High Shear Stress (high + shear_stress)

Distribution by Scientific Domains

Selected Abstracts

Relation between flow, surface-layer armoring and sediment transport in gravel-bed rivers

John Pitlick
Abstract This study investigates trends in bed surface and substrate grain sizes in relation to reach-scale hydraulics using data from more than 100 gravel-bed stream reaches in Colorado and Utah. Collocated measurements of surface and substrate sediment, bankfull channel geometry and channel slope are used to examine relations between reach-average shear stress and bed sediment grain size. Slopes at the study sites range from 0·0003 to 0·07; bankfull depths range from 0·2 to 5 m and bankfull widths range from 2 to 200 m. The data show that there is much less variation in the median grain size of the substrate, D50s, than there is in the median grain size of the surface, D50; the ratio of D50 to D50s thus decreases from about four in headwater reaches with high shear stress to less than two in downstream reaches with low shear stress. Similar trends are observed in an independent data set obtained from measurements in gravel-bed streams in Idaho. A conceptual quantitative model is developed on the basis of these observations to track differences in bed load transport through an idealized stream system. The results of the transport model suggest that downstream trends in total bed load flux may vary appreciably, depending on the assumed relation between surface and substrate grain sizes. Copyright © 2007 John Wiley & Sons, Ltd. [source]

Identification and separation of DNA-hybridized nanocolloids by Taylor cone harmonics

Xinguang Cheng
Abstract A rapid (minutes) electrospray bead-based DNA hybridization detection technique is developed by spraying a mixture of hybridized and unhybridized silica nanocolloids. With proper far-field control by external electrodes, the trajectory of the ejected nanobeads from the electrospray is governed by specific harmonics of the Laplace equation, which select discrete polar angles along well-separated field maxima near the conducting Taylor cone. Due to Rayleigh fission and evaporation, beads of different size acquire different total charge after ejection and suffer different normal electrophoretic displacement such that they are ejected along well-separated field maxima and are deposited in distinct rings on an intersecting plane. As the hybridized DNA is of the same dimension as that of the nanocolloid, the nanocolloids are hence easily differentiated from the unhybridized ones. This technique is highly specific as the high shear stress in the microjet shears away any non-specifically bound DNA from the nanocolloid surface. [source]

Two novel monoclonal antibodies to VWFA3 inhibit VWF-collagen and VWF-platelet interactions

Summary.,Background:,The interaction of collagen-von Willebrand factor (VWF)-GPIb is essential for platelet adhesion, especially under high shear conditions. VWF, which acts as a bridge between platelets and exposed subendothelium, interacts with collagen through its A3 domain, which is a new target for the antithrombotic agent. Objective:,To develop functional blockers that specifically inhibit VWF-dependent adhesion of platelets to collagen under high shear stress. Methods:,To develop murine antihuman VWF A3 monoclonal antibodies (mAbs) by standard hybridoma technology, and characterize their abilities to block interactions between VWF A3 and collagen as well as platelet function. Results:,Thirty anti-VWF-A3 mAbs were obtained. Among them, two mAbs, designated as SZ-123 and SZ-125, were found to inhibit VWF-collagen type III interaction. SZ-123 and SZ-125 inhibited the binding of purified human VWF (1.5 or 3 ,g mL,1) to human placenta collagen type III (IC50 = 0.07 ± 0.02 and 0.15 ± 0.03 ,g mL,1, respectively) or to calf skin collagen type III (IC50 = 0.48 ± 0.06 and 0.51 ± 0.07 ,g mL,1, respectively) coated on plates. Under flow shear condition (1000 s,1), SZ-123 and SZ-125 inhibited platelet adhesion on human placenta collagen- or calf skin collagen-coated surfaces. Both mAbs also inhibited platelet aggregation induced by ristocetin, botrocetin or bovine plasma. Conclusions:,SZ-123 and SZ-125 inhibited VWF-collagen and VWF-platelet interactions. [source]

Purified A2 domain of von Willebrand factor binds to the active conformation of von Willebrand factor and blocks the interaction with platelet glycoprotein Ib,

