Evaluating Stress during Pregnancy: Do We Have the Right Conceptions and the Correct Tools to Assess It?

Gestational stress is believed to increase the risk of pregnancy failure and perinatal and adult morbidity and mortality in both the mother and her child or children. However, some contradictions might arise from methodological issues or even from differences in the philosophical grounds that guide the studies on gestational stress. Biased perspectives could lead us to use and/or design inadequate/incomplete panels of biochemical determinations and/or psychological instruments to diagnose it accurately during pregnancy, a psychoneuroimmune-endocrine state in which allostatic loads may be significant.

Isolation of Leukocytes from the Murine Tissues at the Maternal-Fetal Interface.

Immune tolerance in pregnancy requires that the immune system of the mother undergoes distinctive changes in order to accept and nurture the developing fetus. This tolerance is initiated during coitus, established during fecundation and implantation, and maintained throughout pregnancy. Active cellular and molecular mediators of maternal-fetal tolerance are enriched at the site of contact between fetal and maternal tissues, known as the maternal-fetal interface, which includes the placenta and the uterine and decidual tissues.

Immune cells in term and preterm labor.

Labor resembles an inflammatory response that includes secretion of cytokines/chemokines by resident and infiltrating immune cells into reproductive tissues and the maternal/fetal interface. Untimely activation of these inflammatory pathways leads to preterm labor, which can result in preterm birth. Preterm birth is a major determinant of neonatal mortality and morbidity; therefore, the elucidation of the process of labor at a cellular and molecular level is essential for understanding the pathophysiology of preterm labor.

Polymorphisms in the hypoxia-inducible factor 1 alpha gene in Mexican patients with preeclampsia: A case-control study.

Background: Although the etiology of preeclampsia is still unclear, recent work suggests that changes in circulating angiogenic factors play a key role in its pathogenesis. In the trophoblast of women with preeclampsia, hypoxia-inducible factor 1 alpha (HIF-1α) is over-expressed, and induces the expression of non-angiogenic factors and inhibitors of trophoblast differentiation. This observation prompted the study of HIF-1α and its relation to preeclampsia.

Persistence of decidual NK cells and KIR genotypes in healthy pregnant and preeclamptic women: a case-control study in the third trimester of gestation.

Background: Natural Killer (NK) cells are the most abundant lymphocytes in the decidua during early gestation. The interactions of NK cells with the extravillous cytotrophoblast have been associated with a normal spiral artery remodeling process, an essential event for a successful pregnancy. Recent data indicate that alterations in the amount of decidual NK (dNK) cells contribute to the development of preeclampsia (PE).

[The two leading hypothesis regarding the molecular mechanisms and etiology of preeclampsia, and the Mexican experience in the world context].

Preeclampsia (PE) is one of the most severe complications of pregnancy. PE is responsible for the highest rates of morbidity and mortality for both pregnant women and the neonate. In this review, we first address general aspects of PE and its diagnosis, along with some epidemiological aspects of this disease in the mexican population, in particular the experience from the Instituto Mexicano del Seguro Social.