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Mechanical Disruption (mechanical + disruption)
Selected AbstractsTreatment for Mechanical Valve Thrombosis in the Right Heart: Combined Pharmacological and Mechanical ThrombolysisARTIFICIAL ORGANS, Issue 8 2010Shigeaki Aoyagi Abstract We report clinical results of combined pharmacological and mechanical thrombolysis for mechanical prosthetic valve thrombosis (PVT) in the right heart. Between January 1992 and December 2008, combined thrombolysis, which consisted of an intravenous infusion of urokinase together with mechanical disruption of thrombus in a prosthetic valve by temporarily increasing the cardiac pacing rate, was performed in three patients with four cases of mechanical PVT in the right heart. The prosthetic valve in all three patients was a bileaflet mechanical valve, and was located in the tricuspid position in two patients and in the pulmonary position in the remaining patient. PVT was diagnosed by echocardiography and cineradiography. Thrombolysis was successful in all four cases in the three patients, and no hemorrhagic complications or clinically symptomatic pulmonary embolisms were observed. Mechanical disruption of thrombus using a pacemaker appears to be an effective adjunctive modality to thrombolysis with fibrinolytic agents for PVT in the right heart. Combined pharmacological and mechanical thrombolysis may improve success rates and reduce the time required for thrombolysis of PVT. [source] Ocular penetration of intravenously administered enrofloxacin in the horseEQUINE VETERINARY JOURNAL, Issue 2 2008T. J. DIVERS Summary Reason for performing study: Information on antibiotic concentrations in the equine eye following systemic therapy is limited. Reports that Leptospira spp. are frequently present in the eyes of horses with recurrent uveitis, emphasises a need for studies on ocular concentrations of specific antibiotics. Hypotheses: 1) Enrofloxacin, administered i.v. at 7.5 mg/kg bwt q. 24 h, results in aqueous humour concentrations greater than the reported minimum inhibitory concentration (MIC) for Leptospira pomona. 2) Aqueous humour paracentesis sufficiently disrupts the blood-aqueous humour barrier (BAB) to cause an increase in aqueous humour protein and enrofloxacin concentrations. Methods: Aqueous humour enrofloxacin and total protein concentrations were determined in 6 healthy, mature horses after i.v. administration of enrofloxacin. Paracentesis was performed on the left eye on Days 3 and 4, one hour following enrofloxacin administration, to determine enrofloxacin concentrations in healthy eyes and in eyes with mechanical disruption of the BAB. Paracentesis was also performed on the right eye 23 h after enrofloxacin administration. Blood samples were collected from the horses at identical times to determine enrofloxacin aqueous humour:plasma ratios. Results: Mean ± s.d. enrofloxacin concentration in the aqueous humour one hour post administration on Day 3 was 0.32 ± 0.10 mg/l (range 0.18-0.47); and aqueous humour enrofloxacin, total protein and aqueous humour:plasma enrofloxacin ratios were higher on Day 4 than Day 3. Conclusions and potential relevance: Following disruption of the BAB, enrofloxacin concentrations were above the reported MIC for Leptospira pomona. [source] Redox Cycling of Ni-Based Solid Oxide Fuel Cell Anodes: A ReviewFUEL CELLS, Issue 3 2007D. Sarantaridis Abstract The published literature relating to damage to SOFCs caused by redox cycling of Ni-based anodes is reviewed. The review covers the kinetics of Ni oxidation and NiO reduction (as single phases and as constituents of composites with yttria-stabilised zirconia, YSZ), the dimensional changes associated with redox cycling and the effect of this on the mechanical integrity and electrical performance of cells and stacks. A critical parameter is the expansion strain that is caused by oxidation. Several studies report that the first complete oxidation of a Ni/YSZ composite causes a linear expansion of the order of 1%, but the actual values vary substantially between different investigations. The oxidation strain is the result of microstructural irreversibility during the redox process and leads to strain accumulation over several redox cycles. This can cause mechanical disruption to an anode, anode support or other cell components attached to the anode. A simplified mechanical model of the stress and damage that are likely to be caused by anode expansion is proposed and applied to anode-supported, electrolyte-supported and inert substrate-supported cell configurations. This allows the maximum oxidation strain to avoid damage in each configuration to be estimated. [source] Behavior of Nonselective Cation Channels and Large-Conductance Ca2+ -Activated K+ Channels Induced by Dynamic Changes in Membrane Stretch in Cultured Smooth Muscle Cells of Human Coronary ArteryJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2003PH.D., SHENG-NAN WU M.D. Stretch-Activated Ion Channels. Introduction: The effects of membrane stretch on ion channels were investigated in cultured smooth muscle cells of human coronary artery. Methods and Results: In the cell-attached configuration, membrane stretch with negative pressure induced two types of stretch-activated (SA) ion channels: a nonselective cation channel and a large-conductance Ca2+ -activated K+ (BKCa) channel. The single-channel conductances of SA cation and BKCa