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.
Pełny tekst źródłaMallawaarachchi, Chandike Maithri. "The adventitial response to vascular injury". Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619944.
Pełny tekst źródłaMatter, Christian M. "Molecular and cellular mechanisms of vascular injury /". Zürich, 2007. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253379.
Pełny tekst źródłaMacdonald, Linsay Joanne. "Glucocorticoid metabolism and the vascular response to injury". Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/24084.
Pełny tekst źródłaWahlgren, Carl Magnus. "Mechanisms of thrombosis and restenosis after vascular injury /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-260-8/.
Pełny tekst źródłaBundy, 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.
Pełny tekst źródłaHay, Jennifer R. "Vascular and cellular responses to traumatic brain injury". Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/30819/.
Pełny tekst źródłaOommen, 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.
Pełny tekst źródłaKahn, 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.
Pełny tekst źródłaEvans, 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.
Pełny tekst źródłaGreig, Fiona Helen. "The involvement of modified lipids in vascular injury and disease". Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4229/.
Pełny tekst źródłaKirkby, Nicholas S. "Investigating the role of endothelin receptor subtypes in the response to vascular injury". Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4440.
Pełny tekst źródłaRafi-Janajreh, Asimah. "Role of CD44 in Immune Functions and Endothelial Cell Injury". Diss., Virginia Tech, 1998. http://hdl.handle.net/10919/77996.
Pełny tekst źródłaPh. D.
Amaro, Emilie, Stephen Pophal i Jozef Zoldos. "Vascular Reconstruction in a Neonate after Iatrogenic Injury during Cardiac Catheterization". LIPPINCOTT WILLIAMS & WILKINS, 2017. http://hdl.handle.net/10150/627070.
Pełny tekst źródłaDollery, Clare Margaret. "Matrix metalloproteinase inhibitors in vascular injury : pharmacological and gene transfer approaches". Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286196.
Pełny tekst źródłaLauder, Heather. "Role of endothelins and somatostatin in vascular cell regeneration following injury". Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627199.
Pełny tekst źródłaPadfield, Gareth John. "Role of endothelial progenitor cells in acute vascular injury in man". Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8806.
Pełny tekst źródłaMOORE, ZACHARY W. Q. "APOLIPOPROTEIN E MODULATION OF VASCULAR SMOOTH MUSCLE CELL RESPONSE TO INJURY". University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1127219075.
Pełny tekst źródłaRudström, Håkan. "Iatrogenic Vascular Injuries". Doctoral thesis, Uppsala universitet, Kärlkirurgi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-194346.
Pełny tekst źródłaMthethwa, Mashudu. "The responses of endothelium to insult : does endothelial heterogeneity play a role in in vitro cell models". Thesis, Stellenbosch : Stellenbosch University, 2015. http://hdl.handle.net/10019.1/97832.
