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Purroy, Rodríguez Marina. "Canvis vasculars associats a l'envelliment en models animals de demència vascular." Doctoral thesis, Universitat de Barcelona, 2021. http://hdl.handle.net/10803/673556.
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INTRODUCCIÓ: El deteriorament cognitiu d’origen vascular, i més concretament la demència vascular (DV), s’associa al compromís persistent del flux sanguini cerebral i representa la segona causa més freqüent de demència al món, després de la malaltia d’Alzheimer. La DV és una malaltia caracteritzada per múltiples i discretes lesions isquèmiques, lesions difuses a la substància blanca (leucoaraiosi) i hemorràgies cerebrals, entre d’altres. S’han dedicat gran quantitat d’esforços en la recerca dels mecanismes fisiopatològics subjacents a aquesta patologia però encara no es coneixen amb precisió. Les tècniques de neuroimatge, com la imatge per ressonància (MRI), van suposar un gran avenç en el diagnòstic d’aquesta patologia. Per aquest motiu, en aquest treball de tesi doctoral s’ha proposat l’estudi longitudinal de canvis estructurals i funcionals vasculars al llarg del temps en animals d’experimentació, en el curs dels símptomes de la malaltia, i sota la influència de diversos factors de risc, mitjançant diferents tècniques de MRI per trobar nous biomarcadors no invasius per la DV, i per avançar en l’estudi de la seva fisiopatologia, així com en el diagnòstic precoç i la monitorització de l’efectivitat de noves teràpies.
MATERIAL I MÈTODES: Es van utilitzar un total de 174 ratolins de dues soques, ratolins ApoE-/-, que tenen predisposició a desenvolupar aterosclerosi amb l’edat, i els ratolins control C57Bl6 de tres edats diferents, des de l’adult jove (6 mesos) fins a la vellesa (18 mesos) incloent una edat intermitja (12 mesos). Es va realitzar un seguiment longitudinal amb tècniques de MRI per estudiar diferents característiques de les lesions vasculars, que es van correlacionar proves de comportament. La validació de les tècniques de MRI es va realitzar mitjançant tincions d’immunohistoquímica per MBP i la clarificació de talls gruixuts de cervell (2 mm) per quantificació de la microvasculatura.
RESULTATS: Es van detectar alteracions relacionades amb aterosclerosi i hipoperfusió en longitud i tortuositat de les principals artèries que irriguen el cervell mitjançant angiografia TOF. També en relació a la irrigació del cervell, es van trobar canvis en el flux sanguini cerebral mitjançant perfusió ASL, associats a les tres condicions estudiades (envelliment, aterosclerosi i hipoperfusió). Així mateix, les tres condicions experimentals van provocar alteracions en les fibres de mielina, detectades amb l’anàlisi dels diferents components dels tensors de difusió (DTI). Aquests canvis es van trobar a estructures relacionades amb les alteracions en les proves de conducta, com ara en ansietat,
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memòria de reconeixement, debilitat muscular i pertorbacions en la marxa. D’altra banda, l’índex Q va mostrar menys sensibilitat que l’anàlisi histopatològic per a l’estudi de la densitat microvascular. Tot i això, va servir per detectar canvis en la densitat microvascular associats a l’edat. Els canvis en el gruix de l’escorça cerebral (atròfia cortical) mesurats per MRI va resultar ser un bon biomarcador de la mort neuronal produïda per l’envelliment i la hipoperfusió.
CONCLUSIONS: Els resultats d’aquest estudi confirmen la utilitat de la MRI com a eina per avaluar els canvis estructurals i funcionals de la neuropatologia de l’envelliment, l’aterosclerosi i la hipoperfusió en recerca traslacional.
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Adams, Gregory Nicholas. "Prolylcarboxypeptidase protects from vascular dysfunction and promotes vascular repair." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1346973249.
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Núñez, Do Rio Joan M. "Vascular pattern characterization in colonoscopy images." Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/325145.
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El càncer de còlon és el tercer amb més incidència al món i el segon tipus de tumor maligne més comú a Europa. Les tècniques d'exploració directa del còlon han demostrat la seva eficiència en la reducció del nombre de víctimes mortals, permetent la detecció de pòlips en estadis prematurs. Entre les diferents tècniques d'exploració, la colonoscòpia és considerada actualment l'estàndard clínic, tot i que diferents estudis revelen la incidència d'alguns factors en la qualitat de l'exploració. La navegació al llarg del còlon i el recte evidencia una sèrie de reptes per als endoscopistes que provoquen un augment en la taxa d'errors. L'acurada inspecció del còlon ha de ser certificada per tal de minimitzar les possibilitats que alguna lesió no sigui detectada. La inspecció de les imatges de colonoscòpia pot aportar informació crucial per als endoscopistes i donar suport a la navegació durant el procediment.
Els vasos sanguinis i els seus patrons de ramificació poden aportar potencial descriptiu per desenvolupar marcadors biomètrics. Els marcadors anatòmics basats en vasos sanguinis podrien ser utilitzats per identificar escenes en vídeos de colonoscòpia i donar suport per a la navegació generant una seqüència d'imatges ordenades en el recorregut de les seccions del colon. Verificant la presència de contingut vascular a l'escena endoluminal també és possible certificar una acurada inspecció de les mucoses i millorar la localització de pòlips. Considerant els usos potencials de la descripció dels vasos sanguinis, aquesta contribució estudia la caracterització del contingut vascular i l'anàlisi de la capacitat descriptiva dels seus patrons de ramificació.
La caracterització dels vasos sanguinis en imatges de colonoscòpia suposa reptes importants. L'escena endoluminal inclou diferents objectes amb característiques similars, fet que dificulta el desenvolupament de models diferents per a cadascun d'aquests objectes. Per afrontar aquestes dificultats, proposem l'ús dels patrons de ramificació dels vasos sanguinis com a trets a baix nivell per a la descripció de formes. Hem creat dues bases de dades d'imatges que inclouen la segmentació manual dels arbres vasculars, així com la localització manual de dos tipus de punts d'interès: encreuaments i punts finals. Presentem un model per a la caracterització dels punts d'encreuament en patrons binaris. La implementació del model ens permet desenvolupar un mètode de localització de punts d'encreuament. El mètode supera els algorismes existents a la literatura en experiments en dues bases de dades: una de creació pròpia i la base de dades DRIVE, d'imatges de fons d'ull. En el segon cas, hem creat una extensió amb la localització manual dels punts d'encreuament. Pel fet que volem explorar la capacitat descriptiva de patrons vasculars i punts d'encreuament, proposem una aproximació basada en grafs per crear marcadors anatòmics. En el context de la localització de pòlips, establim un nou mètode per inhibir la influència dels vasos sanguinis en l’extracció d'informació de baix nivell. Els resultats mostren que la nostra metodologia disminueix la influència dels vasos sanguinis, augmenta la informació als pòlips i millora els mètodes de localització de pòlips.Colorectal cancer is the third most common cancer worldwide and the second most common malignant tumor in Europe. Screening tests have shown to be very effective in reducing the amount of deaths since they allow an early detection of polyps. Among the different screening techniques, colonoscopy is considered the gold standard although clinical studies mention several problems that have an impact in the quality of the procedure. The navigation through the rectum and colon track can be challenging for the physicians which can increase polyp miss rates. The thorough visualization of the colon track must be ensured so that the chances of missing lesions are minimized. The visual analysis of colonoscopy images can provide important information to the physicians and support their navigation during the procedure. Blood vessels and their branching patterns can provide descriptive power to potentially develop biometric markers. Anatomical markers based on blood vessel patterns could be used to identify a particular scene in colonoscopy videos and to support endoscope navigation by generating a sequence of ordered scenes through the different colon sections. By verifying the presence of vascular content in the endoluminal scene it is also possible to certify a proper inspection of the colon mucosa and to improve polyp localization. Considering the potential uses of blood vessel description, this contribution studies the characterization of the vascular content and the analysis of the descriptive power of its branching patterns. Blood vessel characterization in colonoscopy images is shown to be a challenging task. The endoluminal scene is conformed by several objects whose similar characteristics hinders the development of particular models for each of them. To overcome such difficulties we propose the use of the blood vessel branching characteristics as low-level features for pattern description. We created two data sets including manually labeled vessel information as well as manual ground truths of two types of keypoint landmarks: junctions and endpoints. We present a model to characterize junctions in binary patterns. The implementation of the junction model allows us to develop a junction localization method. The proposed method outperforms the available algorithms in the literature in experiments in both, our newly created colon vessel data set, and in DRIVE retinal fundus image data set. In the latter case, we created manual ground truth of junction coordinates. Since we want to explore the descriptive potential of junctions and vessels, we propose a graph-based approach to create anatomical markers. In the context of polyp localization, we present a new method to inhibit the influence of blood vessels in the extraction of low-level profile information. The results show that our methodology decreases vessel influence, increases polyp information and leads to an improvement in state-of-the-art polyp localization performance.