channels were 26 and 203 pS, respectively. To elucidate the mechanism of activation of these SA channels and to minimize mechanical disruption, a sinusoidal change in pipette pressure was applied to the on-cell membrane patch. During dynamic changes in pipette pressure, increases in SA cation channel activity was found to coincide with increases in BKCa channel activity. In the continued presence of cyclic stretch, the activity of SA cation channels gradually diminished. However, after termination of cyclic stretch, BKCa channel activity was greatly enhanced, but the activity of SA cation channels disappeared. Conclusion: This study is the first to demonstrate that the behavior of SA cation and BKCa channels in coronary smooth muscle cells is differentially susceptible to dynamic changes in membrane tension. [source] ,-Irradiation of ultrahigh-molecular-weight polyethylene: Electron paramagnetic resonance and nuclear magnetic resonance spectroscopy and imaging studies of the mechanism of subsurface oxidationJOURNAL OF POLYMER SCIENCE (IN TWO SECTIONS), Issue 23 2004Todd M. Alam Abstract The shelf aging of irradiated ultrahigh-molecular-weight polyethylene (UHMWPE) causes subsurface oxidation, which leads to failure in UHMWPE orthopedic components, yet the mechanisms causing subsurface oxidation remain unclear. The shelf aging of ,-irradiated UHMWPE bars has been studied with electron paramagnetic resonance (EPR) and nuclear magnetic resonance (NMR) imaging and with microtoming and Fourier transform infrared microscopy. The bars initially contained only allyl radicals, and upon air exposure, a surface layer of peroxyl radicals formed through the reaction of allyl radicals with oxygen. Importantly, a band of low radical intensity just beneath the peroxyl layer became apparent. NMR imaging showed a zone of altered proton relaxation in this zone. With increasing time, surface peroxyl radicals persisted in comparison with the interior allyl radicals, although oxygen did not appear to penetrate any more deeply into the bar. The area of maximal oxidation and mechanical disruption, measured after 3 years, was at the interface between the zone of exterior peroxyl radicals and the zone of low radical intensity. We present a mechanism involving the intermediacy of sterically strained reactive dialkyl peroxides at this interface to explain subsurface oxidation. We also demonstrate that EPR and NMR imaging provides information that could potentially be used to identify subsurface oxidized UHMWPE components before failure. © 2004 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 42: 5929,5941, 2004 [source] Critical Factors Affecting the Wettability of ,-Alumina by Molten AluminumJOURNAL OF THE AMERICAN CERAMIC SOCIETY, Issue 11 2004Ping Shen The wetting behaviors of ,-Al2O3 single crystals with three different faces,R(0112), A(01120), and C(0001),and polycrystals (PC) by molten aluminum were studied over a wide temperature range using both a conventional and an improved sessile-drop method. The critical factors affecting the wettability, such as temperature, atmosphere, substrate surface roughness, and crystallographic orientation, and the influence from the experimental technique, were thoroughly investigated. The results show that the aluminum surface oxidation and the thickness of the oxide film have a pronounced effect on the wettability, especially at low temperatures. To eliminate this effect, the experimental temperature must be over a critical value. Vacuum favors lowering this value compared with atmosphere, and the improved sessile-drop method, particularly using an impingement-dropping mode (I-mode), helps to weaken this effect by mechanical disruption and removal of the oxide film. However, the dropping distance and the dropping force must be controlled to prevent an overspreading of the drop. The effects of the substrate surface roughness and temperature are not significant in the case of a clean aluminum surface and a fine-prepared alumina surface. On the other hand, the effect of the alumina surface crystallographic orientation is noticeable and the wettability is in the order of R > A > PC > C. The intrinsic contact angles of the Al/,-Al2O3 system in the temperature range of 1000°,1500°C were estimated to be 76°,85° for the R and A faces, 88°,100° for the C face, and 77°,90° for the polycrystal, depending on the temperature. [source] Anatomy, physiology, and pathophysiology of the pedunculopontine nucleus,,MOVEMENT DISORDERS, Issue 3 2009Ned Jenkinson PhD Abstract The pedunculopontine nucleus is composed of cholinergic and non-cholinergic neurones and is located in the caudal pontomesencephalic tegmentum. Evidence suggests that the nucleus plays a role in the production and control of movement. The nucleus has dense interconnections with the basal ganglia, as well as with other areas of the brain associated with motor control. Electrical stimulation of the pedunculopontine nucleus in the decerebrate cat or rat produces organized locomotor movements. Physiological studies show that the pedunculopontine nucleus modulates its activity in response to locomotion, as well as voluntary arm and eye movements. Degeneration of the pedunculopontine nucleus is seen in post-mortem brains in humans with Parkinson's disease and Parkinsonian syndromes. In animal models of Parkinson's disease, metabolic changes are seen in the pedunculopontine nucleus, and chemical