Pełny tekst źródłaENGLISH ABSTRACT: Endothelial injury and dysfunction precede the development of cardiovascular diseases. The endothelium may be regarded as the first line of defence against inflammation / obesity-induced vascular injury, therefore gaining more information on the mechanisms of injury and response to injury, as well as modulating endothelial function may be key in the prevention of cardiovascular diseases. Endothelial cells differ in structure and function, therefore endothelial heterogeneity may be relevant when investigating endothelial function and dysfunction. Understanding endothelial heterogeneity in response to pathophysiological stimuli may be of significance in the prevention of cardiovascular diseases. Oleanolic acid (OA), a plant-derived triterpenoid, has been shown to possess endothelio-protective properties; however, its role in reversing endothelial injury is poorly understood. This study investigated endothelial heterogeneity between aortic endothelial cells (AECs) and cardiac microvascular endothelial cells (CMECs) at baseline and in response to an inflammatory insult via the cytokine, tumour necrosis factor-alpha (TNF-α). An in vitro model of endothelial injury was developed by treating AECs and CMECs with 20 ng/ml TNF-α for 24 hours. Endothelial heterogeneity was investigated by comparing intracellular nitric oxide (NO) and reactive oxygen species (ROS) production, protein expression and phosphorylation, and large-scale protein expression and regulation in AECs and CMECs. The experimental techniques included flow cytometry, western blots and proteomic analyses. An ex vivo model of endothelial injury was included to investigate vascular function in aortic rings from lean and high fat diet (HFD) rats. The role of OA in reversing TNF-α-induced injury and modulating vascular function in the ex vivo model was investigated. Although baseline NO-levels were similar between AECs and CMECs, heterogeneity was observed with regards to the NO biosynthetic pathway in terms of increased eNOS expression in CMECs. Baseline ROS levels were heterogeneous between AECs and CMECs, interestingly CMECs possessed higher anti-oxidant capacity. An in vitro model of TNF-α-induced injury was confirmed by decreased NO-levels, increased ROS-levels and necrosis, up-regulation of apoptotic proteins and activation of inflammatory pathways in AECs and CMECs. Here, heterogeneity between AECs and CMECs was also observed: endothelial activation was mediated through different proteins in AECs (CD9 molecule, galectin) and CMECs (ICAM-1 and IL-36α). Apoptosis was mediated by caspase 3 in AECs and Bid in CMECs. AECs appeared to advance to a dysfunctional state shown by up-regulation of endothelin-converting enzyme and angiotensin II-converting enzyme, while CMECs maintained an activated state. OA reversed TNF-α-induced injury through restoring NO-production, decreasing ROS-production in both AECs and CMECs, and inhibiting necrosis in AECs. In the ex vivo model of injury, aortic rings from 16-week HFD rats showed a pro-contractile response to phenylephrine-induced contraction, a response that was reversed by OA. In conclusion, we demonstrated novel findings with regards to endothelial heterogeneity between AECs and CMECs under baseline and TNF-α-treated conditions. Although reduced NO-bioavailability may be the hallmark of endothelial dysfunction, signalling pathways mediating endothelial injury may differ between cell types as was shown in this study. We demonstrated that OA possess protective properties in AECs and CMECS, an observation which was translated to the ex vivo model.
AFRIKAANSE OPSOMMING: Endoteelbesering en –disfunksie gaan die ontwikkeling van kardiovaskulêre siektes vooraf. Die endoteel word as die eerste linie van verdediging teen inflammasie / vetsug-geïnduseerde vaskulêre skade beskou; dus is die ontginning van nuwe inligting betreffende die meganismes van en respons tot besering, asook die modulering van endoteelfunksie essensieël in die voorkoming van kardiovaskulêre siektes. Endoteelselle verskil t.o.v. struktuur en funksie, en dus is endoteel-heterogeniteit relevant tydens die ondersoek van endoteelfunksie en –disfunksie. ‘n Beter begrip van endoteel-heterogeniteit in die respons tot patofisiologiese stimuli kan betekenisvol tot die voorkoming van kardiovaskulêre siektes bydra. Oleanoliese suur (OA), ‘n triterpenoïed afkomstig van plante is voorheen bewys om