Flow shear stress applied in self-buffered microbial fuel cells

2020 ◽  
Vol 99 ◽  
pp. 324-330
Author(s):  
Chin-Tsan Wang ◽  
Raymond Chong Ong Tang ◽  
Men-Wei Wu ◽  
Akhil Garg ◽  
Aristotle T. Ubando ◽  
...  
Keyword(s):  
Shear Stress ◽  
Fuel Cells ◽  
Microbial Fuel Cells ◽  
Flow Shear ◽  
Flow Shear Stress

scholarly journals The Effect of Fluid Flow Shear Stress and Substrate Stiffness on Yes-Associated Protein (YAP) Activity and Osteogenesis in Murine Osteosarcoma Cells

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3128
Author(s):  
Thomas R. Coughlin ◽  
Ali Sana ◽  
Kevin Voss ◽  
Abhilash Gadi ◽  
Upal Basu-Roy ◽  
...  
Keyword(s):  
Shear Stress ◽  
Fluid Flow ◽  
Bone Cells ◽  
Bone Cancer ◽  
Substrate Stiffness ◽  
Flow Shear ◽  
Fluid Movement ◽  
Flow Shear Stress ◽  
Fluid Flow Shear Stress ◽  
New Treatments

Osteosarcoma (OS) is an aggressive bone cancer originating in the mesenchymal lineage. Prognosis for metastatic disease is poor, with a mortality rate of approximately 40%; OS is an aggressive disease for which new treatments are needed. All bone cells are sensitive to their mechanical/physical surroundings and changes in these surroundings can affect their behavior. However, it is not well understood how OS cells specifically respond to fluid movement, or substrate stiffness—two stimuli of relevance in the tumor microenvironment. We used cells from spontaneous OS tumors in a mouse engineered to have a bone-specific knockout of pRb-1 and p53 in the osteoblast lineage. We silenced Sox2 (which regulates YAP) and tested the effect of fluid flow shear stress (FFSS) and substrate stiffness on YAP expression/activity—which was significantly reduced by loss of Sox2, but that effect was reversed by FFSS but not by substrate stiffness. Osteogenic gene expression was also reduced in the absence of Sox2 but again this was reversed by FFSS and remained largely unaffected by substrate stiffness. Thus we described the effect of two distinct stimuli on the mechanosensory and osteogenic profiles of OS cells. Taken together, these data suggest that modulation of fluid movement through, or stiffness levels within, OS tumors could represent a novel consideration in the development of new treatments to prevent their progression.

Temporal gradient in shear-induced signaling pathway: involvement of MAP kinase, c-fos, and connexin43

2000 ◽  
Vol 278 (5) ◽  
pp. H1598-H1605 ◽  
Author(s):  
Xuping Bao ◽  
Craig B. Clark ◽  
John A. Frangos
Keyword(s):  
Shear Stress ◽  
Mrna Expression ◽  
Signaling Pathway ◽  
Steady Shear ◽  
Flow Shear ◽  
Temporal Gradient ◽  
Step Flow ◽  
Shear Component ◽  
Flow Shear Stress ◽  
Impulse Flow

The effect of a temporal gradient in shear and steady shear on the activity of extracellular signal-regulated protein kinases 1 and 2 (ERK1/ERK2), c- fos, and connexin43 (Cx43) in human endothelial cells was investigated. Three laminar flow profiles (16 dyn/cm2), including impulse flow (shear stress abruptly applied for 3 s), ramp flow (shear stress smoothly transitioned at flow onset), and step flow (shear stress abruptly applied at flow onset) were utilized. Relative to static controls, impulse flow stimulated the phosphorylation of ERK1/ERK2 8.5- to 7.5-fold, respectively at 10 min, as well as the mRNA expression of c- fos 51-fold at 30 min, and Cx43 8-fold at 90 min. These high levels of mRNA expression were sustained for at least 4 h. In contrast, ramp flow was unable to significantly induce gene expression and even inhibited the activation of ERK1/ERK2. Step flow, which contains both a sharp temporal gradient in shear stress and a steady shear component, elicited only moderate and transient responses, indicating the distinct role of these fluid shear stimuli in endothelial signal transduction. The specific inhibitor of mitogen-activated protein kinase kinase PD-98059 inhibited impulse flow-induced c -fos and Cx43 mRNA expression. Thus these findings implicate the involvement of ERK1/ERK2, c -fos, and Cx43 in the signaling pathway induced by the temporal gradient in shear.

