Clinical guidelines for obstetrical practice were first published by the Japan Society of Obstetrics and Gynecology (JSOG) and the Japan Association of Obstetricians and Gynecologists (JAOG) in 2008, and a revised version was published in 2011. The aims of this publication include the determination of current standard care practices for pregnant women in Japan, the widespread use of standard care practices, the enhancement of safety in obstetrical practice, the reduction in burdens associated with medico-legal and medico-economical problems, and a better understanding between pregnant women and maternity-service providers. These guidelines include a total of 87 Clinical Questions followed by several Answers (CQ&A), a Discussion, a List of References, and some Tables and Figures covering common problems and questions encountered in obstetrical practice. Each answer with a recommendation level of A, B or C has been prepared based principally on "evidence" or a consensus among Japanese obstetricians in situations where "evidence" is weak or lacking. Answers with a recommendation level of A or B represent current standard care practices in Japan. All 87 CQ&As are presented herein to promote a better understanding of the current standard care practices for pregnant women in Japan.

In this study, we performed small RNA library sequencing using human placental tissues to identify placenta-specific miRNAs. We also tested the hypothesis that human chorionic villi could secrete miRNAs extracellularly via exosomes, which in turn enter into maternal circulation. By small RNA library sequencing, most placenta-specific miRNAs (e.g., MIR517A) were linked to a miRNA cluster on chromosome 19. The miRNA cluster genes were differentially expressed in placental development. Subsequent validation by real-time PCR and in situ hybridization revealed that villous trophoblasts express placenta-specific miRNAs. The analysis of small RNA libraries from the blood plasma showed that the placenta-specific miRNAs are abundant in the plasma of pregnant women. By real-time PCR, we confirmed the rapid clearance of the placenta-specific miRNAs from the plasma after delivery, indicating that such miRNAs enter into maternal circulation. By using the trophoblast cell line BeWo in culture, we demonstrated that miRNAs are indeed extracellularly released via exosomes. Taken together, our findings suggest that miRNAs are exported from the human placental syncytiotrophoblast into maternal circulation, where they could target maternal tissues. Finally, to address the biological functions of placenta-specific miRNAs, we performed a proteome analysis of BeWo cells transfected with MIR517A. Bioinformatic analysis suggests that this miRNA is possibly involved in tumor necrosis factor-mediated signaling. Our data provide important insights into miRNA biology of the human placenta.

Clinical guidelines for obstetrical practice were first published by the Japan Society of Obstetrics and Gynecology (JSOG) and the Japan Association of Obstetricians and Gynecologists (JAOG) in 2008, and a revised version was published in 2011. The aims of this publication include the determination of current standard care practices for pregnant women in Japan, the widespread use of standard care practices, the enhancement of safety in obstetrical practice, the reduction in burdens associated with medico-legal and medico-economical problems, and a better understanding between pregnant women and maternity-service providers. These guidelines include a total of 87 Clinical Questions followed by several Answers (CQ&A), a Discussion, a List of References, and some Tables and Figures covering common problems and questions encountered in obstetrical practice. Each answer with a recommendation level of A, B or C has been prepared based principally on 'evidence' or a consensus among Japanese obstetricians in situations where 'evidence' is weak or lacking. Answers with a recommendation level of A or B represent current standard care practices in Japan. All 87 CQ&A are presented herein to promote a better understanding of the current standard care practices for pregnant women in Japan.

In 1997, B-Lynch pioneered the use of uterine compression sutures for postpartum hemorrhage. Since then, some researchers, including ourselves, have devised various uterine compression sutures. High-level evidence has not been demonstrated as to whether compression sutures achieve better and safer hemostasis for postpartum hemorrhage than other methods, and, if they do, whether one suture is more efficient and safer than another. However, generally speaking, uterine compression sutures have achieved hemostasis while preserving fertility in many women and thus their efficacy and safety have been timetested. Each suture has both merits and drawbacks: obstetricians must be aware of the fundamental characteristics of various sutures. In this review, we summarize the technical procedures, efficacy, safety and complications of various uterine compression sutures. We add our own experiences and opinions where necessary.