endoteelbeskermende eienskappe te besit; die rol van OA in die omkering van endoteelbesering is egter minder bekend. Hierdie studie het endoteel-heterogeniteit tussen aorta endoteelselle (AECs) en hart mikrovaskulêre endoteeelselle (CMECs) by basislyn en in respons tot ‘n inflammatoriese besering via die sitokien, tumor nekrose faktor-alfa (TNF-α), ondersoek. ‘n In vitro model van endoteelbesering is ontwikkel deur AECs en CMECs met 20 ng/ml TNF-α vir 24 uur te behandel. Endoteel-heterogeniteit was ondersoek deur intrasellulêre stikstofoksied (NO) en reaktiewe suurstofspesies (ROS) produksie, proteïenuitdrukking en fosforilering, en grootskaalse proteïenuitdrukking en regulering in AECs en CMECs te vergelyk. Die eksperimentele tegnieke het ingesluit: vloeisitometrie, western blots en proteomika. ‘n Ex vivo model van endoteelbesering was ook ingesluit deur die vaskulêre funksie in aortaringe van normale en hoë vet dieet-gevoerde (HFD) rotte te meet. Die rol van OA in die omkering van TNF-α-geïnduseerde besering en modulering van vaskulêre funksie was in hierdie model is ondersoek. Alhoewel basislyn NO-vlakke vergelykbaar was in AECs en CMECs, is heterogeniteit wel aangetoon m.b.t. die NO biosintese pad met verhoogde eNOS uitdrukking in die CMECs. Basislyn ROS-vlakke was verskillend in AECs en CMECs en die CMECs het hoër anti-oksidant kapasiteit getoon. ‘n In vitro model van TNF-α-geïnduseerde besering is bevestig met die waarneming van verlaagde NO-vlakke, verhoogde ROS-vlakke en nekrose, opregulering van apoptotiese proteïene en aktivering van inflammatoriese paaie in AECs en CMECs. Hier was heterogeniteit ook opmerkbaar: endoteelaktivering was deur verskillende proteïene in AECs (CD9 molekule, galektien) en CMECs (ICAM-1, IL-36α) bemiddel. Apotose was deur kaspase 3 in AECs en Bid in CMECs bemiddel. Dit het geblyk dat AECs tot ‘n staat van endoteeldisfunksie gevorder het met die opregulering van endotelien-omsettingsensiem en angiotensien II-omsettingsensiem, terwyl CMECs eerder ‘n geaktiveerde staat gehandhaaf het. OA het TNF-α-geïnduseerde besering omgekeer deur NO-produksie te herstel, ROS-produksie te onderdruk in beide AECs en CMECs, en nekrose te inhibeer in AECs. In die ex vivo model van besering, het aortaringe van 16-week HFD rotte ‘n pro-kontraktiele respons tot fenielefrien-geïnduseerde kontraksie getoon, wat deur OA omgekeer is. Ten slotte, nuwe bevindinge is waargeneem m.b.t. endoteel-heterogeniteit tussen AECs en CMECs onder basislyn en TNF-α-behandelde omstandighede. Alhoewel verlaagde NO-biobeskikbaarheid die waarmerk van endoteeldisfunksie is, het hierdie studie getoon dat seintransduksiepaaie wat endoteelbesering medieer verskillend is tussen seltipes. Die studie het verder ook gedemonstreer dat OA beskermende eienskappe toon in AECs en CMECs, ‘n waarneming wat ook in die ex vivo model aangetoon kon word.
Anglin, Sandra Sophia Charmain. "The role of the local renin-angiotensin system in the development of fibrocellular intimal hyperplasia following balloon catheter-induced injury in the rat". Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307441.
Pełny tekst źródłaFlynn, Paul Desmond. "Transgenic rats expressing apolipoprotein(a) : generation, characterisation and response to vascular injury". Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621943.
Pełny tekst źródłaBaker, R. C. "Modulation of peri-operative renal injury in a model of vascular surgery". Thesis, Queen's University Belfast, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396890.
Pełny tekst źródłaArmstrong, Johanna. "C-fos, response to injury and local drug delivery in vascular models". Thesis, University of Sheffield, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312781.
Pełny tekst źródłaMitchell, Andrew Joseph. "Understanding the role of endothelial progenitor cells in vascular injury and repair". Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/33310.
Pełny tekst źródłaDawoud, Hazem Elsaid. "Nanomedical Studies of Angiographic Contrast-Induced Renal and Vascular Injury: Clinical Implications". Ohio University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1522677857523823.
Pełny tekst źródłaAmmann, Kaitlyn R., Katrina J. DeCook, Phat L. Tran, Valerie M. Merkle, Pak K. Wong i Marvin J. Slepian. "Collective cell migration of smooth muscle and endothelial cells: impact of injury versus non-injury stimuli". BioMed Central, 2015. http://hdl.handle.net/10150/610313.
