Calculation and decomposition of regional household energy consumption in China:based on perspectives of urbanization and residents' consumption

Demographic urbanization caused great changes in scale of residents' consumption and residents' lifestyle and then impacted changes of regional household energy consumption. This paper expanded Logarithmic Mean Decomposition Index method through introducing variables of urbanization and residential consumption into the model. It also analyzed the influences of six factors as energy structure, energy intensity, population scale, urbanization, residential consumption, and consumption inhibit on regional household energy consumption. Results showed that in 2003-2012, impact of urbanization on regional household energy consumption of Chinese three areas was significantly higher than population size. The "population gathered in eastern region" phenomenon caused eastern region getting the largest population scale effect. Driving force of residential consumption on regional household energy consumption was much higher than the other five effects. Due to the comparative advantage of residential consumption compared with government consumption, investment, and net export, the decrease of consumption ratio promoted the growth of regional household energy consumption. Energy intensity in Chinese three regions kept reducing in 2003-2012. The progress of energy utilization technology slowed the growth of regional household energy consumption, and energy intensity effect was most significant in the central region.

SRSF1 plays a critical role in invariant natural killer T cell development and function

Invariant natural killer T(iNKT)cells are highly conserved innate-like T lymphocytes that originate from CD4^(+)CD8^(+)double-positive(DP)thymocytes.Here,we report that serine/arginine splicing factor 1(SRSF1)intrinsically regulates iNKT cell development by directly targeting Myb and balancing the abundance of short and long isoforms.Conditional ablation of SRSF1 in DP cells led to a substantially diminished iNKT cell pool due to defects in proliferation,survival,and TCRαrearrangement.The transition from stage 0 to stage 1 of iNKT cells was substantially blocked,and the iNKT2 subset was notably diminished in SRSF1-deficient mice.SRSF1 deficiency resulted in aberrant expression of a series of regulators that are tightly correlated with iNKT cell development and iNKT2 differentiation,including Myb,PLZF,Gata3,ICOS,and CD5.In particular,we found that SRSF1 directly binds and regulates pre-mRNA alternative splicing of Myb and that the expression of the short isoform of Myb is substantially reduced in SRSF1-deficient DP and iNKT cells.Strikingly,ectopic expression of the Myb short isoform partially rectified the defects caused by ablation of SRSF1.Furthermore,we confirmed that the SRSF1-deficient mice exhibited resistance to acute liver injury uponα-GalCer and Con A induction.Our findings thus uncovered a previously unknown role of SRSF1 as an essential post-transcriptional regulator in iNKT cell development and functional differentiation,providing new clinical insights into iNKT-correlated disease.

TCF-1 deficiency influences the composition of intestinal microbiota and enhances susceptibility to colonic inflammation

Dear Editor,The diversity and composition of gut microbiota play critical roles for maintaining the homeostasis of host commensal bacteria which are correlated with mammalian health(Ding and Schloss,2014).Disorder of microbial community is implicated in the pathogenesis of several human diseases,such as autoimmune disease,allergy,diabetes,obesity,and inflammatory bowel disease(IBD),which is clearly demonstrated to relate to gut dysbiosis in patients and mouse models(Saleh and Elson,2011).

Exploring the stage-specific roles of Tcf-1 in T cell development and malignancy at single-cell resolution

Tcf-1(encoded by Tcf7)not only plays critical roles in promoting T cell development and differentiation but also has been identified as a tumor suppressor involved in preventing T cell malignancy.However,the comprehensive mechanisms of Tcf-1 involved in T cell transformation remain poorly understood.In this study,Tcf7^(fl/fl)mice were crossed with Vav-cre,Lck-cre,or Cd4-cre mice to delete Tcf-1 conditionally at the beginning of the HSC,DN2-DN3,or DP stage,respectively.The defective T cell development phenotypes became gradually less severe as the deletion stage became more advanced in distinct mouse models.Interestingly,consistent with Tcf7^(-/-)mice,Tcf^(fl/fl)Vav-cre mice developed aggressive T cell lymphoma within 45 weeks,but no tumors were generated in Tcf7^(fl/fl)Lck-cre or Tcf^(fl/fl)CdA-cre mice.Single-cell RNA-seq(ScRNA-seq)indicated that ablation of Tcf-1 at distinct phases can subdivide DN1 cells into three clusters(C1,C2,and C3)and DN2-DN3 cells into three clusters(C4,C5,and C6).Moreover,Tcf-1 deficiency redirects bifurcation among divergent cell fates,and clusters C1 and C4 exhibit high potential for leukemic transformation.Mechanistically,we found that Tcf-1 directly binds and mediates chromatin accessibility for both typical T cell regulators and proto-oncogenes#including Myb,Mycn,Runxl,and Lyl1 in the DN1 phase and Lefb ld2,Dtxb Fyn,Bclllb,and Zfp36l2 in the DN2-DN3 phase.The aberrant expression of these genes due to Tcf-1 deficiency in very early T cells contributes to subsequent tumorigenesis.Thus,we demonstrated that Tcf-1 plays stage-specific roles in regulating early thymocyte development and transformation,providing new insights and evidence for clinical trials on T-ALL leukemia.