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1
Carter, A. J. "Thromboxane synthesis in human blood platelets and blood vessels." Thesis, University of Nottingham, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355288.
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Au, Pakwai. "Engineering functional blood vessels in vivo." Thesis, Massachusetts Institute of Technology, 2008. http://hdl.handle.net/1721.1/43867.
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Thesis (Ph. D.)--Harvard-MIT Division of Health Sciences and Technology, 2008.Includes bibliographical references.
At the present time, there are many hurdles to overcome in order to create a long-lasting and engineered tissue for tissue transplant in patients. The challenges include the isolation and expansion of appropriate cells, the arrangement of assorted cells into correct spatial organization, and the development of proper growth conditions. Furthermore, the creation of a three dimensional engineered tissue is limited by the fact that tissue assemblies greater than 100-200 micrometers, the limit of oxygen diffusion, require a perfused vascular bed to supply nutrients and to remove waste products and metabolic intermediates. To overcome this limitation, this thesis aims to pre-seed a tissue engineered construct with vascular cells (both endothelial and perivascular cells), so the vascular cells could readily form functional vessels in situ. Previous work in the laboratory had successfully demonstrated the formation of functional microvascular network by co-implantation of human umbilical cord vein endothelial cells (HUVECs) and 10 T 1/2 cells, a line of mouse embryonic fibroblasts. To translate this concept to the clinic, we need to utilize cells that can be secured and used in clinic. To this end, we systematically replace each individual vascular cell type with a readily available source of cells. First, we investigated human embryonic stem cells (hESCs) derived endothelial cells. We demonstrated that when hESCs derived endothelial cells were implanted into SCID mice, they formed blood vessels that integrated into the host circulatory system and served as blood conduits. Second, we compared the formation and function of engineered blood vessels generated from circulating endothelial progenitor cells (EPCs) derived from either adult peripheral blood or umbilical cord blood.
(cont.) We found that adult peripheral blood EPCs formed blood vessels that were unstable and regressed within three weeks. In contrast, umbilical cord blood EPCs formed normal-functioning blood vessels that lasted for more than four months. These vessels exhibited normal blood flow, perm-selectivity to macromolecules and induction of leukocyte-endothelial interactions in response to cytokine activation similar to normal vessels. Third, we evaluated human bone marrow-derived mesenchymal stem cells (hMSCs) as a source of vascular progenitor cells. hMSCs expressed a panel of smooth muscle markers in vitro and cell-cell contact between endothelial cells and hMSCs up-regulated the transcription of smooth muscle markers. hMSCs efficiently stabilized nascent blood vessels in vivo by functioning as perivascular precursor cells. The engineered blood vessels derived from HUVECs and hMSCs remained stable and functional for more than 130 days in vivo. On the other hand, we could not detect differentiation of hMSCs to endothelial cell in vitro and hMSCs by themselves could not form conduit for blood flow in vivo. Similar to normal perivascular cells, hMSCs-derived perivascular cells contracted in response to endothelin-1 in vivo. Thus, our work demonstrates the potential to generate a patent and functional microvascular network by pre-seeding vascular cells in a tissue-engineered construct. It serves as a platform for the addition of parenchymal cells to create a functional and vascularized engineered tissue.
by Pakwai (Patrick) Au.
Ph.D.
3
HYNES, MICHAEL RAY. "ENDOTHELIUM-DEPENDENT RELAXATION OF BLOOD VESSELS." Diss., The University of Arizona, 1987. http://hdl.handle.net/10150/184134.
