Biomedical subjects

Y P Xu

Publications and source records attributed to Y P Xu.

10 recordsLinked to original sources

PubMed1995

Growth hormone amplifies insulin-like growth factor I induced progesterone accumulation and P450scc mRNA expression.

The interaction of growth hormone (GH) and insulin-like growth factor I (IGF-I) in the acquisition of progesterone biosynthetic capacity were examined in cultured porcine granulosa cells. Basal progesterone production was not affected (P > 0.05) by GH treatment. However, concurrent treatment with GH produced a 4.1-fold increase (539 versus 2214 ng/culture) in the IGF-I-stimulated accumulation of progesterone. GH potentiated IGF-I induced progesterone production in a dose and time dependent manner, with a time requirement of 48 h or less. The amplified effect of GH was not attributable to changes in cellular protein, DNA content, cell number, plating efficiency or cell viability. Moreover, Northern blot analyses revealed that GH enhanced IGF-I induced expression of the gene encoding cytochrome P450 side chain cleavage. These observations provide further evidence to support the role of GH in the regulation of ovarian steroidogenesis.

Animals↗

PubMed1994

[A clinical study 39 cases of ovarian pregnancy].

Thirty-nine cases of ovarian pregnancy in our hospital from 1982 to 1992 were analyzed, and compared with the tubal pregnancies admitted during the same period. It showed that the incidence of ovarian pregnancy was 2.6% of all ectopic pregnancies with a trend to increase yearly. The clinical features of ovarian pregnancy revealed that abdominal pain was the major symptom, and history of amenorrhea was obscure. The clinical diagnosis of ovarian pregnancy was more difficult than that of tubal pregnancy. The typical histologic characteristics showed the embryo and chorionic villi surrounded by ovarian tissue or the presence of decidual changes. Ovarian pregnancy was closely related with poor uterine environment, pelvic inflammatory disease and/or endometriosis. The preferred therapeutic procedure was partial ovariectomy or wedge resection, preserving the normal ovarian tissue and tube as much as possible.

Adult↗

PubMed1994

Antitumor effect of alpha isomer of anordrin in vitro and cell cycle arrest at G1 phase.

Alpha isomer of anordrin (2 alpha, 17 alpha-diethyl-A-norandrostane-2 beta, 17 beta-diol dipropionate, alpha-Ano) inhibited mouse hepatoma (Hep A) and P388 cell growth in vitro. alpha-Ano (20 micrograms.ml-1) inhibited the incorporation of [3H]uridine and [3H]thymidine into RNA and DNA within 3 h, but the inhibition of L-[3H]lysine incorporating into protein was not obvious. alpha-Ano had no effect on the DNA-dependent RNA synthesis with purified nuclei of Hep A cells. It is suggested that the inhibition of RNA and DNA syntheses is the major cause of the cytostatic effect. alpha-Ano blocked the P388 cells at G1/G0 phase, and the delay in G1/G0 to S phase transition plays an important role in the inhibition of P388 cell growth.

Animals↗

PubMed1991

Calcium dependency of muscarinic and nicotinic agonist-induced ATP and catecholamine secretion from porcine adrenal chromaffin cells.

The secretion of catecholamines and ATP induced by cholinergic agonists and its dependence on extracellular Ca2+ were studied in cultured porcine adrenal chromaffin cells. Both nicotine and methacholine (a selective muscarinic agonist) induced secretion and increases in cytosolic free Ca2+ concentration ([Ca2+]in), although the activation of nicotinic receptors produced responses that were larger than those produced by activation of muscarinic receptors. The secretion and the increase in [Ca2+]in evoked by nicotine were completely dependent on extracellular Ca2+ and were blocked by prior depolarization of the cells with high extracellular K+ levels. In addition, nicotine induced significant 45Ca2+ influx. In contrast, the secretion and the increase in [Ca2+]in evoked by methacholine were partially dependent on extracellular Ca2+; methacholine also induced 45Ca2+ influx. Prior depolarization of the cells with high extracellular K+ levels did not block methacholine-induced secretion. In general, nicotinic responses were mediated by Ca2+ influx through voltage-dependent pathways. In contrast, muscarinic responses were dependent on both Ca2+ influx through an unknown mechanism that could not be inactivated by high K+ concentration-induced depolarization and presumably also intracellular Ca2+ mobilization.

Adenosine Triphosphate↗

PubMed1989

[P-8502--a new mu selective opioid receptor ligand].

The analgesic potencies of 3-[beta-(p-amino)-phenethyl)-9 beta-methoxy-9 alpha-(m-methoxyphenyl)-3- azabicyclo [3,3,1] nonane (P-8502) and 3-[beta-(p-monoester fumarylamido)-phenethyl]-9 beta-methoxy-9 alpha-(m-methoxyphenyl)-3-azabicyclo [3,3,1] nonane (P-8511) were examined. The analgesic ED50 of P-8502 and P-8511 were 55 and 200 micrograms/kg (mice, ip, hot plate), and 30 and 95 micrograms/kg (rat, sc, tail flick), respectively. The duration of the analgesic action of P-8511 (about 4 h) was longer than that of P-8502 (about 1.5 h, rat, sc, tail flick). Binding assay showed that P-8502 had a high ratio of delta/mu, kappa/mu: IC50 (DPDPE)/IC50 (DAGO) = 399; IC50(DAD-LE)/IC50 (DAGO) = 1498; IC50 (kappa)/IC50 (DAGO) = 159. In conclusion, P-8502 appears to be a new mu selective opioid receptor ligand, whereas P-8511 has no such selectivity.

Analgesics↗

PubMed1988