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Sunman, Wayne. "The role adenosine in vascular steal in peripheral vascular disease." Thesis, University of Liverpool, 1997. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264365.
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Rudström, Håkan. "Iatrogenic Vascular Injuries." Doctoral thesis, Uppsala universitet, Kärlkirurgi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-194346.
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Iatrogenic vascular injuries (IVIs) and injuries associated with vascular surgery can cause severe morbidity and death. The aims of this thesis were to study those injuries in the Swedish vascular registry (Swedvasc), the Swedish medical injury insurance where insurance claims are registered, the Population and Cause of death registries, and in patient records, in order to explore preventive strategies. Among 87 IVIs during varicose vein surgery 43 were venous, mostly causing bleeding in the groin. Among 44 arterial injuries, only 1/3 were detected intraoperatively. Accidental arterial stripping predominated, with poor outcome. Four patients died, all after venous injuries. IVIs increased over time, and constitute more than half of the vascular injuries registered in the Swedvasc. Lethal outcome was more common (4.9%) among patients suffering IVIs than among non-iatrogenic vascular injuries (2.5%). Risk factors for death were age, diabetes, renal insufficiency and obstructive lung-disease. Fifty-two patients died within 30 days after IVI. The most common lethal IVIs were puncture during endovascular procedures (n=24, 46%), penetrating trauma during open surgery (11) and occlusion after compression (6). Symptoms were peripheral ischemia (n=19), external bleeding (14), and hypovolemic chock without external bleeding (10). Most died within two weeks (n=36, 69%). After >2 weeks the IVI as a cause of death was uncertain. Among 193 insurance claims after vascular surgery during 2002-2007, nerve injuries (91) and wound infections (22) dominated. Most patients suffered permanent injuries, three died. Patients with insurance claims were correctly registered in the Swedvasc in 82%. In 32 cases of popliteal artery injury during knee arthroplasty symptoms were bleeding (n=14), ischaemia (n=7) and false aneurysm formation (n=11). Only twelve injuries (38%) were detected intraoperatively. Patency at 30 days was 97%, but only seven (22%) patients had complete recovery. Six of those had intraoperative diagnosis of popliteal injury and immediate vascular repair. In conclusion, registration of IVIs is increasing and outcome is often negatively affected by diagnostic and therapeutic delay. Not all fatalities after IVIs are attributable to the injury itself. The most common causes of insurance claims after vascular surgery were nerve injuries, and 82% were correctly registered in Swedvasc.
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Salanga, Matthew Charles. "EMBRYONIC VASCULAR DEVELOPMENT." Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/203435.
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The formation of the embryonic vasculature is essential for life. The components driving this process are well conserved across vertebrate species. At the core of vascular development is the specification of endothelial precursor cells from nascent mesoderm. Transcription factors of the ETS family are important regulators of endothelial specification. In this document we characterize the role of the ETS transcription factors, ETV2, during embryonic vascular development.Expression analysis shows that Etv2 is highly expressed in hematopoietic and endothelial precursor cells in the Xenopus embryo. In gain-of-function experiments, ETV2 is sufficient to activate ectopic expression of vascular endothelial markers. In addition, ETV2 activated expression of hematopoietic genes representing the myeloid but not the erythroid lineage. Loss-of-function studies indicate that ETV2 is required for expression of all endothelial markers examined. However, knockdown of ETV2 has no detectable effects on expression of either myeloid or erythroid markers. This contrasts with studies in mouse and zebrafish where ETV2 is required for development of the myeloid lineage. Our studies confirm an essential role for ETV2 in endothelial development, but also reveal important differences in hematopoietic development between organisms.Although ETV2 is a pivotal molecule in development it remains unidentified in the chicken genome. We hypothesize that chicken Etv2 is expressed in the early Gallus embryo, and is necessary for endothelial specification consistent with its role in other species. To test this hypothesis we attempted to amplify Etv2 transcripts from Gallus embryos using degenerate PCR. Disappointingly this strategy did not reveal a putative Etv2 candidate. However, some important findings were uncovered, including the cloning of a previously uncharacterized Gallus ETS protein, SPDEF. Additionally the identification of an annotation error mis-identifying Ets gene "Erf" as "Etv3" (also an Ets gene) provided details on gene arrangement previously unknown. The workflow described could be used in future studies for the identification of other members of gene families that exhibit gaps, keeping in mind the goal of the study and the limitations of each technology.
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Lugano, Roberta. "Low density lipoproteins, vascular smooth muscle cell function and vascular remodeling." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/283471.
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High levels of circulating low-density lipoproteins (LDL) are one of the major cardiovascular risk factors. Hypercholesterolemia induces endothelial dysfunction and chronic intimal inflammatory cell accumulation, hallmarks of the initiation of atherosclerosis. Additionally, growing human atherosclerotic plaques show proliferation and migration of vascular smooth muscle cells (VSMC) towards the intima producing remodeling of the vascular wall. However, those plaques that are most prone to rupture show a progressive loss of VSMC becoming soft and vulnerable and these lipid-rich high risk plaques cause clinical episodes resulting in morbid or fatal ischemic events. The mechanisms involved in the transformation of a plaque into a vulnerable VSMC-depleted atheroma have not been completely elucidated. Lipid-rich-VSMC have an impaired vascular repair function due to changes in cytoskeleton proteins. However, the effects of LDL on VSMC function during plaque remodeling and vascular repair are not fully understood. Thus, the aim of this thesis was to investigate early changes directly induced by LDL on VSMC phenotype and function and to identify the molecular mechanisms involved.
