The Lin-Reissner-Tsien equation describes unsteady transonic flows under the transonic approximation. In the present paper, the equation is reduced to an ordinary differential equation via a similarity transformation....The Lin-Reissner-Tsien equation describes unsteady transonic flows under the transonic approximation. In the present paper, the equation is reduced to an ordinary differential equation via a similarity transformation. The resulting equation is then solved analytically and even exactly in some cases. Numerical simulations are provided for the cases in which there is no exact solution. Travelling wave solutions are also obtained.展开更多
Mitochondrial dysfunction is a hallmark of aging that elicits adaptive nuclear responses,yet how chromatin remodeling is coordinated under stress remains unclear.Here,we uncover a phosphorylation-dependent mechanism b...Mitochondrial dysfunction is a hallmark of aging that elicits adaptive nuclear responses,yet how chromatin remodeling is coordinated under stress remains unclear.Here,we uncover a phosphorylation-dependent mechanism by which mitochondrial stress regulates the activity of the Nu RD(nucleosome remodeling and deacetylase)complex via LIN-40,the Caenorhabditis elegans homolog of mammalian MTA proteins.Mitochondrial stress triggers dephosphorylation of LIN-40,enhancing its interaction with the transcription factor DVE-1 to activate the mitochondrial unfolded protein response(UPR mt)and chromatin remodeling.Phosphorylation of LIN-40 is mediated by p38 MAPK/PMK-3 and reversed by PP1c/GSP-2.Furthermore,the LIN-40(T654D)variant abolishes mitochondrial stress-induced lifespan extension.These findings establish a direct link between mitochondrial stress signaling and chromatin remodeling via Nu RD,revealing an evolutionarily conserved strategy to coordinate cellular resilience and organismal longevity.展开更多
文摘The Lin-Reissner-Tsien equation describes unsteady transonic flows under the transonic approximation. In the present paper, the equation is reduced to an ordinary differential equation via a similarity transformation. The resulting equation is then solved analytically and even exactly in some cases. Numerical simulations are provided for the cases in which there is no exact solution. Travelling wave solutions are also obtained.
基金supported by the National Key Research and Development Program of China(2022YFA1303000)the Strategic Priority Research Program of the Chinese Academy of Sciences(XDB39000000)+2 种基金the National Natural Science Foundation of China(32371214,32225025,92254305,32321004,32430025)the CAS Project for Young Scientists in Basic Research(YSBR-076)the Youth Innovation Promotion Association CAS(2021094)。
文摘Mitochondrial dysfunction is a hallmark of aging that elicits adaptive nuclear responses,yet how chromatin remodeling is coordinated under stress remains unclear.Here,we uncover a phosphorylation-dependent mechanism by which mitochondrial stress regulates the activity of the Nu RD(nucleosome remodeling and deacetylase)complex via LIN-40,the Caenorhabditis elegans homolog of mammalian MTA proteins.Mitochondrial stress triggers dephosphorylation of LIN-40,enhancing its interaction with the transcription factor DVE-1 to activate the mitochondrial unfolded protein response(UPR mt)and chromatin remodeling.Phosphorylation of LIN-40 is mediated by p38 MAPK/PMK-3 and reversed by PP1c/GSP-2.Furthermore,the LIN-40(T654D)variant abolishes mitochondrial stress-induced lifespan extension.These findings establish a direct link between mitochondrial stress signaling and chromatin remodeling via Nu RD,revealing an evolutionarily conserved strategy to coordinate cellular resilience and organismal longevity.
