After the progressive collapse of Ronan Point apartment in UK in 1968, intensive research effort had been spent on developing guidelines for design of new or strengthening the existing structures to prevent progressiv...After the progressive collapse of Ronan Point apartment in UK in 1968, intensive research effort had been spent on developing guidelines for design of new or strengthening the existing structures to prevent progressive collapse. However, only very few building design codes provide some rather general guidance, no detailed design requirement is given. Progressive collapse of the Alfred P. Murrah Federal building in Oklahoma City and the World Trade Centre (WTC) sparked again tremendous research interest on progressive collapse of structures. Recently, US Department of Defence (DoD) and US General Service Administration (GSA) issued guidelines for structure progressive collapse analysis. These two guidelines are most commonly used, but their accuracy is not known. This paper presents numerical analysis of progressive collapse of an example frame structure to blast loads. The DoD and GSA procedures are also used to analyse the same example structure. Numerical results are compared and discussed. The accuracy and the applicability of the two design guidelines are evaluated.展开更多
Here, we explore the role of Cbl proteins in regulation of neuronal apoptosis. In two paradigms of neuron apoptosis -- nerve growth factor （NGF） deprivation and DNA damage -- cellular levels of c-Cbl and Cbl-b fell ...Here, we explore the role of Cbl proteins in regulation of neuronal apoptosis. In two paradigms of neuron apoptosis -- nerve growth factor （NGF） deprivation and DNA damage -- cellular levels of c-Cbl and Cbl-b fell well before the onset of cell death. NGF deprivation also induced rapid loss of tyrosine phosphorylation （and most likely, activation） of c-Cbl. Targeting c-Cbl and Cbl-b with siRNAs to mimic their loss/inactivation sensitized neuronal cells to death promoted by NGF deprivation or DNA damage. One potential mechanism by which Cbl proteins might affect neuronal death is by regulation of apoptotic c-Jun N-terminal kinase （JNK） signaling. We demonstrate that Cbl proteins interact with the JNK pathway components mixed lineage kinase （MLK） 3 and POSH and that knockdown of Cbl proteins is sufficient to increase JNK pathway activity. Furthermore, expression of c-Cbl blocks the ability of MLKs to signal to downstream components of the kinase cascade leading to JNK activation and protects neuronal cells from death induced by MLKs, but not from downstream JNK activators. On the basis of these findings, we propose that Cbls suppress cell death in healthy neurons at least in part by inhibiting the ability of MLKs to activate JNK signaling. Apoptotic stimuli lead to loss of Cbl protein/activity, thereby removing a critical brake on JNK activation and on cell death.展开更多
Objective: Early gestational mammalian fetuses possess the amazing ability to heal cutaneous wounds in a scarless fashion. Over the past years, scientists have been working to decipher the mechanisms underlying this r...Objective: Early gestational mammalian fetuses possess the amazing ability to heal cutaneous wounds in a scarless fashion. Over the past years, scientists have been working to decipher the mechanisms underlying this regenerative repair. The remarkable phenotypic differences between fetal and adult healings behoves us to learn their characteristics in genetics, which represents potentially important mechanisms involved in wound repair observed in fetal versus adult tissues. In this sense, it is reasonable to construct subtractive cDNA library for future research. Methods: Middle laparotomy and hysterotomy were performed on pregnant rabbits at 20 day gestation to expose the fetal back, and a longitudinal incision through the skin was made on the back of the fetus. The traumatized fetal skin was harvested 12 hours post operation, the fetus control and traumatized adult skin specimens were taken at the same time. dscDNA was synthesized from total RNA of skin samples with SMART technology. Taking one of the three samples as Tester respectively and the other two as Drivers, we obtained 1 forward and 2 reverse hybridization products. After being amplified with selective polymerase chain reaction, the products were inserted into a vector, and then transferred into E.coli HB101. The colonies were screened afterwards. Results: The wounded fetuses were alive for a long time even after birth. Every determinant step, such as RNA isolation, cDNA synthesis, Rsa I digestion, adaptor ligation and hybridization, was well operated. Subtractive efficiency identification demonstrated that the suppression subtractive hybridization (SSH) was successful. Insertion into vector and transferring to E.coli were satisfactory. Conclusions: Instead of classic SSH, an improved SSH with 2 Drivers was applied for the experiment. Results confirmed that the improved program was reasonable and correct in both theory and practice. The subtractive cDNA library we have obtained is going to be used for future researches to reveal scarless healing related gene(s) and its (their) expression.展开更多
A series of biaxial two-level variable amplitude loading tests are conducted on smooth tubular specimens of LY12CZ alumin- ium alloy. The loading paths of 90° out-of-phase, 45° out-of-phase and 45° in-p...A series of biaxial two-level variable amplitude loading tests are conducted on smooth tubular specimens of LY12CZ alumin- ium alloy. The loading paths of 90° out-of-phase, 45° out-of-phase and 45° in-phase are utilized. The fatigue damage cumulative rules under two-level step loading of three loading paths are analyzed. By introducing a parameter a which is a function of the phase lag angle between the axial and the torsional loading, a new multiaxial nonlinear fatigue damage cumulative model is proposed. The proposed model is evaluated by the experimental aluminium alloy, and multi-level loading of 45 steel. Fatigue lives data for two-level loading, multi-level loading of LY12CZ predicted are within a factor of 2 scatter band.展开更多
基金Supported by National Natural Science Foundation of China(No.50528808)Australian Research Council(No. DP0451966)
文摘After the progressive collapse of Ronan Point apartment in UK in 1968, intensive research effort had been spent on developing guidelines for design of new or strengthening the existing structures to prevent progressive collapse. However, only very few building design codes provide some rather general guidance, no detailed design requirement is given. Progressive collapse of the Alfred P. Murrah Federal building in Oklahoma City and the World Trade Centre (WTC) sparked again tremendous research interest on progressive collapse of structures. Recently, US Department of Defence (DoD) and US General Service Administration (GSA) issued guidelines for structure progressive collapse analysis. These two guidelines are most commonly used, but their accuracy is not known. This paper presents numerical analysis of progressive collapse of an example frame structure to blast loads. The DoD and GSA procedures are also used to analyse the same example structure. Numerical results are compared and discussed. The accuracy and the applicability of the two design guidelines are evaluated.