This thesis demonstrates that the cardiovascular risk of hypercholesterolemia involves the interaction of LDL with VSMC and the regulation at a molecular level of different pathways that converge in the cell’s migratory capacity. Migratory function of lipid-loaded VSMC can be restored by inhibition of 3-hydroxy-methylglutaryl coenzyme A (HMG-CoA) through a Rho kinase and myosin light chain phosphatase dependent mechanism. In addition, the studies performed in this thesis show that LDL affect VSMC adhesion, migration and cytoskeleton dynamics through the abrogation of the urokinase-plasminogen activator (uPA)/uPA receptor (uPAR) system function and by modulation of HSP27 phosphorylation and subcellular localization.El nivel elevado de lipoproteínas de baja densidad (LDL), uno de los principales factores de riesgo cardiovascular, conllevan a una disfunción endotelial y acumulación crónica de células inflamatorias en la íntima arterial en la etapa inicial de desarrollo de la arterosclerosis. Además, la progresión de las placas arterioscleróticas se caracteriza por un proceso de remodelado vascular consecuencia de la proliferación y migración de células musculares lisas vasculares (CML) en la íntima. Sin embargo, las placas ateroscleróticas con mayor susceptibilidad a la ruptura presentan una pérdida progresiva de CML, siendo estas placas ricas en lípidos y altamente vulnerables las que provocan eventos isquémicos mórbidos o fatales. Hoy día desconocemos todavía los mecanismos involucrados en la transformación de las placas en ateromas vulnerables. Las CML ricas en lípidos presentan alteraciones en su capacidad de reparación vascular debido a alteraciones en proteínas del citoesqueleto. Sin embargo, los efectos de las LDL en la función de las CML durante el remodelado de las placas y reparación vascular se desconocen en gran medida. Por ello, el objetivo de esta tesis ha sido investigar los cambios iniciales inducidos directamente por las LDL en el fenotipo y la función de las CML e identificar los mecanismos moleculares involucrados. Esta tesis demuestra que el riesgo cardiovascular de la hipercolesterolemia implica la interacción entre LDL y CML y la regulación a nivel molecular de diferentes vías de señalización que convergen en la migración celular. La capacidad de migración de CML cargadas de lípidos puede restituirse mediante la inhibición de la 3-hidroxi-3-metilglutaril coenzima-A (HMG-CoA), a través de un mecanismo dependiente de la quinasa Rho. Además, los estudios realizados en esta tesis demuestran que las LDL afectan la adhesión, migración y dinámica de formación del citoesqueleto de las CML a través de la alteración de la función del sistema del activador del plasminogeno tipo uroquinasa (uPA)/uPA receptor (uPAR) y mediante la modulación de la fosforilación y localización subcelular de la HSP27.
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Kara, Kerim. "A 3-d Vascular Connectivity Tracking And Vascular Network Extraction Toolkit." Master's thesis, METU, 2011. http://etd.lib.metu.edu.tr/upload/12613201/index.pdf.
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Angiography is an invasive procedure since contrast medium is injected into circulatory system of patients and the mostly preferred technique is X-ray angiography. For diagnosis, treatment planning, and risk assessment purposes, interventional radiologists utilize visual inspection to determine connectivity relations between vessels. This situation leads angiography to be more invasive, since it requires additional injection of contrast medium and X-ray dose.
This thesis work presents a 3-D vascular connectivity tracking toolkit for automated extraction of vascular networks in 3-D medical images. The proposed method automatically extracts the vascular network connected to a user-defined point in a user-defined direction, and requires no further user interaction. The toolkit prevents additional injection of contrast agent and X-ray dose, saves time for the interventional radiologist.
While the algorithm is applicable on all 3-D angiography images, performance of the method is observed on 3-D catheter angiography image of cerebrovascular structures. The algorithm iteratively tracks gravity centers of vascular branches in the user-defined direction, preserving connection to the user-defined point.
Curvy branches are tracked even if they have discontinuous portions. Since this tracking method does not depend on lumen diameter and intensity differences, branches with stenoses and branches having large intensity difference can be successfully tracked. Skeletonization and junction detection methods are described, which are used to detect the sub branches, indirectly connected to the point. These methods are capable of handling bifurcations, trifurcations, and junctions having more branches. However, false junctions occurring due to superposition of vessels are not eliminated.
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Allcock, Graham Harvey. "Functional characterisation of endothelin receptors in vascular and non-vascular tissues." Thesis, Queen Mary, University of London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244194.
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Wardell, Claire Frances. "Mechanisms of transmitter release in vascular and non-vascular smooth muscle." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303665.
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Lugano, Roberta 1983. "Low density lipoproteins, vascular smooth muscle cell function and vascular remodeling." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/283471.
Full textAbstract:
High levels of circulating low-density lipoproteins (LDL) are one of the major cardiovascular risk factors. Hypercholesterolemia induces endothelial dysfunction and chronic intimal inflammatory cell accumulation, hallmarks of the initiation of atherosclerosis. Additionally, growing human atherosclerotic plaques show proliferation and migration of vascular smooth muscle cells (VSMC) towards the intima producing remodeling of the vascular wall. However, those plaques that are most prone to rupture show a progressive loss of VSMC becoming soft and vulnerable and these lipid-rich high risk plaques cause clinical episodes resulting in morbid or fatal ischemic events. The mechanisms involved in the transformation of a plaque into a vulnerable VSMC-depleted atheroma have not been completely elucidated. Lipid-rich-VSMC have an impaired vascular repair function due to changes in cytoskeleton proteins. However, the effects of LDL on VSMC function during plaque remodeling and vascular repair are not fully understood. Thus, the aim of this thesis was to investigate early changes directly induced by LDL on VSMC phenotype and function and to identify the molecular mechanisms involved.
This thesis demonstrates that the cardiovascular risk of hypercholesterolemia involves the interaction of LDL with VSMC and the regulation at a molecular level of different pathways that converge in the cell’s migratory capacity. Migratory function of lipid-loaded VSMC can be restored by inhibition of 3-hydroxy-methylglutaryl coenzyme A (HMG-CoA) through a Rho kinase and myosin light chain phosphatase dependent mechanism. In addition, the studies performed in this thesis show that LDL affect VSMC adhesion, migration and cytoskeleton dynamics through the abrogation of the urokinase-plasminogen activator (uPA)/uPA receptor (uPAR) system function and by modulation of HSP27 phosphorylation and subcellular localization.El nivel elevado de lipoproteínas de baja densidad (LDL), uno de los principales factores de riesgo cardiovascular, conllevan a una disfunción endotelial y acumulación crónica de células inflamatorias en la íntima arterial en la etapa inicial de desarrollo de la arterosclerosis. Además, la progresión de las placas arterioscleróticas se caracteriza por un proceso de remodelado vascular consecuencia de la proliferación y migración de células musculares lisas vasculares (CML) en la íntima. Sin embargo, las placas ateroscleróticas con mayor susceptibilidad a la ruptura presentan una pérdida progresiva de CML, siendo estas placas ricas en lípidos y altamente vulnerables las que provocan eventos isquémicos mórbidos o fatales. Hoy día desconocemos todavía los mecanismos involucrados en la transformación de las placas en ateromas vulnerables. Las CML ricas en lípidos presentan alteraciones en su capacidad de reparación vascular debido a alteraciones en proteínas del citoesqueleto. Sin embargo, los efectos de las LDL en la función de las CML durante el remodelado de las placas y reparación vascular se desconocen en gran medida. Por ello, el objetivo de esta tesis ha sido investigar los cambios iniciales inducidos directamente por las LDL en el fenotipo y la función de las CML e identificar los mecanismos moleculares involucrados. Esta tesis demuestra que el riesgo cardiovascular de la hipercolesterolemia implica la interacción entre LDL y CML y la regulación a nivel molecular de diferentes vías de señalización que convergen en la migración celular. La capacidad de migración de CML cargadas de lípidos puede restituirse mediante la inhibición de la 3-hidroxi-3-metilglutaril coenzima-A (HMG-CoA), a través de un mecanismo dependiente de la quinasa Rho. Además, los estudios realizados en esta tesis demuestran que las LDL afectan la adhesión, migración y dinámica de formación del citoesqueleto de las CML a través de la alteración de la función del sistema del activador del plasminogeno tipo uroquinasa (uPA)/uPA receptor (uPAR) y mediante la modulación de la fosforilación y localización subcelular de la HSP27.
