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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.
Pełny tekst źródłaAdams, 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.
Pełny tekst źródłaNúñez, Do Rio Joan M. "Vascular pattern characterization in colonoscopy images". Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/325145.
Pełny tekst źródłaColorectal 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.
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.
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 źródłaSalanga, Matthew Charles. "EMBRYONIC VASCULAR DEVELOPMENT". Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/203435.
Pełny tekst źródłaLugano, Roberta. "Low density lipoproteins, vascular smooth muscle cell function and vascular remodeling". Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/283471.
Pełny tekst źródłaEl 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.
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.
Pełny tekst źródłaAllcock, 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.
Pełny tekst źródłaWardell, 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.
Pełny tekst źródłaLugano, 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.
Pełny tekst źródłaEl 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.
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.
Pełny tekst źródłaMancini, 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.
Pełny tekst źródłaShen, 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/.
Pełny tekst źródłaDonaldson, 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.
Pełny tekst źródłaStuart, 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.
Pełny tekst źródłaTran, Phan Kiet. "Perlecan in vascular disease /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-195-4/.
Pełny tekst źródłaIghoroje, Ahbor Dolly Awani. "pH and vascular tone". Thesis, University of Glasgow, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293493.
Pełny tekst źródłaVance, C. A. "Laser assisted vascular anastomosis". Thesis, University of Strathclyde, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382424.
Pełny tekst źródłaMartin, Steven Carl. "Homocysteine and vascular disease". Thesis, University of Glasgow, 2003. http://theses.gla.ac.uk/30939/.
Pełny tekst źródłaRobertson, Stephanie. "Vascular responses to adipokines". Thesis, Glasgow Caledonian University, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518238.
Pełny tekst źródłaPostolaki, Yuliana. "Hiperhomocisteínemia e doença vascular". Master's thesis, [s.n.], 2015. http://hdl.handle.net/10284/5172.
Pełny tekst źródłaO 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.
Merriman, Carolyn. "Peripheral Vascular System (PVS)". Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/etsu-works/8533.
Pełny tekst źródłaPedro, Liliana Domingues. "Silício e saúde vascular". Master's thesis, Universidade de Aveiro, 2013. http://hdl.handle.net/10773/11817.
Pełny tekst źródłaThe 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.
Miller, Alex B. "Drug Refillable Vascular Grafts". Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17417569.
Pełny tekst źródłaEngineering Sciences
Ne, Jia Yi Anna. "Obesity and Vascular Health". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/16000.
Pełny tekst źródłaSmith, 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.
Pełny tekst źródłaWarsch, Jessica. "Subclinical Vascular Brain Damage, Vascular Risk Factors, and Depression in Successful Cognitive Aging". Scholarly Repository, 2010. http://scholarlyrepository.miami.edu/oa_dissertations/644.
Pełny tekst źródłaProsdocimo, 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.
Pełny tekst źródłaKrishnamoorthy, 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/.
Pełny tekst źródłaAllcorn, 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.
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 źródłaHarmer, 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.
Pełny tekst źródłaDeshpande, Chinmay Vishwas. "Thermal analysis of vascular reactivity". [College Station, Tex. : Texas A&M University, 2007. http://hdl.handle.net/1969.1/ETD-TAMU-1342.
Pełny tekst źródłaByon, 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.
Pełny tekst źródłaJett, Kimberly Ann. "Vascular function in Neurofibromatosis 1". Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/52244.
Pełny tekst źródłaMedicine, Faculty of
Medical Genetics, Department of
Graduate
Collidge, Tara. "Vascular remodelling in malignant hypertension". Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/27817.
Pełny tekst źródłaDhore, 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.
Pełny tekst źródłaHuijberts, 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.
Pełny tekst źródłaSuylen, 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.
Pełny tekst źródłaPayne, 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.
Pełny tekst źródłaTitle 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.
Breugem, Corstiaan Cornelis. "Progress toward understanding vascular malformations". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/87315.
Pełny tekst źródłaTalbot, Nicholas. "Pulmonary vascular responses to hypoxia". Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404270.
Pełny tekst źródłaModlich, Ute. "Approaches to tumour vascular targeting". Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393467.
Pełny tekst źródłaSouadkia, Nahed. "Hookworms and the vascular endothelium". Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/11412/.
Pełny tekst źródłaAlefishat, Eman. "Nucleotide regulation of vascular system". Thesis, University of Nottingham, 2011. http://eprints.nottingham.ac.uk/12292/.
Pełny tekst źródłaReynolds, Sophie L. "Vascular dysfunction in rheumatoid arthritis". Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/54162/.
Pełny tekst źródłaBills, Victoria Louise. "Vascular permeability in pre-eclampsia". Thesis, University of Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.508075.
Pełny tekst źródłaWimalasundera, Ruwan Chinthaka. "Vascular regulation in pre-eclampsia". Thesis, Imperial College London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.540684.
Pełny tekst źródłaDalton, Matthew W. "Experimental modelling of vascular haemodynamics". Thesis, Nottingham Trent University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273762.
Pełny tekst źródła