inhibition or mechanical disruption of the nucleus can produce an akinetic state in animals and man. In this paper we review the literature in support of the suggestion that some of the symptoms of Parkinson's disease are caused by dysfunction of the pedunculopontine nucleus. In accordance with this view, direct stimulation of the nucleus can ameliorate some symptoms of the disease, as demonstrated in both experimental animals and man. © 2008 Movement Disorder Society [source] Force impairment in calpain 3,deficient mice is not correlated with mechanical disruptionMUSCLE AND NERVE, Issue 5 2003Françoise Fougerousse MD Abstract Defects in human calpain 3 are responsible for limb-girdle muscular dystrophy type 2A, an autosomal-recessive disorder characterized mainly by late-onset proximal muscular atrophy. A corresponding murine model has previously been generated by gene targeting. In this report, muscular activity of calpain 3,deficient (capn3,/,) mice was evaluated at different ages. Growth curves showed a progressive global muscular atrophy. Histological examination throughout the lifespan of mice confirmed the dystrophic lesions. Whole animal tests showed only a mild significant impairment of the forelimbs. Studies of the mechanical properties of selected isolated fast- and slow-twitch muscles demonstrated that slow-twitch muscles were significantly weaker in capn3,/, mice than in wild-type mice. Three different tests showed that there was no membrane disruption, suggesting a nonmechanical etiology of capn3,/, mice dystrophy. These findings are consistent with a mechanism involving signaling systems. Muscle Nerve 27: 616,623, 2003 [source] A sodium dodecyl sulfate,polyacrylamide gel electrophoresis,liquid chromatography tandem mass spectrometry analysis of bovine cartilage tissue response to mechanical compression injury and the inflammatory cytokines tumor necrosis factor , and interleukin-1,ARTHRITIS & RHEUMATISM, Issue 2 2008Anna L. Stevens Objective To compare the response of chondrocytes and cartilage matrix to injurious mechanical compression and treatment with interleukin-1, (IL-1,) and tumor necrosis factor , (TNF,), by characterizing proteins lost to the medium from cartilage explant culture. Methods Cartilage explants from young bovine stifle joints were treated with 10 ng/ml of IL-1, or 100 ng/ml of TNF, or were subjected to uniaxial, radially-unconfined injurious compression (50% strain; 100%/second strain rate) and were then cultured for 5 days. Pooled media were subjected to gel-based separation (sodium dodecyl sulfate,polyacrylamide gel electrophoresis) and analysis by liquid chromatography tandem mass spectrometry, and the data were analyzed by Spectrum Mill proteomics software, focusing on protein identification, expression levels, and matrix protein proteolysis. Results More than 250 proteins were detected, including extracellular matrix (ECM) structural proteins, pericellular matrix proteins important in cell,cell interactions, and novel cartilage proteins CD109, platelet-derived growth factor receptor,like, angiopoietin-like 7, and adipocyte enhancer binding protein 1. IL-1, and TNF, caused increased release of chitinase 3,like protein 1 (CHI3L1), CHI3L2, complement factor B, matrix metalloproteinase 3, ECM-1, haptoglobin, serum amyloid A3, and clusterin. Injurious compression caused the release of intracellular proteins, including Grp58, Grp78, ,4-actinin, pyruvate kinase, and vimentin. Injurious compression also caused increased release and evidence of proteolysis of type VI collagen subunits, cartilage oligomeric matrix protein, and fibronectin. Conclusion Overload compression injury caused a loss of cartilage integrity, including matrix damage and cell membrane disruption, which likely occurred through strain-induced mechanical disruption of cells and matrix. IL-1, and TNF, caused the release of proteins associated with an innate immune and stress response by the chondrocytes, which may play a role in host defense against pathogens or may protect cells against stress-induced damage. [source] Treatment for Mechanical Valve Thrombosis in the Right Heart: Combined Pharmacological and Mechanical ThrombolysisARTIFICIAL ORGANS, Issue 8 2010Shigeaki Aoyagi Abstract We report clinical results of combined pharmacological and mechanical thrombolysis for mechanical prosthetic valve thrombosis (PVT) in the right heart. Between January 1992 and December 2008, combined thrombolysis, which consisted of an intravenous infusion of urokinase together with mechanical disruption of thrombus in a prosthetic valve by temporarily increasing the cardiac pacing rate, was performed in three patients with four cases of mechanical PVT in the right heart. The prosthetic valve in all three patients was a bileaflet mechanical valve, and was located in the tricuspid position in two patients and in the pulmonary position in the remaining patient. PVT was diagnosed by echocardiography and cineradiography. Thrombolysis was successful in all four cases in the three patients, and no hemorrhagic complications or clinically symptomatic pulmonary embolisms were observed. Mechanical disruption of thrombus using a pacemaker appears to be an effective adjunctive modality to thrombolysis with fibrinolytic agents for PVT in the right heart. Combined pharmacological and mechanical thrombolysis may improve success rates and reduce the time required for thrombolysis of PVT. [source] |