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Cunnington, Colin. "The role of plasma and vascular tetrahydrobiopterin in vascular disease states." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:33df2f8a-f16b-4271-988a-4500ed89d35e.
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The endothelial nitric oxide synthase (eNOS) co-factor tetrahydrobiopterin (BH4) has been shown to play a pivotal role in maintaining endothelial function in experimental vascular disease models. In BH4-deficient states, eNOS becomes enzymatically ‘uncoupled’, generating reactive oxygen species instead of nitric oxide, thus promoting endothelial dysfunction. In humans with coronary artery disease (CAD), higher vascular BH4 levels have been shown to be associated with improved endothelial function, and genetic variation in endogenous BH4 synthesis has implicated a causal role. Accordingly, BH4 has been proposed as a potential therapeutic target in vascular disease states. The work in this thesis aims to further elucidate the roles of exogenous and endogenous BH4 in humans. In a randomised, placebo-controlled clinical trial of oral BH4 therapy in patients with CAD, exogenous BH4 had no effect on endothelial function or vascular oxidative stress. Subsequent pharmacokinetic and pharmacodynamic analysis revealed that oral BH4 significantly augmented BH4 levels in plasma and in venous tissue (but not in arterial tissue), but also increased levels of the oxidation product dihydrobiopterin (BH2), which lacks eNOS cofactor activity. Thus, there was a null effect on overall biopterin redox status. To further understand the mechanics of exogenous BH4 oxidation, ex vivo studies of human blood and vascular tissue demonstrated that exogenous BH4 is very rapidly oxidised to BH2; co-administration with an antioxidant had only a modest effect on preventing BH4 oxidation in blood, with no beneficial effect on biopterin redox state in the vasculature. Finally, using a “Mendelian randomisation” approach, I studied the effects of a haplotype of GCH1 (the gene encoding the rate limiting enzyme in BH4 synthesis) on endogenous BH4 bioavailability and vascular function in healthy individuals. In patients with CAD, this haplotype has been associated with decreased BH4 bioavailability and eNOS uncoupling, however in healthy individuals the haplotype exerted no significant effect, likely due to reduced inflammatory stimulation of GCH1.
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Mancini, Maria L. "Novel Roles for Endoglin in Vascular Development and Maintenance of Vascular Integrity." Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/pdf/ManciniML2007.pdf.
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Shen, L. "Vascular function in abdominal adipose tissue : vascular tone, angiogenic and secretory capacity." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1457386/.
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Background Adipose tissue (AT) growth is critically dependant on the functional vascular support. Optimal angiogenesis and functional vascular tone ensure the sufficient supply of oxygen, insulin, and nutrients, thus preventing AT hypoxia and insulin resistance. Meanwhile, vascular function is regulated by vasoactive molecules released from AT. Abdominal AT expansion including subcutaneous and omental depots (SAT and OAT respectively) contributes to increased risks of cardiovascular vascular disease. This thesis investigated: 1. The depot- and diabetes-specific difference in noradrenaline synthesis and noradrenaline-mediated vasoconstriction and tissue fibrosis; 2. The depot- and diabetes-specific differences of angiogenesis and angiogenesis-related mRNA and protein expression; 3. The adipokine secretion from perivascular adipose tissue (PVAT) and vessels. Methods Abdominal SAT and OAT from morbid obese patients were used for 1) cell and tissue culture; 2) histochemistry and immunohistochemistry; 3) myography; 4) real-time PCR and western blot; 5) ELISAs. Results Study 1: In non-diabetic group, SAT showed significantly higher sensitivity to noradrenaline (NA)-induced vasoconstriction compared to OAT and diabetic group, which was concomitant with lower local NE synthesis and collagen deposition. Study 2: SAT of non-diabetic subjects had lower capillary density, angiogenic capacity, and downregulation of angiogenesis-related genes compared with OAT and diabetics. Study 3: In PVAT study, for the first time, we discovered adiponectin expression from human endothelial cells (ECs). Conclusion Study 1: SAT in non-diabetic obese patients was protected by its preserved NA sensitivity, functional vasoreactivity and low levels of tissue fibrosis, while elevated, local, chronic NA levels may desensitise the vessels of OAT and diabetics, and lead to elevated collagen deposition. Study 2: High levels of angiogenesis in OAT and diabetes did not reverse local hypoxia, which may be due to its compromised vascular function. Study 3: Moreover, endothelium-derived adiponectin may be important protecting endothelial function in cardiovascular events.
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Donaldson, Graeme. "Molecular and cellular factors affecting vascular patterning during retinal vascular plexus development." Thesis, Ulster University, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.674916.
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The murine retinal vasculature consists of three co-planar plexi, which develop in the first three weeks of postnatal life (PO-P20). The first to form is the superficial plexus: blood vessels migrate radially outwards from the optic nerve head (ONH) region and along the surface of the retina, guided by a template of astrocytes. This plexus reaches the retinal periphery at around P7, at which time, vertical vascular sprouts begin to project into the deep layers of the retina. Two further plexi then ramify around the inner and outer surfaces of the inner nuclear layer (INL), the deeper of which is the first to form (P7-PI2), whereas the intermediate plexus forms last (PI4-P20). During development, an immature, high calibre capillary-only plexus undergoes differentiation and remodelling to become a mature, low calibre, adult plexus with identifiable arteries and veins. In the first experimental chapter of this project, immunohistochemical (IHC) techniques were used to discover that arteriovenous differentiation is linked to a tightly-patterned process of capillary pruning by caspase-dependent endothelial cell apoptosis. IHC using EFs showed that specific spatio-temporal patterning of hypoxia occurs within the neuroblast layer during deep and intermediate plexus development. Muller glial cell (MGC) and R-Cadherin imaging showed that vertical sprouting of the plexus occurs under the guidance of MGC processes and that the spatio-temporal expression of R-Cadherin defines the locations of the plexi. The second experimental chapter showed that transgenic overexpression of vascular endothelial growth factor 188 (VEGF 188) in the eye ameliorates the vaso-obliteration and pathological neovascularisation associated with oxygen-induced retinopathy (OIR). In the third experimental chapter a novel transgenic mouse strain was created, which over-expresses the VEGFI6Sb isoform in the eye using the same promoter as the aforementioned transgenic mouse. Despite positive identification as transgenics, no ocular perturbations were found in this novel strain.
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Stuart, Persoons Maria Cornelia Johanna. "Cytomegalovirus and vascular pathology." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 1998. http://arno.unimaas.nl/show.cgi?fid=8496.
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Tran, Phan Kiet. "Perlecan in vascular disease /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-195-4/.
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Ighoroje, Ahbor Dolly Awani. "pH and vascular tone." Thesis, University of Glasgow, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293493.
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Vance, C. A. "Laser assisted vascular anastomosis." Thesis, University of Strathclyde, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382424.
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Martin, Steven Carl. "Homocysteine and vascular disease." Thesis, University of Glasgow, 2003. http://theses.gla.ac.uk/30939/.
