Aim:The prevalence of underweight women, who have an increased risk for small-for-gestational-age (SGA) birth, is increasing in Japan. We examined the associations of pre-pregnancy body mass index and gestational weight gain (GWG) with SGA birth among Japanese women. Material and Methods:We conducted a prospective cohort study of 1391 women who delivered full-term singleton babies. SGA was defined as below the 10th percentile of birthweight at each gestational age, baby sex, and parity. We calculated the 5th percentile of birthweight in the same way for another threshold for SGA. According to pre-pregnancy body mass index, we divided the participants into three groups: underweight (<18.5 kg/m 2 ), normal weight (18.5-24.9 kg/m 2 ), and overweight and obese (Ն25.0 kg/m 2 ). Results: SGA birth was observed most frequently among the underweight group (13.8%). Underweight was associated with an increased risk of SGA birth. The multiple-adjusted odds ratio for underweight was 1.96 (95% confidence interval, 1.23-3.11) compared with normal weight. Sufficient GWG reduced the incidence and the multiple-adjusted odds ratio for 1-kg increase of GWG was 0.86 (0.81-0.92). The same tendency was observed for the delivery of infants below the 5th birthweight percentile. Women with underweight and normal weight who had 9.0 kg or less of GWG had a significantly higher risk of SGA birth than women with normal weight who had 9.1-11.0 kg of GWG. Conclusions: Underweight and poor GWG were associated with a higher incidence of SGA birth. However, the incidence of SGA birth among underweight women was not increased significantly if they had sufficient GWG.

We previously reported that human granulosa cells (GC) express integrin alpha6beta1, in large follicles and early corpus luteum (CL). In this study, we examined the expression of integrin alpha5 and fibronectin (FN) by immunohistochemistry. Integrin alpha5 was undetectable on human GC in preovulatory follicles, but it was intensely expressed on luteinizing GC of CL in the early luteal phase, and it was weakly expressed on large luteal cells (LL) in the midluteal phase. FN was similarly expressed between GC/LL. Thus, integrin alpha5 and FN were stage-specifically expressed on/between luteinizing GC in the early luteal phase. Next we examined the effect of human chorionic gonadotrophin (HCG) on expression of integrin alpha5 on luteinizing GC in vitro. GC obtained from preovulatory follicles were cultured for 3 days without (control) or with HCG (1 IU/ml), and expression of integrin alpha5 was examined by flow cytometry. Although the positivity rate did not differ, the mean relative fluorescence intensity was 3.4-fold higher in the HCG-treated group (n = 8, P < 0.01). These findings indicate that integrin alpha5 is rapidly expressed on GC during luteinization, probably under LH stimulation, and suggest that integrin alpha5 is involved in CL formation via interaction with its ligand FN.

Ovulation accompanied by tissue damage can cause an increase in the level of tissue factor (TF) in the follicular fluid, triggering the extrinsic coagulation pathway. However, follicular fluid must block fibrin formation and maintain fluidity until the release of the oocyte at ovulation. The combination of sulfated proteoglycan, antithrombin, and TF pathway inhibitor (TFPI) appears to play a critical role in the hypocoagulability of human follicular fluid. When compared with plasma, folicular fluid differs markedly in the levels of a number of important coagulation proteins. Principal among these are 15-fold, 13-fold, and 3.7-fold increases in free TFPI, thrombin-antithrombin complex, and TF, respectively. The excessively prolonged activated partial thromboplastin time (APTT) and prothrombin time (PT) of human ovarian follicular fluid appear to be primarily due to high concentrations of sulfated proteoglycans, which accelerate the inactivation of thrombin and the anti-Xa activity of TFPI. Thus, heparitinase treatment shortened the clotting times of follicular fluid and reduced the inhibition of thrombin by the proteoglycan fraction combined with a fraction containing antithrombin. The remaining prolongation of APTT and PT may be caused by high levels of free TFPI in follicular fluid, which were confirmed by Northern blotting analysis, demonstrating TFPI mRNA expression by granulosa cells.

No abstract

Splenectomy and TNF-α inhibition both protect the kidney from I/R injury by reducing the accumulation of renal macrophages/monocytes and induction of major inflammatory cytokines.