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Dilation of blood vessels in response to a large number of agents has been shown to be dependent on an intact vascular endothelium. The present studies examine some aspects of endothelium-dependent vasodilation in blood vessels of the rabbit and rat. Using the rabbit ear artery and the subtype-selective muscarinic antagonist pirenzepine, muscarinic receptors of the endothelium and smooth muscle cells were shown to be of the low affinity M₂ subtype. Inhibition of [³H](-)quinuclidinyl benzilate was used to determine affinity for the smooth muscle receptors while antagonism of methacholine induced vasodilation yielded the endothelial cell receptor affinity. The effect of increasing age (1-27 months) on endothelium-dependent relaxation was studied in aortic rings, perfused tail artery and perfused mesenteric bed of the Fisher 344 rat. Both aortic ring segments and perfused caudal arteries showed an age-related increase in sensitivity of endothelium-mediated relaxation to the cholinergic agonist methacholine. This increased sensitivity occurs between the ages of 6 and 12 months, with no further significant increase up to 27 months of age, suggesting this is a consequence of growth and development rather than old age. No difference with age in cholinergic relaxation was observed in the perfused mesenteric bed indicating either no change of sensitivity in smaller resistance vessels or an effect which is hidden in this more complex perfused system. In contrast to findings with cholinergic stimution, responses of the perfused caudal artery to the calcium ionophore A23187 were not altered with age. This suggests that the alteration with age in response to methacholine involves the muscarinic receptor or receptor coupling mechanism rather than the generation of, or response to, endothelium-derived relaxing factor (EDRF). The influence of endothelium on contractile responses was examined using the perfused caudal artery. Endothelium removal significantly increased contraction to the α-adrenergic agonists methoxamine and BH-T 920 as well as to transmural nerve stimulation. Inhibition of contraction to agents which must first cross the smooth muscle layer before reaching the endothelium suggests that a continuous or basal level of EDRF release is responsible for decreased contraction rather than an receptor stimulated release of EDRF.
4
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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Arief, Melissa Suen. "Human Tissue Engineered Small Diameter Blood Vessels." Yale University, 2010. http://ymtdl.med.yale.edu/theses/available/etd-03152010-144428/.
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The engineering of human vascular grafts is an intense area of study since there is crucial need for alternatives to native vein or artery for vascular surgery. This current study sought to prove that a tissue engineered blood vessel (TEBV) 1mm in diameter could be developed from human smooth muscle cells and that endothelial progenitor cells (EPCs) could be cultured and used to endothelialize these grafts. This project had four specific aims: the isolation and characterization of EPCs, the seeding of a novel scaffold with EPCs and exposure to physiologic shear stress in vitro, the development of TEBV from human smooth muscle cells that are strong enough to implant in vivo, and the in vivo implantation of TEBV into the rat aortic model with a comparison of EPC seeded TEBVs pretreated with shear stress and unseeded TEBVs. The results yielded isolation of four EPC lines and a flow system design capable of seeding EPCs onto a novel scaffold with preliminary studies indicating that it is capable of exposing the EPCs to physiologic shear stress, although further studies require more optimization. The development of mechanically strong TEBV was highly successful, yielding TEBVs comparable to native vessels in collagen density and burst pressure, but with much lower compliance. Current implantation studies indicated that unseeded TEBV grafts implanted into the rat aorta without anticoagulation is highly thrombogenic. However, anticoagulation using Plavix may be capable of maintaining graft patency. These TEBVs did not rupture or form aneurysm in vivo and the future completion of the in vivo studies are likely to demonstrate the high potential of these grafts.
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Dritsoula, A. "Regulation of NKX2-5 in blood vessels." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1551692/.
