基于高阶思维能力的物理化学STS习题设计与实践——以“热力学基本定律”为例

在高等教育高质量、现代化发展的趋势下,对学生高阶思维能力的培养成为高等教育发展的重要方向。本文在对高阶思维能力与STS(Science,Technology,Society)教育内涵理解的基础上,梳理STS习题中实物条件、数量条件、特征条件、闲置条件等已知条件与高阶思维能力培养的关系,设计物理化学STS习题。以热力学基本定律为例,结合教学目标、学情、高阶思维能力培养的STS习题设计规划,建立其知识点与STS教育结合的双向明细表,考虑习题题型和难度,采用习题的筛选、改编、自编形式进行STS习题设计,并应用于物理化学教学实践,促使学生高阶思维能力的提升,为物理化学习题内容、形式的改进提供了新思路。

Exosomes secreted from cardiomyocytes suppress the sensitivity of tumor ferroptosis in ischemic heart failure

Heart failure(HF)patients in general have a higher risk of developing cancer.Several animal studies have indicated that cardiac remodeling and HF remarkably accelerate tumor progression,highlighting a cause-and-effect relationship between these two disease entities.Targeting ferroptosis,a prevailing form of non-apoptotic cell death,has been considered a promising therapeutic strategy for human cancers.Exosomes critically contribute to proximal and distant organ-organ communications and play crucial roles in regulating diseases in a paracrine manner.However,whether exosomes control the sensitivity of cancer to ferroptosis via regulating the cardiomyocyte-tumor cell crosstalk in ischemic HF has not yet been explored.Here,we demonstrate that myocardial infarction(MI)decreased the sensitivity of cancer cells to the canonical ferroptosis activator erastin or imidazole ketone erastin in a mouse model of xenograft tumor.Post-MI plasma exosomes potently blunted the sensitivity of tumor cells to ferroptosis inducers both in vitro in mouse Lewis lung carcinoma cell line LLC and osteosarcoma cell line K7M2 and in vivo with xenograft tumorigenesis model.The expression of miR-22-3p in cardiomyocytes and plasma-exosomes was significantly upregulated in the failing hearts of mice with chronic MI and of HF patients as well.Incubation of tumor cells with the exosomes isolated from post-MI mouse plasma or overexpression of miR-22-3p alone abrogated erastin-induced ferroptotic cell death in vitro.Cardiomyocyte-enriched miR-22-3p was packaged in exosomes and transferred into tumor cells.Inhibition of cardiomyocyte-specific miR-22-3p by AAV9 sponge increased the sensitivity of cancer cells to ferroptosis.ACSL4,a pro-ferroptotic gene,was experimentally established as a target of miR-22-3p in tumor cells.Taken together,our findings uncovered for the first time that MI suppresses erastin-induced ferroptosis through releasing miR-22-3p-enriched exosomes derived from cardiomyocytes.Therefore,targeting exosome-mediated cardiomyocyte/tumor pathological communication may offer a novel approach for the ferroptosis-based antitumor therapy.

Mettl13 protects against cardiac contractile dysfunction by negatively regulating C-Cbl-mediated ubiquitination of SERCA2a in ischemic heart failure

