABA receptor binding inhibitor (1 mg), prepared from bovine cerebellum, showed bicuculline-like hypertensive action in a dose-dependent manner. It was antagonized by icv muscimol, but not by the alpha 2-adrenoceptor agonist clonidine. These in vivo results agree quite well with our previous in vitro receptor binding assay experiments.
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