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NKX2-5 is a transcription factor required for the formation of the heart and vessels during development. Postnatal expression is significantly downregulated, and then re-activated in diseased conditions characterised by vascular remodelling. However, the mechanisms regulating NKX2-5 activation in diseased vessels remain unknown. The aim of this thesis is to identify these mechanisms and provide information on how the gene contributes to cardiovascular pathologies, such as sclerodermaassociated pulmonary hypertension. A case-control genetic association study was performed in two independent cohorts of scleroderma patients. Associated SNPs located in the NKX2-5 genomic region were cloned into reporter vectors, and transcriptional activity was assessed by reporter-gene assays. Associated SNPs were further evaluated through proteinDNA binding assays, chromatin immunoprecipitation and RNA silencing. Signalling mechanisms activating NKX2-5 expression were investigated in vascular endothelial and smooth muscle cells using a panel of selective inhibitors. Meta-analysis across the two independent cohorts revealed that rs3131917 was associated with scleroderma. Rs3132139, downstream of NKX2-5, was significantly associated with pulmonary hypertension in both cohorts. The region containing rs3132139 and rs3131917 was shown to be a novel functional enhancer, which increased NKX2-5 transcriptional activity through the binding of GATA6, c-JUN, and MEF-2c. An activator TEAD/YAP1 complex was shown to bind at rs3095870, another functional SNP upstream of NKX2-5 transcription start site, which showed marginal association with scleroderma. Signalling mechanisms, involving TGF-β, ERK5, AKT and hypoxia, stimulated NKX2-5 expression during phenotypic modulation of vascular endothelial and smooth muscle cells. Overall, the data showed that NKX2-5 is genetically associated with scleroderma and pulmonary hypertension. Functional evidence revealed a regulatory mechanism, activated by TGF-β, which results in NKX2-5 transcription in human vascular smooth muscle cells through the interaction of an upstream promoter and a novel downstream enhancer. These regulatory mechanisms can act as a model for NKX2-5 activation in cardiovascular disease characterised by vascular remodelling.
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Kaur, Amaratpal. "Optical remote sensing of hypertensive blood vessels." Thesis, Loughborough University, 1997. https://dspace.lboro.ac.uk/2134/32228.
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The aim of this research is to investigate the effects of hypertension on small artery structure by extending the instrumentation which is available for optical analysis of vessels in-vitro. Conventionally, arterial vessels are pressurised in a perfusion myograph and are analysed by video microscopy. A key objective of this research is to enable the examination of vessels by absorption spectroscopy.
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Omatuku, Emmanuel Ngongo. "Modelling of Residual Stresses of Blood Vessels." Thesis, University of Cape Town, 2015. http://hdl.handle.net/11427/21604.
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The diagnosis of vascular diseases can be achieved with a suitably determined circumferential stress at arterial walls. The stress distribution over arterial walls in blood vessels is affected by residual stresses and stresses due to blood pressure. However, residual stresses are still not reliably determined. For this reason, a suitable incorporation of these stresses is required in order to establish the wall stress as a reliable diagnostic indicator. Thus this study aims to model residual stresses by incorporating them into the wall stress distribution, and to investigate the effect that parameters defining the study constitutive model have on the stress distribution. The constitutive model makes use of the Cosserat fibre continuum in order to account for mechanics of arterial walls. It was developed for cardiac tissues by Skatulla et al. (2014), but it can also be used for a preliminary investigation on arterial tissues as these two types of tissues exhibit comparable mechanics. Residual stresses are incorporated by using three problem definitions, which are derived from the opening angle method, into a three dimensional two-layer artery consisting of the media and adventitia. The first problem incorporates residual stresses that are locked within individual load-free layers. The second problem continues the first problem by incorporating residual stresses acting at the interface surface between arterial layers, and then determine the artery wall stress distribution under blood pressure. The third problem determines the wall stress in the stress-free artery under blood pressure. On the other hand, the effect of parameters defining the constitutive model is investigated by varying the size of parameters in these problems. However, the second problem is not analysed in this study because it requires an analysis implementation that could not be achieved within the study timeline. Similarly, model parameters of problems are not calibrated to available experimental data. Therefore, this study only provides qualitative results. The investigation results on the incorporation of residual stresses into the stress distribution are found to be inconclusive as they provide contradictory results. The characteristic scaling parameters are found to influence the magnitude and gradient of the stress distribution. However, these results are not conclusive to clearly define the influence. Thus it is recommended that further research be conducted in order to gain conclusive results.
9
Williams, Chrysanthi. "Perfusion bioreactor for tissue-engineered blood vessels." Diss., Available online, Georgia Institute of Technology, 2004:, 2003. http://etd.gatech.edu/theses/available/etd-06072004-131410/unrestricted/williams%5Fchrysantyhi%5F200405%5Fphd.pdf.
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Kuzborska, Zyta. "Research of blood flow and stresses in the pathological blood vessels." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2012. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2012~D_20120131_135725-24904.