Pełny tekst źródłaZargham, Ramin. "[Alpha]8[beta]1 integrin and vascular injury : role of [alpha]8[beta]1 integrin in restenosis after balloon injury". Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111876.
Pełny tekst źródłaIn this work, a rat model of carotid angioplasty was used to mimic vascular injury in humans. alpha8beta1 integrin was downregulated in the tunica media concomitantly with loss of the contractile phenotype. In vitro study revealed that it is a differentiation marker of VSMCs. To test the functional significance of the association between alpha8 integrin and the VSMC phenotype, short interference RNA was deployed to silence the alpha8 integrin gene. alpha8 integrin gene silencing heightened VSMC migratory activity as well as modulation of the VSMC phenotype in favour of the noncontractile state. In addition, alpha8 integrin overexpression induced re-differentiation of VSMCs and attenuated their migratory activity. It is, therefore, suggested that alpha8 integrin overexpression after vascular injury might control VSMC migration and neointima formation. On the other hand, alpha8 integrin gene silencing led to a reduced growth rate, which indicated a dichotomy between VSMC migration and proliferation.
In the later stages of neointima formation, constrictive remodeling plays a major role in late lumen loss. Our data demonstrated that alpha8 integrin is upregulated in the neointima during constrictive remodeling with concomitant luminal narrowing. The importance of this finding was highlighted by results showing that alpha8 integrin was required for the VSMC contractile phenotype evoked by transforming growth factor-beta (TFG-beta) and TFG-beta-induced myofibroblastic differentiation of Rat1 fibroblasts. Thus, it appears that alpha8 integrin expression blockade might reduce contractile remodeling and late lumen loss. Although the mechanism of alpha8 integrin signaling is not yet clear, our findings demonstrate that the alpha8 integrin-induced contractile phenotype is blocked by RhoA inhibitors. Furthermore, alpha8 integrin and RhoA are co-immunoprecipitated, and alpha8 integrin gene silencing reduces RhoA activity. Hence, it is postulated that alpha8-RhoA signaling might be closely intertwined.
Altogether, these studies indicate that alpha8 integrin is a contractile marker of VSMCs and a negative regulator of VSMC migration. Therefore, forced alpha8 integrin expression may be applied to reduce neointima formation. However, alpha8 integrin upregulation during constrictive remodeling concomitant with late lumen loss suggest that it could be involved in lumen narrowing. It seems likely that in therapeutic strategies to reduce restenosis the timeline of interference might be very important. Therefore, alpha8 integrin gene silencing in the later stages of neointima formation might be beneficial.
Partridge, Charles Randal. "Identification and molecular characterization of novel genomic targets in oxidant-induced vascular injury". Diss., Texas A&M University, 2005. http://hdl.handle.net/1969.1/5024.
Pełny tekst źródłaChen, Q. "Role of natriuretic peptides in the response of vascular smooth muscle to injury". Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597554.
Pełny tekst źródłaLiu, Zhi Zhao [Verfasser]. "Renal vascular function and contrast media induced acute kidney injury / Zhi Zhao Liu". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1042657602/34.
Pełny tekst źródłaEllison, Stephen Patrick. "THE EFFECTS OF INTERLEUKIN-19 ON ATTENUATION OF THE VASCULAR RESPONSE TO INJURY". Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/253270.
Pełny tekst źródłaPh.D.
