Inverse method for identifying the underlying crack distribution in plates with random strengths

Summary In the current investigation we seek to identify the underlying crack number and crack length distributions in brittle plates with a known strength distribution. The inverse problem in probabilistic fracture mechanics is defined, and the numerical procedure to solve the inverse problem is constructed. The simulation process of generating simulated plates containing simulated random cracks is elaborated. The maximum strain energy release rate criterion (G _max) is applied to each simulated random crack to find the crack strength. The strength of the simulated plate is equated to the strength of the weakest simulated crack in the plate based on the weakest link notion. The underlying crack number and crack length distributions are obtained by minimizing the difference between the simulated plate strengths and the known plate strengths. The gamma, lognormal and two-parameter Weibull distributions are employed for the underlying crack length distribution, and are compared in order to identify the best choice. Numerical examples demonstrate that the three PDFs are all acceptable for reasons to be explained. In the appendix, the direct problem in probabilistic fracture mechanics is presented as part of the demonstration of a method for using the crack distribution identified in the inverse problem to predict the strength and the probability of fracture in a practical application.     

生产二氧化氯的催化工艺及设备

在任意一种氧发生催化剂及无其它酸或不填加还原剂的条件下,采用氯酸与水进行化学还原反应产生二氧化氯和氧气的生产工艺和设备来生产二氧化氯。     

岩心PI值试验研究及应用

主要论述了在多功能采油化学用剂评价仪上进行的岩心ＰＩ值试验的步骤，现象及结论。重点考察了岩心ＰＩ值与渗透率、流量及注入截面面积的关系；平行管岩心复合ＰＩ值和其中单管岩心ＰＩ值的关系。     

Consequences of the photodynamic treatment of resting and activated peripheral T lymphocytes

Silencing of the cryptic mating-type loci HMR and HML requires the recognition of DNA sequence elements called silencers by the Sir1p, one of four proteins dedicated to the assembly of silenced chromatin in Saccharomyces cerevisiae. The Sir1p is thought to recognize silencers indirectly through interactions with proteins that bind the silencer DNA directly, such as the origin recognition complex (ORC). Eight recessive alleles of SIR1 were discovered that encode mutant Sir1 proteins specifically defective in their ability to recognize the HMR-E silencer. The eight missense mutations all map within a 17-amino-acid segment of Sir1p, and this segment was also required for Sir1p's interaction with Orc1p. The mutant Sir1 proteins could function in silencing if tethered to a silencer directly through a heterologous DNA-binding domain. Thus the amino acids identified are required for Sir1 protein's recognition of the HMR-E silencer and interaction with Orc1p, but not for its ability to function in silencing per se. The approach used to find these mutations may be applicable to defining interaction surfaces on proteins involved in other processes that require the assembly of macromolecular complexes.     

The functional role of CrkII in actin cytoskeleton organization and mitogenesis

Crk is a member of a family of adapter proteins predominantly composed of Src homology 2 and 3 domains, whose role in signaling pathways is presently unclear. Using an in situ electroporation system which permits the introduction of glutathione S-transferase (GST) fusion proteins into cells, we found that c-CrkII bound to p130(cas), but not to paxillin in serum-starved rat-1 fibroblasts overexpressing the human insulin receptor (HIRc cells) in vivo. 17 nM insulin stimulation dissociated the binding of c-CrkII to p130(cas), whereas 13 nM insulin-like growth factor-I, 16 nM epidermal growth factor (EGF), and 10% serum each showed little or no effect. We found that stress fiber formation is consistent with a change in the p130(cas).c-CrkII interactions before and after growth factor stimulation. Microinjection of either GST-Crk-SH2 or -Crk-(N)SH3 domains, or anti-Crk antibody each inhibited stress fiber formation before and after insulin-like growth factor-I, EGF, and serum stimulation. Insulin stimulation by itself caused stress fiber breakdown and there was no additive effect of microinjection. Microinjection of anti-p130(cas) antibody also blocked stress fiber formation in quiescent cells. Microinjection of the Crk-inhibitory reagents also inhibited DNA synthesis after insulin-like growth factor-I, EGF, and serum stimulation, but not after insulin. These data suggest that the complex containing p130(cas).c-CrkII may play a crucial role in actin cytoskeleton organization and in anchorage-dependent DNA synthesis.