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Physical load, age and gender influence to blood pressure and maximal stresses in the pathological blood vessel palaces was studies in this work. The main research subject – pathological blood vessel and its blood flow processes that depend on physical load, pathology degree and type, age, gender and blood vessels stress characteristics. The main aim of this work – to examine blood flow characteristics, local blood pressure, stress distribution in the pathological blood vessels dependent physical load assessing blood vessels mechanical properties variations due to age, gender, blood vessel pathology type; to make simplified human efficiency evaluation methodology. The paper analyse a few main tasks:
to explore physical load, blood vessels pathology degree, age and gender influence to blood pressure and tensions increase in the pathological blood vessels locations; experimentally determine blood flow rates changes in pathological blood vessels assessing; additionally investigate blood pressure and heart rate characteristics variations during set physical load and human working age range.
This paper consists of introduction, four chapters, summary, literature and authors publications theses lists and two annexes.
Introductory chapter discusses the test problem, work topicality, research subject, also formulates work subject and tasks, and describes research methodology, work scientific novelty, practical value of the work results, defended propositions. In the introduction end... [to full text]Disertacijoje nagrinėjama fizinio krūvio, amžiaus bei lyties įtaka kraujo spaudimui ir didžiausiems įtempiams pažeistoje kraujagyslės vietoje. Pagrindinis tyrimo objektas – ligos pažeista kraujagyslė ir joje vykstantys kraujo tėkmės procesai, priklausantys nuo fizinio krūvio dydžio, pažeidimo laipsnio ir rūšies, amžiaus, lyties, bei šių veiksnių įtaka didžiausiems įtempiams ir spaudimui pažeistose vietose. Pagrindinis disertacijos tikslas – ištirti kraujo tėkmės charakteristikas, lokalinį kraujo spaudimą, įtempių pasiskirstymą pažeistose kraujagyslėse priklausomai nuo fizinio krūvio, įvertinant kraujagyslių mechaninių savybių pokytį dėl amžiaus, lyties, kraujagyslės pažeidimo rūšies, ir sudaryti supaprastintą darbingumo verti-nimo metodiką. Darbe sprendžiami keli uždaviniai: ištirti fizinės apkrovos dydžio, kraujagyslių pažeidimų laipsnio, amžiaus ir lyties įtaką kraujo spaudimui ir įtempių padidėjimui pažeistose kraujagyslių vietose; ekspe-rimentiniu būdu nustatyti kraujo tėkmės rodiklių pokyčius pažeistose kraujagyslėse; ištirti kraujo spaudimo ir širdies susitraukimų dažnio charakteristikų pokyčius nustatytame fizinio krūvio ir žmogaus darbingo amžiaus intervale. Disertaciją sudaro įvadas, keturi skyriai, rezultatų apibendrinimas, naudotos literatūros ir autorės publikacijų disertacijos tema sąrašai ir du priedai. Įvadiniame skyriuje aptariama tiriamoji problema, darbo aktualumas, aprašomas tyrimų objektas, formuluojamas darbo tikslas bei uždaviniai, aprašoma tyrimų... [toliau žr. visą tekstą]
11
Myers, Daniel. "The Role of Osteopontin in Vascular Remodeling." Fogler Library, University of Maine, 2004. http://www.library.umaine.edu/theses/pdf/MyersDL2004.pdf.
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Scott, Matthew. "The modeling of blood rheology in small vessels." Thesis, University of Waterloo, 2005. http://hdl.handle.net/10012/1149.
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Blood is a dense suspension of flexible red blood cells. In response to a background flow, these cells distribute themselves non-uniformly throughout the vessel. As a result, material properties that are well defined in homogeneous fluids, such as viscosity, are no longer so, and depend upon the flow geometry along with the particle properties. Using a simple model that accounts for the steady-state particle distribution in vessel flow, we derive an expression for the effective viscosity of blood and the suspension flow velocity field in a pressure-driven tube flow. We derive the steady-state particle distribution from a conservation equation with convective flux arising from particle deformation in the flow. We then relate the particle microstructure to the overall flow through a generalized Newtonian stress-tensor, with the particle volume fraction appearing in the expression for the local viscosity. Comparing with experimental data, we show that the model quantitatively reproduces the observed rheology of blood in tube flow.
