Room Temperature Viscous Flow of Amorphous Silica Induced by Electron Beam Irradiation.

The increasing use of oxide glasses in high-tech applications illustrates the demand of novel engineering techniques on nano- and microscale. Due to the high viscosity of oxide glasses at room temperature, shaping operations are usually performed at temperatures close or beyond the point of glass transition Tg . Those treatments, however, are global and affect the whole component. It is known from the literature that electron irradiation facilitates the viscous flow of amorphous silica near room temperature for nanoscale components. At the micrometer scale, however, a comprehensive study on this topic is still pending. In the present study, electron irradiation inducing viscous flow at room temperature is observed using a micropillar compression approach and amorphous silica as a model system. A comparison to high temperature yielding up to a temperature of 1100 °C demonstrates that even moderate electron irradiation resembles the mechanical response of 600 °C and beyond. As an extreme case, a yield strength as low as 300 MPa is observed with a viscosity indicating that Tg has been passed. Those results show that electron irradiation-facilitated viscous flow is not limited to the nanoscale which offers great potential for local microengineering.

Local Deformation of Glasses is Mediated by Rigidity Fluctuation on Nanometer Scale.

Microscopic deformation processes determine defect formation on glass surfaces and, thus, the material's resistance to mechanical failure. While the macroscopic strength of most glasses is not directly dependent on material composition, local deformation and flaw initiation are strongly affected by chemistry and atomic arrangement. Aside from empirical insight, however, the structural origin of the fundamental deformation modes remains largely unknown. Experimental methods that probe parameters on short or intermediate length-scale such as atom-atom or superstructural correlations are typically applied in the absence of alternatives. Drawing on recent experimental advances, spatially resolved Raman spectroscopy is now used in the THz-gap for mapping local changes in the low-frequency vibrational density of states. From direct observation of deformation-induced variations on the characteristic length-scale of molecular heterogeneity, it is revealed that rigidity fluctuation mediates the deformation process of inorganic glasses. Molecular field approximations, which are based solely on the observation of short-range (interatomic) interactions, fail in the prediction of mechanical behavior. Instead, glasses appear to respond to local mechanical contact in a way that is similar to that of granular media with high intergranular cohesion.

Atrial myocardium is the predominant inotropic target of adrenomedullin in the human heart.

Adrenomedullin (ADM) is an endogenous peptide with favorable hemodynamic effects in vivo. In this study, we characterized the direct functional effects of ADM in isolated preparations from human atria and ventricles. In electrically stimulated human nonfailing right atrial trabeculae, ADM (0.0001-1 micromol/l) increased force of contraction in a concentration-dependent manner, with a maximal increase by 35 +/- 8% (at 1 micromol/l; P < 0.05). The positive inotropic effect was accompanied by a disproportionate increase in calcium transients assessed by aequorin light emission [by 76 +/- 20%; force/light ratio (DeltaF/DeltaL) 0.58 +/- 0.15]. In contrast, elevation of extracellular calcium (from 2.5 to 3.2 mmol/l) proportionally increased force and aequorin light emission (DeltaF/DeltaL 1.0 +/- 0.1; P < 0.05 vs. ADM). Consistent with a cAMP-dependent mechanism, ADM (1 micromol/l) increased atrial cAMP levels by 90 +/- 12%, and its inotropic effects could be blocked by the protein kinase A (PKA) inhibitor H-89. ADM also exerted positive inotropic effects in failing atrial myocardium and in nonfailing and failing ventricular myocardium. The inotropic response was significantly weaker in ventricular vs. atrial myocardium and in failing vs. nonfailing myocardium. In conclusion, ADM exerts Ca(2+)-dependent positive inotropic effects in human atrial and less-pronounced effects in ventricular myocardium. The inotropic effects are related to increased cAMP levels and stimulation of PKA. In heart failure, the responsiveness to ADM is reduced in atria and ventricles.

Insulin causes [Ca2+]i-dependent and [Ca2+]i-independent positive inotropic effects in failing human myocardium.

BACKGROUND: Insulin has been shown to exert positive inotropic effects in several in vitro and in vivo models, but signal transduction and substrate dependency remain unclear. We examined inotropic responses and signal transduction mechanisms of insulin in human myocardium. METHODS AND RESULTS: Experiments were performed in isolated trabeculae from end-stage failing hearts of 58 nondiabetic and 3 diabetic patients undergoing heart transplantation. The effect of insulin (0.3 and 3 IU/L) on isometric twitch force (37 degrees C, 1 Hz) was tested in the presence of glucose or pyruvate as energetic substrate. Furthermore, intracellular Ca2+ transients (aequorin method), sarcoplasmic reticulum (SR) Ca2+ content (rapid cooling contractures), and myofilament Ca2+ sensitivity (semiskinned fibers) were assessed. In addition, potential signaling pathways were tested by blocking glycolysis, PI-3-kinase, protein kinase C, diacylglycerol kinase, insulin-like growth factor-1 receptors, or transsarcolemmal Ca2+ entry via the Na+/Ca2+ exchanger. Insulin exerted concentration-dependent and partially substrate-dependent positive inotropic effects. The phosphatidylinositol-3-kinase inhibitor wortmannin and the Na2+/Ca2+ exchanger reverse-mode inhibitor KB-R7943 completely or partially prevented the functional effects of insulin. In contrast, insulin-like growth factor-1 receptor blockade, protein kinase C inhibition, and diacylglycerol kinase blockade were without effect. The inotropic response was associated with increases in intracellular Ca2+ transients, SR Ca2+ content, and increased myofilament Ca2+ sensitivity. CONCLUSIONS: Insulin exerts Ca2+-dependent and -independent positive inotropic effects through a phosphatidylinositol-3-kinase-dependent pathway in failing human myocardium. The increased [Ca2+]i originates at least in part from enhanced reverse-mode Na+/Ca2+ exchange and consequently increased SR-Ca2+ load. These nongenomic functional effects of insulin may be of clinical relevance, eg, during insulin-glucose-potassium infusions.