Mass Transport with Asymmetric Peristaltic Propulsion Coated with Synovial Fluid

This article aims to model two-dimensional, incompressible asymmetric peristaltic propulsion coated with Synovial fluid (“non-Newtonian model”) with mass transport. Due to the coating of the same base-fluid at the surface of the channel, the boundaries become non-porous and exert no slip on the fluid particles. Two illustrative models for the viscosity, namely, shear-thinning (Model 1) and shear-thickening (Model 2), are considered, which reveal the presence and integrity of coating. The perturbation method has been applied to linearize the complicated differential equations. Model 1 predicted higher viscosity values and more significant non-Newtonian behavior than Model 2. It is also observed that the shear-thinning model behaved in quite the opposite manner for the shear thickening model. The converse behavior of Model 1 and Model 2 occurs due to a curvature of the flow domain. Moreover, Model 1 is not able to capture the correct exponential viscosity dependence on concentration for the whole range of shear rates. On the other hand, the second model shows a strong relationship with accurate power. Solutions are attained for velocity field, concentration profile, and pressure gradient. The novelty of all the essential parameters is analyzed through graphical results. Furthermore, streamlines are also drawn to determine the trapping mechanism. The present analysis is beneficial in the study of intrauterine fluid dynamics; furthermore, it is applicable in vivo diagnostic; drug delivery; food diagnostics; protein chips; and cell chips and packaging, i.e., smart sensors.

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The Effect of Rheology of Viscoelastic Polymer on Pressure Transient Response in Near-Wellbore Regions

Geofluids ◽

10.1155/2021/5568336 ◽

2021 ◽

Vol 2021 ◽

pp. 1-12

Author(s):

Jia Zhang ◽

Shiqing Cheng ◽

Jie Zhan ◽

Qi Han

Keyword(s):

Shear Thickening ◽

Shear Thinning ◽

Polymer Flooding ◽

High Shear ◽

Pressure Data ◽

Transient Pressure ◽

Pressure Derivative ◽

Shear Rates ◽

Viscoelastic Polymer ◽

Thickening Behavior

Viscoelastic polymer solution shows shear thinning behavior at low shear rates and shear thickening behavior at high shear rates in reservoirs. However, models that ignored shear thickening behavior were commonly employed to interpret transient pressure data derived from tested wells in viscoelastic polymer flooding systems; although, viscoelastic polymer solutions show shear thickening behavior in the near-wellbore region due to high shear rate. To better characterize the oilfield with pressure transient analysis in viscoelastic polymer flooding systems, we developed a numerical model that takes into account both shear thinning behavior and shear thickening behavior. A finite volume method was employed to discretize partially differential flow equations in a hybrid grid system including PEBI mesh and Cartesian grid, and the Newton-Raphson method was used to solve the fully implicit nonlinear system. To illustrate the significance of our model, we compared our model with a model that ignores the shear thickening behavior by graphing their solutions on log-log plots. In the flow regime of near-wellbore damage, the pressure derivative computed by our model is distinctly larger than that computed by the model ignoring shear thickening behavior. Furthermore, the effect of shear thickening behavior on pressure derivative differs from that of near-wellbore damage. We then investigated the influence of shear thickening behavior on pressure derivative with different polymer injection rates, injection rates, and permeabilities. The results can provide a benchmark to better estimate near-wellbore damage in viscoelastic polymer flooding systems. Besides, we demonstrated the applicability and accuracy of our model by interpreting transient pressure data from a field case in an oilfield with viscoelastic polymer flooding treatments.

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Shear Thinning and Thickening of Alumina Suspensions

Advanced Materials Research ◽

10.4028/www.scientific.net/amr.105-106.833 ◽

2010 ◽

Vol 105-106 ◽

pp. 833-836

Author(s):

Xiang Yang Lu ◽

Li Ming Zhang ◽

Yong Huang

Keyword(s):

Zeta Potential ◽

Particle Surface ◽

Shear Thickening ◽

Shear Thinning ◽

High Shear ◽

Shear Rates ◽

High Shear Rates ◽

Stern Potential ◽

Thickening Behavior ◽

Alumina Suspensions

The rheological behavior of alumina suspension stabilized with Tri-ammonia citrate (TAC) was studied. It was thought that there would form some particle clusters due to the collisions between particles caused by their relative motion in the suspension, and such particle clusters are classified as thermodynamic clusters and hydrodynamic clusters by their origin. Shear thinning is the result of decomposition of the thermodynamic clusters, while shear thickening is the result of formation of the hydrodynamic clusters. From the view of cluster-forming potential barrier, it was deemed that the viscosities of alumina suspensions at low and high shear rates are respectively determined by zeta potential and Stern potential on the particle surface, and shear thickening behavior can be suppressed with some excessive TAC.

