Immediate postpartum glycemic control and risk of surgical site infection.

OBJECTIVE: Nearly one-third of all births in the United States in 2013 were by cesarean delivery, with 6% complicated by diabetes. The purpose of this study was to correlate immediate postoperative hyperglycemia with wound morbidity in diabetic women who underwent cesarean delivery. METHODS: This retrospective case-control study was performed at UC Irvine Health and Miller Women's & Children's Hospital Long Beach between 2009 and 2015. Subjects included women with at least Class B diabetes mellitus who underwent cesarean birth. Fasting and postprandial blood glucose levels (BGL) were recorded daily during postoperative days one through four. Outcomes included abscess formation, cellulitis, wound separation, fascial dehiscence, hospital readmission, secondary wound closure, antibiotic treatment, and a composite of the above. RESULTS: Outcomes were evaluated for 176 subjects. Twenty-nine experienced wound complications. Women readmitted for wound complications and those with composite morbidity experienced significantly higher mean fasting BGL, however, BGL during the immediate postoperative setting were not predictive of wound morbidity. CONCLUSION: In our cohort of diabetic women who underwent cesarean delivery, immediate postoperative hyperglycemia was not associated with wound morbidity.

Prenatally Diagnosed Vasa Previa: A Single-Institution Series of 96 Cases.

OBJECTIVE: To describe outcomes for a large cohort of women with prenatally diagnosed vasa previa, determine the percentage in patients without risk factors, and compare delivery timing and indications for singletons and twins. METHODS: This was a retrospective case series of women with prenatally diagnosed vasa previa delivered at a single tertiary center over 12 years. Potential participants were identified using hospital records and perinatal databases. Patients were included if vasa previa was confirmed at delivery and by pathologic examination. Maternal and newborn data were gathered from medical records. RESULTS: There were 77 singleton and 19 twin pregnancies with a prenatal diagnosis of vasa previa. There was one neonatal death from congenital heart disease. Perinatal management of recommended elective hospitalizations with corticosteroid administration and elective early delivery resulted in average gestational age for delivery in singletons at 34.7±1.6 weeks and 32.8±2.2 weeks for twins. Among the 77 singletons, delivery was elective in 48, as a result of contractions or labor in 21, bleeding in four, nonreassuring tracing in two, asymptomatic cervical shortening in one, and preeclampsia in one. Among 19 twins, delivery was elective in six and for contractions or labor in 13. Sixty-eight percent of twins compared with 37% of singletons had nonelective delivery (P<.05). Delivery occurred by 32 weeks of gestation in 6.4% of singletons and 26% of twins (P<.05) and by 34 weeks of gestation in 11% of singletons and 58% of twins (P<.001). Six neonates (5.2%) had major anomalies, all prenatally detected. Respiratory distress syndrome occurred in 57.1% of singletons and 65.7% of twins. Nineteen singletons (24.7%) had no risk factors for vasa previa. CONCLUSION: Planned preterm delivery for women with prenatally diagnosed vasa previa resulted in elective delivery for singletons in 62% and for twins 32%. Gestational age at birth on average was 34.7 weeks for singletons and 32.8 weeks of gestation for twins. Major anomalies were frequent as was respiratory distress syndrome. Elective delivery between 34 and 35 weeks of gestation for singletons is reasonable. As a result of the high rate of nonelective delivery in twins, delivery at 32-34 weeks of gestation may be risk-beneficial. The high rate of singletons without risk factors for vasa previa reinforces the recommendation to screen routinely for cord insertion site.

S-nitrosylation of cofilin-1 mediates estradiol-17ß-stimulated endothelial cytoskeleton remodeling.

Rapid nitric oxide (NO) production via endothelial NO synthase (eNOS) activation represents a major signaling pathway for the cardiovascular protective effects of estrogens; however, the pathways after NO biosynthesis that estrogens use to function remain largely unknown. Covalent adduction of a NO moiety to cysteines, termed S-nitrosylation (SNO), has emerged as a key route for NO to directly regulate protein function. Cofilin-1 (CFL1) is a small actin-binding protein essential for actin dynamics and cytoskeleton remodeling. Despite being identified as a major SNO protein in endothelial cells, whether SNO regulates CFL-1 function is unknown. We hypothesized that estradiol-17ß (E2ß) stimulates SNO of CFL1 via eNOS-derived NO and that E2ß-induced SNO-CFL1 mediates cytoskeleton remodeling in endothelial cells. Point mutation studies determined Cys80 as the primary SNO site among the 4 cysteines (Cys39/80/139/147) in CFL1. Substitutions of Cys80 with Ala or Ser were used to prepare the SNO-mimetic/deficient (C80A/S) CFL1 mutants. Recombinant wild-type (wt) and mutant CFL1 proteins were prepared; their actin-severing activity was determined by real-time fluorescence imaging analysis. The activity of C80A CFL1 was enhanced to that of the constitutively active S3/A CFL1, whereas the other mutants had no effects. C80A/S mutations lowered Ser3 phosphorylation. Treatment with E2ß increased filamentous (F)-actin and filopodium formation in endothelial cells, which were significantly reduced in cells overexpressing wt-CFL. Overexpression of C80A, but not C80S, CFL1 decreased basal F-actin and further suppressed E2ß-induced F-actin and filopodium formation compared with wt-CFL1 overexpression. Thus, SNO(Cys80) of cofilin-1 via eNOS-derived NO provides a novel pathway for mediating estrogen-induced endothelial cell cytoskeleton remodeling.

Antimyoclonic and neuroprotective effects of lamotrigine in an animal model of cardiac arrest.

A major consequence of severe cardiac arrest is impairment of neurological functions. Posthypoxic myoclonus and seizures are two of the major neurological problems following ischemic and hypoxic insults. This condition affects motor function to different degrees of severity ranging from mild to serious debilitation. The pathophysiological mechanism(s) associated with these neurological conditions remain elusive. Glutamate-mediated neuronal overexcitation is thought to play a major role in the neuronal damage and in the neurological consequences of the posthypoxic state. Therefore, lamotrigine, a new anticonvulsant that indirectly modulates glutamatergic neurotransmission by interfering with voltage-dependent sodium channels, was tested for its effectiveness in controlling the neurological and histopathological changes in the animal model of cardiac arrest-induced myoclonus. Lamotrigine dose-dependently attenuated the audiogenic seizures and action myoclonus seen in this rat model. Histological analysis using Nissl staining and the novel Fluoro-Jade histochemistry in cardiac-arrested rats showed an extensive neuronal degeneration in the hippocampus and cerebellum. Lamotrigine treatment significantly attenuated the neuronal degeneration in these brain areas. The neuroprotective effect was more pronounced in hippocampal pyramidal and cerebellar Purkinje neurons. The therapeutic window of lamotrigine in this model was 8 hours. These results suggest that lamotrigine can be viewed as a potential antimyoclonic and neuroprotective agent for the treatment of posthypoxic myoclonus and seizures. The study also suggests that neuronal hyperexcitability may play a role in the etiology of posthypoxic myoclonus and seizure.