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Cardiovascular disease is multifactorial. The main risk factors for developing cardiovascular disease (age, sex, smoking, diabetes, hyperlipidaemia and hypertension) do not explain its development in everyone. New risk factors are continually being sought in order to better understand and treat the disease process. In recent years homocysteine has been proposed as a risk factor for the development of premature cardiovascular disease as a consequence of the accelerated arterial and venous thrombotic disease seen in homocystinuria as a result of a single gene defect. This theory has been difficult to test because patients with premature cardiovascular disease are thankfully rare and because of the difficulties in measuring homocysteine itself. We propose that, if homocysteine is a causative risk factor for atherothrombosis, it will be involved in the development of cardiovascular disease regardless of age and have therefore studied affected patients from routine hospital clinics. Homocysteine analysis has become easier over the past decade with the development of HPLC methods utilising fluorescent detection, but these methods involve toxic chemicals and suffer from high background fluoresence. I have developed an HPLC method more suited to a routine hospital laboratory utilising coulometric detection for measuring plasma total homocysteine and used it to investigate the relationship between homocysteine levels and both micro- and macro-vascular atherothrombotic disease.
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Robertson, Stephanie. "Vascular responses to adipokines." Thesis, Glasgow Caledonian University, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518238.
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Postolaki, Yuliana. "Hiperhomocisteínemia e doença vascular." Master's thesis, [s.n.], 2015. http://hdl.handle.net/10284/5172.
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Projeto de Pós-Graduação/Dissertação apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Ciências FarmacêuticasO objetivo foi estudar a ligação entre a homocisteína (Hcy) e a doença vascular, assim como os possíveis danos na saúde que podem ser causados devido ao seu aumento. O metabolismo da Hcy acontece através de duas vias: a via de transulfuração e a via de remetilação, sendo a coenzima tetra-hidrofolato (THF) e a S-adenosilmetionina (SAM) compostos importantes deste metabolismo. O piridoxal fosfato, um derivado de vitamina B6, é necessário para a atividade da cistationina β – sintase, e o tetra-hidrofolato e a vitamina B12 auxiliam a metilação da homocisteina a metionina. A determinação da concentração da Hcy parece ser de vital importância porque o aumento desta pode provocar danos vasculares nos seres humanos difíceis de recuperar. Além disso, e como consequência destes danos, o aumento da Hcy pode danificar um variado conjunto de órgãos tais como, o coração (artérias), fígado, cérebro (nervos) e também as articulações, causando assim uma ampla variedade de doenças (doenças arteriais coronárias, AVC, doenças vasculares periféricas, doenças cerebrovasculares etc). Assim, a hiperhomocisteínemia (HHcy) derivada logicamente do aumento da Hcy, não deve ser descurada. O controlo HHcy passa por uma alimentação equilibrada e um aporte correto de nutrientes e vitaminas. This thesis was elaborated for the conclusion of Master Degree in Pharmaceutical Sciences. The subject was chosen taken into account the connection between hyperhomocysteinemia (HHcy) and vascular diseases. Thus described the importance of the homocysteine (Hcy) in the everyday life, its determination and possible damage to health that can be caused due to its increase. It is described the metabolism of homocysteine (Hcy ) through its two pathways: the pathway of transsulfuration and the pathway remethylation . Also mentioned was the importance of coenzyme tetrahydrofolate (THF) and S-Adenosyl methionine (SAM) in the metabolism of Hcy. The pyridoxal phosphate, a derivative of vitamin B6 is required for the activity of cystathionine β - synthase, and tetrahydrofolate and vitamin B12 assist the methylation of homocysteine to methionine. The evaluation of Hcy it has vital importance because its increase may cause vascular damage of difficult recover. The increase of Hcy may damage several vital organs, such as the heart (arteries), liver, brain (nerves) and also articulations, causing a wide variety of diseases (coronary artery disease, stroke, peripheral vascular disease, etc). The HHcy can’t be neglected since it may have harmful health consequences. However it can be controlled by a balanced diet and a proper supply of nutrients and vitamins by which may be evidenced in the researched studies for the completion of this article.
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Merriman, Carolyn. "Peripheral Vascular System (PVS)." Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/etsu-works/8533.
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Pedro, Liliana Domingues. "Silício e saúde vascular." Master's thesis, Universidade de Aveiro, 2013. http://hdl.handle.net/10773/11817.
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Mestrado em Biotecnologia - Biotecnologia MolecularThe involvement of Si in cardiovascular diseases has been suggested by several authors. However, only a small number of studies have investigated the Si content of human aortic tissue. The aim of this study was to investigate age- and gender-related changes in silicon levels of the human aorta. Moreover, associations were sought between silicon and structural components, e.g. elastin of the aortic wall, as to enlighten possible associations between silicon and aortic health. Forty thoracic aortas, obtained post-mortem from female and male subjects between 45 and 83 years old, were analysed for Si content and other elements (Al, B, Cu, Fe, Mn, Zn, Ca, K, Mg, Na and P) by ICP-OES. Elastin was quantified using a colorimetric dye-binding method Fastin™ Elastin assay. Silicon levels in the aorta samples did not vary significantly with age or gender. Relevant correlations with the Si concentration in the aorta were observed for (1) Cu in the female samples with a significant positive correlation, and (2) a negative correlation with P levels, although this was not significant. Analysis of the elastin concentration in the aorta samples revealed no gender- or age-related changes, although a trend for a decrease in older subjects (< 66 years) was observed. Elastin levels did not correlate with the Si concentrations in the aorta samples, but a negative correlation was observed with Cu in samples from female donors and with K (male and female). Additionally, Si levels in the aorta were also similar to levels analysed in skin biopsy samples (male and female: n = 47, age range = 19 – 72), where a trend for increasing Si levels with ageing was observed in female subjects. Results from the present study could be used to support the suggestion that silicon affects factors that are involved in progression of aortic stiffness, including the utilization of copper, essential in preventing oxidative damage to adult elastin fibres, and decreasing the adsorption of phosphorus to the matrix proteins and thereby prevent the calcification of the aortic wall.
O envolvimento do silício em doenças cardiovasculares, particularmente aterosclerose, foi sugerido por vários autores. No entanto, apenas um número reduzido de estudos investigaram a concentração de Si em aortas humanas. Este estudo teve como objectivo investigar alterações no conteúdo de Si e elastina com a idade e sexo em amostras de aortas humanas. Foram também investigadas correlações entre as concentrações de silício e elastina. Silício e outros elementos (Al, B, Cu, Fe, Mn, Zn, Ca, K, Mg, Na e P) foram quantificados, através de ICP-OES, em 40 aortas torácicas, obtidas post-mortem de indivíduos de sexo masculino e feminino com idades compreendidas entre os 54 e 83 anos. O conteúdo de elastina destas amostras foi determinado através do método colorimétrico Fastin™ Elastin assay. Não foram observadas correlações significativas entre a concentração de Si nas amostras de aorta com a idade ou sexo dos indivíduos. Correlações entre a concentração de Si e outros elementos foram também investigadas e, para além de uma correlação positiva e significativa, observada entre Si e Cu em amostras provenientes de indivíduos do sexo feminino, foi também identificada uma correlação negativa entre Si e P, embora não significantiva. A quantificação de elastina nas amostras de aorta não demonstrou alterações significantivas com a idade ou sexo dos pacientes, no entanto foi observado um decréscimo na concentração de elastina em individuos de idade avançada (< 66 anos). Correlações negativas relevantes foram observadas entre a elastina e K, e entre elastina e Cu em amostras de indivíduos do sexo feminino. Não foram identificadas correlações significativas entre a concentração de elastina e Si nas amostras de aorta analisadas. Adicionalmente, a concentração de Si na aorta humana foi semelhante à quantidade determinada em amostras de biópsias da pele humana (indivíduos do sexo feminino e masculino: n = 47, faixa etária = 19 – 72), onde foi observada uma tendência para o aumento da concentração de Si com o envelhecimento em indivíduos do sexo feminino. Os resultados deste estudo poderão ser usados para apoiar a hipótese de que o Si interage com factores que estão envolvidos no envelhecimento vascular e progressivo aumento da rigidez da aorta. Estes incluém a utilização de cobre, essencial na prevenção de danos oxidativos em fibras elásticas maduras (elastina), e também a diminuição da absorção de fósforo em proteínas da matriz extracelular, consequentemente, impedindo a calcificação da parede da aorta.
