Gotowe bibliografie tematyczne / Vascular injury

Gotowa bibliografia na temat „Vascular injury”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 20 lutego 2023

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Artykuły w czasopismach na temat "Vascular injury"

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Benzel, Edward C. "Vascular injury". Journal of Neurosurgery: Spine 95, nr 1 (lipiec 2001): 152. http://dx.doi.org/10.3171/spi.2001.95.1.0152.

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Webster, Robert O. "Lung Vascular Injury". Critical Care Medicine 23, nr 7 (lipiec 1995): 1310. http://dx.doi.org/10.1097/00003246-199507000-00031.

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Mirvis, Stuart E. "Thoracic Vascular Injury". Radiologic Clinics of North America 44, nr 2 (marzec 2006): 181–97. http://dx.doi.org/10.1016/j.rcl.2005.10.007.

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Newman, J. H. "Lung vascular injury". Chest 93, nr 3 (1.03.1988): 139S—146. http://dx.doi.org/10.1378/chest.93.3.139s.

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Newman, John H. "Lung Vascular Injury". Chest 93, nr 3 (marzec 1988): 139S—146S. http://dx.doi.org/10.1378/chest.93.3_supplement.139s.

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Mattox, Kenneth L., Jon M. Burch, Robert Richardson i R. Russell Martin. "Retroperitoneal Vascular Injury". Surgical Clinics of North America 70, nr 3 (czerwiec 1990): 635–53. http://dx.doi.org/10.1016/s0039-6109(16)45134-0.

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Slama, Richard, i Frank Villaume. "Penetrating Vascular Injury". Emergency Medicine Clinics of North America 35, nr 4 (listopad 2017): 789–801. http://dx.doi.org/10.1016/j.emc.2017.06.005.

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Rasmussen, Todd, Zsolt Stockinger, Jared Antevil, Christopher White, Nathaniel Fernandez, Joseph White i Paul White. "Wartime Vascular Injury". Military Medicine 183, suppl_2 (1.09.2018): 101–4. http://dx.doi.org/10.1093/milmed/usy138.

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Orcutt, Michael B. "Iatrogenic Vascular Injury". Archives of Surgery 120, nr 3 (1.03.1985): 384. http://dx.doi.org/10.1001/archsurg.1985.01390270122021.

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YARADILMIŞ, Yüksel Uğur, Mert KARADUMAN, Süleyman ALBAYRAK i Murat ALTAY. "Vascular injury following revision knee arthroplasthy: A case report". Journal of Surgical Case Reports and Images 4, nr 7 (7.10.2021): 01–06. http://dx.doi.org/10.31579/2690-1897/062.

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Acute arterial occlusions are uncommon complications in total knee arthroplasty (TKA). This complication is seen more in TKA revision surgery, and when appropriate treatment cannot be made, amputation may be necessary. The present case is here presented of a patient applied with TKA revision because of instability following a simple fall one year after primary TKA, and popliteal artery occlusion developed in the early postoperative period. The patient was a 70-year old female not actively working. In the patient history there was deep vein thrombosis in the ipsilateral lower extremity after primary TKA and associated with that, pulmonary embolism. The diagnosis of popliteal artery occlusion, which formed after the revision surgery, was diagnosed with advanced tests in the 3rd hour postoperatively, and in the 4th hour, exploration was made. No arterial active bleeding had been observed intraoperatively. Popliteal thrombectomy were applied of popliteal artery trombosis. Acute arterial occlusion is a rarely encountered complication, but it requires emergency intervention. To prevent the development of acute occlusive disease in revision knee surgery, preoperative evaluation of arterial status is recommended, especially in patients with a history of surgery.
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Rozprawy doktorskie na temat "Vascular injury"

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Millar, Christopher G. "Endothelial progenitor cells and vascular injury". Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/24977.

