Shear-Stress Formulas and the Shear Center for Curved Beams

1978 ◽  
Vol 45 (2) ◽  
pp. 438-439
Author(s):  
R. Schmidt
2002 ◽  
Vol 5 (4) ◽  
pp. 195-209 ◽  
Author(s):  
Genshu Tong ◽  
Qiang Xu

Currently available theories for thin-walled curved beams lack rigorous theoretical development. This paper provides a detailed derivation of an exact theory for biaxial bending and torsion of thin-walled circularly curved beams with any open profile. The derivation is based on two well-accepted assumptions in the theory of thin-walled members. Exact expressions for longitudinal displacement, longitudinal normal stress and shear stress and their resultants are presented. Simplified theories are also given for practical applications.


2012 ◽  
Vol 80 (1) ◽  
Author(s):  
Eduardo Velazquez ◽  
J. B. Kosmatka

In-plane bending of curved beams produces substantial through-thickness normal and shear stresses that can result in structural failures. A half-elliptic curved beam, having a known prescribed variable radius of curvature, is studied as an extension of the previously published circular arc beam. The equations for the normal, tangential, and shear stresses are developed for a curved beam outlined by two confocal half ellipses loaded by a pair of concentrated perpendicular forces on its ends. Closed-form analytical solutions for the stresses are found using an elasticity approach, where the solution is found by using selected terms of the biharmonic equation in elliptic coordinates. For the case of an elliptic beam with an aspect ratio of very close to unity, the solution closely agrees with published circular beam solutions. For other elliptic beam aspect ratios, the calculated stresses display good correlation to detailed finite element model solutions for thickness to semi-axis ratios < 0.1. A parametric study revealed that the maximum normal stress is located at the midplane for high-aspect ratio (a/b ≥ 1) half-elliptic beams, but shifts toward the load tip for low aspect ratio (a/b < 1) beams due to local curvature effects. Moreover, the peak shear stress location moves toward the midplane and the magnitude greatly increases as the aspect ratio is increased. Thus, there are large normal and shear stress interactions occurring near the midplane for high-aspect ratio half-elliptic beams, which is not observed for circular beams. These stress interactions can produce unique failures in materials having low shear strength and through-thickness strength. The current closed-form solution is an improvement on previously published approximate solutions.


2020 ◽  
Vol 134 (17) ◽  
pp. 2399-2418
Author(s):  
Yoshito Yamashiro ◽  
Hiromi Yanagisawa

Abstract Blood vessels are constantly exposed to mechanical stimuli such as shear stress due to flow and pulsatile stretch. The extracellular matrix maintains the structural integrity of the vessel wall and coordinates with a dynamic mechanical environment to provide cues to initiate intracellular signaling pathway(s), thereby changing cellular behaviors and functions. However, the precise role of matrix–cell interactions involved in mechanotransduction during vascular homeostasis and disease development remains to be fully determined. In this review, we introduce hemodynamics forces in blood vessels and the initial sensors of mechanical stimuli, including cell–cell junctional molecules, G-protein-coupled receptors (GPCRs), multiple ion channels, and a variety of small GTPases. We then highlight the molecular mechanotransduction events in the vessel wall triggered by laminar shear stress (LSS) and disturbed shear stress (DSS) on vascular endothelial cells (ECs), and cyclic stretch in ECs and vascular smooth muscle cells (SMCs)—both of which activate several key transcription factors. Finally, we provide a recent overview of matrix–cell interactions and mechanotransduction centered on fibronectin in ECs and thrombospondin-1 in SMCs. The results of this review suggest that abnormal mechanical cues or altered responses to mechanical stimuli in EC and SMCs serve as the molecular basis of vascular diseases such as atherosclerosis, hypertension and aortic aneurysms. Collecting evidence and advancing knowledge on the mechanotransduction in the vessel wall can lead to a new direction of therapeutic interventions for vascular diseases.


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