The effects of hydrogen sulfide (H 2 S) on blood-brain barrier (BBB) and brain edema after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) remain poorly understood. We investigated the effects of exogenous 80-p.p.m. H 2 S gas on BBB, brain water content, neurologic outcome, and survival rate after CA and CPR. Cardiopulmonary resuscitation followed CA induced in rats by ventricular fibrillation for 6 minutes. Results show that inhalation of 80-p.p.m. H 2 S significantly reduced the permeability of the BBB in both in the cortex and hippocampus at 24 hours after resuscitation. Hydrogen sulfide also lessened brain edema in the cortex and hippocampus, ameliorated neurologic outcome as evaluated by neurologic deficit score and tape removal test, and improved the 14-day survival rate. Hydrogen sulfide also attenuated CA and CPR-induced increases of matrix metalloproteinase-9 (MMP-9) activity and vascular endothelial growth factor (VEGF) expression, and increased the expression of angiogenin-1 (Ang-1). These results indicate that inhalation of 80-p.p.m. H 2 S immediately after CPR attenuated BBB permeability and brain edema, and improved neurologic outcome and 14-day survival of rats after CA. The therapeutic benefits of H 2 S could be associated with suppression of MMP-9 and VEGF expression and increased expression of Ang-1.

Uncultivable microorganisms account for over 99% of all species on the planet, but their functions are yet not well characterized. Though many cultivable degraders for n-alkanes have been intensively investigated, the roles of functional n-alkane degraders remain hidden in the natural environment. This study introduces the novel magnetic nanoparticle-mediated isolation (MMI) technology in Nigerian soils and successfully separates functional microbes belonging to the families Oxalobacteraceae and Moraxellaceae, which are dominant and responsible for alkane metabolism in situ. The alkR-type n-alkane monooxygenase genes, instead of alkA- or alkP-type, were the key functional genes involved in the n-alkane degradation process. Further physiological investigation via a BIOLOG PM plate revealed some carbon (Tween 20, Tween 40 and Tween 80) and nitrogen (tyramine, l-glutamine and d-aspartic acid) sources promoting microbial respiration and n-alkane degradation. With further addition of promoter carbon or nitrogen sources, the separated functional alkane degraders significantly improved n-alkane biodegradation rates. This suggests that MMI is a promising technology for separating functional microbes from complex microbiota, with deeper insight into their ecological functions and influencing factors. The technique also broadens the application of the BIOLOG PM plate for physiological research on functional yet uncultivable microorganisms.

This is an Open Access article licensed under the terms of the Creative Commons AttributionNonCommercial 3.0 Unported license (CC BY-NC) (www.karger.com/OA-license), applicable to the online version of the article only. Distribution permitted for non-commercial purposes only. AbstractBackground/Aims: The effects of H 2 S on cerebral inflammatory reaction after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) remain poorly understood. In this study, we investigated the effects of exogenous 40 ppm and 80 ppm H 2 S gas on inflammatory reaction and neurological outcome after CA/CPR. Methods: CA was induced by ventricular fibrillation and followed by CPR. Forty or 80 ppm H 2 S was inhaled for 1 h immediately following CPR. The levels of IL-1β, IL-6 and TNF-α, the myeloperoxidase (MPO) activity, the expression of iNOS and ICAM-1, and the phosphorylation and translocation of NF-κB were evaluated at 24 h after CA/ CPR. The tape removal test, survival rate and hippocampal neuronal counts were investigated at 14 d after CA/CPR. Results: CA/CPR induced significant increases in IL-1β, IL-6, TNF-α and MPO activity. The phosphorylation and translocation of NF-κB, and the expression of iNOS and ICAM-1 were increased significantly. Inhalation of 40 or 80 ppm H 2 S gas decreased these inflammatory cytokines. Furthermore, 40 or 80 ppm H 2 S inhibited the activation of NF-κB and the downstream proinflammatory mediators iNOS and ICAM-1. H 2 S inhalation also improved neurological function, 14-d survival rate, and reduced hippocampal neuronal loss. Conclusion: These results indicated that inhalation of H 2 S protected against brain injury after CA/CPR. The mechanisms underlying protective effects of H 2 S were associated with the inhibition of CA/ CPR-induced inflammation reactions by reducing IL-1β, IL-6 and TNF-α, and concomitantly inhibiting the activation and infiltration of neutrophils. The beneficial effects of H 2 S might be mediated by downregulation of NF-κB and the downstream proinflammatory signaling pathway.

Background/Aims: Hydrogen sulfide (H₂S) can decrease blood-brain barrier (BBB) permeability after cardiac arrest (CA) and resuscitation; however, the underlying mechanisms are not understood clearly. Methods: We investigated the effects of inhalation of H₂S on CA and resuscitation in a rat model of CA. We used Evans blue to detect the integrity of BBB and Western blot to assess the activation of protein kinase c (PKC) isozymes and the expression of Claudin-5, Occludin, and ZO-1. Neurological deficit scales and the 14-days survival rate were measured. Results: We determined that inhalation of 40 p.p.m or 80 p.p.m H₂S significantly decreased brain water content and Evans blue leakage, ameliorated neurologic deficit scale and improved 14-days survival rate. H₂S inhibited the activation of PKC-α, β I, β II and δ, impelled the activation of PKC-ε, and increased the expression of Claudin-5, Occludin and ZO-1. Conclusions: H₂S improved the integrity of BBB, mitigated brain edema; improved neurological outcome and 14-days survival rate in rats after CA and resuscitation. The beneficial effects of H₂S may be associated with inhibiting the activation of PKC-α, β I, β II and δ, promoting the activation of PKC-ε, and increasing the expression of Claudin-5, Occludin and ZO-1.