No abstract

The present study reveals that inhalation of 80 ppm H(2)S reduced neurohistopathological damage and improves early neurological function after CA and resuscitation in rabbits. The increased CEO(2) and decreased AJVD(glu) and enhanced lactate clearance may be involved in the protective effects.

Atrial septal defect (ASD) is one of the most prevalent types of congenital heart disease (CHD). The pathogenic role of miRNAs in the development of ASD has not yet been fully elucidated. The aim of this study was to examine the miRNA profile of ASD patients, and to identify the role of miRNAs in the pathogenesis of ASD. We performed a miRNA comparison between the atrial septa of three normal fetuses and three ASD patients by microarray, followed by chromosome clustering and bioinformatic analysis to identify the dysregulated miRNA clusters between these two groups. Furthermore, qRT-PCR in the mouse developing heart was used to exclude differences resulting from the use of unpaired stage patient samples. After normalization, 70 dysregulated miRNAs were detected between the two groups. Advanced chromosome clustering and bioinformatic analysis showed that two upregulated miRNA clusters (miR-29 and miR-143/145) and three downregulated miRNA clusters (miR-17-92, miR-106b-25 and miR-503/424) were associated with ASD. Further qRT-PCR in the mouse developing heart found that the dysregulated expression levels of all the clusters, except the miR-143/145 cluster, were associated with the occurrence of ASD. This study reveals four dysregulated miRNA clusters, which will enable further elucidation of the pathogenic mechanism of ASD.

Background Mitochondrial dysfunction results in poor organ quality, negatively affecting the outcomes of lung transplantation. Whether hydrogen benefits mitochondrial function in cold-preserved donors remain unclear. The present study assessed the effect of hydrogen on mitochondrial dysfunction in donor lung injury during cold ischemia phase (CIP) and explored the underlying regulatory mechanism. Methods Left donor lungs were inflated using 40% oxygen + 60% nitrogen (O group), or 3% hydrogen + 40% oxygen + 57% nitrogen (H group). Donor lungs were deflated in the control group and were harvested immediately after perfusion in the sham group (n = 10). Inflammation, oxidative stress, apoptosis, histological changes, mitochondrial energy metabolism, and mitochondrial structure and function were assessed. The expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were also analyzed. Results Compared with the sham group, inflammatory response, oxidative stress, histopathological changes, and mitochondrial damage were severe in the other three groups. However, these injury indexes were remarkably decreased in O and H groups, with increased Nrf2 and HO-1 levels, elevated mitochondrial biosynthesis, inhibition of anaerobic glycolysis and restored mitochondrial structure and function compared with the control group. Moreover, inflation using hydrogen contributed to stronger protection against mitochondrial dysfunction and higher levels of Nrf2 and HO-1 when comparing with O group. Conclusions Lung inflation using hydrogen during CIP may improve donor lung quality by mitigating mitochondrial structural anomalies, enhancing mitochondrial function, and alleviating oxidative stress, inflammation, and apoptosis, which may be achieved through activation of the Nrf2/HO-1 pathway.