scholarly journals Effect of Bundled Tubular System on Response of Building Subjected to Dynamic Wind Loads

Author(s):  
Purva B. Ghodam
Keyword(s):  
Author(s):  
H. W. Tieleman ◽  
M. A. K. Elsayed ◽  
M. R. Hajj
Keyword(s):  

2021 ◽  
Author(s):  
Thomas G. Ivanco ◽  
Donald F. Keller ◽  
Jennifer L. Pinkerton

Author(s):  
Emil Simiu ◽  
Rene D. Gabbai

Current approaches to the estimation of wind-induced wind effects on tall buildings are based largely on 1970s and 1980s technology, and were shown to result in some cases in errors of up to 40%. Improvements are needed in: (i) the description of direction-dependent aerodynamics; (ii) the description of the direction-dependent extreme wind climate; (iii) the estimation of inertial wind effects induced by fluctuating aerodynamic forces acting on the entire building envelope; (iv) the estimation of uncertainties inherent in the wind effects; and (v) the use of applied wind forces, calculated inertial forces, and uncertainty estimates, to obtain via influence coefficients accurate and risk-consistent estimates of wind-induced internal forces or demand-to-capacity ratios for any individual structural member. Methods used in current wind engineering practice are especially deficient when the distribution of the wind loads over the building surface and their effects at levels other than the building base are not known, as is the case when measurements are obtained by the High-Frequency Force Balance method, particularly in the presence of aerodynamic interference effects due to neighboring buildings. The paper describes a procedure that makes it possible to estimate wind-induced internal forces and demand-to-capacity ratios in any individual member by: developing aerodynamic and wind climatological data sets, as well as aerodynamic/climatological directional interaction models; significantly improving the quality of the design via rigorous structural engineering methods made possible by modern computational resources; and properly accounting for knowledge uncertainties. The paper covers estimates of wind effects required for allowable stress design, wherein knowledge uncertainties pertaining to the parameters that determine the wind loading are not considered, as well as estimates required for strength design, in which these uncertainties need to be accounted for explicitly.


2019 ◽  
Vol 26 ◽  
pp. 100884
Author(s):  
Kelly Samara ◽  
Mingyu Sun ◽  
Eun Jeong Cha ◽  
James LaFave

1977 ◽  
Author(s):  
Jonathan M. Gerrard ◽  
James G. White

Evidence that the dense tubular system (DTS) is the site of platelet prostaglandin synthesis derives from several observations. First platelet peroxidase is localized in the DTS. Aminotriazole which inhibits the platelet peroxidase, inhibits prostaglandin biosynthesis at the same concentration. Secondly, a similar peroxidase occurs in the secretory cells of the sheep vesicular gland (SVG) and other cells known to be involved in prostaglandin synthesis. Third, the DTS is smooth endoplasmic reticulum (SER) and SER, which is abundant in the prostaglandin synthesizing columnar cells of the SVG secretory units, is known to be involved in lipid synthesis and metabolism in other tissues. Evidence that calcium is stored in the DTS derives from ultrastructural studies showing that the DTS is analagous to the sarcotubules of skeletal muscle, and that the DTS has the capacity to bind divalent cations. Evidence that calcium flux and prostaglandin synthesis are closely linked comes from several observations which suggest 1) that movement of calcium ions to the site where arachidonic acid (AA) is released from the precursor phospholipids to be used for synthesis of prostaglandins, stimulates the AA release and 2) that synthesized prostaglandin G2, prostaglandin H2, and/or thromboxane A2 initiate platelet contraction by moving calcium from the site of synthesis to the vicinity of the contractile actin and myosin. The results suggest that the DTS, prostaglandin and thromboxane synthesis, and calcium flux are integral parts of the system modulating platelet activation.


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