An integrated, selective interlayer structure is developed to further mitigate the diffusion of polysulfides, simply by coating the surface of a C–S cathode with a graphene/TiO2 film. It is found that the application of the graphene/TiO2 film as an interlayer enables the porous carbon nanotubes–S cathode to exhibit a high reversible specific capacity and extraordinarily excellent cycling stability.

Molecular mechanisms underlying the role of statins in the induction of brain plasticity and subsequent improvement of neurologic outcome after treatment of stroke have not been adequately investigated. Here, we use both in vivo and in vitro studies to investigate the potential roles of two prominent factors, vascular endothelial growth factor (VEGF) and brain-derived neurotrophic factor (BDNF), in mediating brain plasticity after treatment of stroke with atorvastatin. Treatment of stroke in adult mice with atorvastatin daily for 14 days, starting at 24 hours after MCAO, shows significant improvement in functional recovery compared with control animals. Atorvastatin increases VEGF, VEGFR2 and BDNF expression in the ischemic border. Numbers of migrating neurons, developmental neurons and synaptophysin-positive cells as well as indices of angiogenesis were significantly increased in the atorvastatin treatment group, compared with controls. In addition, atorvastatin significantly increased brain subventricular zone (SVZ) explant cell migration in vitro. Anti-BDNF antibody significantly inhibited atorvastatin-induced SVZ explant cell migration, indicating a prominent role for BDNF in progenitor cell migration. Mouse brain endothelial cell culture expression of BDNF and VEGFR2 was significantly increased in atorvastatin-treated cells compared with control cells. Inhibition of VEGFR2 significantly decreased expression of BDNF in brain endothelial cells. These data indicate that atorvastatin promotes angiogenesis, brain plasticity and enhances functional recovery after stroke. In addition, VEGF, VEGFR2 and BDNF likely contribute to these restorative processes.

Background and Purpose-We tested the hypothesis that sildenafil, a phosphodiesterase type 5 (PDE5) inhibitor, promotes functional recovery and neurogenesis after stroke. Methods-Male Wistar rats were subjected to embolic middle cerebral artery occlusion. Sildenafil (Viagra) was administered orally for 7 consecutive days starting 2 or 24 hours after stroke onset at doses of 2 or 5 mg/kg per day. Ischemic rats administered the same volume of tap water were used as a control group. Functional outcome tests (foot-fault, adhesive removal) were performed. Rats were killed 28 days after stroke for analysis of infarct volume and newly generated cells within the subventricular zone and the dentate gyrus. Brain cGMP levels, expression of PDE5, and localized cerebral blood flow were measured in additional rats. Results-Treatment with sildenafil significantly (PϽ0.05) enhanced neurological recovery in all tests performed. There was no significant difference of infarct volume among the experimental groups. Treatment with sildenafil significantly (PϽ0.05) increased numbers of bromodeoxyuridine-immunoreactive cells in the subventricular zone and the dentate gyrus and numbers of immature neurons, as indicated by ␤III-tubulin (TuJ1) immunoreactivity in the ipsilateral subventricular zone and striatum. The cortical levels of cGMP significantly increased after administration of sildenafil, and PDE5 mRNA was present in both nonischemic and ischemic brain. Conclusions-Sildenafil increases brain levels of cGMP, evokes neurogenesis, and reduces neurological deficits when given to rats 2 or 24 hours after stroke. These data suggest that this drug that is presently in the clinic for sexual dysfunction may have a role in promoting recovery from stroke.

Intravenous administration of human bone marrow stromal cells (hMSCs) after middle cerebral artery occlusion (MCAo) in rats provides functional benefit. We tested the hypothesis that these functional benefits are derived in part from hMSC production of growth and trophic factors. Quantitative sandwich enzyme-linked immunosorbent assay (ELISA) of hMSCs cultured with normal and MCAo brain extracts were performed. hMSCs cultured in supernatant derived from ischemic brain extracts increased production of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF). These neurotrophins and angiogenic growth factors increased in a post-ischemia time-dependent manner. The hMSC capacity to increase expression of growth and trophic factors may be the key to the benefit provided by transplanted hMSCs in the ischemic brain.

The oxygen evolution reaction (OER) is a key reaction for many electrochemical devices. To date, many OER electrocatalysts function well in alkaline media, but exhibit poor performances in neutral and acidic media, especially the acidic stability. Herein, sodium‐decorated amorphous/crystalline RuO2 with rich oxygen vacancies (a/c‐RuO2) was developed as a pH‐universal OER electrocatalyst. The a/c‐RuO2 shows remarkable resistance to acid corrosion and oxidation during OER, which leads to an extremely high catalytic stability, as confirmed by a negligible overpotential increase after continuously catalyzing OER for 60 h at pH=1. Besides, a/c‐RuO2 also exhibits superior OER activities to commercial RuO2 and most reported OER catalysts under all pH conditions. Theoretical calculations indicated that the introduction of Na dopant and oxygen vacancy in RuO2 weakens the adsorption strength of the OER intermediates by engineering the d‐band center, thereby lowering the energy barrier for OER.

In this communication, we have demonstrated that SiO(2) nanoparticles can be generated by simply scratching the quartz or silicon wafer with a SiO(2) layer and confirmed it to be active for the growth of SWNTs for the first time. Furthermore, the SWNTs from SiO(2) has a much narrower size distribution. This may open a way to control the diameter of the SWNTs. More importantly, our work has found a series of oxides including Al(2)O(3), TiO(2), and rare earth oxides to be active for SWNT growth as well. These findings not only provide an alternative new type of catalysts for the growth of SWNTs but also give more insight into the role of the catalysts and a deeper understanding of the growth mechanism of SWNTs. The effective catalysts and catalytic activity for SWNT growth seem to be more size-dependent than the catalysts. Long oriented SWNTs generated from these catalysts enable us to rule out the relationship between the catalysts and the structures of the SWNTs. Thus controlled growth of SWNTs including the diameter and chirality is expected to be eventually realized.

Severe immunological damage in lung tissue is responsible for the clinical features of SARS.

Treatment of traumatic brain injury (TBI) with bone marrow stromal cells (MSCs) improves functional outcome in the rat. However, the specific mechanisms by which introduced MSCs provide benefit remain to be elucidated. Currently, the ability of therapeutically transplanted MSCs to replace injured parenchymal CNS tissue appears limited at best. Tissue replacement, however, is not the only possible compensatory avenue in cell transplantation therapy. Various growth factors have been shown to mediate the repair and replacement of damaged tissue, so trophic support provided by transplanted MSCs may play a role in the treatment of damaged tissue. We therefore investigated the temporal profile of various growth factors, brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and hepatocyte growth factor (HGF), within cultures of human MSCs (hMSCs) conditioned with cerebral tissue extract from TBI. hMSCs were cultured with TBI extracts of rat brain in vitro and quantitative sandwich enzyme-linked immunosorbent assays (ELISAs) were performed. TBI-conditioned hMSCs cultures demonstrated a time-dependent increase of BDNF, NGF, VEGF, and HGF, indicating a responsive production of these growth factors by the hMSCs. The ELISA data suggest that transplanted hMSCs may provide therapeutic benefit via a responsive secretion of an array of growth factors that can foster neuroprotection and angiogenesis.