Summary.,Background:,von Willebrand factor (VWF) does not interact with circulating platelets unless it is induced to expose the binding site for platelet glycoprotein (GP)Ib, in the A1 domain by high shear stress, immobilization, and/or a modulator. Previous studies have implied indirectly that the A2 domain may be involved in regulating A1,GPIb, binding. Objective and methods:,Because the relationship between the A1 and A2 domains has not been defined, we have investigated the effect of the A2 domain on the binding activity of the A1 domain using recombinant A domain polypeptides, multimeric VWF, and monoclonal antibodies (mAb). Results:,The A2 domain polypeptide bound specifically to the immobilized A1 domain polypeptide or full-length VWF, with half-maximal binding being obtained at 60 or 168 nm, respectively. This A1,A2 interaction was inhibited by mAb against the A2 or A1 domain and by the A1 domain polypeptide. The A2 domain polypeptide effectively blocked GPIb,-mediated platelet adhesion under high flow conditions. The A2 domain polypeptide specifically recognizes the GPIb,-binding conformation in the A1 domain, as it only interacted with VWF activated by the modulator ristocetin or immobilized VWF. Furthermore, in contrast to plasma VWF, the ultra-large (UL)VWF multimers or a recombinant VWF,A1A2A3 polypeptide containing a gain-of-function mutation (R1308 L) of type 2B von Willebrand disease bound to the A2 domain polypeptide without the need for ristocetin. Conclusions:,The recombinant A2 domain polypeptide specifically binds to the active conformation of the A1 domain in VWF and effectively blocks the interaction with platelet GPIb, under high-flow conditions. [source]

A novel nitric oxide-releasing statin derivative exerts an antiplatelet/antithrombotic activity and inhibits tissue factor expression,

Summary.,Background:,NO-releasing statins are new chemical entities, combining HMG-CoA reductase inhibition and slow NO release, that possess stronger anti-inflammatory and antiproliferative activities than the native statins. Objective:,We evaluated the antithrombotic effects of nitropravastatin (NCX-6550) by assessing its activity on platelet activation and tissue factor (TF) expression by mononuclear cells in vitro and in vivo. Methods and results:,In vitro, NCX-6550 inhibited (1) U46619- and collagen-induced platelet aggregation in buffer and plasma; (2) collagen-induced P-selectin expression in whole blood and (3) platelet adhesion to collagen-coated coverslips under high shear stress. These effects were displayed at concentrations of NCX-6550 ranging from 25 to 100 ,m, and were totally reverted by the guanylylcyclase inhibitor ODQ (10 ,m). Equimolar concentrations of pravastatin had no influence on these parameters of platelet function. LPS- and PMA-induced TF expression by blood mononuclear cells was also inhibited by NCX-6550 (IC50 13 ,m), but not by pravastatin, as assessed by functional and immunological assays and by real-time PCR. In a mouse model of platelet pulmonary thromboembolism, induced by the i.v. injection of collagen plus epinephrine, pretreatment with NCX-6550 (24,48 mg kg,1) significantly reduced platelet consumption, lung vessel occlusion and mortality. Moreover, nitropravastatin markedly inhibited the generation of procoagulant activity by spleen mononuclear cells and peritoneal macrophages in mice treated with LPS. In these in vivo models too, pravastatin failed to affect platelet activation and monocyte/macrophage procoagulant activity. Conclusions:,Our results show that nitropravastatin exerts strong antithrombotic effects in vitro and in vivo, and may represent an interesting antiatherothrombotic agent for testing in acute coronary syndromes. [source]

Cleavage of platelet endothelial cell adhesion molecule-1 (PECAM-1) in platelets exposed to high shear stress

