Gestational diabetes is one of the most prevalent medical complications of pregnancy and causes increased fetal wastage. Investigation of placentas from diabetic mothers indicate chronic disturbances in intervillous, circulation, dilatation of capillaries, and a relatively immature villous structure. Abnormal levels of nitric oxide (NO) may contribute to maternal disorders such as the pathogenesis of diabetic vascular complications. In the normal placenta NO is generated only by endothelial NOS, which apparently serves to regulate vascular tone in the fetoplacental circulation. In contrast, studies have reported the absence of inducible nitric oxide synthase (iNOS) in human placentas under normal conditions. The aim of our study was to investigate whether iNOS is expressed in placentas from patients with gestational diabetes. Reverse transcription-polymerase chain reaction and Western blot analysis demonstrated iNOS mRNA and protein expression in placental tissue only from patients with gestational diabetes. Immunohistochemistry localized iNOS staining to endothelial cells and trophoblasts. We conclude that iNOS can be expressed in human placenta. Its expression might play an important role in placental pathophysiology.

Abstract-Neutrophil activation and increased migration is associated with preeclampsia and is resolved after delivery.Preeclampsia is an inflammatory disorder where altered levels of vascular endothelial growth factor (VEGF) and the circulating soluble fms-like tyrosine kinase 1 (sFlt-1) have a pathogenic role. VEGF, by binding to FLT-1, induces leukocytic chemotaxis. We studied expression and function of FLT-1 in maternal neutrophils during preeclampsia and normal pregnancies. Analysis of maternal neutrophils showed the relationship between FLT-1 expression and week of gestation. Preeclamptic women express lower FLT-1 and sFLT-1 in neutrophils. In contrast, serum levels of sFLT-1 in patients with preeclampsia are increased and, therefore, inhibit upregulation of FLT-1 in neutrophils by neutralizing VEGF. VEGF-dependent FLT-1 expression is regulated by changing FLT-1-promoter activity. Promoter activity is decreased by sFLT-1. In vitro experiments demonstrated that migration of neutrophils is regulated by VEGF via FLT-1 and excess of sFLT-1. Thus, VEGF-dependent migration of neutrophils is decreased during preeclampsia as a consequence of excess circulating sFlt1. But, they still increase migration by fMLP and, therefore, migration of neutrophils from preeclamptic women is highly activated when compared with the normotensive group. In conclusion, besides being involved in inducing an antiangiogenic state in the serum, excess of sFLT-1 seems to prevent activated neutrophils from women with preeclampsia from additional migration by VEGF. We provide evidence that neutrophils may be involved in the pathophysiology of pregnancy-related hypertensive disorders. Key Words: migration Ⅲ neutrophils Ⅲ preeclampsia Ⅲ pregnancy Ⅲ VEGF receptor 1 P reeclampsia (PE) is a hypertensive disorder of unknown etiology affecting 5% to 10% of all pregnancies. Pathophysological changes include elevated systemic vascular resistance, generalized vasoconstriction, activation of the coagulation cascade, maternal endothelial dysfunction, and a poorly perfused fetoplacental unit. 1 Preeclampsia is characterized by altered cytokine production 2 and marked neutrophil activation. 3-6 They release proteases and reactive oxygen species, which can cause vascular endothelial injury, inappropriate endothelial activation or transformation. 7-9 The latter processes are important for physiological adaptations during normal pregnancy creating a low-resistance arteriolar system, which allows adequate blood supply to the growing fetus. 10,11 Recently, case-control studies have shown associations between polymorphisms of the vascular endothelial growth factor (VEGF) gene and preeclampsia. 12 VEGF is a multifunctional cytokine that plays a pivotal role in angiogenesis in vivo. 13 VEGF is expressed by different cells, eg, smooth muscle, endothelial cells, monocytes/macrophages, and polymorphonuclear neutrophils (PMNs). VEGF exerts its biological effects through Fms-like tyrosine kinase 1 (FLT-1)/ VEGF receptor-1 and VEGF receptor-2 (FLK-1/KDR). 13 KDR is con...

As a important part of endocrine surgery, laparoscopic surgery has become the gold standard for the treatment of benign symptomatic ovarian cysts refractory to medical treatment. In fact, the stripping technique seems to be the most common technique used for ovarian cyst surgery. After stripping the cystic wall, the subsequent bleeding of the ovarian stromal wound ground is usually controlled by bipolar coagulation or/and by suturing. Potentially, the surgery-induced ovarian tissue damage will be increased by heat and/or by sutures. In respect to intraovarian hemostasis, the use of gelantine-thrombin-matrix might protect from additional ovarian tissue damage, which is of great importance for the ovarian reproductive function in woman. For the first time, our data do support a promising laparoscopic technique demonstrating ovarian cystectomy without any bipolar coagulation and/or suturing of ovarian tissue using a gelantine-thrombin-matrix sealant (FloSeal) as a new tool to control post-cystectomy ovarian wound bleeding.

Antibiotic administration following preterm premature rupture of membranes is associated with a prolongation of pregnancy and a reduction of neonatal infectious morbidity.

Loss of nNOS expression is associated with preeclampsia. It may alter the regulation of blood flow in the fetal and maternal placental vasculature in preeclampsia. However, the impact of NO produced by nNOS on the vascular tone of umbilical veins remains to be elucidated.