We reconsider the problem in an alternate geometry corresponding to the flow between two concentric cylinders. The steady-state particle distribution, suspension velocity field and the measured effective viscosity are all very different from their counterparts in tube flow, casting serious doubt upon the practice of using data from a Couette viscometer to parameterize constitutive models applied to vascular blood flow.
Finally, we calculate the effect of random fluctuations in the particle velocity on the averaged behaviour of the particle conservation equation. Using a smoothing method for linear stochastic differential equations, we derive a correction to the free Einstein-Stokes diffusion coeffcient that is due to the interaction of the particles with their neighbours.
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Pate, Michael Alastair. "Characterisation of endothelin receptors in human blood vessels." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392486.
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Fierro, Murga Leobardo. "Analysis of countercurrent exchange between paired blood vessels." Diss., The University of Arizona, 1993. http://hdl.handle.net/10150/186130.
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Throughout much of the blood circulatory system, supply vessels (arteries and arterioles) are situated adjacent to corresponding draining vessels (veins and venules), which flow in the opposite direction. In this dissertation, mathematical models are developed to describe diffusive exchange of heat, oxygen and inert gases between such paired countercurrent blood vessels and surrounding tissue. In preliminary analyses, exchange between a single vessel and surrounding tissue is considered. The concept of equilibration length is developed. Then a well-known solution for two-dimensional diffusion between two vessels situated in an infinite domain is presented. This provides a basis for developing semianalytic solutions for two vessels situated in a cylindrical tissue region with Dirichlet or zero-flux conditions at the outer boundary. A general approach is then developed for obtaining semianalytic solutions for domains with non-circular cross-sections, and applied to the case of a rectangular domain. The governing equations for paired blood vessels are then solved to obtain the axial variation of temperature or concentration for a variety of cases, including Dirichlet and zero-flux boundary conditions, with and without deposition or consumption of heat or gas. For the Dirichlet case, the equilibration length is compared to that for a single vessel, showing that equilibrium is achieved more rapidly when a single vessel is replaced by two vessels with the same diameter as the single vessel. For the zero-flux case, particular solutions to the full three-dimensional diffusion equation in the tissue are obtained from the two-dimensional solutions. The total transport (convective and diffusive) in the axial direction is evaluated, with and without consumption/deposition, and the results are interpreted in terms of an enhanced diffusivity. Finally, the complementary roles of convection and diffusion in mass and heat transport in the axial direction are considered. It is shown that as vessel diameter decreases, countercurrent exchange eventually results in a reduction of convective transport. Axial diffusion becomes significant at approximately the same range of diameters. This finding is interpreted in terms of the efficiency by which a branching network can transport heat and mass to its extremities.
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Kristo, Aleksandra S. "The Effect of Wild Blueberries on Endothelium-Dependent Vasodilation in Spontaneously Hypertensive Rats." Fogler Library, University of Maine, 2008. http://www.library.umaine.edu/theses/pdf/KristoAS2008.pdf.
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Yuan, Yuan. "Multi-scale vessel enhancement using local line integrals and variational optimization /." View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?CSED%202008%20YUAN.
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Robertson, Zoe. "An in vitro study of the effect of silicon and magnesium ions on bone repair and angiogenesis." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25934.
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Clark, Kateryna. "Wild Blueberries Affect Endothelium-dependant Vasodilation in Sprague-Dawley and Spontaneously Hypertensive Rats." Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/pdf/ClarkK2007.pdf.
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Zoellner, Hans. "The vascular response in chronic periodontitis." Thesis, The University of Sydney, 1990. http://hdl.handle.net/2123/4468.