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Miller, Alex B. "Drug Refillable Vascular Grafts." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17417569.
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When dealing with cardiovascular disease, vascular devices are used to expand the vascular opening and maintain proper flow. However, current vascular grafts have a high rate of occlusion due to biological responses to the foreign body. By coating these devices with thrombomodulin (TM), an anti-clotting protein, the graft is protected from plaque accumulation. But since TM naturally degrades in the body over time, the risk of thrombosis is merely delayed. My project aims to mitigate the risk of long-term thrombosis for small diameter vascular grafts by providing a system to replenish the TM surface coating once it begins to degrade. In order to accomplish this, DNA was used as the homing mechanism and a process call DNA toehold exchange was utilized. By specially designing the sequence of primary and secondary strands of DNA, secondary strands bound to the drug or protein could displace one another from primary strands bound to the surface of the graft, resulting in the recoating of the surface with active drug. This process fully replaced the necessary amount of TM on the surface to prevent long-term thrombosis with over 100-fold excess. This high safety factor allows for more time between surface replacement procedures. This system can ultimately be applied to any system with a drug or protein coated surface, providing an effective means of sustained and controlled drug expression.Engineering Sciences
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Ne, Jia Yi Anna. "Obesity and Vascular Health." Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/16000.
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Background: Obesity is an established risk factor for cardiovascular disease. The mechanisms by which obesity confers increased cardiovascular risk have not been fully elucidated but may involve arterial endothelial dysfunction and atherosclerosis among others. Studies examining the association of obesity with markers of atherosclerotic vascular disease have had mixed findings. Accordingly, we undertook two comprehensive systematic reviews of the published literature on obesity and vascular health, specifically one on obesity, brachial flow-mediated dilatation (FMD) and fingertip plethysmography using the EndoPAT device and one on obesity and carotid intima-media thickness (IMT). For vascular measures with sufficient studies (flow-mediated dilatation and carotid intima-media thickness), meta-analysis was undertaken to determine whether these two measures of vascular health differ between obese and healthy weight adults, and the estimated magnitude of the association. Methods: Electronic searches for “Obesity and flow-mediated dilatation”, “Obesity and intima-media thickness” and “Obesity and fingertip plethysmography” were performed using Ovid Medline and Embase databases. Meta-analysis was undertaken for brachial flow-mediated dilatation and carotid intima-media thickness to obtain pooled estimates for the obese and healthy weight adults. Results: Of the 4990 articles (1700 for FMD, 3122 for IMT and 168 for EndoPAT) retrieved, we identified 19 studies that met the study inclusion criteria for flow-mediated dilatation, 19 studies for intima-media thickness and 2 studies for EndoPAT. Meta-analysis demonstrated that obesity was associated with lower flow-mediated dilatation (-1.92 % [95% CI -2.92, -0.92], = 0.0002), and greater carotid intima-media thickness (0.07 mm [95% CI 0.05, 0.08], < 0.00001). Conclusion: Obesity is associated with significant differences in both functional and structural measures of vascular health, suggesting a likely mechanistic pathway through which obesity affects risk of clinical cardiovascular disease.
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Smith, James Douglas. "Cyclic stretch-mediated release of vascular endothelial growth factor by vascular smooth muscle cells : a role in improved vascular graft patency." Master's thesis, University of Cape Town, 1999. http://hdl.handle.net/11427/26456.
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In the light of studies which show the upregulation of VEGF in contractile cells subjected to cyclic stretch and the profound effects which cyclic stretch has been shown to have on the release of other cytokines by SMC, this study investigates the role which cyclic stretch might play in VEGF expression by SMC in a compliant environment. Furthermore, following observations of receptor phosphorylation in response to cyclic stretch in vascular cells, the effect of cyclic strain on the KDR-mediated endothelial response to locally-released VEGF was also investigated. Low passage number bovine aortic SMC and EC were plated on collagen-coated elastomer plates and subjected to 10% repetitive strain at 1 Hz. The mRNA expression of VEGF in SMC and the phosphorylation of KDR on EC were determined by northern blotting and western blotting respectively. The biological activity on EC and levels of VEGF secreted into the medium by SMC under cyclic stretch were investigated using a migration assay and ELISA respectively. Cyclic stretch was found to cause a 3.3 (±1.5 p < 0.005) fold increase in VEGF mRNA levels over unstretched controls at 4 hours. This biomechanically-induced expression was found to drop slightly by 24 hours and to be approximately equivalent to expression induced by the cytokine bFGF over the same time course. These results correlated with an increase in VEGF levels in media from stretched SMC capable of inducing migration of EC by 1.6 fold although additional EC chemotactic factors appear to be released by stretch. Furthermore, although the levels of KDR remained constant under cyclic stretch, average KDR phosphorylation was found to increase weakly over time due to cyclic stretch. These results show that cyclic stretch affects the VEGF communication between SMC and EC at both the level of VEGF expression by SMC and at the level of VEGF recognition by the KDR receptor on EC. It is possible that through the nitric oxide (NO) pathway, VEGF release may alleviate abnormally high levels of cyclic strain. It is hoped that a better understanding of the role of VEGF communication between stretched SMC and EC will enable the design of a graft in which the level of compliance encourages SMC to maintain a functional endothelium. Following this it is hoped that the low levels of SMC and pericytes invading the graft, pacified by endothelial cell mediation, will not result in intimal hyperplasia but rather play a role in microvessel maintenance and more complete healing.
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Warsch, Jessica. "Subclinical Vascular Brain Damage, Vascular Risk Factors, and Depression in Successful Cognitive Aging." Scholarly Repository, 2010. http://scholarlyrepository.miami.edu/oa_dissertations/644.
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Currently, about one in every eight Americans is age 65 or older; by the year 2050, it will be one in five people. Given this graying of the population, research into successful aging is of increasing relevance. The question of how to precisely define successful aging, however, has not been completely answered. Likewise, the role of vascular risk factors, subclinical vascular brain damage, and other biopsychosocial characteristics in normal cognitive aging are not well understood. This Dissertation focused on the identification of some of the physiological, behavioral, and social risk factors that distinguish people able to maintain extraordinary health at an advanced age. Specifically, we aimed to create an ecologically valid definition of successful aging that incorporates both physical well-being and cognitive abilities, and to report the prevalence of successful cognitive aging in a population-based multi-ethnic cohort of older adults. We sought to describe how the prevalence varies by several sociodemographic and psychosocial determinants, and to investigate global vascular risk, depressive symptomatology, and MRI markers of subclinical vascular brain damage as correlates of successful cognitive aging. We observed the prevalence of successful cognitive aging to be 37% in the study sample (N=1,162) of a diverse racial/ethnic population in Northern Manhattan (NYC, NY). The prevalence decreased with increasing age; we did not observe any differences by racial/ethnic group, but did note a lower prevalence with lower socioeconomic status. Several social resources and self-reported quality of life were related to successful cognitive aging, and appeared more important than demographic variables alone. We found that the likelihood of successful cognitive aging decreases with increasing global vascular risk score, more severe depressive symptomatology, and greater white matter damage. The field of successful aging requires further study. Consideration of such biopsychosocial factors as socioeconomic status, social support, quality of life, and depressive symptoms alongside novel indicators of disease and disability including global vascular risk and white matter hyperintensity burden is essential. It may lead to a more robust definition of successful cognitive aging replete with opportunities to modify the aging process, as many of the factors investigated in this study are modifiable.
