Construction of Industrialization Development Model for"1+4+X"Community-Based Elderly Care in Gannan Old Revolutionary Base Area in the Context of Population Aging

In the context of controlling population development in a planned way,China entered an aging society in the early 21 st century.In this context,how to meet the needs of the elderly care and form an effective elderly care model has become a key problem to be solved urgently by local government departments.With the continuous advancement of the elderly care policy,the community-based elderly care has gradually become the mainstream and is in the stage of vigorous promotion.Taking the Gannan old revolutionary base area in Jiangxi Province as an example,this study puts forward"1+4+X"community-based elderly care model based on the policy system of community-based elderly care,the physical and mental health of the elderly,the material space and the construction of evaluation system,and explores how to promote the application of this community model efficiently in the form of industrialization,so as to drive the economic growth of the Gannan old revolutionary base area,promote the employment development and improve the community-based elderly care service.

Lignin valorization toward value-added chemicals and fuels via electrocatalysis:A perspective

Developing efficient approaches for lignin upgrading is of interest for the industrial production of chemicals and fuels from renewable biomass.Electrocatalytic lignin upgrading powered by renewable electricity operating under gentle conditions(at or near ambient pressures and temperatures)enables a decentralized production of chemicals and fuels.Herein,we will cover the structures of lignin and review the recent advances in the electrocatalytic lignin upgrade,the electrocatalytic depolymerization of lignin,and the electrocatalytic upgrading of lignin monomers to value-added chemicals and fuels.Finally,we provide insights into the main challenges and future perspectives of this field.

PRMT6 promotes tumorigenicity and cisplatin response of lung cancer through triggering 6PGD/ENO1 mediated cell metabolism

Metabolic reprogramming is a hallmark of cancer,including lung cancer.However,the exact underlying mechanism and therapeutic potential are largely unknown.Here we report that protein arginine methyltransferase 6(PRMT6)is highly expressed in lung cancer and is required for cell metabolism,tumorigenicity,and cisplatin response of lung cancer.PRMT6 regulated the oxidative pentose phosphate pathway(PPP)flux and glycolysis pathway in human lung cancer by increasing the activity of 6-phosphogluconate dehydrogenase(6PGD)and a-enolase(ENO1).Furthermore,PRMT6 methylated R324 of 6PGD to enhancing its activity;while methylation at R9 and R372 of ENO1 promotes formation of active ENO1 dimers and 2-phosphoglycerate(2-PG)binding to ENO1,respectively.Lastly,targeting PRMT6 blocked the oxidative PPP flux,glycolysis pathway,and tumor growth,as well as enhanced the antitumor effects of cisplatin in lung cancer.Together,this study demonstrates that PRMT6 acts as a posttranslational modification(PTM)regulator of glucose metabolism,which leads to the pathogenesis of lung cancer.It was proven that the PRMT6-6PGD/ENO1 regulatory axis is an important determinant of carcinogenesis and may become a promising cancer therapeutic strategy.

Incorporation of a histone mutant with H3K56 site substitution perturbs the replication machinery in mouse embryonic stem cells

Sense mutations in several conserved modifiable sites of histone H3 have been found to be strongly correlated with multiple tissuespecific clinical cancers.These clinical site mutants acquire a distinctively new epigenetic role and mediate cancer evolution.In this study,we mimicked histone H3 at the 56th lysine(H3K56)mutant incorporation in mouse embryonic stem cells(mESCs)by lentivirus-mediated ectopic expression and analyzed the effects on replication and epigenetic regulation.The data show that two types of H3K56 mutants,namely H3 lysine 56-to-methionine(H3K56M)and H3 lysine 56-to-alanine(H3K56A),promote replication by recruiting more minichromosome maintenance complex component 3 and checkpoint kinase 1 onto chromatin compared with wild-type histone H3 and other site substitution mutants.Under this condition,the frequency of genomic copy number gain in H3K56M and H3K56A cells globally increases,especially in the Mycl1 region,a known molecular marker frequently occurring in multiple malignant cancers.Additionally,we found the disruption of H3K56 acetylation distribution in the copy-gain regions,which indicates a probable epigenetic mechanism of H3K56M and H3K56A.We then identified that H3K56M and H3K56A can trigger a potential adaptation to transcription;genes involved in the mitogen-activated protein kinase pathway are partially upregulated,whereas genes associated with intrinsic apoptotic function show obvious downregulation.The final outcome of ectopic H3K56M and H3K56A incorporation in mESCs is an enhanced ability to form carcinomas.This work indicates that H3K56 site conservation and proper modification play important roles in harmonizing the function of the replication machinery in mESCs.