Microfluidic models of physiological or pathological flow shear stress for cell biology, disease modeling and drug development

2019 ◽  
Vol 117 ◽  
pp. 186-199 ◽  
Author(s):  
Huaying Chen ◽  
Zhihang Yu ◽  
Siwei Bai ◽  
Huaxiu Lu ◽  
Dong Xu ◽  
...  
Keyword(s):  
Shear Stress ◽  
Drug Development ◽  
Cell Biology ◽  
Disease Modeling ◽  
Flow Shear ◽  
Flow Shear Stress

scholarly journals Advanced human carotid plaque progression correlates positively with flow shear stress using follow-up scan data: An in vivo MRI multi-patient 3D FSI study

2010 ◽  
Vol 43 (13) ◽  
pp. 2530-2538 ◽  
Author(s):  
Chun Yang ◽  
Gador Canton ◽  
Chun Yuan ◽  
Marina Ferguson ◽  
Thomas S. Hatsukami ◽  
...  
Keyword(s):  
Shear Stress ◽  
Carotid Plaque ◽  
Plaque Progression ◽  
Flow Shear ◽  
Flow Shear Stress ◽  
Scan Data ◽  
Human Carotid

The Influence of Temperature and Humidity on the ABS Contaminations

2014 ◽  
Author(s):  
Fuhao Cui ◽  
Jinhong Hu ◽  
Yue Peng ◽  
Hui Li ◽  
Shengnan Shen ◽  
...  
Keyword(s):  
Shear Stress ◽  
Flow Pattern ◽  
Air Flow ◽  
Disk Drive ◽  
Flying Height ◽  
Flow Shear ◽  
Slip Boundary ◽  
Temperature And Humidity ◽  
Flow Shear Stress ◽  
The Impact

In order to increase the areal recording density of hard disk drive beyond 1 Tb/in2, the flying height has to be reduced to several nanometers. At such a low flying height, particles and lube contaminations, which could lead to a transient vibration and flying height modulation in a hard disk drive, are becoming more and more serious. In this work, it studies the influence of temperature and humidity on the air flow pattern, velocity and shear stress distribution on the air bearing surface (ABS) of slider using a self-developed simulator. It first solves the generalized steady state Reynolds equation with slip boundary conditions. Then it solves the reduced Navier-Stokes (N-S) equation with slip boundary conditions to get the air velocity distribution, i.e., identify the air flow pattern on the ABS. The stagnation lines and areas of air flow are calculated to judge the contamination area. On the other hand, it calculates the air shear stress distribution on the ABS since the air shear stress is the main driving force for the lubricant and particles migration and contaminations. After that, the impact of the temperature and humidity on the air flow pattern is analyzed by applying the Sutherland equation and mixed gas viscosity calculation equation. The simulation results indicate that the impact of temperature and humidity on the air flow pattern is un-conspicuous. However, the peak velocity of the air flow, which contains no vapor, reduces almost 10%, and the peak air flow shear stress increases less than 1.5%, with the increase of operational temperature from 298.15 K to 343.15 K. In addition, the peak velocity of the air flow increasing almost 4%, and the peak air flow shear stress keeps almost same, with the increase of the operational mole fraction of vapor from 5% to 15%.