Ischemic heart failure(HF)remains a leading cause of morbidity and mortality.Maintaining homeostasis of cardiac function and preventing cardiac remodeling deterioration are critical to halting HF progression.Methyltransferase-like protein 13(Mettl13)has been shown to regulate protein translation efficiency by acting as a protein lysine methyltransferase,but its role in cardiac pathology remains unexplored.This study aims to characterize the roles and mechanisms of Mettl13 in cardiac contractile function and HF.We found that Mettl13 was downregulated in the failing hearts of mice post-myocardial infarction(MI)and in a cellular model of oxidative stress.Cardiomyocyte-specific overexpression of Mettl13 mediated by AAV9-Mettl13 attenuated cardiac contractile dysfunction and fibrosis in response to MI,while silencing of Mettl13 impaired cardiac function in normal mice.Moreover,Mettl13 overexpression abrogated the reduction in cell shortening,Ca^(2+)transient amplitude and SERCA2a protein levels in the cardiomyocytes of adult mice with MI.Conversely,knockdown of Mettl13 impaired the contractility of cardiomyocytes,and decreased Ca^(2+)transient amplitude and SERCA2a protein expression in vivo and in vitro.Mechanistically,Mettl13 impaired the stability of c-Cbl by inducing lysine methylation of c-Cbl,which in turn inhibited ubiquitination-dependent degradation of SERCA2a.Furthermore,the inhibitory effects of knocking down Mettl13 on SERCA2a protein expression and Ca^(2+)transients were partially rescued by silencing c-Cbl in H_(2)O_(2)-treated cardiomyocytes.In conclusion,our study uncovers a novel mechanism that involves the Mettl13/c-Cbl/SERCA2a axis in regulating cardiac contractile function and remodeling,and identifies Mettl13 as a novel therapeutic target for ischemic HF.

Hydrothermal growth of hydroxyapatite and ZnO bilayered nanoarrays on magnesium alloy surface with antibacterial activities

Magnesium alloy(MgA)has been extensively used as orthopedic and cardiovascular scaffolds in virtue of its good biocompatibility,unique biodegradability and excellent mechanical properties.However,poor corrosion resistance and easy infection after implantation seriously limit the potential applications of MgA in the biomedical field.Herein,we fabricated bilayered nanoarrays of hydroxyapatite nanorods(HANRs)and ZnO nanorods(ZnONRs)onto the surface of MgA(MgA-MgO-HANRs-ZnONRs)via micro-arc oxidation(MAO)treatment,microwave-assisted hydrothermal and hydrothermal methods.The morphology and chemical composition of MgA-MgO-HANRs-ZnONRs was characterized by FE-SEM,XRD and EDS,indicating that HANRs-ZnONRs bilayered nanoarrays were fabricated on the surface of MgA-MgO.The surface of MgA-MgO-HANRs-ZnONRs exhibited excellent hydrophilicity as evidenced by the low water contact angle of 3°.Compared with the original MgA,the corrosion resistance of MgA-MgO-HANRs-ZnONRs was obviously improved with decreasing the corrosive current density(icorr)of 2 orders of magnitude.The MgA-MgO-HANRs-ZnONRs performed excellent antibacterial properties with the bactericidal rate of 96.5%against S.aureus and 94.3%against E.coli.

Unraveling structure evolution failure mechanism in MoS_(2)anode for improving lithium storage stability

2 H phase molybdenum disulfide(2 H-MoS_(2))possesses the two-dimensional layered structure and high theoretical capacity,presenting excellent lithiation-delithiation property.However,the violent capacity decay within dozens of cycles still remains a great challenge due to lacking of in-depth failure mechanism.Herein,a novel decay-recovery-decay failure phenomenon upon long-term cycles is reported for the first time,which originates from the slow size change of Mo nanoparticles(NPs).Decay stages are triggered by many irregular-shaped Mo NPs with the increasing size up to~15 nm,leading to prominent pseudocapacitance failure and capacity loss.Subsequent recovery stages are attributed to the pulverization of coarse Mo NPs through surface sulfurization and accompanying lithiation.To overcome the instability issue,proper modifiers should be introduced to restrain the spontaneous growth of Mo NPs,such as aluminum oxide(Al_(2)O_(3)).The strong Mo-Al_(2)O_(3)bond gradually"drags"Al_(2)O_(3)fragments into the active material as the cycle continuously proceeds,resulting in the efficient refinement and the reversible conversion between Mo and MoS_(2).Therefore,the enhanced cycling stability and the capacity retention are successfully achieved.It is expected to provide a new insight into the energy storage of transition metal chalcogenide anode materials in rechargeable batteries.