BACKGROUND: Despite aggressive dietary modification, lipid lowering medications, and other medical therapy, vascular proliferative diseases continue to account for 50% of all mortality in the United States. It is a significant medical and socioeconomic problem contributing to the mortality of multiple diseases including myocardial infarction (MI), stroke, renal failure, and peripheral vascular disease. With a growing number of children becoming obese and an increase in the number of patients with co-morbidities such as metabolic syndrome and Type 2 diabetes mellitus, epidemiological studies project the morbidity and mortality of these diseases to increase. Among these vascular proliferative diseases are primary atherosclerosis, vascular restenosis, and allograft vasculopathy, all of which are the result of chronic inflammation believed to stem from initial endothelial injury. Once activated by any number of potential injurious agents, endothelial cells (ECs) secrete cytokines that act on multiple cell types. Stimulation of resident vascular smooth muscle cells (VSMCs) results in a phenotypic switch from a normally contractile state to a proliferative state. Following this phenotypic shift, VSMCs migrate from the media to the intima of the artery where they begin secretion of both pro- and anti-inflammatory cytokines. Vascular proliferative disease ensues as a result of the autocrine and paracrine signaling of these cytokines between many different cell types including ECs, VSMCs, macrophages, and T-cells. As a result of the integral role pro- and anti-inflammatory cytokines play in the development of vascular proliferative diseases, they have become the subject of intense study in the field of cardiovascular research. Interleukin-19 (IL-19) is a newly described member of the IL-10 sub-family of anti-inflammatory cytokines. Discovered in 2000, it was originally only thought to be basally expressed in monocytes and lymphocytes, however in 2005 our lab discovered that while uninjured arteries have no detectable IL-19, arteries of patients with vascular proliferative diseases have notable IL-19 expression. Since its discovery in multiple cell types of injured arteries, our lab has subsequently shown that IL-19 inhibits proliferation, migration, spreading, production of reactive oxygen species (ROSs), and expression of pro-inflammatory genes in VSMCs, while in ECs IL-19 has been shown to promote angiogenesis, proliferation, migration, and spreading. AIMS and HYPOTHESIS: The first aim of the current study is to show that IL-19 is expressed in atherosclerotic plaque, and to test that IL-19 can reduce experimental atherosclerosis in susceptible mice. The second aim of the study is to show that IL-19 can regulate development of intimal hyperplasia in a murine model of restenosis. For both aims, we sought to identify potential intracellular signaling mechanisms of IL-19 which produce the observed effect. These aims directed our overall hypothesis that the anti-inflammatory properties of IL-19 can attenuate the vascular response to injury in various animal models of vascular proliferative disease. METHODS and RESULTS: The first aim of this dissertation showed that LDLR-/- mice fed an atherogenic diet and injected with either 1.0ng/g/day or 10.0ng/g/day rmIL-19 had significantly less plaque area in the aortic arch compared with controls (p<0.0001). Weight gain and serum lipid levels were not significantly different. IL-19 could halt, but not reverse expansion of existing plaque. Gene expression in splenocytes from IL-19 treated mice demonstrated immune cell Th2 polarization, with decreased expression of T-bet, IFNgamma, IL-1β and IL-12β, and increased expression of GATA3 messenger ribonucleic acid (mRNA). A greater percentage of lymphocytes were Th2 polarized in IL-19 treated mice. Cellular characterization of plaque by immunohistochemistry demonstrated IL-19 treated mice have significantly less macrophage infiltrate compared with controls (p<0.001). Intravital microscopy revealed significantly less leukocyte adhesion in wild-type mice injected with IL-19 and fed an atherogenic diet compared with controls. Treatment of cultured EC, VSMC, and bone marrow-derived macrophages (BMDM) with IL-19 resulted in a significant decrease in chemokine mRNA, and in the mRNA-stability protein HuR. In the second aim of this dissertation we showed that IL-19 attenuates vascular restenosis in response to carotid artery ligation. Carotid artery ligation of hyper-responsive friend leukemia virus B (FVB) wild-type mice injected with 10ng/g/day rIL-19 had significantly lower neointima/media ratio (I/M) compared with phosphate buffered saline (PBS) controls (p=0.006). Conversely, carotid artery of IL-19-/- mice demonstrated significantly higher I/M ratio compared with wild-type mice (p=0.04). Importantly, the increased I/M ratio in the knockout mice could be rescued by injection of 10ng/g/day IL-19 (p=0.04). VSMC explanted from IL-19-/- mice proliferated significantly more rapidly compared with wild-type (p=0.04). Surprisingly, in this model, IL-19 does not modulate adoptive immunity. Rather, addition of IL-19 to cultured wild-type VSMC did not significantly decrease VSMC proliferation, but could rescue proliferation in IL-19-/- VSMC to wild-type levels (p=0.02). IL-19-/- VSMC expressed significantly greater levels of inflammatory mRNA including IL-1β, TNFα, and MCP-1 in response to TNFα stimulation (p<0.01 for all). No polarization of adaptive immunity was noted in these mice. CONCLUSIONS: These data are the first to report that IL-19 is a potent inhibitor of experimental atherosclerosis via diverse mechanisms including immune cell polarization, decrease in macrophage adhesion, and decrease in gene expression. In addition, these data are also the first to show that IL-19 plays a previously unrecognized protective role in vascular restenosis. Together, these data suggest IL-19 is both anti-atherogenic and anti-restenotic and may identify IL-19 as a novel therapeutic to limit vascular inflammation.
