Peripheral arteriogenesis is distinctly enhanced by increased fluid shear stress. Thus, the aim of this study was to investigate in the rat brain whether increased fluid shear stress can also stimulate cerebral arteriogenesis. To increase fluid shear stress in the cerebral circulation, we developed different shear stress models as the ligature of both common carotid arteries (Double-Ligature model), bilateral carotid ligature followed by creation of a unilateral arterio-venous fistula (two-stage protocol, Ligature-Shunt model), and unilateral arterio-venous fistula-creation alone (Solo-Shunt model). Blood flow changes were monitored in vivo by quantitative magnetic resonance imaging-analysis. Cerebral arteriogenesis was analyzed by magnetic resonance imaging and contrast agent-angiography. For proliferation and accumulation of mononuclear cells, immunohistochemistry was performed. During the 14 days-observation period, blood flow increased maximal by 5.5-fold in the A. basilaris and 10.3-fold in the fistula-sided A. cerebri posterior of the Ligature-Shunt model. Considerable vessel growth was found in all shear stress-stimulated arteries. Comparative analysis of vessel length and diameter versus blood flow indicated a correlation between the growth of cerebral collaterals and rising intravascular flow rates (R2=0.90/0.96). Immunohistochemistry showed the typical phases of arteriogenesis and accumulation of mononuclear cells. In conclusion, we provide evidence that fluid shear stress is not only the pivotal trigger of peripheral but also of cerebral arteriogenesis.
Damage models have significantly advanced predictions of ductile fractures in large, thin-walled structures like automobiles, ships, and aircraft. However, accurately predicting these fractures remains challenging due to variations in strain localization, ranging from biaxial compression to tension. This study introduces a specialized damage model for shell elements, utilizing data from shear, uniaxial, and plane tension tests.
The A1 domain in Von Willebrand Factor (VWF) initiates coagulation through binding to platelet glycoprotein GPIbα receptors. Von Willebrand Disease (VWD)-Mutations in A1 that either impair (type 2M) or enhance (type 2B) platelet adhesion to VWF can locally destabilize and even misfold the domain. We leveraged misfolding in the gain-of-function type 2B VWD phenotype as a target, distinct from the normal conformation.
Background And Objective: Deep vein thrombosis (DVT) of the lower limbs is a critical global vascular disease. Accurately assessing and predicting the efficacy of DVT treatment remains a significant challenge due to a lack of understanding of the mechanisms by which the level of patient-specific embolization and the rate of drug injection affect thrombolytic therapy.
Methods: In this study, we used the computed tomographic venography (CTV) clinical method to obtain patient-specific parameters, and the flow-solid interaction (FSI) method combined with biochemical response modeling of thrombolysis to analyze patient-specific hemodynamic and biomechanical characteristics and to quantitatively assess the effects of three vessel embolism levels (VEL) versus two drug injection rates (DIR) on bifurcated femoral venous thrombolytic therapy.
The State Key Laboratory for Artificial Microstructures and Mesoscopic Physics, School of Physics, Peking University, Beijing 100871, China; Center for Quantitative Biology, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing 100871, China;; Wenzhou Institute, University of Chinese Academy of Sciences, Wenzhou, Zhejiang 325001, China. Electronic address:
In the circulatory system, the microenvironment surrounding cancer cells is complex and involves multiple coupled factors. We selected two core physical factors, shear stress and hydraulic resistance, and constructed a microfluidic device with dual negative inputs to study the trade-off movement behavior of cancer cells when facing coupled factors. We detected significant shear stress escape phenomena in the MDA-MB-231 cell line and qualitatively explained this behavior using a cellular force model.
