Morbilidad materna: hospitalización ante-parto / Maternal morbidity: ante partum hospitalization

Determinar la incidencia de admisiones antenatales en gestantes portadoras de enfermedades severas que implican un tratamiento intrahospitalario, revelando así la morbilidad materna, además de conocer sus repercusiones perinatales. Estudio observacional, descriptivo, analítico realizado durante el trienio 2008-2010. Hubo 5 815 nacimientos, 1 033 admisiones antenatales, 230 neonatos con morbilidad neonatal y 34 muertes feto-neonatales. Las embarazadas debían tener 20 semanas o más de gestación, hospitalizadas 2 días o más, fueron dadas de alta sin parir y luego regresaron para su asistencia obstétrica definitiva. Departamento de Obstetricia y Ginecología, Hospital "Dr. Adolfo Prince Lara", Departamento Clínico Integral de la Costa, Universidad de Carabobo. Puerto Cabello. Hubo una incidencia de 17,76 pacientes hospitalizadas antenatalmente por cada 100 nacimientos o 1 cada 5,6 nacimientos. Las patologías más frecuentes fueron las propias del embarazo (57,41 por ciento): la amenaza de parto prematuro (18,20 por ciento), preeclampsia (9,78 por ciento), hemorragia placentaria (6,68 por ciento), oligohidramnios (6,58 por ciento) y anemia (5,52 por ciento). Las patologías asociadas al embarazo (33,98 por ciento): infección urinaria (14,13 por ciento) y diabetes(9,49 por ciento) La morbilidad neonatal global fue 22,26 por ciento, aportada principalmente por patologías propias del embarazo: amenaza parto pretérmino (20,43 por ciento), preeclampsia (13,04 por ciento), y hemorragia placentaria (10 por ciento); de las asociadas: infección urinaria 14,35 por ciento y diabetes 14,35 por ciento. La mortalidad feto-neonatal fue de 3,3 por ciento, contribuyendo predominante prematurez y malformación fetal (29,41 por ciento), preeclampsia (26,47 por ciento), el desprendimiento prematuro de placenta y la placenta previa (17,65 por ciento). Hubo una incidencia elevada de admisiones antenatales, causadas por entidades que obligan a un diagnóstico precoz...

To determine the incidence of antenatal admissions in pregnant women carrying a severe illness involving hospital management, revealing maternal morbidity, in addition to knowing their impact perinatal outcomes. An observational, descriptive, analytical study, made during the 2008-2010 period. There were 5 815 births, 1 033 antenatal admissions, 230 infants with neonatal morbidity and 34 fetal and neonataldeaths. Pregnant women should take 20 weeks or more gestation, hospitalized 2 days or more, were discharged without giving birth and then returned for final delivery care. Department of Obstetrics and Gynecology, Hospital "Dr. Adolfo Prince Lara". Departamento Clinico de la Costa. University of Carabobo. Puerto Cabello, Estado Carabobo, Venezuela. There was an incidence of patients hospitalized antenatally 17.76 per 100 births or 1 in 5.6 children. The most frequent pathologies were typical of pregnancy (57.41 percent): preterm delivery threatens (18.20 percent), pre-eclampsia (9.78 percent), placental hemorrhage (6.68 percent), oligohydramnios (6.58 percent) and anemia (5.52 percent). Pregnancy-associated pathologies (33.98 percent): urinary tract infection (14.13 percent) and diabetes (9.49 percent). Neonatal morbidity rate was 22.26 percent, contributed mainly by pathologies of pregnancy: preterm delivery threatens (20.43 percent), pre-eclampsia (13.04 percent), and placental hemorrhage (10 percent), associated: urinary tract infection 14.35 percent and diabetes 14.35 percent. Feto-neonatal mortality was 3.3 percent, contributing predominant: prematurity and fetal malformation (29.41 percent), pre-eclampsia (26.47 percent), abruptio placenta and placenta previous (17.65 percent). There was a high incidence of antenatal admissions caused by entities that require early diagnosis and better management in order to lessen the economic impact and the serious repercussions hospital perinatal evidenced

[Experimental and pathological changes of the neuromuscular junction]. / Remaniements expérimentaux et pathologiques de la jonction neuromusculaire.

The objective of our study was to investigate the cellular communication between the axon and its postsynaptic targets in the synapse. We used the neuromuscular junction (NMJ) model, which is a highly specialized structure between the nerve, the muscle, and the Schwann cell terminal where the motor neuron orders the muscle to contract. We used experimental models of motor nerve reimplantation in a denervated muscle to determine whether 1) the formation of new NMJ could participate in reinnervation of the muscle necessary to contraction or 2) the blockage of neurotransmitter release using botulinum toxin could be compensated by the formation of new NMJ. We also studied human genetic diseases that affect neuromuscular transmission--congenital myasthenic syndromes--to identify the mutations in the genes coding for synaptic molecules and to analyze the compensatory processes involved in NMJ dysfunction so that muscle contraction can occur in these conditions.

Mutation causing congenital myasthenia reveals acetylcholine receptor beta/delta subunit interaction essential for assembly.

We describe a severe postsynaptic congenital myasthenic syndrome with marked endplate acetylcholine receptor (AChR) deficiency caused by 2 heteroallelic mutations in the beta subunit gene. One mutation causes skipping of exon 8, truncating the beta subunit before its M1 transmembrane domain, and abolishing surface expression of pentameric AChR. The other mutation, a 3-codon deletion (beta426delEQE) in the long cytoplasmic loop between the M3 and M4 domains, curtails but does not abolish expression. By coexpressing beta426delEQE with combinations of wild-type subunits in 293 HEK cells, we demonstrate that beta426delEQE impairs AChR assembly by disrupting a specific interaction between beta and delta subunits. Studies with related deletion and missense mutants indicate that secondary structure in this region of the beta subunit is crucial for interaction with the delta subunit. The findings imply that the mutated residues are positioned at the interface between beta and delta subunits and demonstrate contribution of this local region of the long cytoplasmic loop to AChR assembly.