Survival Following Veno-Venous Extracorporeal Membrane Oxygenation and Mortality in a Diverse Patient Population

Racial and ethnic disparities in cardiovascular disease are well established; however, there is limited information about survival differences following veno-venous extracorporeal membrane oxygenation (VV-ECMO) in contemporary adult populations. The purpose of this study was to assess survival at discharge, 30 days, and at 1 year following institution of VV-ECMO in an ethnically diverse population, and to examine potential risk factors for mortality. This was a single-center study of 41 patients (49% female, 27% minorities, 7% > 65 years) who received VV-ECMO between the years 2004 and 2013 at an academic medical center. Kaplan–Meier estimates were calculated to assess survival up to 1 year, and cox proportional hazard models were used to evaluate the association between risk factors, mortality, and confounders. Overall, 76% (n = 31) of VV-ECMO patients survived to discharge and 30 days and 71% (n = 29) survived to 1 year. Whites (n = 30) had a higher survival at 1 year compared to minorities (n = 11) (83% vs. 36%, respectively, p = .01). Minorities had a significantly increased risk of mortality at 30 days (hazard ratio [HR] = 5.07, 95% confidence interval [CI] = 1.42–18.09) and at 1 year (HR = 5.19, 95% CI = 1.63–16.55). Race/ethnicity remained a significant independent predictor of survival at 30 days except when history of shock or lung transplantation was included in adjusted regression models. VV-ECMO was associated with an excellent overall survival up to 1 year. Racial/ethnic minorities had a 5-fold increased risk for 30-day mortality, which was largely explained by a lower likelihood of lung transplantation and increased risk of shock

The skeleton : biochemical, genetic and molecular interactions in development and homeostasis. : Effects of boric acid on Hox gene expression and the axial skeleton in the developing rat.

Gestational exposure to boric acid (BA) causes reduced incidences of supernumerary ribs and shortening/absence of the 13th rib in the progeny of multiple laboratory species. To further explore this, Sprague-Dawley rats received 500 mg/kg b.i.d. on gestation days (GD) 6, 7, 8, 9, 10, or 11 (plug day = GD 0). GD-21 fetuses were stained for skeletal examination. BA's most noteworthy effects were apparent homeotic shifts in the axial skeleton; i.e., a given vertebra anatomically resembled an adjacent vertebra, thus leading to altered numbers of cervical, thoracic, or lumbar vertebrae. Whereas most groups generally had no such effect, about 90% of the GD-9 exposed fetuses had only six cervical vertebrae. Deficiencies in the C3-C5 region, C6, or C7 were observed in 67%, 1%, and 23% of the exposed fetuses, respectively. In contrast, GD-10 treatment caused agenesis of a thoracic/lumbar vertebra in over 60% of the fetuses. In these fetuses, the deficient region was usually T11. In view of the 90% incidence of six-cervical vertebrae in GD-9 exposed fetuses, we used this exposure regimen (500 mg/kg b.i.d. on GD 9) as an experimental model for the study of homeotic shifts. We sought to determine if these skeletal alterations could be explained by modifications of the hox code, involved in the establishment of positional information along the cranio-caudal axis of the embryo. Embryos were collected on GD 13.5 and processed for in situ hybridization. Several hox genes were selected according to the position of their cranial limit of expression in the cervical and thoracic region. A cranial shift in the cranial limit of expression of hoxc6 and hoxa6 was evident in the prevertebrae, whereas no difference was observed between control and treated embryos in the expression of hoxd4, hoxa4, hoxc5, and hoxa5. Anteriorization of the expression domain of hoxc6 and hoxa6 is consistent with the posterior transformation of cervical vertebrae, and may partially account for the phenotype observed on GD 21 in BA-exposed fetuses

Fertility of rat epididymal sperm after chemically and surgically induced sympathectomy

Guanethidine, a chemical that selectively blocks sympathetic noradrenergic neurons, was used to investigate the role of sympathetic innervation in the fertility of rat epididymal sperm, using both natural mating and in utero insemination protocols. This animal model correlates, at least in part, with spinal cord injury (SCI) in men. Adult male rats were treated daily by i.p. injections, for 21 or 42 days, with 0 or 6.25 mg/kg guanethidine. To compare the effects of guanethidine-induced sympathectomy with those following surgically induced sympathectomy, the inferior mesenteric ganglion and the proximal hypogastric nerves were removed in another group of rats. Both chemically and surgically induced sympathectomy increased the weight of the epididymis and seminal vesicles/coagulating glands as well as the number and the transit time of cauda epididymal sperm. Neither serum testosterone levels nor LH was affected by treatment with guanethidine. Using natural mating, no litters were produced by guanethidine-treated rats. Chemically denervated rats failed to produce copulatory plugs or ejaculate into the uterus. However, distal cauda epididymal sperm from chemically or surgically denervated rats displayed normal fertilization ability (80%) using in utero inseminations. In addition, the sperm of denervated rats did not show abnormal sperm chromatin structure using an assay that detects DNA damage. We conclude that sympathectomy delays the transit of sperm through the cauda epididymidis and produces ejaculatory dysfunction but does not compromise sperm quality in the distal cauda epididymidis. Moreover, these data provide compelling evidence that there is no association between the prolonged transit time of sperm within the epididymis, i.e., pre-ejaculatory sperm aging, and the fertility of those sperm, which has important implications for artificial insemination using sperm from men with SCI