Encuesta perinatal de la Sociedad Gallega de Obstetricia y Ginecología 2010-2011 / Perinatal survey of the Galician Society of Obstetrics and Gynecology 2010-2011

Objetivo. Obtener y evaluar los datos de la asistencia perinatal en Galicia. Material y métodos. Estudio descriptivo, retrospectivo y multicéntrico. Se solicitó la colaboración de todos los centros sanitarios gallegos con asistencia al parto para la realización de la base de datos perinatales de los años 2010 y 2011. Resultados. Realizamos el estudio estadístico epidemiológico de 29.254 nacimientos acontecidos en nuestra comunidad en el bienio 2010-2011, lo cual representa el 67,2% del total de nacimientos de Galicia en ese periodo. Analizamos las siguientes variables: edad materna, estática fetal, amenorrea en el momento del parto, tipo de parto, indicaciones de cesáreas, y mortalidad perinatal y materna (AU)

Objective. To obtain and evaluate information on perinatal care in Galicia (Spain). Material and methods. We performed a descriptive, retrospective, multicenter study. All centers in Galicia involved in deliveries were requested to collaborate in the perinatal database for 2010 and 2011. Results. We performed a statistical, epidemiological study of 29,254 births in our region in the 2-year period from 2010 to 2011, representing 67.2% of all births in Galicia in this period. The following variables were analyzed: maternal age, fetal statics, amenorrhea at delivery, type of delivery, indications for cesarean section, and perinatal and maternal mortality (AU)

Procyanidins from grape pomace are suitable inhibitors of human endothelial NADPH oxidase.

Procyanidins have been associated with a reduced risk of cardiovascular diseases such as atherosclerosis. However, the molecular mechanisms underlying this benefit are not fully understood. Increased reactive oxygen species (ROS) production generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is a common problem in different cardiovascular diseases. Our objective was to evaluate the effects of procyanidin-rich fractions from distilled grape pomace on NADPH oxidase activity in human umbilical vein endothelial cells (HUVEC). Three differently polymerized and galloylated procyanidin fractions were analyzed for their NADPH oxidase inhibitory activity in cell lysates and in HUVEC cultures. All of the three fractions, up to 1 µg/ml, equally inhibited isolated NADPH oxidase in HUVEC lysates in a concentration-dependent manner and independently of any superoxide anion scavenging activities. The procyanidin fractions even blocked NADPH oxidase activity in intact HUVEC, inhibiting ROS production at both extra- and intracellular levels. The fractions achieved the same effects that known NADPH oxidase inhibitors, such as diphenylene iodonium and apocynin, but they presented better hydrosolubility. Our results demonstrated that procyanidin from grape pomace inhibit human endothelial NADPH oxidase regardless of their polymerization degree and galloylation percentage. Therefore, procyanidins are suitable NADPH oxidase inhibitors which could serve as models for therapeutic alternatives for cardiovascular diseases.

Glycated albumin, a precursor of advanced glycation end-products, up-regulates NADPH oxidase and enhances oxidative stress in human endothelial cells: molecular correlate of diabetic vasculopathy.

BACKGROUND: Hyperglycaemia induces non-enzymatic glycation reactions in proteins which generate Amadori products and advanced glycation end-products; the latter are thought to participate in the vascular complications of diabetic patients. However, the exact mechanisms concerning the effects of glycated proteins on vascular tissue remain to be determined. Therefore, the effects of glycated human serum albumin on human umbilical vein endothelial cells were studied. METHODS: Reactive oxygen species production was measured by the cytochrome C reduction method and by 5(6)-carboxy-2',7'-dichlorofluorescein diacetate (c-DCF-DA) fluorescence after treating human umbilical vein endothelial cells with glycated human serum albumin (6-200 µg/mL). The expression of Nox4 and p22phox mRNAs were analysed by reverse transcription-quantitative polymerase chain reactions and the levels of their proteins were measured by immunofluorescence. RESULTS: Low concentrations of glycated human serum albumin enhanced reactive oxygen species production in human umbilical vein endothelial cells after 4 h of treatment at both extracellular and intracellular sites. This enhanced production was sustained, although to a lesser extent, after 6 and 12 h of treatment. The gene expression study revealed that Nox4 and p22phox mRNA levels were elevated after 4 h of treatment with glycated human serum albumin. This mRNA elevation and enhanced reactive oxygen species production correlated with an increased expression of the Nox4 protein. CONCLUSIONS: The results revealed that a circulating and abundant modified glycated human serum albumin protein in diabetic patients induced a sustained reactive oxygen species production in human endothelial cells. This effect may have been due to an up-regulation of Nox4, the main subunit of NADPH oxidase in the endothelium.

Pravastatin counteracts angiotensin II-induced upregulation and activation of NADPH oxidase at plasma membrane of human endothelial cells.

Endothelial dysfunction has been linked to reactive oxygen species (ROS) production by nicotinamide adenine dinucleotide phosphate reduced (NADPH) oxidase. Angiotensin II (ANG), which levels are elevated in some cardiovascular diseases, can stimulate this enzyme, whereas statins have been demonstrated pleiotropic effects related with the restoration of endothelial function. Therefore, our purpose was to study the mechanism of the possible beneficial effects of pravastatin on ANG-activated human umbilical vein endothelial cells (HUVEC). ANG induced an increase in the extracellular superoxide anion produced by NADPH oxidase but had no effect in the intracellular ROS production. Pravastatin, which alone did not have any effect on ROS production, totally blocked the stimulating effects of ANG when combined with it. These effects were not due to a direct action of ANG or pravastatin on the activity of NADPH oxidase measured in HUVEC lisates. On the contrary, the results correlated well with other effects of ANG: a Nox4 and p22phox upregulated expression and an enhanced Nox4 translocation to the cell membrane. All these effects were inhibited by pravastatin, which had no effect when incubated alone. These data reveal for the first time that pravastatin interrupts the signaling pathway activated by ANG that leads to an enhanced NADPH oxidase activity at the cell membrane of HUVEC. For that, pravastatin inhibits ANG-induced upregulation of catalytic NADPH oxidase subunits and blocks the migration of them to the endothelial cell membrane.