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Studies on the Haemostatic Defect in a Complicated Syndrome

Thrombosis and Haemostasis ◽

10.1055/s-0038-1649920 ◽

1995 ◽

Vol 74 (05) ◽

pp. 1244-1251 ◽

Cited By ~ 37

Author(s):

H Stormorken ◽

H Holmsen ◽

R Sund ◽

K S Sakariassen ◽

T Hovig ◽

...

Keyword(s):

Ex Vivo ◽

Bleeding Tendency ◽

Clot Retraction ◽

Abnormal Finding ◽

Shear Rates ◽

Perfusion Chamber ◽

Coagulant Activity ◽

5 Ht Uptake ◽

And Storage

SummaryThe Stormorken syndrome is a multifacetted syndrome including a bleeding tendency. No deviations were found in the coagulation- or fibrinolytic systems. Platelet number was low normal, and size abnormal, whereas EM findings were unremarkable. Survival time was half normal. Clot retraction was initially rapid, but clearly decreased, whereas prothrombin consumption was also initially rapid, but complete. Membrane GP’s were normal, so was AA metabolism, PI-cycle, granule storage and secretion, and c-AMP function, whereas 5-HT uptake and storage was decreased. Optical platelet aggregation was low normal with all physiological agonists. The only clearly abnormal finding was that coagulant activity was present on non stimulated platelets at the same level as kaolin-stimulated normal platelets. This indicated a platelet abnormality which should lead to a thrombogenic, not to a haemorrhagic trait. This paradox may have its origin in rheology, because when challenged with in vivo shear rates in an ex vivo perfusion chamber, platelet cohesion was abnormally low. Further studies to better delineate the membrane abnormality are underway.

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Exosomes derived from miR-126-3p-overexpressing synovial fibroblasts suppress chondrocyte inflammation and cartilage degradation in a rat model of osteoarthritis

Cell Death Discovery ◽

10.1038/s41420-021-00418-y ◽

2021 ◽

Vol 7 (1) ◽

Author(s):

Yan Zhou ◽

Jianghua Ming ◽

Yaming Li ◽

Bochun Li ◽

Ming Deng ◽

...

Keyword(s):

Synovial Fluid ◽

Apoptotic Cell ◽

Synovial Fibroblasts ◽

Cartilage Degeneration ◽

Cartilage Degradation ◽

Exosomal Mirnas ◽

Exosomal Mirna ◽

And Control ◽

And Cartilage

AbstractMicroRNAs (miRNAs) encapsulated within exosomes can serve as essential regulators of intercellular communication and represent promising biomarkers of several aging-associated disorders. However, the relationship between exosomal miRNAs and osteoarthritis (OA)-related chondrocytes and synovial fibroblasts (SFCs) remain to be clarified. Herein, we profiled synovial fluid-derived exosomal miRNAs and explored the effects of exosomal miRNAs derived from SFCs on chondrocyte inflammation, proliferation, and survival, and further assessed their impact on cartilage degeneration in a surgically-induced rat OA model. We identified 19 miRNAs within synovial fluid-derived exosomes that were differentially expressed when comparing OA and control patients. We then employed a microarray-based approach to confirm that exosomal miRNA-126-3p expression was significantly reduced in OA patient-derived synovial fluid exosomes. At a functional level, miRNA-126-3p mimic treatment was sufficient to promote rat chondrocyte migration and proliferation while also suppressing apoptosis and IL-1β, IL-6, and TNF-α expression. SFC-miRNA-126-3p-Exos were able to suppress apoptotic cell death and associated inflammation in chondrocytes. Our in vivo results revealed that rat SFC-derived exosomal miRNA-126-3p was sufficient to suppress the formation of osteophytes, prevent cartilage degeneration, and exert anti-apoptotic and anti-inflammatory effects on articular cartilage. Overall, our findings indicate that SFC exosome‐delivered miRNA-126-3p can constrain chondrocyte inflammation and cartilage degeneration. As such, SFC-miRNA-126-3p-Exos may be of therapeutic value for the treatment of patients suffering from OA.

