In order to overcome the embrittlement of metastable titanium alloys caused by the precipitation ofωiso phase during aging,regulation of isothermalωprecipitation was investigated in Ti−15Mo alloy.The results show th...In order to overcome the embrittlement of metastable titanium alloys caused by the precipitation ofωiso phase during aging,regulation of isothermalωprecipitation was investigated in Ti−15Mo alloy.The results show that the sample is brittle when direct aging(A)is applied at 350℃for 1 h after solution treatment(ST).If pre-deformation(D)is performed on the ST sample to induce{332}twins and secondaryα″phase,subsequent aging at 350℃(STDA350)improves the strength to 931 MPa with a good ductility of about 20%maintained.However,when aging is performed at 400℃or 450℃(STDA400/450),the strength can be further improved,but the ductility is dramatically reduced.Atomic-scale characterizations show that the partial collapse ofωphase in the STDA350 sample effectively eliminates aging-induced embrittlement,but complete collapse leads to poor ductility in the STDA400/450 sample.展开更多
Exercise significantly enhances bone mass.However,whether exercise can alter the bone microenvironment through exosomes and the underlying molecular mechanisms remains unclear.This study aims to investigate the role o...Exercise significantly enhances bone mass.However,whether exercise can alter the bone microenvironment through exosomes and the underlying molecular mechanisms remains unclear.This study aims to investigate the role of exercise in mitigating osteoporosis and to elucidate the molecular mechanisms of exercise-intervened bone marrow mesenchymal stromal cells(BMSCs)exosomes in the treatment of osteoporosis.In this study,18-month-old male mice were subjected to 8 weeks of treadmill exercise for 1 h daily.Changes in bone mass were assessed using micro-computed tomography(micro-CT),real-time polymerase chain reaction(RT-PCR),hematoxylin and eosin(H&E),calcein,immunohistochemistry,and immunofluorescence staining.The distribution and therapeutic effects of exosomes on osteoporosis were evaluated using immunofluorescence staining and small-animal imaging systems.Finally,the molecular mechanisms by which BMSC-derived exosomes regulate bone mass were explored through RNA sequencing,PCR,luciferase assays,and alkaline phosphatase(ALP)and alizarin red S(ARS)staining.Exercise alleviated the symptoms of bone loss through an increase in the number of osteoblasts and type H vessels.Blocking exosome release from BMSCs significantly reversed exercise-induced improvements in bone mass.Furthermore,exercise-intervened BMSCs exosomes could promote osteoblast differentiation and effectively target bone and ameliorate osteoporosis induced by aging.Mechanistically,miR-206 was found to regulate osteoblast differentiation by binding to yes-associated protein(YAP1)and promoting the nuclear translocation ofβ-catenin.Inhibition of miR-206 abolished the exercise-induced improvements in bone mass.This study demonstrates that exercise-intervened BMSCs exosomes can alleviate osteoporosis by delivering miR-206 to regulate the YAP1/β-catenin pathway.These findings provide new insights into the mechanisms by which exercise ameliorates osteoporosis and offer potential therapeutic strategies for future osteoporosis treatments.展开更多
基金the financial support from the National Natural Science Foundation of China (No. 52374380)the China Postdoctoral Science Foundation (Nos. 2023M730234, 2024T171126)。
文摘In order to overcome the embrittlement of metastable titanium alloys caused by the precipitation ofωiso phase during aging,regulation of isothermalωprecipitation was investigated in Ti−15Mo alloy.The results show that the sample is brittle when direct aging(A)is applied at 350℃for 1 h after solution treatment(ST).If pre-deformation(D)is performed on the ST sample to induce{332}twins and secondaryα″phase,subsequent aging at 350℃(STDA350)improves the strength to 931 MPa with a good ductility of about 20%maintained.However,when aging is performed at 400℃or 450℃(STDA400/450),the strength can be further improved,but the ductility is dramatically reduced.Atomic-scale characterizations show that the partial collapse ofωphase in the STDA350 sample effectively eliminates aging-induced embrittlement,but complete collapse leads to poor ductility in the STDA400/450 sample.
基金supported by grants from the National Natural Science Foundation of China(Nos.82201748,82202674,and 82272490)Shanghai Sailing Program(No.21YF1459200)Natural Science Foundation of Xiamen,China(No.3502Z20227124).
文摘Exercise significantly enhances bone mass.However,whether exercise can alter the bone microenvironment through exosomes and the underlying molecular mechanisms remains unclear.This study aims to investigate the role of exercise in mitigating osteoporosis and to elucidate the molecular mechanisms of exercise-intervened bone marrow mesenchymal stromal cells(BMSCs)exosomes in the treatment of osteoporosis.In this study,18-month-old male mice were subjected to 8 weeks of treadmill exercise for 1 h daily.Changes in bone mass were assessed using micro-computed tomography(micro-CT),real-time polymerase chain reaction(RT-PCR),hematoxylin and eosin(H&E),calcein,immunohistochemistry,and immunofluorescence staining.The distribution and therapeutic effects of exosomes on osteoporosis were evaluated using immunofluorescence staining and small-animal imaging systems.Finally,the molecular mechanisms by which BMSC-derived exosomes regulate bone mass were explored through RNA sequencing,PCR,luciferase assays,and alkaline phosphatase(ALP)and alizarin red S(ARS)staining.Exercise alleviated the symptoms of bone loss through an increase in the number of osteoblasts and type H vessels.Blocking exosome release from BMSCs significantly reversed exercise-induced improvements in bone mass.Furthermore,exercise-intervened BMSCs exosomes could promote osteoblast differentiation and effectively target bone and ameliorate osteoporosis induced by aging.Mechanistically,miR-206 was found to regulate osteoblast differentiation by binding to yes-associated protein(YAP1)and promoting the nuclear translocation ofβ-catenin.Inhibition of miR-206 abolished the exercise-induced improvements in bone mass.This study demonstrates that exercise-intervened BMSCs exosomes can alleviate osteoporosis by delivering miR-206 to regulate the YAP1/β-catenin pathway.These findings provide new insights into the mechanisms by which exercise ameliorates osteoporosis and offer potential therapeutic strategies for future osteoporosis treatments.
