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The fracture strength and cyclic crack-growth properties of surface-flawed, shot-peened D6AC steel plate were investigated. For short crack lengths (up to 1.5 mm) simple linear elastic fracture mechanics - based only on applied loading - did not predict the fracture strengths. Also, Paris' Law for cyclic crack growth did not correlate the crack-growth behavior. To investigate the effect of shot-peening, additional fracture and crack-growth tests were performed on material which was precompressed to remove the residual stresses left by the shot-peening. Both tests and analysis show that shot-peening residual stresses influence the fracture and crack-growth properties of the material. This report presents the analytical method of compensating for residual stresses and the fracture and cyclic crack-growth test results and predictions.
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The fracture strength and cyclic crack-growth properties of surface-flawed, shot-peened D6AC steel plate were investigated. For short crack lengths (up to 1.5mm) simple linear elastic fracture mechanics - based only on applied loading - did not predict the fracture strengths. Also, Paris' Law for cyclic crack growth did not correlate the crack-growth behavior. To investigate the effect of shot-peening, additional fracture and crack-growth tests were performed on material which was precompressed to remove the residual stresses left by the shot-peening. Both tests and analysis show that the shot-peening residual stresses influence the fracture and crack-growth properties of the material. The analytical method of compensating for residual stresses and the fracture and cyclic crack-growth test results and predictions are presented.
Leucine Carboxyl Methyltransferase-1 (LCMT-1) 3 methylates the carboxy-terminal leucine α-carboxyl group of the catalytic subunits of the protein phosphatase 2A (PP2A) subfamily of protein phosphatases, PP2Ac, PP4c, and PP6c. LCMT-1 differentially regulates the formation and function of a subset of the heterotrimeric complexes that PP2A and PP4 form with their regulatory subunits. Global LCMT-1 knockout causes embryonic lethality in mice, but LCMT-1 function in development is unknown. In the current study, we analyzed the effects of global LCMT-1 loss on embryonic development. LCMT-1 knockout causes loss of PP2Ac methylation, indicating that LCMT-1 is the sole PP2Ac methyltransferase. PP2A heterotrimers containing the Bα and Bδ B-type subunits are dramatically reduced in whole embryos, and the steady-state levels of PP2Ac and the PP2A structural A subunit are also down 30%. Strikingly, global loss of LCMT-1 causes severe defects in fetal hematopoiesis and death by embryonic day 16.5 (E16.5). Fetal livers of homozygous lcmt-1 knockout embryos display hypocellularity, elevated apoptosis, and greatly reduced numbers of hematopoietic stem and progenitor cell-enriched Kit + Lin - Sca1 + (KLS) cells. The percent cycling cells and mitotic indexes of wild-type and lcmt-1 knockout fetal liver cells are similar, suggesting that hypocellularity may be due to a combination of apoptosis and/or defects in specification, self-renewal, or survival of stem cells. Indicative of a possible intrinsic defect in stem cells, non-competitive and competitive transplantation experiments reveal that lcmt-1 loss causes a severe multi-lineage hematopoietic repopulating defect. Therefore, this study reveals a novel role for LCMT-1 as a key player in fetal liver hematopoiesis. Published under license by The American Society for Biochemistry and Molecular Biology, Inc. 2ff7e9595c
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