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An Evidence-Based Systematic Review of Human Knee Post-Traumatic Osteoarthritis (PTOA): Timeline of Clinical Presentation and Disease Markers, Comparison of Knee Joint PTOA Models and Early Disease Implications

International Journal of Molecular Sciences ◽

10.3390/ijms22041996 ◽

2021 ◽

Vol 22 (4) ◽

pp. 1996 ◽

Cited By ~ 1

Author(s):

Christine M. Khella ◽

Rojiar Asgarian ◽

Judith M. Horvath ◽

Bernd Rolauffs ◽

Melanie L. Hart

Keyword(s):

Synovial Fluid ◽

Knee Joint ◽

Ex Vivo ◽

Disease Process ◽

Early Disease ◽

Knee Trauma ◽

Post Traumatic ◽

Acute Knee

Understanding the causality of the post-traumatic osteoarthritis (PTOA) disease process of the knee joint is important for diagnosing early disease and developing new and effective preventions or treatments. The aim of this review was to provide detailed clinical data on inflammatory and other biomarkers obtained from patients after acute knee trauma in order to (i) present a timeline of events that occur in the acute, subacute, and chronic post-traumatic phases and in PTOA, and (ii) to identify key factors present in the synovial fluid, serum/plasma and urine, leading to PTOA of the knee in 23–50% of individuals who had acute knee trauma. In this context, we additionally discuss methods of simulating knee trauma and inflammation in in vivo, ex vivo articular cartilage explant and in vitro chondrocyte models, and answer whether these models are representative of the clinical inflammatory stages following knee trauma. Moreover, we compare the pro-inflammatory cytokine concentrations used in such models and demonstrate that, compared to concentrations in the synovial fluid after knee trauma, they are exceedingly high. We then used the Bradford Hill Framework to present evidence that TNF-α and IL-6 cytokines are causal factors, while IL-1β and IL-17 are credible factors in inducing knee PTOA disease progresssion. Lastly, we discuss beneficial infrastructure for future studies to dissect the role of local vs. systemic inflammation in PTOA progression with an emphasis on early disease.

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Stability of Shear-Thickening Liquids Between Rotating Cylinders

Volume 8: Dynamic Systems and Control, Parts A and B ◽

10.1115/imece2010-39854 ◽

2010 ◽

Author(s):

Nariman Ashrafi ◽

Habib Karimi Haghighi

Keyword(s):

Couette Flow ◽

Dynamical Behavior ◽

Shear Thickening ◽

Shear Thinning ◽

Taylor Vortex ◽

Shear Dependent Viscosity ◽

Shear Thinning Fluids ◽

Shear Thickening Fluids ◽

The Stability ◽

Dependent Viscosity

The effects of nonlinearities on the stability are explored for shear thickening fluids in the narrow-gap limit of the Taylor-Couette flow. It is assumed that shear-thickening fluids behave exactly as opposite of shear thinning ones. A dynamical system is obtained from the conservation of mass and momentum equations which include nonlinear terms in velocity components due to the shear-dependent viscosity. It is found that the critical Taylor number, corresponding to the loss of stability of Couette flow becomes higher as the shear-thickening effects increases. Similar to the shear thinning case, the Taylor vortex structure emerges in the shear thickening flow, however they quickly disappear thus bringing the flow back to the purely azimuthal flow. Naturally, one expects shear thickening fluids to result in inverse dynamical behavior of shear thinning fluids. This study proves that this is not the case for every point on the bifurcation diagram.

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Rheological properties of hydroxypropylmethyl cellulose/sodium dodecylsulfate mixtures

Journal of the Serbian Chemical Society ◽

10.2298/jsc130807132k ◽

2014 ◽

Vol 79 (4) ◽

pp. 457-468 ◽

Cited By ~ 5

Author(s):

Jaroslav Katona ◽

Sandra Njaradi ◽

Verica Sovilj ◽

Lidija Petrovic ◽

Brankica Marceta ◽

...