Abstract-In this study, to search for novel preeclampsia (PE) biomarkers, we focused on microRNA expression and function in the human placenta complicated with PE. By comprehensive analyses of microRNA expression, we identified 22 microRNAs significantly upregulated in preeclamptic placentas, 5 of which were predicted in silico to commonly target the mRNA encoding hydroxysteroid (17-␤) dehydrogenase 1 (HSD17B1), a steroidogenetic enzyme expressed predominantly in the placenta. In vivo HSD17B1 expression, at both the mRNA and protein levels, was significantly decreased in preeclamptic placentas. Of these microRNAs, miR-210 and miR-518c were experimentally validated to target HSD17B1 by luciferase assay, real-time PCR, and ELISA. Furthermore, we found that plasma HSD17B1 protein levels in preeclamptic pregnant women reflected the decrease of its placental expression. Moreover, a prospective cohort study of plasma HSD17B1 revealed a significant reduction of plasma HSD17B1 levels in pregnant women at 20 to 23 and 27 to 30 weeks of gestation before PE onset compared with those with normal pregnancies. The sensitivities/specificities for predicting PE at 20 to 23 and 27 to 30 weeks of gestation were 0.75/0.67 (cutoff valueϭ21.9 ng/mL) and 0.88/0.51 (cutoff valueϭ30.5 ng/mL), and the odds ratios were 6.09 (95% CI: 2.35-15.77) and 7.83 (95% CI: 1.70 -36.14), respectively. We conclude that HSD17B1 is dysregulated by miR-210 and miR-518c that are aberrantly expressed in preeclamptic placenta and that reducing plasma level of HSD17B1 precedes the onset of PE and is a potential prognostic factor for PE. (Hypertension. 2012;59:265-273.) • Online Data Supplement Key Words: preeclampsia Ⅲ microRNA Ⅲ biomarker Ⅲ placenta Ⅲ prospective cohort study T he pathophysiology and etiology of preeclampsia (PE) remain largely unknown, and its final diagnosis can only be made when symptoms have regressed after delivery. 1 Thus, it is of clinical significance to predict PE before its onset. Dysregulation of the serum levels of angiogenic/ antiangiogenic factors has been demonstrated previously; examples include placental growth factor (PlGF), soluble fms-like tyrosine kinase 1 (sFlt-1), and soluble endoglin. [2][3][4] However, these proteins may not sufficiently characterize the clinical features and pathophysiological mechanisms of PE onset. 5 If there are any other parameters of which serum levels change in PE, they may illustrate the pathophysiology of PE in a manner different from the previous studies.MicroRNAs (miRNAs), small noncoding RNAs of Ϸ22 nucleotides in length, play a critical role in posttranscriptional gene regulation. 6,7 Although many miRNAs are ubiquitously expressed in mammals, some miRNAs exhibit specific expression patterns in an organ-or cell-type-dependent manner. 8 For instance, miRNAs derived from the miRNA cluster in human chromosome 19, a primate-specific miRNA cluster encompassing 46 miRNAs in the human genome, 9 have been demonstrated to exhibit a placenta-specific expression pattern. 10 Although a few studi...

For cesarean hysterectomy with placenta previa accreta, "universally achievable" measures are required. We propose eight measures: (i) placement of intra-iliac arterial occlusion balloon catheters; (ii) placement of ureter stents; (iii) "holding the cervix" to identify the site to be transected; (iv) uterine fundal incision; (v) avoidance of uterotonics; (vi) "M cross double ligation" for ligating the ovarian ligament; (vii) "filling the bladder" to identify the bladder separation site and "opening the bladder" for placenta previa accreta with bladder invasion; and (viii) to continue to clamp the medial side of the parametrium or the cervix or employment of the "double edge pick-up" to ligate it. These eight measures are simple, easy, effective, and thus "universally achievable".

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Abstract-The first aim of our study was to develop a pregnant mouse model for preeclampsia using adenoviral vector containing mouse full-length soluble fms-like tyrosine kinase 1 (sFlt-1) but not truncated sFlt-1. The second aim was to evaluate effects of recombinant mouse (rm) vascular endothelial growth factor (VEGF) and rm placental growth factor (PlGF) on a preeclampsia model induced by adenoviral vector containing mouse full-length sFlt-1. We injected adenoviral vector containing mouse full-length sFlt-1 on day 8.5 or 9.5 of gestation into pregnant Institute of Cancer Research mice, resulting in hypertension, proteinuria, and similar glomerular histological changes as those seen in human preeclamptic women with glomerular endotheliosis on day 16.5 or 17.5 of gestation. The preeclampsia models were treated with 100 g/kg of rmVEGF164 (nϭ5), 100 g/kg of rmPlGF-2 (nϭ5), or vehicle (nϭ7) twice a day for 2 days IP. The rmVEGF164 treatment significantly decreased the mean blood pressure on day 16.5 or 17.5 of gestation compared with the vehicle treatment (85Ϯ4 versus 97Ϯ2 mm Hg; Pϭ0.018). The rmPlGF-2 treatment also significantly decreased the mean blood pressure on day 16.5 or 17.5 of gestation compared with the vehicle treatment (86Ϯ3 versus 97Ϯ2 mm Hg; Pϭ0.018). However, proteinuria was not affected by either rmVEGF164 or rmPlGF-2. In conclusion, we, for the first time, created a mouse preeclampsia model using mouse full-length sFlt-1. VEGF and PlGF may be promising for ameliorating hypertension in women with preeclampsia. Additional study of PlGF as a potential drug for preeclampsia is warranted. Key Words: adenoviral vector Ⅲ soluble fms-like tyrosine kinase 1 Ⅲ vascular endothelial growth factor Ⅲ placental growth factor Ⅲ preeclampsia Ⅲ animal models Ⅲ therapy P reeclampsia is associated with maternal and infantile morbidity and mortality. 1,2 It has been shown that the concentration of soluble fms-like tyrosine kinase 1 (sFlt-1), a circulating antiangiogenic protein, is increased in women with preeclampsia, 3,4 and increased levels of sFlt-1 and reduced levels of free placental growth factor (PlGF) are potentially useful for predicting the subsequent development of preeclampsia. 4,5 SFlt-1 acts by adhering to the receptorbinding domains of vascular endothelial growth factor (VEGF)-A and PlGF, preventing their interaction with endothelial receptors on the cell surface. Recent studies have indicated that patients with cancer receiving anti-VEGF antibody therapy may have an increased incidence of proteinuria and hypertension because of a decrease in their circulating VEGF levels. 6 Nonpregnant and pregnant rodents administered anti-VEGF antibodies or sFlt-1 manifested proteinuria and hypertension. 3,7,8 These results strongly indicate that increases in sFlt-1 and decreases in VEGF/PlGF in the maternal circulation may cause the occurrence of preeclampsia.SFlt-1, a human natural soluble form of the VEGF receptor (VEGFR) 1, is produced in conditioned culture medium of human umbilical vein endothelial cells 9 an...