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Endothelial progenitor cells (EPCs) are bone marrow derived cells that contribute towards neovascularisation. I have primarily used real time polymerase chain reaction (PCR), but also flow cytometry and cell culture techniques, to investigate the effect of vascular injury on the expression of the putative markers of EPCs (CD34, CD133, VEGFR-2 and VE-cadherin) and their number in peripheral blood. In the first study I investigated the effect of percutaneous coronary intervention (PCI) on EPCs in a group of patients with stable coronary disease. After PCI, EPC markers did not conclusively demonstrate a rise in expression, although the number of VEGFR-2+ cells did increase. However, the number of EPC colony forming units (CFUs) increased significantly. In the next study, I investigated the effect of open aortic aneurysm repair on EPCs in a group of elective surgical patients. There were changes in the level of expression of EPC markers, using both real-time PCR and flow cytometry, but statistical significance was not reached. However, there were significant increases in the mean fluorescent intensities (MFI) of VEGFR-2 and VE-cadherin expression. EPC-CFUs did not change significantly. The next study investigated the effect of type 1 diabetes on EPC levels. The percentage of CD34+ cells, the RQ of VE-cadherin mRNA and the number of EPC-CFUs were significantly reduced in the diabetic cohort compared with control groups. Finally, the effect of chronic renal impairment and administration of human recombinant erythropoietin (Epo) on EPC levels was investigated. The RQs of CD34, VEGFR-2 and VE-cadherin mRNA species increased over the period analysed, but this increase did not correspond with an increase in VEGF expression. This thesis provides further insight into the effect of endogenous and exogenous causes of vascular injury on EPCs.
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Mallawaarachchi, Chandike Maithri. "The adventitial response to vascular injury". Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619944.

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Matter, Christian M. "Molecular and cellular mechanisms of vascular injury /". Zürich, 2007. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253379.

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Macdonald, Linsay Joanne. "Glucocorticoid metabolism and the vascular response to injury". Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/24084.

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In order to study the influence of glucocorticoids on vascular lesion formation, a model of intra-luminal, wire-induced vascular injury in the mouse femoral artery was developed. This model caused extensive stretching of the arterial wall and denudation of the endothelium, followed by the time-dependent formation of smooth muscle-rich neointimal lesions. Systemic administration of dexamethasone by sub-cutaneous injection (1 mg/kg/day, 21 days) reduced the size of smooth muscle-rich lesions after injury, but also promoted the formation of large thrombotic lesions. These occluded the lumen, leading to a similar reduction in luminal diameter to that seen in vehicle-treated controls. In contrast, local application of cortisol at the vessel wall via sustained release from an implanted pellet (21 days), significantly reduced neointimal lesion growth when compared to contra-lateral vehicle controls, without the development of thrombotic lesions. The influence of endogenous glucocorticoid activity on neointimal proliferation in the femoral artery was assessed using administration of a glucocorticoid receptor antagonist (RU38486, via implanted pellet for 21 days) or via selective pharmacological inhibition of 11βHSD1 (60mg/kg/day via oral gavage, 14 days) and the use of mice with transgenic disruption of 11βHSD1. Neither glucocorticoid receptor antagonism nor 11βHSD1 inhibition or deletion altered neointimal lesion development after injury. These results indicate that exogenous glucocorticoids do inhibit proliferation in this model but their effectiveness depends upon whether they are administered systemically or locally at the vessel wall. Whereas the manipulation of endogenous glucocorticoid generation in the vessel wall may not represent a novel therapeutic target, the application of glucocorticoids locally at this site may be beneficial in the treatment of arterial remodelling.
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Wahlgren, Carl Magnus. "Mechanisms of thrombosis and restenosis after vascular injury /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-260-8/.

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Bundy, Ruth Eldeca. "Redox modulation of vascular cell injury and adaptation". Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414511.

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Hay, Jennifer R. "Vascular and cellular responses to traumatic brain injury". Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/30819/.

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There is growing evidence that suggests Traumatic brain injury (TBI) may initiate long-term neurodegenerative processes. Exposure to a single moderate or severe TBI, or to repetitive TBI, reveals a complex of pathologies including abnormalities of tau, amyloid-β and TDP-43; neuronal loss; neuroinflammation; and white matter degradation. The mechanisms driving these late post-TBI neurodegenerative pathologies remain elusive. Firstly, a potential association between blood-brain barrier (BBB) disruption and TBI was investigated. Results showed that increased and widespread BBB disruption was observed in material from patients dying in the acute phase following a single, moderate to severe TBI and persisted in a high proportion of patients surviving years following injury. Furthermore, there was preferential distribution to the deep layers of the cortex and to the crests of the gyri rather than the depths of the sulci. This post-TBI BBB disruption was investigated further within a paediatric TBI cohort. BBB disruption was noted in both paediatric and adult TBI in a similar pattern and distribution, however, interestingly, in sharp contrast to adult TBI cases, BBB disruption in paediatric cases appears preferentially distributed to capillary sized vessels. This vulnerability of the small vessels was rarely observed in adult material. In addition to the post-TBI vascular change observed, the cellular response was investigated, which interestingly, demonstrated regional differences. Specifically, in the grey matter, reactive astrogliosis was observed subpially, around cortical vessels, at the grey and white matter boundaries and subependymally. This astrogliosis was evident in a proportion of acute and continued into the late phase following TBI. In contrast, microglial activation was observed as a delayed response and localised to the white matter tracts. In addition, this delayed microglial response expressed an M2-like phenotype. Furthermore, there was an increased population of inactivated perivascular microglia beyond the perivascular space in the grey matter regions, observed in the acute phase and persisted in a proportion of patients surviving years following injury. Collectively these findings are interesting and indicate TBI induces both a vascular and cellular responses which may contribute to the long-term post-TBI neurodegenerative processes.
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Oommen, Anson Jacob. "Assessing the role of Polyphenols as a vascular protectant against Drug Induced Vascular Injury". Wright State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=wright1560292217772559.