Y. Naganuma
Platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31) is a 130 kDa transmembrane glycoprotein that belongs to the immunoglobulin superfamily and is expressed on the surface of endothelial cells, platelets, and other blood cells. Although the importance of this adhesion molecule in various cell,cell interactions is established, its functional role in platelets remains to be elucidated. In this study, we examined whether PECAM-1 underwent changes in platelets exposed to high shear stress. Platelet PECAM-1 was cleaved under high shear stress and was released into the extracellular fluid as a fragment with an approximate molecular weight of 118 kDa. The cleavage was inhibited by an anti-VWF MoAb, but not by recombinant VWF A1 domains. These findings suggest that the GPIb,VWF interaction is involved in PECAM-1 cleavage under high shear stress, and that the cleavage is independent of GPIb clustering by VWF multimers. Furthermore, EGTA or calpeptin inhibited PECAM-1 cleavage. This finding provides evidence for the involvement of calpain in PECAM-1 cleavage. Flow-cytometric analysis revealed that PECAM-1 expression on the platelet surface was decreased under high shear stress. This reduction occurred exclusively in a specific population of platelets, which corresponded to platelet-derived microparticles (PMP). In conclusion, PECAM-1 cleavage under high shear stress is closely related to the activation of calpain and the process of PMP formation mediated by the GPIb,VWF interaction. [source]

von Willebrand factor stimulates thrombin-induced exposure of procoagulant phospholipids on the surface of fibrin-adherent platelets

J. J. Briedé
Summary., Studies from our laboratory have demonstrated that von Willebrand factor (VWF) stimulates thrombin generation in platelet-rich plasma. The precise role of VWF and fibrin in this reaction, however, remained to be clarified. In the present study we utilized thrombin-free planar fibrin layers and washed platelets to examine the relationship between platelet,fibrin interaction and exposure of coagulation-stimulating phosphatidylserine (PS) under conditions of low and high shear stress. Our study confirms that platelet adhesion to fibrin at a shear rate of 1000 s,1 requires fibrin-bound VWF. The cytosolic calcium concentration ([Ca2+]i) of stationary platelets was not elevated and PS exposing platelets were virtually absent (2 ± 2%). However, thrombin activation resulted in a marked increase in the number of PS exposing platelets (up to 85 ± 14%) along with a transient elevation in [Ca2+]i from 0.05 µmol L,1 up to 1.1 ± 0.2 µmol L,1. Platelet adhesion to fibrin at a shear rate of 50 s,1 is mediated by thrombin but not by fibrin-bound VWF. The [Ca2+]i of these thrombin-activated platelets was elevated (0.2 ± 0.1 µmol L,1), but only a minority of the platelets (11 ± 8%) exposed PS. The essential role of VWF in this thrombin-induced procoagulant response became apparent from low shear rate perfusion studies over fibrin that was incubated with VWF and botrocetin. After treatment with thrombin, the majority of the adherent platelets (57 ± 23%) exposed PS and had peak values of [Ca2+]i of about 0.6 µmol L,1. Taken together, these results demonstrate that thrombin-induced exposure of PS and high calcium response on fibrin-adherent platelets depends on shear- or botrocetin-induced VWF,platelet interaction. [source]

Decreased Platelet Function in Cavalier King Charles Spaniels with Mitral Valve Regurgitation

Inge Tarnow
With aggregometry, increased platelet activity has been reported in Cavalier King Charles Spaniels (CKCS) without mitral regurgitation (MR). In contrast, dogs with MR have been found to have decreased platelet activity. The purpose of this study was to test an easy bedside test of platelet function (the Platelet Function Analyzer [PFA-100]) to see if it could detect an increase in platelet activity in CKCS without MR and a decrease in platelet activity in CKCS with MR. This study included 101 clinically healthy dogs 1 year of age: 15 control dogs of different breeds and 86 CKCS. None of the dogs received medication or had a history of bleeding. The PFA-100 evaluates platelet function in anticoagulated whole blood under high shear stress. Results are given as closure times (CT): the time it takes before a platelet plug occludes a hole in a membrane coated by agonists. The CT with collagen and adenosine-diphosphate as agonists was similar in control dogs (median 62 seconds; interquartile interval 55,66 seconds) and CKCS with no or minimal MR (55; 52,64 seconds). The CT was higher in CKCS with mild MR (regurgitant jet occupying 15,50% of the left atrial area) (75; 60,84 seconds; P= .0007) and in CKCS with moderate to severe MR (jet 50%) (87; 66,102 seconds; P < .0001). CKCS with mild, moderate, and severe, clinically inapparent MR have decreased platelet function. The previous finding of increased platelet reactivity in nonthrombocytopenic CKCS without MR could not be reproduced with the PFA-100 device. [source]

