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Y F Shi

Publications and source records attributed to Y F Shi.

94 records · Page 6Linked to original sources

Increased plasma and pituitary prolactin concentrations in adult male rats with selective elevation of FSH levels may be explained by reduced testosterone and increased estradiol production.

The roles of testosterone and estradiol in regulating prolactin concentrations were studied in acutely castrated adult male rats receiving subcutaneous Silastic implants of the sex steroids. Testosterone was administered in increasing doses, from subphysiologic to intact levels, both alone and in combination with a small, single dose of estradiol. The study was designed to assess whether a change in the relative rates of sex steroid production could account for an increase in PRL release in the absence of other testicular factors. At very low levels of plasma testosterone, FSH and LH levels were indistinguishable from castrate controls. As plasma testosterone concentration increased, both plasma FSH and LH levels were suppressed progressively to intact levels. When a subphysiologic dose of testosterone was coadministered with a small dose of estradiol, the combined effects produced a midcastrate level of FSH but maintained a normal level of LH similar to the selective increase in FSH concentration observed in men with germinal aplasia. Although PRL levels were indistinguishable in intact and castrate controls, testosterone replacement by capsule increased prolactin in a dose-related manner so that, at the physiologic level of testosterone, prolactin was elevated two-fold (P less than 0.01), similar to the level achieved with estradiol replacement alone. Pituitary prolactin levels also increased with increasing doses of testosterone but values remained within the range measured in intact controls. When estradiol was coadministered with testosterone, the combination produced different effects depending on the testosterone dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Apoptosis: the quiet death silences the immune system.

Apoptosis plays an essential role in maintaining cellular homeostasis during development, differentiation, and pathophysiological processes. In the immune system, recent investigations reveal that during the course of T-cell development in the thymus, negative selection of autoreactive immature T-cells is a typical apoptotic process. In addition, apoptosis is also involved in cytotoxic killing of target cells and the regulation of lymphocyte homeostasis during immune responses. Interestingly, recent evidence has suggested that cells dying by apoptosis are actively involved in immunosuppression in various circumstances. We have shown that apoptotic cells could inhibit the expression of CD69 during T-cell activation. Furthermore, apoptotic cells phagocytosed by macrophages and/or dendritic cells are immunosuppressive, a process likely mediated by the production of transforming growth factor-beta1. Since apoptosis is a common mechanism by which excessive cells in many tissues and organs are eliminated in various pathophysiological processes, we believe that further investigation into the mechanisms by which apoptotic cells affect the immune system will not only lead to a better understanding of the significance of apoptosis during immune responses, but will also provide novel strategies for the management of autoimmune diseases and transplantation.

Apoptosis↗

The changes of gene expression profiles in hydatidiform mole and choriocarcinoma with hyperplasia of trophoblasts.

The purpose of this study is to investigate changes of gene expression profiles in hydatidiform moles (HM) and choriocarcinoma and to explore causes of trophoblastic hyperplasia. Using cDNA microarray, 4,096 genes were analyzed in two pairs of the tissues of HM versus normal villi and in two pairs of normal primary culture trophoblasts versus JAR cell line of choriocarcinoma. The expressions of two genes in normal villi and HM, as well as in JAR and JEG-3, were examined with the help of immunohistochemistry, immunoblot, and reverse transcriptase-polymerase chain reaction in order to confirm the findings of cDNA microarray. Twenty-four genes were upregulated and 65 genes were downregulated in all HM. Four hundred thirty-three genes were upregulated and 380 genes were downregulated in JAR. Forty-six genes were upregulated in both HM and choriocarcinoma, whereas 13 genes were downregulated. Genes associated with the inhibition of cell proliferation were significantly downregulated, whereas genes associated with cell proliferation, malignant transformation, metastasis, and drug resistance were upregulated. Thymidine kinase-1 (TK-1) and small subunit ribonucleotide reductase (RRM-2) were overexpressed in HM, JAR, and JEG-3. The expressions of TK-1 and RRM-2 in moles were positively correlated with proliferative index of trophoblasts. Our results suggest that altered expression of genes exist in HM and choriocarcinoma. Trophoblastic hyperplasia may be involved in the overexpression of DNA synthetic enzymes.

Adult↗

The influence of aquaporin-1 and microvessel density on ovarian carcinogenesis and ascites formation.

This study aimed at investigating aquaporin-1 (AQP1) distribution and expression in primary ovarian epithelial tumors, correlating with clinicopathologic variables and intratumoral microvessel density (IMD). The AQP1 expression and IMD in 105 cases with primary epithelial ovarian tumors were measured by semiquantitative immunohistochemical technique. AQP1 was located mainly in microvessels and small vessels but seldom in tumor cells. Expression of AQP1 and IMD in ovarian malignant tumors was significantly higher than that in borderline tumors (P= 0.000, P= 0.001, respectively), and that in borderline tumors was higher than in benign tumors (P= 0.008, P= 0.028, respectively). The expression of AQP1 in FIGO stage III-IV was more than that in stage I-II (P= 0.001), and cases with ascites volume greater than 1000 mL were more than cases with ascites volume less than 1000 mL (P= 0.000). There is a positively correlated relationship between expression of AQP1 and IMD (correlation coefficient 0.60, P= 0.000) and between expression of AQP1 and ascites volume (correlation coefficient 0.57, P= 0.000). These data implicate that high AQP1 expression may play an important role in the ovarian carcinogenesis, progression, and ascites formation. Further studies into the mechanism of AQP1 regulation and the relationship between AQP1 expression and tumor angiogenesis may lead to novel therapies for ovarian carcinoma.

Adenocarcinoma↗