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Prosdocimo, Domenick A. "Extracellular Pyrophosphate Homeostasis and Regulation of Vascular Calcification in Vascular Smooth Muscle Cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1266605413.
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Krishnamoorthy, Suresh. "Arterial stiffness, macro-vascular, micro-vascular endothelial function and cardiac remodelling in arterial fibrillation." Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/5957/.
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In patients with atrial fibrillation (AF) there appears a close link between arterial stiffness, endothelial function and cardiac remodelling thereby contributing to the development and progression of AF as well as to its complications. However this complex interaction(s) is not well understood. In the cross-sectional study with PAF patients, higher arterial stiffness (PP, Pr) is strongly associated with endothelial-dependent macro-vascular dysfunction (Δ%AIx Salbutamol). Similarly a strong relationship observed between arterial stiffness (PP, PWV cf, Pr) and abnormal LA remodelling (LAV and LAD) in PAF patients. Higher levels of vWf and soluble E-Selectin at baseline are independently associated with increased risk of adverse clinical events (including AMI and ischaemic stroke) in ‘real world’ AF patients, and may aid clinical risk stratification towards identifying patients at higher risk. In the longitudinal study of dual chamber pacemaker patients there was a close relationship observed between arterial stiffness (PP, PWV cf, Pr), macro-vascular (Δ%AIx Sal) / micro-vascular (∆%LDF Ach) endothelial function and cardiac remodelling (EF, E/A ratio, E_M, A_M). These findings support the close interaction between ventricular contraction, arterial system and endothelial function towards the development of AF in pacemaker patients, beyond the adverse effects of pacing per se.
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Allcorn, Richard John. "An investigation of some aspects of sympathetic neurotransmission in non-vascular and vascular tissue." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382564.
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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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Harmer, Jason Anthony. "Non-Invasive assessment of subclinical vascular disease in at risk populations using vascular ultrasound." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/13965.
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Early arterial changes preceding the late stages of atherosclerosis often appear decades before the onset of clinically evident cardiovascular disease (CVD). Flow-mediated dilatation (FMD), a non-invasive method used to assess arterial endothelial vasodilator function, is impaired in the presence of early arterial endothelial damage. Carotid intima-media thickness (IMT), a non-invasive method used to assess arterial wall thickness – a surrogate measure of subclinical vascular disease – occurs later in the sequence of atherosclerosis disease progression. These methods were used to assess CVD risk and associations with traditional CVD risk factors. Specifically, the aims of this thesis were: i) to study agreement in carotid IMT measurements, comparing a clinic-based mainframe and a portable, laptop-based ultrasound machine; ii) to investigate the effects of ‘westernisation’ on traditional CVD risk factors and carotid IMT, comparing rural Indians (in India) to migrant Australian-Indians, using a portable ultrasound machine; iii) to investigate the determinants of carotid IMT in children aged 8-years, using a portable ultrasound machine; iv) to explore the effects of fenofibrate on carotid IMT in adults with T2DM; v) to study the determinants of arterial function in adults with T2DM; and vi) to investigate the effects of fenofibrate on arterial endothelial function in adults with T2DM.
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Deshpande, Chinmay Vishwas. "Thermal analysis of vascular reactivity." [College Station, Tex. : Texas A&M University, 2007. http://hdl.handle.net/1969.1/ETD-TAMU-1342.
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Byon, Chang Hyun. "Oxidative stress-stimulated vascular calcification." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2010r/byon.pdf.
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Jett, Kimberly Ann. "Vascular function in Neurofibromatosis 1." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/52244.
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Neurofibromatosis 1 (NF1) is an autosomal dominant disorder with an estimated prevalence of 1/3000. NF1 is characterized by multiple café-au-lait spots, iris hamartomas, and multiple nerve sheath tumors. Patients may also present with heart disease, cerebrovascular disease, ischemia, or aneurysm. Though well documented, vascular disease in NF1 patients remains poorly understood.
Previous in vitro studies suggest that endothelial and vascular smooth muscle function is altered in Nf1+/- mice; however, it is unknown how these alterations affect vascular function in vivo. Haploinsufficiency for neurofibromin, the protein affected in patients with NF1, results in prolonged Ras hyperactivation. We hypothesized that this may result in vascular endothelial dysfunction and impaired cardiac function.
To study this hypothesis we examined vascular function in Nf1+/- and control mice using wire myography. Isometric force measurements in thoracic and abdominal aorta at 6-months of age were similar, with Nf1+/- mice demonstrating altered smooth muscle function, enhanced relaxation, and upregulation of the PI3K/Akt/eNOS pathway. To determine if the alterations observed at 6 months of age remain stable or progress to a more dysfunctional state, we examined the abdominal aorta in older mice. Interestingly, we observed increased contraction and reduced relaxation in 9-to-12 month old Nf1+/-mice compared to control littermates, indicative of endothelial dysfunction and progression to a more dysfunctional state.
Vascular dysfunction is likely to impact cardiac performance, and Ras hyperactivation has also been linked to cardiac dysfunction. We, therefore, used 2-dimensional echocardiography with color Doppler to measure cardiac function in Nf1+/- and control littermates. We found that Nf1+/- mice have increased left ventricular wall thickness and reduced cardiac contractility. We also observed alterations in cardiomyocyte organization in Nf1+/- animals.
The results presented in this thesis support the hypothesis that neurofibromin haploinsufficiency in Nf1+/- mice results in vascular endothelial and cardiac dysfunction. Whether these findings extend to humans with NF1, who have the same genetic defect, is unknown, but if so, our observations may have important clinical implications. The role of neurofibromin in other kinds of vascular disease needs to be studied, and the possibility that neurofibromin may provide a novel therapeutic target should be explored.Medicine, Faculty of
Medical Genetics, Department of
Graduate
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Collidge, Tara. "Vascular remodelling in malignant hypertension." Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/27817.
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Recently a highly controllable and reproducible animal model of MH was developed in the rat. The Inducible Hypertensive Rat (IHR) exploits conditional transgenic technology allowing renin expression to be switched on, and hypertension to develop, following exposure to a dietary inducing agent. The resulting phenotype resembles human MH, where inappropriate activation of the renin angiotensin system is also seen. This study used the IHR to characterise the development of MH with specific reference to the renal vasculature. Histological injury and hypertension were pre-dated by adventitial fibroblast proliferation and inflammatory cell infiltration. In order to determine the role of inflammatory cells the immunosuppressant FK506 was administered pre-emptively, resulting in the total abolition of hypertension and end-organ injury. To allow further investigation of inflammation, the MH phenotype was developed in mice using subcutaneous angiotensin II infusion. When MH was superimposed on a transgenic line susceptible to conditional macrophage depletion, vascular remodelling failed to occur in the mesenteric circulation where depletion was greatest. The effect of volume expansion on the IHR was assessed. Transgenic animals craved saline and the resulting fluid overload overcame cerebral autoregulation resulting in ischaemic stroke without alteration in systemic hypertension or pathology. The onset of stroke was tightly predictable and reproducible. Accordingly, the saline-loaded IHR represents a novel and inducible model of ischaemic stroke. In conclusion, this study has identified inflammation as an early and important event in the pathogenesis of MH in two rodent models. Additionally, cerebral autoregulation in the IHR could be overcome by fluid overload resulting in the dissociation of central and systemic pathology.