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Kahn, Matthew Benjamin. "Effects of insulin resistance on endothelial regeneration following vascular injury". Thesis, University of Leeds, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.550287.

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Insulin resistance, the primary metabolic abnormality underpinning type 2 diabetes mellitus and obesity, is an important risk factor for the development of cardiovascular disease. Endothelial dysfunction represents one of the earliest phases in the natural . history of atherosclerosis and is normally offset in health by various endogenous repair processes. Circulating endothelial progenitor cells (EPCs) participate in endothelial repair following arterial injury. Type 2 diabetes is associated with fewer circulating EPCs, EPC dysfunction and impaired endothelial-repair. I set out to determine whether insulin-resistance per se adversely affects EPC mediated endothelial-regeneration using mice hemizygous for knockout of the insulin receptor (IRKO) and wild-type (WT) littermate controls. The metabolic phenotype of IRKO mice was consistent with compensated insulin resistance. Flow cytometry demonstrated that IRKO mice had fewer circulating EPCs than WT mice. Culture of mononuclear-cells confirmed that IRKO mice had fewer EPCs in peripheral-blood, but not in bone-marrow or spleen, suggesting a mobilization defect. Defective VEGF-stimulated EPC mobilization was confirmed in IRKO mice, consistent with reduced eNOS expression in bone marrow and impaired vascular eNOS activity. Paracrine angiogenic activity of EPCs from IRKO mice was impaired compared to those from WT animals. Endothelial-regeneration of the femoral artery following denuding wire-injury was delayed in IRKO mice compared to WT. Transfusion of mononuclear-cells and c-kit bone-marrow cells from WT mice normalized the impaired endothelial-regeneration in IRKO mice. However, transfusion of c-kit+ cells from IRKO mice was less effective at improving endothelial-repair. My data suggest that insulin-resistance impairs EPC function and delays endothelial-regeneration following arterial injury. These findings support the hypothesis that insulin-resistance per se is sufficient to jeopardise endogenous vascular repair. Defective endothelial-repair may be normalised by transfusion of EPCs from insulin- sensitive animals but not from insulin-resistant animals. These data may have important implications for the development of therapeutic strategies for insulin- resistance associated cardiovascular disease.
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Evans, Steven Martin. "Role of nitric oxide isoenzymes in inflammation and vascular injury". Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267851.

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Książki na temat "Vascular injury"

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Simon, Daniel I., i Campbell Rogers. Vascular Disease and Injury. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/1592590039.

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Love, Graham P. Endothelin-I as a mediator of injury in vascular endothelial cells. Dublin: University College Dublin, 1997.

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Brace, Sarah. A guide to ozone injury in vascular plants of the Pacific Northwest. Portland, Or. (333 S.W. First Avenue, P.O. Box 3890 Portland, 97208-3890): U.S. Department of Agriculture, Forest Service, Pacific Nortwest Research Station, 1999.

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The clinical neuropsychiatry of stroke: Cognitive, behavioral, and emotional disorders following vascular brain injury. Cambridge: Cambridge University Press, 1998.

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V, Schaff Hartzell, red. Vasoactive factors produced by the endothelium: Physiology and surgical implications. Austin: R.G. Landes, 1994.

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Kim, Tony Tae Yub. Vascular growth after balloon catheter injury in normal rats treated with high fat diet and insulin implants. Ottawa: National Library of Canada, 2002.

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Vascular Disease And Injury. Humana Press, 2010.

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Vascular endothelium: Responses to injury. New York: Plenum Press, 1996.

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John D. Catravas Allan D. Callow. Vascular Endothelium: Responses to Injury. Brand: Springer, 2011.

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Ryan, Una S., Allan D. Callow i John D. Catravas. Vascular Endothelium: Responses to Injury. Springer, 2012.

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Części książek na temat "Vascular injury"

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Davenport, Andrew, Todd W. Costantini, Raul Coimbra, Marc M. Sedwitz, A. Brent Eastman, David V. Feliciano, David V. Feliciano i in. "Vascular Injury". W Encyclopedia of Intensive Care Medicine, 2390. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_2389.