Interactions of Platelets with Subendothelium and Endothelium

ABSTRACT In this review, the authors summarize how platelets interact with subendothelium when the vessel wall is damaged or with intact endothelium in the inflammatory state. When subendothelium is exposed to rapidly flowing blood upon vessel damage, platelets adhere rapidly to the exposed surface, decelerate, and aggregate to arrest bleeding. Under high shear stress, such as is found in the microcirculation, the interaction between subendothelial von Willebrand factor (VWF) and its platelet receptor, glycoprotein (GP) Ib-IX-V, is required to slow down platelets and allow the platelet collagen receptors ,2,1 and GP VI to bind to collagen. GP VI and ,2,1 play important roles to activate platelets in the early stage and work with GP Ib-IX-V to fully activate platelets to form thrombi. GP Ib-IX-V and GP VI employ similar signaling pathways for platelet activation and the signals from both receptors are down-modulated by PECAM-1 (platelet,endothelial,cell adhesion molecule 1) to prevent unnecessary platelet activation under high shear. During inflammatory states, intact endothelial cells release VWF and P-selectin from their Weibel-Palade bodies. Both molecules are ligands for GP Ib-IX-V. The newly released VWF is larger and stickier than the form normally found in plasma and binds platelets spontaneously. Normally, VWF is processed by proteolysis by the plasma metalloprotease ADAMTS-13. Failure of this processing results in the microvascular thrombotic disorder thrombotic thrombocytopenic purpura. In this review, the authors also use available crystal structures of platelet receptors and ligands to explain the details of their interactions. [source]

Investigation of the relationships between die build up and die swell

Todd A. Hogan
Die build up (DBU) is a common problem encountered during extrusion of polymers where material accumulates around the die exit and may cause defects in the surface of the product. This study was initiated to better understand the fundamental relationships between DBU and die swell. The study was conducted on a strand die extrusion system using an ethylene-octene polyolefin elastomer resin. This study demonstrated that die swell is not a root cause of DBU. It was shown that at constant shear rate, increasing the die L/D ratio results in an increase in DBU, while die swell decreases. The important variables influencing DBU for the resin used in this study were: the shear rate or shear stress in capillary portion of the die, the nominal residence time that the resin is exposed to the high shear stress in the die capillary, and the concentration of oligomers present in the resin or generated during processing. These data support the conclusion that DBU is due to the shear-induced migration of oligomeric species in the polymer to the die surface. Higher shear rates and stresses in the die promote this migration and result in a higher concentration of oligomeric species near the die wall. POLYM. ENG. SCI., 2009. © 2008 Society of Plastics Engineers [source]

Using Macrophytes in Urban Stream Rehabilitation: A Cautionary Tale

Alastair M. Suren
Abstract Native macrophytes were transplanted into a small urban stream as part of a rehabilitation program, that also meandered the previously channeled stream, naturalized stream banks, and planted native riparian vegetation. Transplanted macrophytes minimized spread of introduced macrophytes and were viewed beneficially by residents, as was the stream rehabilitation. We transplanted the native macrophyte Myriophyllum triphyllum into five larger streams dominated by exotic macrophytes,some of which were weeded prior to transplanting,to see whether Myriophyllum could prevent regrowth of weeded plants. Transplanted Myriophyllum plants were washed away in two streams, reflecting high shear stresses there. Myriophyllum cover in the other streams decreased as weeded plants regrew. Our attempt at eliminating exotic macrophytes in patches in large streams was unsuccessful. Furthermore, council authorities weeded other experimental sections following complaints from residents of excess macrophyte growth. This problem highlighted conflicting multiple values placed on urban streams by managers and the public. A repeat survey of residents living near the original rehabilitated stream showed that many respondents were now critical of excessive plant growth,both in-stream and riparian. A recurring comment made concerned the apparent lack of maintenance to the stream, giving it an untidy appearance. Difficulties with propagating and transplanting native macrophytes into larger streams, coupled with a negative perception of native vegetation (both in-stream and riparian) if it looks unmanaged, suggest that planting macrophytes or riparian plants as part of urban stream rehabilitation programs may be more problematic than realized. [source]