基金Acknowledgments This work was supported by grants from the NIH/NINDS （NS33689） （L.A.G.） and from the National Science Foundation of China （NSFC） （30525007/30670663）, the Ministry of Science and Technology of China （2006AA02Z173/2007CB947202） and the Chinese Academy of Sciences （KSCX1-YW-R-59） （Z.X.）.
文摘Here, we explore the role of Cbl proteins in regulation of neuronal apoptosis. In two paradigms of neuron apoptosis -- nerve growth factor （NGF） deprivation and DNA damage -- cellular levels of c-Cbl and Cbl-b fell well before the onset of cell death. NGF deprivation also induced rapid loss of tyrosine phosphorylation （and most likely, activation） of c-Cbl. Targeting c-Cbl and Cbl-b with siRNAs to mimic their loss/inactivation sensitized neuronal cells to death promoted by NGF deprivation or DNA damage. One potential mechanism by which Cbl proteins might affect neuronal death is by regulation of apoptotic c-Jun N-terminal kinase （JNK） signaling. We demonstrate that Cbl proteins interact with the JNK pathway components mixed lineage kinase （MLK） 3 and POSH and that knockdown of Cbl proteins is sufficient to increase JNK pathway activity. Furthermore, expression of c-Cbl blocks the ability of MLKs to signal to downstream components of the kinase cascade leading to JNK activation and protects neuronal cells from death induced by MLKs, but not from downstream JNK activators. On the basis of these findings, we propose that Cbls suppress cell death in healthy neurons at least in part by inhibiting the ability of MLKs to activate JNK signaling. Apoptotic stimuli lead to loss of Cbl protein/activity, thereby removing a critical brake on JNK activation and on cell death.
文摘Objective: Early gestational mammalian fetuses possess the amazing ability to heal cutaneous wounds in a scarless fashion. Over the past years, scientists have been working to decipher the mechanisms underlying this regenerative repair. The remarkable phenotypic differences between fetal and adult healings behoves us to learn their characteristics in genetics, which represents potentially important mechanisms involved in wound repair observed in fetal versus adult tissues. In this sense, it is reasonable to construct subtractive cDNA library for future research. Methods: Middle laparotomy and hysterotomy were performed on pregnant rabbits at 20 day gestation to expose the fetal back, and a longitudinal incision through the skin was made on the back of the fetus. The traumatized fetal skin was harvested 12 hours post operation, the fetus control and traumatized adult skin specimens were taken at the same time. dscDNA was synthesized from total RNA of skin samples with SMART technology. Taking one of the three samples as Tester respectively and the other two as Drivers, we obtained 1 forward and 2 reverse hybridization products. After being amplified with selective polymerase chain reaction, the products were inserted into a vector, and then transferred into E.coli HB101. The colonies were screened afterwards. Results: The wounded fetuses were alive for a long time even after birth. Every determinant step, such as RNA isolation, cDNA synthesis, Rsa I digestion, adaptor ligation and hybridization, was well operated. Subtractive efficiency identification demonstrated that the suppression subtractive hybridization (SSH) was successful. Insertion into vector and transferring to E.coli were satisfactory. Conclusions: Instead of classic SSH, an improved SSH with 2 Drivers was applied for the experiment. Results confirmed that the improved program was reasonable and correct in both theory and practice. The subtractive cDNA library we have obtained is going to be used for future researches to reveal scarless healing related gene(s) and its (their) expression.
基金supported by the National Natural Science Foundation of China(Grant No.10702027)Aviation Science Funds of China(Grant No.2011ZA52016)Program for Changjiang Scholars and Innovative Research Team in University(Grant No.Irt0906)
文摘A series of biaxial two-level variable amplitude loading tests are conducted on smooth tubular specimens of LY12CZ alumin- ium alloy. The loading paths of 90° out-of-phase, 45° out-of-phase and 45° in-phase are utilized. The fatigue damage cumulative rules under two-level step loading of three loading paths are analyzed. By introducing a parameter a which is a function of the phase lag angle between the axial and the torsional loading, a new multiaxial nonlinear fatigue damage cumulative model is proposed. The proposed model is evaluated by the experimental aluminium alloy, and multi-level loading of 45 steel. Fatigue lives data for two-level loading, multi-level loading of LY12CZ predicted are within a factor of 2 scatter band.