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Neff, Lucas P., i Todd E. Rasmussen. "Vascular Injury". W Fundamentals of Pediatric Surgery, 189–94. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27443-0_23.

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Gaines, Barbara A. "Vascular Injury". W Fundamentals of Pediatric Surgery, 157–60. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6643-8_21.

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Beard, Jonathan D. "Vascular Injury". W Medicolegal Issues in Obstetrics and Gynaecology, 253–58. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78683-4_45.

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Davenport, Andrew, Todd W. Costantini, Raul Coimbra, Marc M. Sedwitz, A. Brent Eastman, David V. Feliciano, David V. Feliciano i in. "Vascular Injury, Classification". W Encyclopedia of Intensive Care Medicine, 2390–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_539.

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Zabka, Tanja S., i Kaïdre Bendjama. "Vascular Injury Biomarkers". W Drug Discovery Toxicology, 397–406. Hoboken, NJ: John Wiley & Sons, Inc, 2016. http://dx.doi.org/10.1002/9781119053248.ch25.

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Wendorff, Heiko, Benedikt Reutersberg i Hans-Henning Eckstein. "Varia: Vascular Injury". W Acute Elbow Trauma, 119–26. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-97850-5_10.

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Peterson, Hamlet A. "Vascular Deficiency". W Physeal Injury Other Than Fracture, 1–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-22563-5_1.

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Gänger, K. H., i A. Senn. "Injury of the Large Veins". W Vascular Surgery, 687–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-72942-3_58.

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Kumar, Anand, Helen Lavretsky i Ebrahim Haroon. "Neuropsychiatric Correlates of Vascular Injury". W Vascular Dementia, 157–69. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-824-2:157.

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Streszczenia konferencji na temat "Vascular injury"

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Shatos, M., J. Doherty, D. Allen i J. Hoak. "ALTERATIONS IN VASCULAR ENDOTHELIAL CELL FUNCTION BY OXYGEN-FREE RADICALS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643365.

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The vascular endothelium is a target for oxidant-induced damage in many disease states including hyperoxia, inflammation, ischemia and reperfusion injury. However, little is known concerning oxidant injury to endothelial cells and its relationship to hemostasis. Our studies have focused on the ability of oxygen free radicals to injure and/or alter selected vascular endothelial cell functions pertinent to the regulation of hemostasis. Xanthine and xanthine oxidase, a well-characterized generating system for the production of the superoxide anion radical (O− 2) was used to sublethally injure human umbilical vein endothelial cells (HUVE) in vitro. We examined the effects of a 15 min exposure of HUVE cells to xanthine (50μM), and xanthine oxidase (2.5-100mU) (previously determined to be non-toxic using trypan blue dye exclusion) on platelet adherence, and prostacyclin release using established assays. The antioxidant enzymes superoxide dismutase (SOD) 200μg/ml and catalase 50μg/ml were added to endothelium incubation systems to evaluate any protective effects upon O− 2-induced alterations. All experiments were conducted in a serum-free HEPES-Tyrode's buffer, pH 7.4 incubation system. Our results show that exposure of HUVE cells to sublethal concentrations of oxygen free radical generating systems causes significant enhancement of platelet adherence (65%) to injured endothelium. A 12-fold increase in prostacyclin release resulted after a 15 min treatment with xanthine and xanthine oxidase. The addition of exogenous PGI2 (150nM) to platelet-endothelial systems did not completely prevent the enhanced platelet adherence suggesting that lack of prostacyclin was not completely responsible for the adherence of platelets to O− 2 injured cells. When SOD and catalase, scavengers of O− 2 and H2O− 2, were added to treated cells, platelet adherence decreased by 42-77% and prostacyclin release approached that of control cultures. These data implicate an active participation of activated metabolites of molecular oxygen in the alteration of vascular endothelial cell function.
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Bhattacharya, Mallar, George Su, Juan Oses-Prieto, John Li, Amha Atakilit, Hilda Barry, Nanyan Wu, Alma Burlingame i Dean Sheppard. "IQGAP1 Prevents Vascular Leak In Murine Acute Lung Injury". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1339.

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Sequeira, M., O. Bhadra, D. Kalbacher, N. Schofer, F. Deuschl, A. Schäfer, Y. Schneeberger i in. "Percutaneous Management of Vascular Injury after Transfemoral Aortic Valve Implantation". W 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678873.

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Barbee, Kenneth A., i Amit Bhavnani. "Strain and Strain Rate Dependence of Vascular Smooth Muscle Injury". W ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23155.

