Consequences of gold nanoparticles of MHD blood flow in a wavy tube with wall properties

Author(s):  
Naheeda Iftikhar ◽  
Hina Sadaf ◽  
Abdul Rehman
2008 ◽  
Vol 20 (9) ◽  
pp. 21
Author(s):  
L. A. Vodstrcil ◽  
J. Novak ◽  
M. Tare ◽  
M. E. Wlodek ◽  
L. J. Parry

During pregnancy, the uteroplacental circulation undergoes dramatic alterations to allow for the large increase in blood flow to the feto-placental unit. These alterations are achieved through several mechanisms including structural changes in the uterine artery wall and endothelium-dependent vasodilation. Small renal arteries of relaxin-deficient mice and rats have enhanced myogenic reactivity and decreased passive compliance, and are relatively vasoconstricted (Novak et al. 2001, 2006). To date, no study has identified relaxin receptors (Rxfp1) in arteries or investigated the effects of relaxin deficiency in pregnancy on uterine artery function. The aims of this current study were to: 1) localise Rxfp1 in the uterine arteries, 2) measure myogenic reactivity in small uterine arteries after relaxin treatment, and 3) test the hypothesis that blocking circulating relaxin in late pregnancy will increase uterine artery wall stiffness. We demonstrated that Rxfp1 is expressed in the uterine arteries of pregnant mice and rats. Brightfield immunohistochemistry and immunofluorescence using antibodies specific for rat Rxfp1, α-smooth muscle actin and CD31 localised Rxfp1 protein predominantly to the vascular smooth muscle in the uterine artery of pregnant rats. Administration of recombinant human H2 relaxin (4 ug/h) for 6 h or 5 days in intact and ovariectomised rats reduced myogenic reactivity of small uterine arteries in vitro. Pregnant rats were treated with a monoclonal antibody against circulating relaxin (MCA1) or control (MCAF) for 3 days (Days 17–19) and uterine arteries were mounted on a pressure myograph to assess passive mechanical wall properties. Neutralising circulating relaxin in late pregnancy resulted in a significant increase in uterine artery wall stiffness. These data demonstrate that relaxin acts on the vascular smooth muscle cells in the uterine artery and may be involved in the pregnancy-specific vascular remodelling of uterine arteries to increase vasodilation and blood flow to the uterus and placenta. (1) Novak J et al. (2001). J Clin Invest 107: 1469–75 (2) Novak J et al. (2006). FASEB J 20: 2352–62


Author(s):  
Guanglei Xiong ◽  
C. Alberto Figueroa ◽  
Nan Xiao ◽  
Charles A. Taylor

Previous efforts to simulate blood flow in patient-specific models either assumed rigid vessel walls or deformable walls with constant mechanical property [1]. We have developed a new workflow to enable blood flow and vessel dynamics simulations using subject-specific geometry and variable wall properties. The geometric model construction is based on 3D segmentation and geometric processing which greatly reduce human labor and increase the objectivity of the model. Variable wall properties are assigned to the model based on combining centerline-based and surface-based methods. This new approach was successfully applied to simulate blood flow and wall dynamics in models with abdominal, thoracic, and cerebral aneurysms.


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