Effects of cold-rolling deformation on texture evolution and mechanical properties of Ti-29Nb-9Ta-10Zr alloy

International audienceThe crystallographic texture of Ti-29Nb-9Ta-10Zr alloy is studied after cold-rolling with different amounts of thickness reduction, up to 60%. The major texture components developed during cold-rolling were: γ-fibre components: {111}〈View the MathML source〉, {111}〈View the MathML source〉, {111}〈View the MathML source〉 and {111}〈View the MathML source〉; texture component: {112}〈View the MathML source〉 and texture components: {001}〈View the MathML source〉 and {010}〈001〉. Besides crystallographic texture the resulted mechanical properties were studied by nanoindentation. It was showed that the decrease in Young's modulus after different cold-rolling stages is mainly attributed to the stress-induced α″-Ti phase formation. At 60% cold-rolling thickness reduction obtained an elastic modulus close to 45.29±3.81 GPa, coupled with an average Vickers microhardness close to 279.83±4.28 HV

β1A Integrin Is a Master Regulator of Invadosome Organization and Function

Use of patterned surfaces, reverse genetics, and time-controlled photoinactivation showed that β1 but not β3 integrins are required for invadosome formation, self-assembly, and stabilization into a ring structure. The activation state of β1 as well as its phosphorylation by protein kinase C on Ser785 control these process and link to the degradative function

Texture evolution during ARB (Accumulative Roll Bonding) processing of Ti-10Zr-5Nb-5Ta alloy

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Texture evolution in a Ti-Ta-Nb alloy processed by severe plastic deformation

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The Membrane-targeted Alkylphosphocholine Erufosine Interferes with Survival Signals from the Extracellular Matrix

Integrin-dependent adhesion of tumor cells to extracellular matrix proteins provides anchorage-dependent protection from cell death. In the present investigation we aimed to understand whether and how the paradigmatic membrane-targeted synthetic phospholipid analog erufosine is relevant for tumor cell adhesion to extracellular matrix proteins, cell survival and migration. The antineoplastic action of erufosine was analyzed with glioblastoma and prostate cancer cells adhering to fibronectin or collagen I using proliferation, adhesion and migration assays. The composition of adhesion contacts containing activated beta 1 integrins was studied using immunofluorescence. The importance of beta 1 integrins for the observed effects was analyzed in fibroblasts proficient or deficient in beta 1 integrin expression. Adhesion to collagen I and fibronectin increased the death threshold in serum-deprived tumor cells. Moreover, beta 1 integrin-deficient cells were more sensitive to erufosine-treatment compared to beta 1 integrin proficient cells suggesting a role of beta 1 integrins for matrix-mediated death resistance. Most importantly, erufosine disturbed the maturation of the cell adhesion complexes containing paxillin, activated beta 1 integrins and phosphorylated FAK, leading to a reduction of survival signals and inhibition of tumor cell adhesion and migration. These findings suggest that membrane-targeted synthetic phospholipids analogs may be of value for counteracting matrix-mediated treatment resistance in combined treatment approaches with radiotherapy or chemotherapy