A New Hypothesis for Human Atherosclerotic Plaque Progression Based on Serial In Vivo MRI and Computational Modeling Method

2007 ◽  
Author(s):  
Sayan Mondal ◽  
Chun Yang ◽  
Joseph D. Petruccelli ◽  
Chun Yuan ◽  
Fei Liu ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Thickness ◽  
Computational Models ◽  
Ex Vivo ◽  
Maximum Principal Stress ◽  
Magnetic Resonance Images ◽  
Shear Stresses ◽  
Flow Shear ◽  
Flow Shear Stress

It has been well-accepted that atherosclerosis initiation and progression correlate positively with low and oscillating flow wall shear stresses. However, this shear stress mechanism cannot fully explain why advanced plaques continue to grow under elevated flow shear stress conditions. Our previous investigations using 3D computational models with fluid-structure interactions (FSI) based on in vivo/ex vivo magnetic resonance images (MRI) of human carotid atherosclerotic plaques indicated that there is a negative correlation between advanced plaque wall thickness and structural maximum principal stress (Stress-P1) in the plaque and a positive correlation between plaque wall thickness and flow shear stress [3].

Reversed Correlations Between Atherosclerotic Carotid Plaque Progression and Flow Shear Stress/Plaque Wall Stress Based on Past and Current Scan Data: In Vivo MRI-Based 3D FSI Studies

2010 ◽  
Author(s):  
Chun Yang ◽  
Gador Canton ◽  
Chun Yuan ◽  
Thomas Hatsukami ◽  
Dalin Tang
Keyword(s):  
Shear Stress ◽  
Wall Stress ◽  
Significant Negative Correlation ◽  
Shear Stresses ◽  
Plaque Progression ◽  
Flow Shear ◽  
Carotid Plaques ◽  
Flow Shear Stress ◽  
The Difference

It has been well accepted that low and oscillating blood flow shear stresses (LFSS) correlate positively with intimal thickening and atherosclerosis initiation [1,2]. However, the LFSS hypothesis cannot explain why advanced plaques continue to grow under elevated high flow shear stress conditions [3]. For patient tracking studies, plaque progression is often measured by the difference of plaque geometries between two scans (“past” and “current” scans) when medical imaging is used. Mechanical flow shear stress (FSS) and plaque wall stress (PWS) conditions from the two scans may have different correlations with plaque progression. Using 2D structure models based on in vivo magnetic resonance imaging (MRI) human carotid plaques, Tang et al. showed that 18 out of 21 patients had significant negative correlation between plaque progression measured by wall thickness increase (WTI) and plaque wall stress from current scan [3]. The correlation was reversed when plaque wall stress from past scan was used. In this paper, 3D fluid-structure interactions (FSI) models for 32 matched “past-current” scan pairs of human atherosclerotic carotid plaques based on in vivo MRI data were solved and plaque wall stress (PWS) and flow shear stress (FSS) data were obtained to quantify their correlations with plaque progression measured by WTI.

Devlopment of a Cell Coculture Microfluidic Shear Device for Mechano-Transmission Study

2007 ◽  
Author(s):  
Devon Scott ◽  
Aaron Richman ◽  
Craig Lanning ◽  
Robin Shandas ◽  
Wei Tan
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Pulmonary Vascular Disease ◽  
Interstitial Tissue ◽  
Endothelial Lining ◽  
Flow Shear ◽  
Flow Shear Stress

We have developed a microfluidic shear device that allows for the study of cell communication in a dynamically controlled biochemical and biomechanical environments simulating cells’ living environments in vivo. Such study may help to improve our understanding in the effects of hypertension-relevant and vascular development-relevant flow shear stress on cell behaviors. Endothelial cells may be a key factor for transmitting the blood flow conditions from the endothelial lining to interstitial layers and smooth muscle cells. The interstitial flow stress and the shear stress induced signaling factors may greatly alter vascular biology of these deep layers. Endothelial cells act as a mechano-transducer by converting shear stress into biochemical signaling factors. The biochemical factors diffuse to smooth muscle cells and further alter the biological structure of vascular tissues. Also, the flow shear stress will be transmitted to the interstitial tissue layer through the pores resulted from the pores in the fenestrated endothelial lining. Studies in both the mechano-transduction process and the mechano-transmission process will benefit from a biomimetic flow shear device with co-cultured cells. Our device will allow the co-culture of endothelial cells and smooth muscle cells to study these biomechanical processes. The pulmonary arterial cells are used as a model in the study. The microfluidic device developed here will be used to enhance the understanding of pulmonary vascular disease pathogenesis due to the variations in the flow shear stress.

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