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I-girders with circular corrugated webs are considered as a new fabrication technology. The corrugation of the web considerably increases the stiffness of the cross-section to resist shear forces and also increases the out-of-plane stiffness. However, investigations on the lateral-torsional buckling behavior of the circular corrugated web girders are still scarce. Therefore, the present study focuses on the lateral-torsional buckling performance of these types of girders. A numerical study is performed in order to simulate the inelastic lateral-torsional buckling behavior of the I-girders with the circular corrugated web using ABAQUS software. A parametric study is carried out taking into account both linear and non-linear buckling analyses, to investigate the effect of different geometrical parameters on the inelastic lateral-torsional buckling behavior using three different corrugated web profiles. The results indicate that increasing the corrugation depth, flange width, flange thickness, and web height increases the moment capacity of these girders. The results of the parametric study show that the moment capacity of the I-girders with the circular corrugated web is higher than those with flat web girders.

We investigated the mechanism by which a1-adrenergic activation regulates basal and stimulated whole cell L-type Ca current (ICa) in rat ventricular myocytes using the physiological neurotransmitter, norepinephrine (NE, 10µM). Stimulation of a1-adrenoceptors, achieved by NE+10µM esmolol (a ß-receptor antagonist), had no significant effect on basal ICa. a1-adrenergic activation had a marked inhibitory effect on ICa elevated by ß activation (NE+1µM) prazosin, an a1-receptor antagonist) or activation of adenylyl cyclase by forskolin (25µM); the inhibitory effect was reversible upon washout. However, a1-adrenergic stimulation had no significant effect on ICa previously increased by intracellular application of cAMP (25µM). The inhibitory effect seen on ICa elevated by NE showed no significant shift of either I–V or inactivation curves. It is unlikely that the inhibitory effect of a1-adrenergic stimulation on NE or forskolin-elevated ICa is mediated through activation of Ca-dependent protein kinase C or changes in intracellular free Ca (pCa=8.5, EGTA 5 mM) or cAMP-dependent phosphodiesterase. We conclude that a1-adrenergic inhibition of ß-adrenergic stimulated-ICa is probably mediated through an as yet unknown G-protein. This inhibitory effect could serve as a regulatory feedback mechanism in physiological and pathophysiological settings.

Objective: The hypothesis being tested in the present study is that increased anisotropic properties occurs in the remodeled post-infarction heart due to spatial alterations in Kv channels expression and K+ currents of the remodeled myocardium. Methods: Three to 4 weeks post myocardial infarction (MI) in the rat, we measured the two components of the outward K+ current, Ito-fast (f) and Ito-slow(s) in the epicardium (epi) and endocardium (endo) of noninfarcted remodeled left ventricle (LV) using patch clamp techniques. Alterations in mRNA and/or protein levels of potassium channel genes Kv1.4, Kv1.5, Kv2.1, Kv4.2 and Kv4.3 were measured in epi, midmyocardium (mid), and endo regions of LV and in the right ventricle (RV). Results: In sham operated rat heart, the density of Ito-f was 2.3 times greater in epi compared to endo myocytes. In post-MI heart, the density of Ito-f and Ito-s decreased to a similar degree in LV epi and endo but the difference in Ito-f density between epi and endo persisted. The mRNA and/or protein levels of Kv1.4, Kv2.1, Kv4.2 and Kv4.3 but not Kv1.5 decreased to a varying extent in different regions of LV but not in RV of post-MI heart. Conclusions: Our results suggest that regional downregulation of Kv channels expression and density of K+ currents can be a significant determinant of increased spatial electrophysiological heterogeneity and contribute to increased electrical instability of the post-MI heart.