Successful In Situ Growth of Conductive MOFs on 2D Cobalt-Based Compounds and Their Electrochemical Performance.

Conductive metal-organic frameworks (cMOFs), as a kind of porous material, are considered to be highly promising materials in the field of electrochemistry due to their excellent conductivity. However, due to the low specific capacitance of pure cMOFs, their application in supercapacitors is limited. By virtue of the high theoretical capacity and excellent chemical stability of Co-based compounds, in this work, cMOFs' M-HHTP (M = Ni, Co, NiCo, HHTP = 2,3,6,7,10,11-hexahydroxytriphenylene) are grown in situ on Co(OH)2, CoP, and Co3O4 nanosheets, resulting in a series of electroactive compounds as electrode materials used in supercapacitors. Among all of the compounds, Ni-HHTP@Co(OH)2 shows the most excellent energy storage performance and outstanding cyclic stability in the application of aqueous asymmetric supercapacitors.

Inhibition of Structural Transformation and Surface Lattice Oxygen Activity for Excellent Stability Li-Rich Mn-Based Layered Oxides.

Li-rich Mn-based layered oxides (LLOs) are one of the most promising cathode materials, which have exceptional anionic redox activity and a capacity that surpasses 250 mA h/g. However, the change from a layered structure to a spinel structure and unstable anionic redox are accompanied by voltage attenuation, poor rate performance, and problematic capacity. The technique of stabilizing the crystal structure and reducing the surface oxygen activity is proposed in this paper. A coating layer and highly concentrated oxygen vacancies are developed on the material's surface, according to scanning electron microscopy, transmission electron microscopy, and X-ray photoelectron spectroscopy. In situ EIS shows that structural transformation and oxygen release are inhibited during the first charge and discharge. Optimized 3@LRMA has an average attenuation voltage of 0.55 mV per cycle (vs 1.7 mV) and a capacity retention rate of 93.4% after 200 cycles (vs 52.8%). Postmortem analysis indicates that the successful doping of Al ions into the crystal structure effectively inhibits the structural alteration of the cycling process. The addition of oxygen vacancies reduces the surface lattice's redox activity. Additionally, surface structure deterioration is successfully halted by N- and Cl-doped carbon coating. This finding highlights the significance of lowering the surface lattice oxygen activity and preventing structural alteration, and it offers a workable solution to increase the LLO stability.

Cystathionine γ-lyase S-sulfhydrates SIRT1 to attenuate myocardial death in isoprenaline-induced heart failure.

OBJECTIVE: Hydrogen sulfide (H2S), the third gasotransmitter, plays a critical role in protecting against heart failure. Sirtuin-1 (SIRT1) is a highly conserved histone deacetylase that has a protective role in the treatment of heart failure by regulating the deacetylation of some functional proteins. This study investigates the interaction between SIRT1 and H2S in heart failure and the underlying mechanisms. METHODS AND RESULTS: Using endogenous H2S-generating enzyme cystathionine γ-lyase (CSE) knockout mice, we found that CSE deficiency aggravated isoprenaline-induced cardiac injury. Treatment with H2S attenuated atrial natriuretic peptide level, brain natriuretic peptide level, improved cardiac function. Moreover, H2S treatment potentiated myocardial SIRT1 expression. Silencing CSE abolished intracellular SIRT1 expression. Furthermore, CSE/ H2S S-sulfhydrated SIRT1 at its zinc finger domains and augmented its zinc ion binding activity to stabilize the alpha-helix structure. DISCUSSION: In conclusion, these results uncover that a novel mechanism that CSE/H2S S-sulfhydrated SIRT1 to prevent heart dysfunction through modulating its activity.

Enhanced Interfacial Kinetics and High Rate Performance of LiCoO2 Thin-Film Electrodes by Al Doping and In Situ Al2O3 Coating.

The structure and surface-interface instability of LiCoO2 thin-film electrodes during charge-discharge cycles are one of the main factors leading to the deterioration of electrochemical performance. Element doping and surface coating are effective strategies to tackle this issue. In this work, Al-doped and in situ Al2O3-coated LiCoO2 composite thin-film electrodes are prepared by magnetron sputtering. The results show that the resultant composite thin-film electrodes exhibited excellent cycling stability, with a discharge specific capacity of 40.2 µAh um-1 cm-2 after 240 cycles at 2.5 µA cm-2, with a capacity retention rate of 94.14%, compared to a discharge capacity of the unmodified sample of only 37.7 µAh um-1 cm-2 after 110 cycles, with a capacity retention rate of 80.04%. In addition, the rate performance of the prepared LiCoO2 film is significantly improved, and the discharge specific capacity of the Al-doped sample reaches 43.5 µAh um-1 cm-2 at 100 µA cm-2, which is 38.97% higher than that of the unmodified sample (31.3 µAh um-1 cm-2). The enhancement of electrochemical performance is mainly attributed to the synergistic effect of Al doping and in situ Al2O3 coating. The metal Al forms a conductive network in the film, while part of the Al will enter the LiCoO2 lattice to form a LiAl y Co1-y O2 solid solution, promoting the transport of lithium ions and improving the stability of the electrode structure. The in situ continuous deposition of the coating optimizes the active material coating-electrolyte interface.

