No abstract

Compression has been regarded as the main haemostatic mechanism of compression sutures; however, we suggest that reduced uterine blood flow may be another important action. We suggest that our 'double vertical compression sutures' may have dual actions: haemostatic compression of the bleeding surface and reduced uterine blood flow.

No abstract

The precise reporting of fetal station is important in the decision-making regarding whether instrumental vaginal delivery or cesarean section should be performed. However, accurate evaluation of fetal station is difficult because it is defined on the basis of a hypothetical vertical midline to the ischial spines. Moreover, during delivery, the fetal head descends anteriorly into the pelvis along the pelvic axis and not in the vertical direction. DeLee's concept of fetal station, first reported in 1924, has been revised by taking into account the fetal head descent along the pelvic axis, and this concept has been in clinical use at the University of Tokyo Hospital since the 1970s. In this review, we assess the problems associated with conventional fetal station and explain the new concept of fetal station based on the trapezoidal plane and assessment of head descent upon instrumental delivery.

The function of CD44-v3 and heparin/heparan sulfate (HS) signaling was investigated during trophoblast cell migration to identify their role in the renewal of syncytial layer damage caused by increased hemodynamic turbulence in the intervillous space and maintenance of syncytial integrity in pre-eclampsia. We evaluated the effect of heparin/HS/CD44-v3-mediated processes during scratch wound closure in monolayer immortalized human trophoblast cells derived from term placenta (TCL-1 cells). Western blot analysis showed that these cultured human trophoblast cells express the epidermal growth factor receptor and CD44-v3 but do not express syndecan 4. An in vitro scratch wound healing assay showed enhanced migration of trophoblast cells in a dose-dependent manner in the presence of heparin compared with controls when cultured under serum-free conditions. Conversely, an anti-CD44 function-blocking antibody and CD44 siRNA suppressed the migration of trophoblast cells in the presence of heparin in a similar scratch assay. Furthermore, both heparin treatment and in vitro scratch wounding induced the phosphorylation of p21-activated kinase 1 (PAK1), whereas the anti-CD44-v3 antibody suppressed the heparin-induced phosphorylation of PAK1 in trophoblast cells. These results indicate that heparin/HS/CD44-v3-mediated signaling, in the absence of growth factor networks, enhances the direct repair of the damaged trophoblast layer through the migration of trophoblast cells. This renewed cell coverage may lead to the maintenance of syncytiotrophoblast cell function and an associated reduction in pathogenic soluble factors derived from the damaged trophoblast cells.