Here, we consider the role of infection during pregnancy in fetal development including placental development and function, which can lead to fetal growth restriction. The classical group of teratogenic pathogens is referred to as ‘TORCH’ (Toxoplasma gondii, others like Treponema pallidum, rubella virus, cytomegalovirus, and herpes simplex virus) but should include a much broader group this website of pathogens including Parvovirus B19, Varicella zoster virus, and Plasmodium falciparum to name a few. In this review, we describe the influence of different infections in utero on fetal development and the short-and long-term outcomes for the neonate. In some cases, the mechanisms used

by these pathogens to disrupt fetal development are well known. Bacterial infection of the developing fetal lungs

and brain begins with an inflammatory cascade resulting in cytokine injury and oxidative stress. For some pathogens like P. falciparum, the mechanisms involve oxidative stress and apoptosis to disrupt placental and fetal growth. An in utero infection may also affect the long-term health of the infant; in many cases, a viral infection in utero selleckchem increases the risk of developing type 1 diabetes in childhood. Understanding the varied mechanisms employed by these pathogens may enable therapies to attenuate changes in fetal development, decrease preterm birth, and improve survival.”
“Preterm birth is defined as birth before 37 weeks’ gestational age. With an incidence of 7% to 11%, it is one of the major causes of perinatal mortality and morbidity. Preterm birth is considered a clinical

syndrome, which arises from different pathological processes that activate prematurely one or more components of the mechanisms leading to parturition. The premature activation of labor may be caused by multiple pathological conditions; in particular a deregulation of the immune system and an exaggeration of inflammatory processes represent common central mechanisms. The complex pathogenesis, the main risk factors and the different therapeutic options will be described in the present review. Since its incidence is still increasing in the last decades, the goal is to improve the primary and secondary prevention.”
“The spindle apparatus is a vital structure and must be structurally Avelestat (AZD9668) intact for proper segregation of the oocyte’s genetic material during metaphase II. Endometriosis, oxidative stress, and cryopreservation can all adversely affect the structural integrity of the spindle, potentially resulting in aneuploidy and spontaneous abortion of the embryo. Advances in spindle imagery have made it possible to visualize the effects of environmental stresses on spindle structure. Deviation from an oocyte’s normal environment can seriously impair the positioning and integrity of the spindle. Oocytes cryopreservation causes depolymerization and repolymerization of the spindle.