Patient-Specific Numerical Simulations of Coronary Artery Hemodynamics and Biomechanics: A Pathway to Clinical Use.

Purpose: Numerical models that simulate the behaviors of the coronary arteries have been greatly improved by the addition of fluid-structure interaction (FSI) methods. Although computationally demanding, FSI models account for the movement of the arterial wall and more adequately describe the biomechanical conditions at and within the arterial wall. This offers greater physiological relevance over Computational Fluid Dynamics (CFD) models, which assume the walls do not move or deform.

A spatiotemporal analysis of the left coronary artery biomechanics using fluid-structure interaction models.

Biomechanics plays a critical role in coronary artery disease development. FSI simulation is commonly used to understand the hemodynamics and mechanical environment associated with atherosclerosis pathology. To provide a comprehensive characterization of patient-specific coronary biomechanics, an analysis of FSI simulation in the spatial and temporal domains was performed.

An in situ inferior vena cava ligation-stenosis model to study thrombin generation rates with flow.

Background: Blood flow-induced shear stress affects platelet participation in coagulation and thrombin generation. We aimed to develop an in vivo model to characterize thrombin generation rates under flow.

Methods: An in situ inferior vena cava (IVC) ligation-stenosis model was established using C57BL/6 mice.

SARS-CoV-2 Exacerbates COVID-19 Pathology Through Activation of the Complement and Kinin Systems.

Infection with SARS-CoV-2 triggers the simultaneous activation of innate inflammatory pathways including the complement system and the kallikrein-kinin system (KKS) generating in the process potent vasoactive peptides that contribute to severe acute respiratory syndrome (SARS) and multi-organ failure. The genome of SARS-CoV-2 encodes four major structural proteins - the spike (S) protein, nucleocapsid (N) protein, membrane (M) protein, and the envelope (E) protein. However, the role of these proteins in either binding to or activation of the complement system and/or the KKS is still incompletely understood.

gC1qR Antibody Can Modulate Endothelial Cell Permeability in Angioedema.

Angioedema is characterized by swelling of the skin or mucous membranes. Overproduction of the vasodilator bradykinin (BK) is an important contributor to the disease pathology, which causes rapid increase in vascular permeability. BK formation on endothelial cells results from high molecular weight kininogen (HK) interacting with gC1qR, the receptor for the globular heads of C1q, the first component of the classical pathway of complement.

SARS-CoV-2 and Plasma Hypercoagulability.

Hypercoagulability has emerged as a prominent consequence of COVID-19. This presents challenges not only in the clinic, but also in thrombosis research. Health and safety considerations, the status of the blood and plasma supply, the infection status of individual donors, and the mechanisms by which SARS-CoV-2 activates coagulation are all of concern.