新能源汽车智能化能量管理是先进汽车技术研究的重要领域,是进一步提升整车燃油经济性能的关键。针对插电式混合动力汽车(Plug-in hybrid electric vehicle,PHEV)能量全局化管理与控制的实时性和最优性难以兼顾的难题,开展了基于能耗预...新能源汽车智能化能量管理是先进汽车技术研究的重要领域,是进一步提升整车燃油经济性能的关键。针对插电式混合动力汽车(Plug-in hybrid electric vehicle,PHEV)能量全局化管理与控制的实时性和最优性难以兼顾的难题,开展了基于能耗预测的全路径自适应能量管理研究,提出了以等效燃油消耗最小化为目标的全规划路径PHEV自适应控制算法。最后,基于MATLAB/Simulink的建模与仿真分析验证了所提控制算法对实际行驶工况、里程和整车能量状态的变化具有较好的跟随性和自适应性,全路径近似全局性优化控制效果明显,较好地改善了整车的燃油经济性。展开更多
Objective The nucleolar protein PES1(Pescadillo homolog 1)plays critical roles in ribosome biogenesis and cell cycle regulation,yet its involvement in cellular senescence remains poorly understood.This study aimed to ...Objective The nucleolar protein PES1(Pescadillo homolog 1)plays critical roles in ribosome biogenesis and cell cycle regulation,yet its involvement in cellular senescence remains poorly understood.This study aimed to comprehensively investigate the functional consequences of PES1 suppression in cellular senescence and elucidate the molecular mechanisms underlying its regulatory role.Methods Initially,we assessed PES1 expression patterns in two distinct senescence models:replicative senescent mouse embryonic fibroblasts(MEFs)and doxorubicin-induced senescent human hepatocellular carcinoma HepG2 cells.Subsequently,PES1 expression was specifically downregulated using siRNA-mediated knockdown in these cell lines as well as additional relevant cell types.Cellular proliferation and senescence were assessed by EdU incorporation and SA-β-gal staining assays,respectively.The expression of senescence-associated proteins(p53,p21,and Rb)and SASP factors(IL-6,IL-1β,and IL-8)were analyzed by Western blot or qPCR.Furthermore,Northern blot and immunofluorescence were employed to evaluate pre-rRNA processing and nucleolar morphology.Results PES1 expression was significantly downregulated in senescent MEFs and HepG2 cells.PES1 knockdown resulted in decreased EdU-positive cells and increased SA-β-gal-positive cells,indicating proliferation inhibition and senescence induction.Mechanistically,PES1 suppression activated the p53-p21 pathway without affecting Rb expression,while upregulating IL-6,IL-1β,and IL-8 production.Notably,PES1 depletion impaired pre-rRNA maturation and induced nucleolar stress,as evidenced by aberrant nucleolar morphology.Conclusion Our findings demonstrate that PES1 deficiency triggers nucleolar stress and promotes p53-dependent(but Rb-independent)cellular senescence,highlighting its crucial role in maintaining nucleolar homeostasis and regulating senescence-associated pathways.展开更多
文摘新能源汽车智能化能量管理是先进汽车技术研究的重要领域,是进一步提升整车燃油经济性能的关键。针对插电式混合动力汽车(Plug-in hybrid electric vehicle,PHEV)能量全局化管理与控制的实时性和最优性难以兼顾的难题,开展了基于能耗预测的全路径自适应能量管理研究,提出了以等效燃油消耗最小化为目标的全规划路径PHEV自适应控制算法。最后,基于MATLAB/Simulink的建模与仿真分析验证了所提控制算法对实际行驶工况、里程和整车能量状态的变化具有较好的跟随性和自适应性,全路径近似全局性优化控制效果明显,较好地改善了整车的燃油经济性。
文摘Objective The nucleolar protein PES1(Pescadillo homolog 1)plays critical roles in ribosome biogenesis and cell cycle regulation,yet its involvement in cellular senescence remains poorly understood.This study aimed to comprehensively investigate the functional consequences of PES1 suppression in cellular senescence and elucidate the molecular mechanisms underlying its regulatory role.Methods Initially,we assessed PES1 expression patterns in two distinct senescence models:replicative senescent mouse embryonic fibroblasts(MEFs)and doxorubicin-induced senescent human hepatocellular carcinoma HepG2 cells.Subsequently,PES1 expression was specifically downregulated using siRNA-mediated knockdown in these cell lines as well as additional relevant cell types.Cellular proliferation and senescence were assessed by EdU incorporation and SA-β-gal staining assays,respectively.The expression of senescence-associated proteins(p53,p21,and Rb)and SASP factors(IL-6,IL-1β,and IL-8)were analyzed by Western blot or qPCR.Furthermore,Northern blot and immunofluorescence were employed to evaluate pre-rRNA processing and nucleolar morphology.Results PES1 expression was significantly downregulated in senescent MEFs and HepG2 cells.PES1 knockdown resulted in decreased EdU-positive cells and increased SA-β-gal-positive cells,indicating proliferation inhibition and senescence induction.Mechanistically,PES1 suppression activated the p53-p21 pathway without affecting Rb expression,while upregulating IL-6,IL-1β,and IL-8 production.Notably,PES1 depletion impaired pre-rRNA maturation and induced nucleolar stress,as evidenced by aberrant nucleolar morphology.Conclusion Our findings demonstrate that PES1 deficiency triggers nucleolar stress and promotes p53-dependent(but Rb-independent)cellular senescence,highlighting its crucial role in maintaining nucleolar homeostasis and regulating senescence-associated pathways.