Keyword(s):

Rheological Properties ◽

Sodium Dodecylsulfate ◽

Shear Thinning ◽

Cellulose Ether ◽

Flow Profile ◽

Hydroxypropylmethyl Cellulose ◽

Shear Rates ◽

Newtonian Liquids ◽

Shear Induced Structure ◽

Induced Structure

Rheological properties of mixtures of hydroxypropylmethyl cellulose (HPMC), a nonionic associative cellulose ether, and sodium dodecylsulfate (SDS), an anionic surfactant, were investigated by viscosity measurements performed at different shear rates (0.1-6000 s-1). HPMC/SDS mixtures containing different concentrations of SDS (CSDS=0.00-3.50 % w/w) and HPMC concentrations which corresponded to the overlap parameter c/c*=3, 6, and 12 were prepared. All HPMC/SDS mixtures were found to be shear-thinning when examined in a low-end-to mid-range of the applied shear rates. The degree of shear-thinning, n, and viscosity of the mixtures were influenced by composition of HPMC/SDS mixtures and HPMC-SDS complex formation. The changes in n ranged from values typical for highly shear thinning to almost perfectly Newtonian liquids, and were more pronounced as c/c* was increased from 3 to 6 and 12. A change in flow profile and a buildup of the first normal stress difference (N1) was observed in HPMC/SDS mixtures with c/c*=6 and 12 and CSDS 0.55-1.00 % and 0.55-2.50 %, respectively, when a critical shear rate, crit. was exceeded, suggesting that a shear-induced structure formation in the mixtures took place.

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in vivo catabolism of [4–14c] cortisol in synovial fluid of the rheumatoid and osteoarthritic knee

Arthritis & Rheumatism ◽

10.1002/art.1780110208 ◽

1968 ◽

Vol 11 (2) ◽

pp. 178-183 ◽

Cited By ~ 4

Author(s):

Tawfik M. A. Elattar ◽

William R. Murray ◽

Carl E. Anderson

Keyword(s):

Synovial Fluid ◽

Osteoarthritic Knee

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Cationic Amino Acid Transporter-1 (CAT-1) Promotes Fibroblast-Like Synoviocytes Proliferation and Cytokine Secretion by Taking Up L-Arginine in Rheumatoid Arthritis

10.21203/rs.3.rs-1147918/v1 ◽

2021 ◽

Author(s):

Ying Lu ◽

Chongbo Hao ◽

Shanshan Yu ◽

Zuan Ma ◽

Xuelian Fu ◽

...

Keyword(s):

Rheumatoid Arthritis ◽

Amino Acid ◽

Synovial Fluid ◽

Culture Conditions ◽

Cytokine Secretion ◽

Cationic Amino Acid Transporter ◽

Cationic Amino Acid ◽

The Relationship ◽

Fibroblast Like Synoviocytes

Abstract Background: Abnormal proliferation of fibroblast-like synoviocytes (FLSs) in the synovial lining layer is the primary cause of synovial hyperplasia and joint destruction in rheumatoid arthritis (RA). Currently, the relationship between metabolic abnormalities and FLS proliferation is a new focus of investigation. However, little is known regarding the relationship between amino acid metabolism and RA. Methods: The concentrations of amino acids and cytokines in the synovial fluid of RA (n=9) and osteoarthritis (OA,n=9) were detected by LC-MS/MS and CBA assay, respectively. The mRNA and protein expression of CAT-1 were determined in FLSs isolated from RA and OA patients by real-time PCR and western blotting. MTT assay, cell cycle, apoptosis, invasion and cytokine secretion were determined in FLSs knocked down of CAT-1 using siRNA or treated with D-arginine under normoxic and hypoxic culture conditions. A mouse collagen-induced arthritis (CIA) model was applied to test the therapeutic potential of blocking the uptake of L-arginine in vivo.Results: L-arginine was upregulated in the synovial fluid of RA patients and was positively correlated with elevation of the cytokines IL-1β, IL-6 and IL-8. Further examination demonstrated that cationic amino acid transporter-1 (CAT-1) was the primary transporter for L-arginine and was overexpressed on RA FLSs compared to OA FLSs. Moreover, knockdown of CAT-1 using siRNA or inhibition of L-arginine uptake using D-arginine significantly suppressed L-arginine metabolism, cell proliferation, migration and cytokine secretion in RA FLSs under normoxic and hypoxic culture conditions in vitro but increased cell apoptosis in a dose-dependent manner. Meanwhile, in vivo assays revealed that an L-arginine-free diet or blocking the uptake of L-arginine using D-arginine suppressed arthritis progression in CIA mice. Conclusion: CAT-1 is upregulated and promotes FLS proliferation by taking up L-arginine, thereby promoting RA progression.

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