Role of harmful impurities in failure of high-strength steels

Conclusions The high-strength, medium-alloy, martensitic steels subjected to low-temperature tempering are characterized by intragranular adsorption of harmful impurities, which reduces the microductility of intragranular failure. Two types of failure take place in this case: fine-dimpled for the steels with _B 1700 MPa, and quasicleavage with _B 1850 MPa.Fine-dimpled failure is associated with adsorption of harmful impurities at the carbide-matrix and fine nonmetallic inclusion-matrix interfacial boundaries. Quasicleavage is supported by adsorption of phosphorus and sulfur on intragranular interfaces: inherited austenite boundaries, subboundaries, martensite crystal boundaries.A reduction of the content of free phosphorus and sulfur increases the microductility of the fracture surfaces of the high-strength steels and greatly increases the fracture toughness and reliability of the steel in service.Translated from Fiziko-Khimicheskaya Mekhanika Materialov, Vol. 27, No. 5, pp. 89–94, September–October, 1991.     

Metabolism of native and naturally occurring multiple modified low density lipoprotein in smooth muscle cells of human aortic intima

The subfraction of low density lipoprotein (LDL) with low sialic acid content that caused accumulation of cholesterol esters in human aortic smooth muscle cells has been found in the blood of coronary atherosclerosis patients. It was demonstrated that this subfraction consists of LDL with small size, high electronegative charge, reduced lipid content, altered tertiary structure of apolipoprotein B, etc. LDL of this subfraction is naturally occurring multiple-modified LDL (nomLDL). In this study we compared the binding, uptake and proteolytic degradation of native LDL and nomLDL by smooth muscle cells cultured from human grossly normal intima, fatty streaks, and atherosclerotic plaques. Uptake of nomLDL by normal and atherosclerotic cells was 3.5- and 6-fold, respectively, higher than uptake of native LDL. Increased uptake of nomLDL was due to increased binding of this LDL by intimal smooth muscle cells. The enhanced binding is explained by the interaction of nomLDL with cellular receptors other than LDL-receptor. Modified LDL interacted with the scavenger receptor, asialoglycoprotein receptor, and also with cell surface proteoglycans. Rates of degradation of nomLDL were 1.5- and 5-fold lower than degradation of native LDL by normal and atherosclerotic cells, respectively. A low rate of nomLDL degradation was also demonstrated in homogenates of intimal cells. Activities of lysosomal proteinases of atherosclerotic cells were decreased compared with normal cells. Pepstatin A, a cathepsin D inhibitor, completely inhibited lipoprotein degradation, while serine, thiol, or metallo-proteinase inhibitors had partial effect. This fact reveals that cathepsin D is involved in initial stages of apoB degradation by intimal smooth muscle cells. Obtained data show that increased uptake and decreased lysosomal degradation of nomLDL may be the main cause of LDL accumulation in human aortic smooth muscle cells, leading to foam cell formation.