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Abstract Over 350,000 percutaneous translumenal coronary angioplasty (balloon angioplasty) procedures are performed each year. This procedure offers a less invasive alternative to coronary by-pass surgery for patients whose coronary vessels have become occluded due to the process of atherosclerosis. Its potential has not been fully realized due to the high rate of restenosis — the rapid reocclusion of the vessel due to the pathological growth of the vascular smooth muscle (VSM) in response to the trauma of the balloon inflation. Despite the recognition of smooth muscle injury as an initiating event in the process of restenosis, there has been no systematic study to determine the mechanical loading conditions required to produce VSM injury and elicit the restenosis response. In this study, a cell culture model was developed to define the loading conditions required to produce VSM injury. The model system allows precise control of the applied strain and strain rate and quantification of the injury severity in terms of membrane damage. The determination of the threshold criteria for cell injury will allow the angioplasty procedure to be modified, and possibly automated, to minimize VSM injury and avoid the restenosis response.
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Yeoh, Stewart, Vishwas Mathur i Kenneth L. Monson. "Vascular Injury and Cortical Deformation in a Model of Brain Contusion". W ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53833.

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Traumatic brain injury (TBI) is a leading cause of death and disability, affecting 1.7 million Americans annually, 50,000 of whom die [1]. Victims who survive the initial injury often suffer debilitating neurologic deficits. The total annual cost of TBI in the United States has been estimated at $60 billion [2]. While damage to brain tissue is of primary concern in TBI, nearly all head trauma includes some element of vascular injury or dysfunction [3], putting neural tissue uninjured in the primary event at subsequent risk. Contusion, which includes injury to both brain and vessel tissue in the cortex, is considered the hallmark of head injury, but little is known about the specific mechanisms of vascular injury in contusion. Previous efforts to elucidate mechanisms and thresholds for contusion, including inanimate gel, animal, and computational models [e.g. 4–7], have defined bulk tissue deformations that are associated with contusion, but the relationship to vascular injury is not clear. In order to address this question, our laboratory is studying acute disruption of the blood-brain barrier using a controlled cortical impact (CCI) mouse model. The objective of this study was to compare acute vascular injury in CCI with cortical mechanics predicted by a computational model of the experiment. This comparison is then discussed in the context of results from isolated vessels testing in our laboratory.
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Tan, Y. Y., K. P. O'Dea i M. Takata. "Circulating Neutrophil-Derived Microvesicles During Endotoxaemia Induce Pulmonary Vascular Injury". W American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2670.

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Tuncer, HA. "EP1314 Laparoscopic management of major vascular injury during paraaortic lymphadenectomy". W ESGO Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-esgo.1318.

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Veress, Livia A. "Airway Obstruction And vascular Injury After Sulfur Mustard Analog Inhalation". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4683.

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Hernandez, J., J. Acosta, L. Almeciga i S. Vieira. "SF019/#636 Vascular injury in robot-assisted para-aortic lymphadenectomy". W IGCS 2021 Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/ijgc-2021-igcs.63.

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Welch, Tre, Robert C. Eberhart i Cheng-Jen Chuong. "Thermal Treatment Effects on a PLLA Bioresorbable Stent". W ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176640.

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Stent navigation and expansion may injure vascular endothelium, including vulnerable plaque lesions. Balloon expansion and deployment of a stent can lead to injury or the endothelial lining and stretching of the arterial wall [1]. Understanding the traction forces an expanding stent imparts on the vascular wall at the endothelial surface, the underlying plaque lesions and other tissue components during expansion is an important step in improving short term stent-wall mechanics. More importantly, the long term influence of stent-vascular wall mechanical interactions in restenosis remains unknown, and this analysis may shed light on the process.
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Raporty organizacyjne na temat "Vascular injury"

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Arthurs, Zachary. Joint Global War on Terror (GWOT) Vascular Injury Study 2. Fort Belvoir, VA: Defense Technical Information Center, luty 2015. http://dx.doi.org/10.21236/ada613646.

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Brace, Sarah, David L. Peterson i Darci Bowers. A guide to ozone injury in vascular plants of the Pacific Northwest. Portland, OR: U.S. Department of Agriculture, Forest Service, Pacific Northwest Research Station, 1999. http://dx.doi.org/10.2737/pnw-gtr-446.

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Percival, Thomas J., Shimul Patel, Nickolay P. Markov, Jerry R. Spencer, Gabriel E. Burkhardt, Lorne H. Blackbourne i Todd E. Rasmussen. Fasciotomy Reduces Compartment Pressures and Improves Recovery in a Porcine Model of Extremity Vascular Injury and Ischemia/Reperfusion. Fort Belvoir, VA: Defense Technical Information Center, październik 2012. http://dx.doi.org/10.21236/ada568830.

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