Metabolic Response of Adult Male Offspring Rats to Prenatal Caffeine Exposure.

Caffeine is the most widely consumed psychoactive substance, with recommendations from health associations and regulatory bodies for limiting caffeine consumption during pregnancy being increasingly common. Prenatal exposure to caffeine has been shown to increase the risk of developing abnormalities in lipid metabolism in adult life. We further investigated the effect of prenatal caffeine exposure (PCE) (20 mg/kg of body weight) on the metabolic "reserve" of male Sprague Dawley offspring fed on a high fructose diet in adult life. Male adult PCE offspring were assigned to four groups; Nw and Nf: offspring of control mothers (N group of mothers), having received tap water or high fructose water respectively; Cw and Cf: offspring exposed to caffeine during gestation (C group of mothers) and receiving tap water or a high fructose water solution, respectively. Cf rats presented increased serum triglyceride level, as well as raised systolic and diastolic blood pressure levels, together with extensive renal tissue oedema in adulthood, compared to the other groups (p<0.05 for all comparisons). These findings show further evidence for potential detrimental metabolic effects of prenatal caffeine exposure during adulthood in this animal model.

Retention of cervical cerclage after preterm premature rupture of the membranes: a critical appraisal.

PURPOSE: The present meta-analysis aims to assess the efficacy of cervical cerclage retention after the occurrence of preterm premature rupture of the membranes by analyzing the observed maternal and neonatal perinatal outcomes. METHODS: We searched Medline (1966-2014), Scopus (2004-2014), Clinicaltrials.org (1997-2014), Cochrane Central Register of Controlled Trials (CENTRAL) (1999-2014) and Google Scholar (2004-2014) search engines, as well as reference lists from all included studies. The statistical analysis was performed using the RevMan software. RESULTS: Six studies were finally included in the present review, involving 293 parturient. Cerclage retention did not significantly prolong the gestational latency period (MD 2.56 days, 95% CI - 1.06, 6.71). It did, however, increased the rates of delivery after the first 48 h (OR 6.27, 95% CI 1.08, 36.24). As a technique, it did not significantly increase the rates of neonatal sepsis (OR 1.42, 95% CI 0.65, 3.12) or the neonatal death rates (OR 1.09, 95% CI 0.48, 2.47).Maternal chorioamnionitis was, however, significantly more prevalent among women offered cerclage retention (OR 1.78, 95% CI 1.02, 3.12), although the same was not observed in the case of postpartum endometritis (REM OR 4.73, 95 % CI 0.74, 30.09). CONCLUSIONS: Current evidence is insufficient to support the retention of cervical cerclage after the occurrence of PPROM, therefore, its implementation should be exceptionally instituted in everyday clinical practice, until further evidence becomes available.

Fetal alcohol spectrum disorders and cognitive functions of young children.

Fetal alcohol spectrum disorder (FASD) is one of the main causes of mental retardation worldwide. Nearly 1% of children in North America are affected from antenatal exposure to ethanol. Its economic burden in industrialized countries is increasing. It is estimated that, in the United States, 4.0 billion dollars are annually expended in the treatment and rehabilitation of these patients. As a pathologic entity, they present with a broad symptomatology. Fetal alcohol syndrome (FAS) is the most readily recognized clinical manifestation of these disorders. Various factors seem to contribute in the pathogenesis of FASD-related cognitive disorders. During the last 20 years, several potential pretranslational and posttranslational factors have been extensively studied in various experimental animal models. Research has specifically focused on several neurotransmitters, insulin resistance, alterations of the hypothalamic-pituitary-adrenal (HPA) axis, abnormal glycosylation of several proteins, oxidative stress, nutritional antioxidants, and various epigenetic factors. The purpose of the present review is to summarize the clinical manifestations of this disorder during childhood and adolescence and to summarize the possible pathophysiologic and epigenetic pathways that have been implicated in the pathophysiology of FASD.