Temple University--Theses
Ohashi, Naohiro. "Role of p38 Mitogen-Activated Protein Kinase in Neointimal Hyperplasia After Vascular Injury". Kyoto University, 2001. http://hdl.handle.net/2433/150561.
Pełny tekst źródłaSayers, Rebecca Lynn Taylor Joan M. "Focal adhesion kinase and its endogenous inhibitor, FRNK, in vascular development and injury". Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,2089.
Pełny tekst źródłaTitle from electronic title page (viewed Feb. 17, 2009). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Cell and Molecular Physiology." Discipline: Cell and Molecular Physiology; Department/School: Medicine.
Ali, Ziad A. "Regulation of endothelial nitric oxide synthase by tetrahydrobiopterin in the response to vascular injury". Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437385.
Pełny tekst źródłaRobinson, Hollie Christine. "Investigation of the role of microRNA-143 and microRNA-145 in acute vascular injury". Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5221/.
Pełny tekst źródłaLow, Emma Louise. "Dissecting transforming growth factor-beta signalling pathways in the context of acute vascular injury". Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/30703/.
Pełny tekst źródłaXu, Yang. "Role of bone marrow-derived progenitor cells in cuff-induced vascular injury in mice". Kyoto University, 2004. http://hdl.handle.net/2433/147517.
Pełny tekst źródłaMalabanan, Kristine Paz Centre for Vascular Research Faculty of Medicine UNSW. "Roles of activation transcription factor 4 (ATF4) and YrdC in the response of vascular smooth muscle cells to injury". Publisher:University of New South Wales. Centre for Vascular Research, 2008. http://handle.unsw.edu.au/1959.4/41338.
Pełny tekst źródłaCarvalho, Maria Dulce Ribeiro. "In vitro studies of functional effects of antiendothelial cell autoantibodies". Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244285.
Pełny tekst źródłaOlby, Natasha J. "An experimental model of rat spinal cord injury : its development and studies on manipulation of its glial environment". Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243014.
Pełny tekst źródłaPay, Salih, Meral Calguneri, Zafer Caliskaner, Ayhan Dinc, Sule Apras, Ihsan Ertenli, Sedat Kiraz i Veli Cobankara. "Evaluation of vascular injury with proinflammatory cytokines, thrombomodulin and fibronectin in patients with primary fibromyalgia". Nagoya University School of Medicine, 2000. http://hdl.handle.net/2237/5359.
Pełny tekst źródłaBrickler, Thomas Read. "The Role of Age and Model Severity on Cortical Vascular Response Following Traumatic Brain Injury". Diss., Virginia Tech, 2017. http://hdl.handle.net/10919/85566.
Pełny tekst źródłaPh. D.