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Dhore, Cherida Rachel. "Molecular regulation of vascular calcification." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 2005. http://arno.unimaas.nl/show.cgi?fid=6374.
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Huijberts, Maria Simone Petra. "Vascular dysfunction in experimental diabetes." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1994. http://arno.unimaas.nl/show.cgi?fid=6811.
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Suylen, Robert Jan van. "Vascular remodeling in pulmonary hypertension." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 1999. http://arno.unimaas.nl/show.cgi?fid=6859.
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Payne, Martha Elizabeth Haines Pamela S. "Nutritional factors of vascular depression." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2006. http://dc.lib.unc.edu/u?/etd,312.
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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2006.Title from electronic title page (viewed Oct. 10, 2007). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Nutrition." Discipline: Nutrition; Department/School: Public Health.
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Breugem, Corstiaan Cornelis. "Progress toward understanding vascular malformations." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/87315.
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Talbot, Nicholas. "Pulmonary vascular responses to hypoxia." Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404270.
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Modlich, Ute. "Approaches to tumour vascular targeting." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393467.
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Souadkia, Nahed. "Hookworms and the vascular endothelium." Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/11412/.
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Background. Necator americanus is one of the major causes of human hookworm infection, affecting over 800 million people worldwide. Hookworm infections cause gastro-intestinal bleeding, anaemia and iron deficiency, and are associated with high rates of morbidity, especially in children. Although chemotherapy has proven effective, high rates of reinfection are reported in socioeconomically developing countries, possibly due to the short-term efficacy of anthelmintic drugs in addition to individual predisposition to these infections, raising interests in developing suitable alternatives to chemotherapy which are capable of providing complete, long-term protection against hookworms. Understanding of the molecular mechanisms used by Necator americanus larvae to penetrate the human skin and the vasculature would therefore aid the development of effective vaccines against this important pathogen. Methods. First, Necator americanus larval exsheathing fluid (EF) and excretory/secretory products (ES) were profiled using gel electrophoresis and enzyme assays. Protease inhibitors against the main protease classes were used to determine which proteases are present in larval products. Second, the interaction of larval EF and ES products with human skin and extracellular matrix (ECM) macromolecules including collagens I, III, IV and V, fibronectin and laminin was investigated using western blots and protein separation by gel electrophoresis. Third, the impact of Necator americanus larval EF and ES on the endothelial barrier was examined using human umbilical vein endothelial cells (HUVEC). Permeability, an essential endothelial barrier function, was assessed during treatment with larval products, using transendothelial electrical resistance (TEER), and post-treatment using albumin-tracer flux. Finally, at the cellular level, responses to treatment with larval products were assessed by investigating molecular changes at cell-cell vascular endothelial (VE)-cadherin junctions and actin filaments, and by determining levels of secreted inflammatory cytokines, IL-6 and IL-8, and vascular endothelial growth factor (VEGF) in the culture medium. Results. It would appear that a repertoire of larval proteases, including serine, cysteine, aspartyl and metalloprotinases, caused partial degradation of skin macromolecules, collagens I, III, IV and laminin while fibronectin was fully degraded. Proteolysis of skin- and ECM macromolecules was related to the characteristic presence of proteolytic enzymes in larval products. The presence of transglutaminase activity was confirmed in both EF and ES products. Larval proteases caused a dose related increase in endothelial permeability, characterised by a decrease in monolayer resistance (TEER) with increased permeation of albumin tracer, which was minimal in the presence of a cocktail of protease inhibitors. These barrier changes were associated with disruption of junctional VE-cadherin and F-actin, the formation of intercellular gaps and an increase in endothelial secretion of IL-6 and IL-8. Conclusions. Necator americanus larvae produce a repertoire of proteolytic enzymes which could play an important role in negotiating the skin and breaching the endothelium to gain access to the host’s blood circulation.
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Alefishat, Eman. "Nucleotide regulation of vascular system." Thesis, University of Nottingham, 2011. http://eprints.nottingham.ac.uk/12292/.
Full textAbstract:
Previously, acyl derivatives of CoA were shown to antagonise human native and recombinant P2Y1 purine receptors. The main aim of this thesis was to study the effect of these endogenous nucleotide derivatives at endogenous P2Y1 receptors in blood vessels. Using isometric tension recordings, CoA, acetyl-CoA and palmitoyl-CoA (PaCoA) appeared to show selectivity for P2Y1 receptors (over P2Y2 and adenosine receptors) in the rat isolated thoracic aorta, with PaCoA being the most potent of the CoA derivatives used. In porcine isolated mesenteric arteries (PMA) and porcine isolated coronary arteries (PCA), isometric tension recordings indicated that ADP mediated endothelium-dependent and endothelium-independent relaxations, respectively. Relaxations in PMA were blocked by the P2Y1 receptor antagonist MRS2500 and PaCoA, whilst these were ineffective against ADP relaxations in the PCA. A FlexStation was used to monitor calcium responses in native HEK293 cells expressing P2Y1 and P2Y2 receptors using ADP and UTP, respectively. Responses to UTP were not significantly altered in the presence of PaCoA. In contrast, ADP-evoked responses were significantly inhibited in the presence of either MRS2500 or PaCoA. These data raise the possibility of an endogenous selective antagonism of P2Y1 receptors via CoA compounds, irrespective of species or cellular environment. Nicotinamide adenine dinucleotide (NAD) is an intracellular nucleotide which has been identified as an agonist at P2Y1, P2Y11, P2X and adenosine receptors. NAD evoked endothelium-independent concentration-dependent contractions of the pre-contracted PMA, which were unaltered in the presence of PaCoA. In contrast, αβ-methylene ATP (a desensitizing P2X receptor agonist) significantly reduced these responses suggesting the involvement of P2X1-like receptors. In both RTA and PCA, NAD evoked endothelium-independent concentration-dependent relaxations of the pre-contracted vessels, which were attenuated by SCH58261, but not PaCoA, which suggests the involvement of smooth muscle A2A receptors. These results together emphasise the possibility of a tissue and receptor-specific role of NAD as an endogenous extracellular nucleotide in purinergic signalling.
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Reynolds, Sophie L. "Vascular dysfunction in rheumatoid arthritis." Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/54162/.
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These findings suggest that systemic and vascular wall levels of matrix metalloproteinase-9, related to inflammation at the joint site, may play a prominent role in the development of vascular dysfunction in this experimental model. This thesis goes someway to elucidating the potential mechanisms of vascular dysfunction in rheumatoid arthritis.
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Bills, Victoria Louise. "Vascular permeability in pre-eclampsia." Thesis, University of Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.508075.
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Wimalasundera, Ruwan Chinthaka. "Vascular regulation in pre-eclampsia." Thesis, Imperial College London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.540684.
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Dalton, Matthew W. "Experimental modelling of vascular haemodynamics." Thesis, Nottingham Trent University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273762.
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