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The much publicized conflict hypothesis for understanding fetal-maternal interaction during pregnancy often invokes a 'battle' metaphor, rather than a well orchestrated interplay occurring as a series of well controlled moves and counter-moves as happens in a game of chess. Such stepwise interaction is particularly obvious in the spiral artery remodelling process, and it would be interesting to trace the history of the successive steps in histological adaptation throughout primate phylogeny. The restricted invasion observed in a few species on a 'lower' evolutionary scale suggests a tendency of progressive deeper invasion during primate evolution. Unfortunately, our knowledge of invasive processes in the placental bed in nonhuman primates is highly inadequate. A paradigm underscoring the stepwise interaction between mother and fetus may be provided by the Red Queen hypothesis, which is a useful model to explain co-evolutionary processes between different species. The apparent association between preeclampsia and restricted endovascular trophoblast invasion, combined with the absence of the disease in primate species showing shallow invasion, suggests that preeclampsia may result from a failure in one or more interactive steps necessary for deeper invasion. Evidence for a genetic component invokes the puzzling question as to why “preeclampsia genes” are not eliminated from human populations. As in other fields of medicine, a proper understanding of Darwinian selection processes may throw some light on the causes of preeclampsia. [ABSTRACT FROM AUTHOR]

Looks at the modern-day reproductive technologies as they were anticipated by the advanced state of Aldous Huxley's science fiction horror story, "Brave New World." Overview of the concept of reproduction in the book; Information on the standard set-up for in vitro fertilization; Details of the laboratory set-up for the actual insemination procedure as described by Huxley in the book.

Implantation and placentation present an immune challenge because of the semi-allogeneic nature of the conceptus. In this review, histological evidence for maternal immune cellular responses at the implantation site is summarized. Decidualization of the endometrium itself has features in common with an inflammatory response. During decidualization, infiltration by uterine natural killer (NK) cells occurs, and these interact with the non-polymorphic human leukocyte antigen (HLA) class I antigens expressed by invading extravillous trophoblasts. In humans, extension of trophoblast invasion beyond the decidual layer into the myometrium presents an additional challenge, which might be relevant for pregnancy complications such as pre-eclampsia. How far maternal cellular responses to invading trophoblasts seen at later stages of pregnancy can be traced back to the implantation period is an open question. [ABSTRACT FROM AUTHOR]

We here review the evolution of invasive placentation in primates towards the deep penetration of the endometrium and its arteries in hominoids. The strepsirrhine primates (lemurs and lorises) have non-invasive, epitheliochorial placentation, although this is thought to be derived fromamore invasive type. In haplorhine primates, there is differentiation of trophoblast at the blastocyst stage into syncytial and cellular trophoblast. Implantation involves syncytiotrophoblast that first removes the uterine epithelium then consolidates at the basal lamina before continuing into the stroma. In later stages of pregnancy, especially in Old World monkeys and apes, cytotrophoblast plays a greater role in the invasive process. Columns of trophoblast cells advance to the base of the implantation sitewhere they spread out to forma cytotrophoblastic shell. In addition, cytotrophoblasts advance into the lumen of the spiral arteries. They are responsible for remodelling these vessels to form wide, low-resistance conduits. In human and great apes, there is additional invasion of the endometrium and its vessels by trophoblasts originating from the base of the anchoring villi. Deep trophoblast invasion that extends remodelling of the spiral arteries to segments in the inner myometrium evolved in the common ancestor of gorilla, chimp and human. [ABSTRACT FROM AUTHOR]

Functional diversity of protein phosphatase 2A (PP2A) enzymes mainly results from their association with distinct regulatory subunits. To analyze the functions of one such holoenzyme in vivo, we generated mice lacking PR61/B'δ (B56δ), a subunit highly expressed in neural tissues. In PR61/B'δ-null mice the microtubule-associated protein tau becomes progressively phosphorylated at pathological epitopes in restricted brain areas, with marked immunoreactivity for the misfolded MC1-conformation but without neurofibrillary tangle formation. Behavioral tests indicated impaired sensorimotor but normal cognitive functions. These phenotypical characteristics were further underscored in PR61/B'δ-null mice mildly overexpressing human tau. PR61/B'δ-containing PP2A (PP2AT61δ) poorly dephosphorylates tau in vitro, arguing against a direct dephosphorylation defect. Rather, the activity of glycogen synthase kinase-3β a major tau kinase. was found increased, with decreased phosphorylation of Ser-9, a putative cyclin-dependent kinase 5 (CDK5) target. Accordingly, CDK5 activity is decreased, and its cellular activator p35, strikingly absent in the affected brain areas. As opposed to tau. p35 is an excellent PP2AT61δ substrate. Our data imply a nonredundant function for PR61/B'δ in phospho-tau homeostasis via an unexpected spatially restricted mechanism preventing p35 hyperphosphorylation and its subsequent degradation. [ABSTRACT FROM AUTHOR]