Cardioprotective effects of hydrogen sulfide in attenuating myocardial ischemia­reperfusion injury (Review).

Ischemic heart disease is one of the major causes of cardiovascular­related mortality worldwide. Myocardial ischemia can be attenuated by reperfusion that restores the blood supply. However, injuries occur during blood flow restoration that induce cardiac dysfunction, which is known as myocardial ischemia­reperfusion injury (MIRI). Hydrogen sulfide (H2S), the third discovered endogenous gasotransmitter in mammals (after NO and CO), participates in various pathophysiological processes. Previous in vitro and in vivo research have revealed the protective role of H2S in the cardiovascular system that render it useful in the protection of the myocardium against MIRI. The cardioprotective effects of H2S in attenuating MIRI are summarized in the present review.

JAK2/STAT3 regulates estrogen-related senescence of bone marrow stem cells.

Emerging evidence has indicated that estrogen deficiency contributes to osteoporosis by affecting the level of inflammation. The inflammation microenvironment affects many cellular physiological processes, one of which may be cellular senescence according to previous studies. Senescent cells cannot function normally and secrete inflammatory cytokines and degradative proteins, which are referred to as senescence-associated secretory phenotype (SASP) factors, inducing further senescence and inflammation. Thus, stopping this vicious cycle may be helpful for postmenopausal osteoporosis treatment. Here, we used ovariectomized (OVX) mice as an estrogen-deficient model and confirmed that OVX bone marrow mesenchymal stem cells (BMSCs) displayed a senescent phenotype and upregulated SASP factor secretion both in vitro and in vivo. Furthermore, JAK2/STAT3, an important cytokine secretion-related signalling pathway that is associated with SASP secretion, was activated. Estrogen addition and estrogen receptor blockade confirmed that the JAK2/STAT3 axis participated in OVX BMSC senescence by mediating SASP factors. And JAK inhibition reduced SASP factor expression, alleviated senescence and enhanced osteogenic differentiation. Intraperitoneal injection of a JAK inhibitor, ruxolitinib, prevented bone loss in OVX mice. Collectively, our results revealed that JAK2/STAT3 plays an important role in the inflammation-senescence-SASP feedback loop in OVX BMSCs and that JAK inhibition could be a new method for treating postmenopausal osteoporosis.

miR-199a-3p is involved in estrogen-mediated autophagy through the IGF-1/mTOR pathway in osteocyte-like MLO-Y4 cells.

To date, evidence indicates that estrogen partially modulates cellular processes through microRNAs. Autophagy is a catabolic process that is regulated by multiple factors and is associated with skeletal diseases. However, whether estrogen regulates osteocyte autophagy via microRNAs is largely unknown. In this study, we observed the up-regulation of microRNA-199a-3p, a post-transcriptional regulatory factor, in osteocytic areas in ovariectomized (OVX) mice. The mature forms of miR-199a-3p and pri-miR-199a were produced in response to estrogen signaling in osteocyte-like MLO-Y4 cells. Western blotting, autophagic flux detection, mRFP-GFP-LC3 fluorescence, and electron microscopy confirmed that miR-199a-3p induced autophagy in MLO-Y4 cells, although cellular apoptosis was not affected. Additionally, we documented the ability of estrogen to mediate osteocyte autophagy. Based on our in vivo data, estrogen deficiency induced autophagy in osteocytes. Treatment of starved MLO-Y4 cells with 17ß-estradiol suppressed the excess autophagy induced by starvation via activation of mammalian target of rapamycin (mTOR)-related signaling cascades, while administration of rapamycin reversed the effects of 17ß-estradiol. Meanwhile, miR-199a-3p overexpression reversed 17ß-estradiol-mediated regulation of autophagy in MLO-Y4 cells. According to mechanistic studies, miR-199a-3p inhibited the mTOR pathway by directly binding to the 3'-untranslated regions of insulin growth factor-1 (IGF-1) and mTOR. However, overexpression of miR-199a-3p inhibited IGF-1 phosphorylation and mTOR-related pathways. Knockdown of mTOR and IGF-1 abolished estrogen signaling and restored LC3-II expression through mTOR re-activation, respectively. Thus, miR-199a-3p appears to be involved in the estrogen regulatory networks that mediate bone cell autophagy, potentially by targeting IGF-1 and mTOR.