This paper proposes the assumption that the flow with viscous friction is the stretch of part of the sheet that lies along the walls of a die during the process of superplastic bulging according to superplastic flow e...This paper proposes the assumption that the flow with viscous friction is the stretch of part of the sheet that lies along the walls of a die during the process of superplastic bulging according to superplastic flow equation and geometrical model of bulging of a sheet into a long trapezoid groove or truncated cone, by introducing the friction-factor P which describes the friction effect on the process. Also, the paper proposes the method of controlling thickness nonuniformity and develops the equipment which for uniform thickness of bulging, is automatically controlled with a computerl it also analyzes the important innuence of lubrication on thickness distribution of bulging materials. By the assumption, the relationship between bulging pressure and time is obtained in bulging of a sheet into the groove and cone, and p-t curve of multi-mould-cavity complicated bulging is discussed based on the analysis of single-mould-cavity bulging characteristics.展开更多
The tumor suppressor p53 is a multifunctional, highly regulated, and promoter-specific transcriptional factor that is uniquely sensitive to DNA damage and cellular stress signaling. The mechanisms by which p53 directs...The tumor suppressor p53 is a multifunctional, highly regulated, and promoter-specific transcriptional factor that is uniquely sensitive to DNA damage and cellular stress signaling. The mechanisms by which p53 directs a damaged cell down either a cell growth arrest or an apoptotic pathway remain poorly understood. Evidence suggests that the in vivo functions of p53 seem to balance the cell-fate choice with the type and severity of damage that occurs. The concept of antirepression, or inhibition of factors that normally keep p53 at bay, may help explain the physiological mechanisms for p53 activation. These factors also provide novel chemotherapeutic targets for the reactivation of p53 in tumors harboring a wild-type copy of the gene.展开更多
Mesenchymal stem cells （MSCs） are considered as the developmental origin of multiple Uneage cells including osteocytes, adipocytes, and muscle cells. Previous studies demonstrated that the PH domain.containing prote...Mesenchymal stem cells （MSCs） are considered as the developmental origin of multiple Uneage cells including osteocytes, adipocytes, and muscle cells. Previous studies demonstrated that the PH domain.containing protein CKIP-1 plays an important role in the devel- opment of osteobiasts and cardiomyocytes. However, whether CKIP-1 is involved in the generation of adipocytes as weU as the MSC differentiation remains unknown. Here we show that CKIP-1 is a novel regulator of MSCs differentiating into adipocytes. MSCs derived from CKIP-l-deficient mice display enhanced adipogenesis upon induction. Further analysis showed that CKIP-1 interacts with the histone deacetylase HDAC1 in the nucleus and inhibits the transcription of CCAAT/enhancer-binding protein α （C/EBPcx）, which is a crucial adipogenic transcription factor. Ectopic expression of CKI P-1 in a MSC-Uke cell line C3H/10T1/2 reduced the gener- ation of adipocytes due to suppression of adipogenic factors, including C/EBPα. Moreover, CKI P-l-deficient mice showed an increase in body weight and white adipose tissue gains when fed on a high-fat diet. Collectively, these results suggest that CKIP-1 is a novel inhibitor of MSC-originated adipogenesis by enhancing HDACl-associated repression of C/EBPα.展开更多
文摘This paper proposes the assumption that the flow with viscous friction is the stretch of part of the sheet that lies along the walls of a die during the process of superplastic bulging according to superplastic flow equation and geometrical model of bulging of a sheet into a long trapezoid groove or truncated cone, by introducing the friction-factor P which describes the friction effect on the process. Also, the paper proposes the method of controlling thickness nonuniformity and develops the equipment which for uniform thickness of bulging, is automatically controlled with a computerl it also analyzes the important innuence of lubrication on thickness distribution of bulging materials. By the assumption, the relationship between bulging pressure and time is obtained in bulging of a sheet into the groove and cone, and p-t curve of multi-mould-cavity complicated bulging is discussed based on the analysis of single-mould-cavity bulging characteristics.
文摘The tumor suppressor p53 is a multifunctional, highly regulated, and promoter-specific transcriptional factor that is uniquely sensitive to DNA damage and cellular stress signaling. The mechanisms by which p53 directs a damaged cell down either a cell growth arrest or an apoptotic pathway remain poorly understood. Evidence suggests that the in vivo functions of p53 seem to balance the cell-fate choice with the type and severity of damage that occurs. The concept of antirepression, or inhibition of factors that normally keep p53 at bay, may help explain the physiological mechanisms for p53 activation. These factors also provide novel chemotherapeutic targets for the reactivation of p53 in tumors harboring a wild-type copy of the gene.
文摘Mesenchymal stem cells （MSCs） are considered as the developmental origin of multiple Uneage cells including osteocytes, adipocytes, and muscle cells. Previous studies demonstrated that the PH domain.containing protein CKIP-1 plays an important role in the devel- opment of osteobiasts and cardiomyocytes. However, whether CKIP-1 is involved in the generation of adipocytes as weU as the MSC differentiation remains unknown. Here we show that CKIP-1 is a novel regulator of MSCs differentiating into adipocytes. MSCs derived from CKIP-l-deficient mice display enhanced adipogenesis upon induction. Further analysis showed that CKIP-1 interacts with the histone deacetylase HDAC1 in the nucleus and inhibits the transcription of CCAAT/enhancer-binding protein α （C/EBPcx）, which is a crucial adipogenic transcription factor. Ectopic expression of CKI P-1 in a MSC-Uke cell line C3H/10T1/2 reduced the gener- ation of adipocytes due to suppression of adipogenic factors, including C/EBPα. Moreover, CKI P-l-deficient mice showed an increase in body weight and white adipose tissue gains when fed on a high-fat diet. Collectively, these results suggest that CKIP-1 is a novel inhibitor of MSC-originated adipogenesis by enhancing HDACl-associated repression of C/EBPα.
