Co3O4 nanocage derived from metal-organic frameworks: An excellent cathode catalyst for rechargeable Li-O2 battery

Rechargeable non-aqueous Li-O2 battery is regarded as one of the most promising energy-storage technologies on account of its high energy density.It is believed that the rational design of three-dimensional (3D) architecture for catalyst is a key factor for the remarkable performance.Metal-organic frameworks (MOFs) derived materials possess excellent architecture,which is beneficial for Li-O2 batteries.In this work,ZIF-67 is used as precursor template and calcinated under different temperature to produce Co3O4 crystals.When the anneal treatment is under 350℃,the derived Co3O4 nanocage holds the most complete skeleton,which provides better charge transfer ability as well as O2 and Li^+ diffusion.Meanwhile,the Co3O4 nanocage owns more oxygen vacancies,offering more active sites.With the synergistic effect of nanocage structure and active sites,the Co3O4 nanocage stably delivers a large specific capacity of 15,500 mAh·g^-1 as well as a long cycle-life of 132 cycles at limited discharge capacity of 1,000 mAh·g^-1 under discharge/charge current density of 0.5 A·g^-1.

Cardiac fibroblast heat shock protein 47 aggravates cardiac fibrosis post myocardial ischemia-reperfusion injury by encouraging ubiquitin specific peptidase 10 dependent Smad4 deubiquitination

Despite complications were significantly reduced due to the popularity of percutaneous coronary intervention(PCI) in clinical trials, reperfusion injury and chronic cardiac remodeling significantly contribute to poor prognosis and rehabilitation in AMI patients. We revealed the effects of HSP47 on myocardial ischemia-reperfusion injury(IRI) and shed light on the underlying molecular mechanism.We generated adult mice with lentivirus-mediated or miRNA(mi1/133TS)-aided cardiac fibroblastselective HSP47 overexpression. Myocardial IRI was induced by 45-min occlusion of the left anterior descending(LAD) artery followed by 24 h reperfusion in mice, while ischemia-mediated cardiac remodeling was induced by four weeks of reperfusion. Also, the role of HSP47 in fibrogenesis was evaluated in cardiac fibroblasts following hypoxia-reoxygenation(HR). Extensive HSP47 was observed in murine infarcted hearts, human ischemic hearts, and cardiac fibroblasts and accelerated oxidative stress and apoptosis after myocardial IRI. Cardiac fibroblast-selective HSP47 overexpression exacerbated cardiac dysfunction caused by chronic myocardial IRI and presented deteriorative fibrosis and cell proliferation.HSP47 upregulation in cardiac fibroblasts promoted TGFβ1-Smad4 pathway activation and Smad4 deubiquitination by recruiting ubiquitin-specific peptidase 10(USP10) in fibroblasts. However, cardiac fibroblast specific USP10 deficiency abolished HSP47-mediated fibrogenesis in hearts. Moreover, blockage of HSP47 with Col003 disturbed fibrogenesis in fibroblasts following HR. Altogether, cardiac fibroblast HSP47 aggravates fibrosis post-myocardial IRI by enhancing USP10-dependent Smad4 deubiquitination,which provided a potential strategy for myocardial IRI and cardiac remodeling.

The RIP3-RIP1-NF-κB signaling axis is dispensable for necroptotic cells to elicit cross-priming of CD8^(+) T cells

Apoptosis and necroptosis are two types of programmed cell death with distinct morphological features.Necroptosis has been assumed to be more inflammatory than apoptosis,but a recent paper1 concluded that necroptotic cells cannot elicit cross-priming of CD8^(+)T cells and that NF-κB activation in necroptotic cells is required for maximal CD8^(+)T-cell cross-priming.