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Biomedical subjects

X Bian

Publications and source records attributed to X Bian.

60 records · Page 4Linked to original sources
PubMed1994

A case-control epidemiologic study of endometriosis.

A case-control study involving 203 cases of pelvic endometriosis seen from 1987-1989, and 406 randomly selected and age-matched community controls was conducted in order to provide information relevant to effective prophylaxis of the disease. The diagnosis was confirmed by pathology from laparotomy and/or laparoscopy. A questionnaire focused on menstrual, marital and reproductive status, professional exposure and physical activities, and the results were analyzed by a conditional logistic regression model. Women characterized by earlier menarche (< or = 12 years) and longer period (> or = 8 days) were found to be associated with an elevated incurring risk, and a trend of increasing risk associated with primary dysmenorrhea (RR = 2.1 for mild to moderate and RR = 5.2 for severe dysmenorrhea), energetic physical activity during menstruation (RR = 2.1), and allergic diathesis (RR = 1.8) was seen. An inverse relationship was observed between the number of pregnancies and risk of endometriosis, and the protective effect was most significant when only the number of full-term pregnancies was counted. The risk factors of endometriosis are discussed, and intensive treatment of primary dysmenorrhea and avoidance of strenuous exercise during menstruation are identified as important measures in the prevention of endometriosis.

Adult↗
PubMed1993

Fetal dexamethasone exposure interferes with establishment of cardiac noradrenergic innervation and sympathetic activity.

Endogenous glucocorticoids provide natural differentiation signals for adrenergic neurons, and exposure to high exogenous steroid levels thus disrupts the timing of neuronal maturation. In the current study, pregnant rats were given 0.05, 0.2, or 0.8 mg/kg dexamethasone on gestational days 17, 18, and 19, and the effects on development of cardiac sympathetic function were assessed postnatally in the offspring. Dexamethasone produced a dose-dependent retardation of body and heart weight gains; at the highest dose, heart weight deficits were smaller than those for body weight, producing a relative cardiomegaly. The weight effects were accompanied by abnormalities of noradrenergic innervation, as assessed with measurements of norepinephrine levels and turnover. Norepinephrine levels were significantly reduced at all doses of dexamethasone, with the magnitude of effect exceeding that on heart or body weights; thus the levels were reduced even when corrected for tissue weight (ng norepinephrine/g heart weight). Norepinephrine turnover, a measure of neuronal impulse activity, showed delayed development at the lowest dose of dexamethasone and displayed profound suppression throughout development at the higher doses. Adverse effects of dexamethasone on norepinephrine turnover were still apparent in young adulthood, despite the recovery of weight variables to within 15% of normal values. In light of the release of steroids during maternal stress and the use of steroids in the therapy of neonatal respiratory distress, developing adrenergic neurons are likely to be targeted for adverse effects even when standard growth indices have normalized.

Abnormalities, Drug-Induced↗
PubMed1993

Effects of fetal dexamethasone exposure on postnatal control of cardiac adenylate cyclase: beta-adrenergic receptor coupling to Gs regulatory protein.

In the adult, glucocorticoids have been shown to upregulate beta-adrenergic control of adenylate cyclase by a variety of mechanisms; glucocorticoids are also thought to play a role in development of cardiac adrenergic function. In the current study, pregnant rats were given 0.2 mg/kg of dexamethasone on gestational days 17, 18, and 19 and the effects on the development of cardiac beta-receptors and their linkage to the stimulatory G-protein, Gs, were examined at 4 days postpartum. beta-Receptor numbers and affinity were unaffected by dexamethasone exposure, nor was there any change in the ability of the GTP analog, Gpp(NH)p, to shift the affinity state of the receptor. Addition of Gpp(NH)p to cardiac membranes enhanced basal and isoproterenol-stimulated adenylate cyclase activity, but the total response to isoproterenol, with or without Gpp(NH)p, represented a very small fraction of total enzymatic activity. Quantitative analysis of Gs indicated no changes attributable to dexamethasone treatment. Although prenatal dexamethasone has been shown to increase adenylate cyclase reactivity to beta-adrenergic input, the effect appears to be at the level of the catalytic subunit of adenylate cyclase, rather than at receptor or G-protein stages.

Adenylyl Cyclases↗
PubMed1992

Glucocorticoids accelerate the ontogenetic transition of cardiac ventricular myosin heavy-chain isoform expression in the rat: promotion by prenatal exposure to a low dose of dexamethasone.

Cardiac myosin heavy chain expression undergoes a perinatal transition from predominance of beta-MHC to alpha-MHC. In the current study, we tested the effects of glucocorticoids in this early transition period, by treating pregnant rats with dexamethasone on gestational days 17, 18 and 19, using doses below (0.05 mg/kg), at (0.2 mg/kg) or above (0.8 mg/kg) the threshold for growth retardation. Cardiac MHC isoforms were resolved with a denaturing SDS-PAGE system, followed by quantitative densitometry. In normal animals alpha-MHC was only 10% of the total on gestational day 18 but rose to 35% by postnatal day 1, and to 95% by the end of the first month postpartum. During the early phase of this transition, the lowest dose of dexamethasone significantly promoted alpha-MHC expression without inhibiting body or heart growth; regression analysis indicated a 40% increase in the slope of MHC isoform transition with respect to tissue weight. In contrast, the higher, growth-retarding doses of dexamethasone either failed to enhance alpha-MHC expression or caused biphasic changes, with inhibition at ages corresponding to the onset of weight deficits; regression analysis indicated that the effects of the higher doses on MHC could all be accounted for by changes in tissue weight. Glucocorticoid levels rise substantially in the period surrounding parturition, and serve to program the development and coupling of adenylate cyclase to membrane receptors; because adenylate cyclase has been shown to elicit the beta-MHC to alpha-MHC transition in vitro, our results suggest that glucocorticoids, along with thyroid hormone and beta-adrenergic stimulation, influence the ontogenetic program of MHC isoform transition.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1990

[Exploration of the clinical management of prolonged pregnancy].

This study was designed to address the effect of induced labor using pitocin iv drip in decreasing the incidence of perinatal complications and perinatal mortality of prolonged pregnancy. Induced labor was used in a study group which included 126 prolonged pregnant nullipara without complication. One hundred and twenty-eight prolonged pregnant nullipara in natural labor were defined as the control group. The perinatal mortality was 0 in the study group and 3.125% in the control. Also, the asphyxia rate was 8.7% in the study group and 13.3% in the control. The percentage of caesarean deliveries was the same in the both groups. The results of this study suggest that induced labor is safe, effective and practical in the management of prolonged pregnancies.

Asphyxia Neonatorum↗