Stacy, Mitchel R. "The Effect of Eccentric Exercise-Induced Muscle Injury on Vascular Function and Muscle Blood Flow". University of Toledo / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1302229144.
Pełny tekst źródłaRamachandra, Rakshit. "Injury and Impact Responses of the Abdomen Subjected to Seatbelt Loading". The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1480497361350603.
Pełny tekst źródłaAshawesh, Mohamed. "Ultrasound enhanced gene delivery of secreted Interleukin 1 receptor antagonist in a murine vascular injury model". Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/18481/.
Pełny tekst źródłaKobuke, Kazuhiro. "ESDN, A Novel Neuropilin-like Membrane Protein Cloned from Vascular Cells with the Longest Secretory Signal Sequence among Eukaryotes, Is Up-regulated after Vascular Injury". Kyoto University, 2002. http://hdl.handle.net/2433/150206.
Pełny tekst źródłaSeeger, Joost. "Ischaemic preconditioning in exercise and disease : one size fits all?" Thesis, Liverpool John Moores University, 2016. http://researchonline.ljmu.ac.uk/4550/.
Pełny tekst źródłaPereira, Aline Carvalho. "Mecanismos celulares que influenciam a sinalização por receptores 1-adrenérgicos na carótida contra-lateral à lesão por cateter balão". Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/60/60138/tde-20102009-132757/.
Pełny tekst źródłaIn rat carotid arteries, balloon catheter injury results in neurocompensatory response in contralateral carotid, leading to increased levels of substance P and CGRP (calcitonin gene-related peptide), beside alterations in reactiveness to vasoconstrictor agonists. The aim of this work was to study the mechanisms involved in alterations in phenylephrine (Phe) responsiveness in contralateral carotid, 1, 2, 4 and 15 days after injury. Histological analysis showed that contralateral carotid was similar to control. Endothelium was absent in ipsilateral arteries, but 15 days after lesion it was observed the neointima. Concentration-response curves to Phe (contraction) were performed in isolated carotid rings, control and contralateral, 1, 2, 4 and 15 days after lesion. In the fourth day after lesion, it was observed increase in maximum effect (Emax) to Phe in contralateral compared to control arteries. In order to verify if the increase in Emax to Phe was related to calcium mobilization by this agonist, it was used free-calcium Krebs solution containing or not EGTA, and concentration-response curves to CaCl2. It was observed that intracellular calcium mobilization by Phe was similar to control, but calcium influx was reduced in contralateral. Confocal microscopy, using carotid rings loaded with Fluo-3AM, was also utilized to corroborate this result. In presence of specific inhibitors, it was observed that endothelial isoform of nitric oxide synthase, calcium-activated potassium channels, prostanoids from COX-2, superoxide anions and Gap-junctions are involved on reduction of Phe-induced calcium influx. However, neither nitric oxide, guanylate cyclase nor sarcoendoplasmic reticulum Ca-ATPase participate in this response. Superoxide anions, COX-2 and Gap-junctions also play a role on increased Emax to Phe in contralateral carotid. Futhermore, superoxide anions promote increase in Rho-kinase activity in contralateral carotid compared to control, as it was observed in relaxation curves with Y-27632 (Rho-kinase inhibitor), after Phe pre-contraction. Phe and CaCl2 potency in contralateral were similar to control, like acetylcholine relaxation and KCl-induced contraction. Results obtained in this work indicate that the neurocompensatory response to balloon catheter injury leads to alterations in the signaling pathway downstream alpha1-adrenoceptor activation in contralateral carotid. These alterations are endothelium dependent and, probably, triggered by oxidative stress due to superoxide anions. Taken together, data suggest the existence of compensatory mechanisms to maintain the vascular tonus.
Young, Yun Wai. "Pro-inflammatory growth factors reduce secondary degeneration after traumatic spinal cord injury". Thesis, Queensland University of Technology, 2013. https://eprints.qut.edu.au/60875/1/Yun%20Wai_Young_Thesis.pdf.
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