The protective effect of RES against DOX-induced cardiomyocyte apoptosis is associated with the up-regulation of SIRT1-mediated p53 deacetylation.

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Currently, because of higher theoretical capacity compared with other materials, the research of Fe2O3 as an anode electrode material for lithium-ion batteries (LIBs) has been widely reported. By using a microwave-assisted-template method, the Fe-based metal–organic framework (Fe-MIL-88A) material with a spindle-like morphology was prepared by a microwave-assisted method. Via the one-step pyrolysis of Fe-MIL-88A-MW (microwave-assisted synthesis) in air, uniform Fe2O3-MW-4h nanoparticles with a multicavity structure were obtained. The influence of microwave holding time on the formation of internal cavity in Fe-MIL-88A-MW-derived Fe2O3 nanoparticles was investigated. The resulting Fe2O3-MW-4h nanoparticles exhibit the unique advantages of nanomaterials, with a high surface area and large pore volume. These features facilitate the movement of the electrolyte and reduce the resistance of the material. Most importantly, the multicavity structure of Fe2O3-MW-4h nanoparticles could reduce the volume change during the Li+ insertion and extraction process. When materials were used as anode materials for LIBs, the Fe2O3-MW-4h nanoparticles exhibit excellent electrochemical performance. Therefore, the microwave-assisted-template method is promising in manufacturing metal oxides with multicavity structures for the next generation of LIB anode electrode materials.

Petroclival meningiomas (PCMs) are regarded as one of the most formidable challenges in neurosurgery. We retrospectively assessed the surgical outcomes of PCMs based on a tumor classification to evaluate the long-term outcomes. A series of 168 patients with PCMs from July 1996 to January 2017. On the basis of the difference in the origin of dural attachment and patterns of growth, the PCMs were classified into 4 different types. The clinical characteristics, surgical record, and follow-up data of each type were reviewed. The study included 138 females (82.1%) with an average age of 49.9 ± 16.2 years. And 138 cases (82.1%) had developed neurological deficits preoperatively with the average tumor size of 44.0 ± 10.6 mm. Specific surgical approaches were applied depended on the tumor classification. Gross total resection (GTR) was achieved in 119 cases (70.8%) with the complications of 46 cases (27.7%). With a median follow-up of 86.5 months, there were 41 cases of recurrence/progress (25.7%) and 39 cases of morbidity (26.4%). Compared with the non-GTR group, the GTR significantly decreased the R/P rate (P = 0.001), prolonged the R/P-FS time (P = 0.032) and improved the follow-up neurological status (P = 0.026). Favorable outcomes and acceptable morbidity were achieved with the treatment strategy of the choice of specific approaches for each type. Meanwhile, the differences of each type in diverse clinical characteristic were verified. Individualized assessment and suitable approach choice should be based on the tumor classification to improved the GTR and quality of life for patients.

Heat shock proteins (HSPs) play important roles in cellular stress resistance. Previous reports had already suggested that HSP27 played multiple roles in preventing doxorubicin-induced cardiotoxicity. Although HSP25 might have biological functions similar to its human homolog HSP27, the mechanism of HSP25 is still unclear in doxorubicin-induced cardiomyocyte apoptosis. To investigate HSP25 biological function on doxorubicin-induced apoptosis, flow cytometry was employed to analyze cell apoptosis in over-expressing HSP25 H9c2 cells in presence of doxorubicin. Unexpectedly, the H9c2 cells of over-expressing HSP25 have no protective effect on doxorubicin-induced apoptosis. Moreover, no detectable interactions were detected by coimmunoprecipitation between HSP25 and cytochrome c, and HSP25 over-expression failed in preventing cytochrome c release induced by doxorubicin. However, down-regulation of endogenous HSP25 by a specific small hairpin RNA aggravates apoptosis in H9c2 cells. Subsequent studies found that HSP25, but not HSP90, HSP70, and HSP20, interacted with SIRT1. Knockdown of HSP25 decreased the interaction between SIRT1 and p53, leading to increased p53 acetylation on K379, up-regulated pro-apoptotic Bax protein expression, induced cytochrome c release, and triggered caspase-3 and caspase-9 activation. These findings indicated a novel mechanism by which HSP25 regulated p53 acetylation through dissociation of SIRT1 from p53 in doxorubicin-induced H9c2 cell apoptosis.

Cardiomyocytes can resist ischemia/reperfusion (I/R) injury through ischemic postconditioning (IPoC) which is repetitive ischemia induced during the onset of reperfusion. Myocardial ischemic preconditioning up-regulated protein 2 (MIP2) is a member of the WD-40 family proteins, we previously showed that MIP2 was up-regulated during ischemic preconditioning (IPC). As IPC and IPoC engaged similar molecular mechanisms in cardioprotection, this study aimed to elucidate whether MIP2 was up-regulated during IPoC and contributed to IPoC-mediated protection against I/R injury. The experiment was conducted on two models, an in vivo open chest rat coronary artery occlusion model and an in vitro model with H9c2 myogenic cells.In both models, 3 groups were constituted and randomly designated as the sham, I/R and IPoC/hypoxia postconditioning (HPoC) groups. In the IPoC group, after 45 min of ischemia, hearts were allowed three cycles of reperfusion/ischemia phases (each of 30 s duration) followed by reperfusion. In the HPoC group, after 6 h of hypoxia, H9c2 cells were subjected to three cycles of 10 minute reoxygenation and 10 minute hypoxia followed by reoxygenation. IPoC significantly reduced the infarct size, plasma level of Lactate dehydrogenase and creatine kinase MB in rats. 12 h after the reperfusion, MIP2 mRNA levels in the IPoC group were 10 folds that of the sham group and 1.4 folds that of the I/R group. Increased expression of MIP2 mRNA and attenuation of apoptosis were similarly observed in the HPoC group in the in vitro model. These effects were blunted by transfection with MIP2 siRNA in the H9c2 cells. This study demonstrated that IPoC induced protection was associated with increased expression of MIP2. Both MIP2 overexpression and MIP2 suppression can influence the IPoC induced protection.

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