The article offers clinical information on pre-eclampsia, a pregnancy-specific disease characterized by de-novo development of concurrent hypertension and proteinuria. The cause of pre-eclampsia remains unknown, although it is being related to disturbed placental function during early pregnancy. Its signs and symptoms include new proteinuria, headache, epigastric pain, hypertension and reduced fetal movements. The author emphasizes the importance of early prediction of pre-eclampsia and the need for clinicians not to undervalue the clinical signs and symptoms that may be related to the disorder. Clinical management of preeclampsia may include laboratory tests, hospital admission and/or induction of labor.

While there is a growing realization that the origins of major obstetrical complications associated with defective deep placentation, such as pre-term labour, fetal growth restriction and pre-eclampsia, may lie in the very early pregnancy events, the underlying mechanisms are not understood. Impaired deep placentation is foremost a vascular pathology, characterized by a lack of endovascular trophoblast invasion and remodelling of a segment of the spiral arteries embedded within the inner myometrium of the uterus. Outside pregnancy, the inner myometrium represents a highly specialized, hormone-dependent structure, termed the junctional zone (JZ), which plays an integral part in the implantation process. The JZ changes with age and is disrupted in several reproductive disorders, such as endometriosis and adenomyosis, which in turn may account for the increased risk of adverse pregnancy outcome. Unlike the endometrium, the myometrial JZ is not readily accessible to biochemical or molecular studies, yet its structure and function can be assessed using imaging techniques, such as high-resolution ultrasound and magnetic resonance imaging. Thus, non-invasive assessment of the JZ prior to conception may turn out to be useful in identifying those women at risk of major obstetrical complications. [ABSTRACT FROM PUBLISHER]

Background: The process of physiological conversion of spiral arteries is dependent on the invasion of the interstitium and spiral arteries of the uterine wall by invasive extravillous trophoblast thereby creating a high flow-low resistance vessel. Quantitative data on restriction of trophoblast invasion and failure of spiral artery transformation are limited in preeclampsia.Aim: This study morphometrically analyzes interstitial trophoblast cells and trophoblast cells embedded in the wall of the converted spiral arteries within the decidua and myometrium of normotensive and preeclamptic Black African pregnant women.Methods: Placental bed biopsies were obtained from 25 normotensive pregnant women and 30 pregnant women complicated with hypertensive disorders. Biopsies were processed and immunostained for trophoblast cell identification, using anti-MNF 116 antibody. Image analysis of the trophoblast population within the decidua, myometrium and the spiral arteries was performed in the normotensive and in the severe proteinuric hypertensive groups.Results: The mean field area percentage of trophoblast cells observed in the decidua of the normotensive women was 22.79 +/- 2.1% in comparison to 18.14 +/- 1.53% in the severe hypertensive group (p < 0.01). In the myometrium, the mean field area percentage of interstitial trophoblast cells (both mononuclear and multinuclear) was 10.04 +/- 2.1% of the field area of the normotensive group compared to 2.81 +/- 0.67% in the severe hypertensive group (p < 0.001). The mean field area percentage occupied by trophoblast cells in myometrial spiral arteries was 10.15% in the normotensive group compared to none in the severe hypertensive group. The latter group displayed medial disorganization, hyperplasia and endothelial vacuolation.Conclusion: This study demonstrates restricted invasion of the trophoblastic cells in preeclampsia. This inadequate invasion may influence vascular remodeling required for delivering adequate volumes of maternal blood to the placenta. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to an article by Eric Steegers and colleagues on pre-eclampsia in the August 21, 2010 issue