4-Methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene,a Major Active Metabolite of Bisphenol A,Triggers Pancreatic β-Cell Death via a JNK/AMPKα Activation-Regulated Endoplasmic Reticulum Stress-Mediated Apoptotic Pathway

4-methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene (MBP), a major active metabolite of bisphenol A (BPA), is generated in the mammalian liver. Some studies have suggested that MBP exerts greater toxicity than BPA. However, the mechanism underlying MBP-induced pancreatic β-cell cytotoxicity remains largely unclear. This study demonstrated the cytotoxicity of MBP in pancreatic β-cells and elucidated the cellular mechanism involved in MBP-induced β-cell death. Our results showed that MBP exposure significantly reduced cell viability, caused insulin secretion dysfunction, and induced apoptotic events including increased caspase-3 activity and the expression of active forms of caspase-3/-7/-9 and PARP protein. In addition, MBP triggered endoplasmic reticulum (ER) stress, as indicated by the upregulation of GRP 78, CHOP, and cleaved caspase-12 proteins. Pretreatment with 4-phenylbutyric acid (4-PBA; a pharmacological inhibitor of ER stress) markedly reversed MBP-induced ER stress and apoptosis-related signals. Furthermore, exposure to MBP significantly induced the protein phosphorylation of JNK and AMP-activated protein kinase (AMPK)α. Pretreatment of β-cells with pharmacological inhibitors for JNK (SP600125) and AMPK (compound C), respectively, effectively abrogated the MBP-induced apoptosis-related signals. Both JNK and AMPK inhibitors also suppressed the MBP-induced activation of JNK and AMPKα and of each other. In conclusion, these findings suggest that MBP exposure exerts cytotoxicity on β-cells via the interdependent activation of JNK and AMPKα, which regulates the downstream apoptotic signaling pathway.     

What Can We Learn from FGF-2 Isoform-Specific Mouse Mutants? Differential Insights into FGF-2 Physiology In Vivo

Fibroblast growth factor 2 (FGF-2), ubiquitously expressed in humans and mice, is functionally involved in cell growth, migration and maturation in vitro and in vivo. Based on the same mRNA, an 18-kilo Dalton (kDa) FGF-2 isoform named FGF-2 low molecular weight (FGF-2LMW) isoform is translated in humans and rodents. Additionally, two larger isoforms weighing 21 and 22 kDa also exist, summarized as the FGF-2 high molecular weight (FGF-2HMW) isoform. Meanwhile, the human FGF-2HMW comprises a 22, 23, 24 and 34 kDa protein. Independent studies verified a specific intracellular localization, mode of action and tissue-specific spatiotemporal expression of the FGF-2 isoforms, increasing the complexity of their physiological and pathophysiological roles. In order to analyze their spectrum of effects, FGF-2LMW knock out (ko) and FGF-2HMWko mice have been generated, as well as mice specifically overexpressing either FGF-2LMW or FGF-2HMW. So far, the development and functionality of the cardiovascular system, bone formation and regeneration as well as their impact on the central nervous system including disease models of neurodegeneration, have been examined. This review provides a summary of the studies characterizing the in vivo effects modulated by the FGF-2 isoforms and, thus, offers a comprehensive overview of its actions in the aforementioned organ systems.     

机械合金化FeS/Cu复合材料的摩擦磨损性能

以FeS和CuSn8Ni1粉末为原料，利用机械合金化技术和粉末冶金技术制备了FeS/Cu复合材料，探讨了不同载荷情况下所制备的FeS/Cu复合材料的摩擦学性能及润滑膜与转移膜特征。结果表明：机械合金化提高了FeS与铜合金基体界面结合性能，进而提高了材料减摩耐磨性能；当载荷较小时，摩擦副表面接触不稳定，复合转移膜不连续，摩擦因数波动大；载荷较大时，复合转移膜易破损，材料的减摩耐磨性能变差；当载荷为150 N时，载荷适宜，材料表面软化，复合转移膜更加完整，摩擦因数较小。     

Increasing Volumetric CO2 Uptake of Hypercrosslinked Polymers through Composite Formation

To overcome the drawbacks of solid microporous materials for CO₂ capture, this proof‐of‐concept study demonstrates a low‐cost and rapid method for producing composites consisting of hypercrosslinked polymers (HCP) with a polyethyleneimine (PEI) binder. The resulting materials capture CO₂ through physical and chemical absorption simultaneously. Compared with HCP, the composites exhibit higher CO₂ uptake, higher volumetric density, and improved tolerance to water which is attributed to the PEI binder.     

锂-二氧化碳电池阴极催化剂的研究进展

锂-二氧化碳电池通过捕获、转化二氧化碳为储能物质，既可以减少二氧化碳排放量又可以作为创新的储能装置，引起了研究者们的广泛关注。本文简单介绍了锂-二氧化碳电池的工作机理、发展历程和目前研究存在的难题，通过对研究工作的总结、电池性能的对比，将不同类型的催化剂进行了系统的分类和简单的概括，综述了催化剂的设计理念和研究现状，提出了催化剂目前存在的难题与挑战，并展望了催化剂未来的发展方向。本文主要针对锂-二氧化碳电池阴极催化剂的最新研究进展进行了详细的阐述，指出高效的阴极催化剂是促进锂-二氧化碳电池电化学反应动力学、降低充电平台和过电势的关键所在。     

耦合膜分离的新型CO2低温捕集系统性能优化

CO₂捕集作为温室气体排放控制的有效手段已成为重要研究课题。作为新兴捕集技术之一，低温CO₂捕集因产品纯度高、无附加污染等优势受到关注。然而，该技术能耗和捕集率对于气体中CO₂浓度十分敏感，对于高CO₂浓度气体可获得较高的CO₂捕集率和较低能耗水平。基于此，本文提出了耦合膜分离的新型CO₂低温捕集系统，通过膜材料选择渗透性实现待捕集气体CO₂浓度主动调控，并在最优浓度下进行CO₂低温捕集。首先基于不同传统低温捕集系统特点，对比分析了不同耦合系统模式，从而确定了最优耦合系统结构。针对最优耦合系统进行了运行参数优化，并分别基于实现系统捕集能耗最低与捕集率最高的目标，获得了膜渗透侧CO₂浓度与进气CO₂浓度间的关系式，为该耦合系统中膜组件选型提供指导。研究表明，本文提出的耦合系统捕集能耗为1.92MJ/kgCO₂，相比于传统单一低温系统捕集能耗可降低16.5%。