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This thesis describes work done at the Institute of Dental Research in Sydney between February of 1986 and January 1990. The broad subject of the work is the role of vascular endothelial cells (ECs) in chronic inflammation. Periodontitis has been used as an example of chronic inflammatory disease, and provides the focus for this study of endothelial biology. In Chapter 1, aspects of the endothelial literature which provide relevant background information for work described in later chapters are reviewed. In Chapter 2, literature relating to aetiology and pathogenesis of chronic inflammatory periodontal disease is discussed. To maintain relevance of literature reviews to experimental work, each subsequent chapter contains a small literature review of material relating to the subject of the specific chapter. Early laboratory work is described in Chapter 3, and consisted of a morphological survey of the vascular changes occurring in gingival tissues with development of chronic periodontitis. Expansion of the vasculature and appearance of phenotypically specialised high endothelial cells (HECs), were associated with progression of the disease. Vessels with HECs and had a similar appearance to those known to be responsible for lymphocyte recirculation described in lymphoid tissues and chronic inflammatory sites. In the course of performing this survey, a perivascular hyaline material was noted surrounding capillaries close to the bacterial plaque irritant. The incidence, distribution, extent, ultrastructre and immuo-histochemistry of this material was more closely investigated, and the possible pathogenesis and significance of the material discussed in Chapter 4. In Chapter 5, the ultrastructural, histochemical and functional properties of gingival HECs are described, and compared with the well characterised HECs of rat lymph nodes. It was found that periodontal vessels were very similar to those in rat lymph nodes, with the exception however, that the gingival vessels appeared to exchange polymorphonuclear leukocytes almost exclusively, while vessels with HECs in lymph nodes and other locations are known as sites of lymphocyte recirculation. This observation indicated that the function of HECs requires further investigation, with particular regard to the synthetic activity of the cells. HECs were consistently alkaline phosphatise (AP) negative. The negative association between leukocyte emigration and AP activity (APA), as well as evidence in the literature illustrating both the wide substrate specificity of this enzyme and the importance of phosphorylation in the control of protein activation, suggested that AP could play a role in regulating leukocyte emigration. A pre-requisite for the investigation of this possibility, is the identification of a rich source of the identical iso-enzyme of AP to what is present in ECs. In Chapter 6, the sensitivity of endothelial AP to a panel of inhibitors is compared with that of a number of tissues for which isoenzyme has been identified. Endothelial AP was identified as the liver/bone/kidney isoenzyme. This allows the use of kidney tissue as a relevant source of AP for use in further study of the role of this enzyme in EC biology. It was clear that in order to study both the synthetic activity of HECs, as well as the role of AP in the control of leukocyte emigration, a method for obtaining high density primary cultures of HECs had to be established. Chapter 7 describes work done towards the development of such a culture system. The availability in the latter phase of the work of suitable probe for the technique of the in-situ hybridization allowed the possibility of testing the hypothesis that HECs are important cytokine producers. It was felt that this would provide some basis for the further study of those cells in-virtro. This work is described in the appendix. The general discussion in Chapter 8, summarises the work, and develops potential areas of study arising from the finding of this thesis.
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Zoellner, Hans. "The vascular response in chronic periodontitis." University of Sydney, 1990. http://hdl.handle.net/2123/4468.
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Doctor of PhilosophyThis thesis describes work done at the Institute of Dental Research in Sydney between February of 1986 and January 1990. The broad subject of the work is the role of vascular endothelial cells (ECs) in chronic inflammation. Periodontitis has been used as an example of chronic inflammatory disease, and provides the focus for this study of endothelial biology. In Chapter 1, aspects of the endothelial literature which provide relevant background information for work described in later chapters are reviewed. In Chapter 2, literature relating to aetiology and pathogenesis of chronic inflammatory periodontal disease is discussed. To maintain relevance of literature reviews to experimental work, each subsequent chapter contains a small literature review of material relating to the subject of the specific chapter. Early laboratory work is described in Chapter 3, and consisted of a morphological survey of the vascular changes occurring in gingival tissues with development of chronic periodontitis. Expansion of the vasculature and appearance of phenotypically specialised high endothelial cells (HECs), were associated with progression of the disease. Vessels with HECs and had a similar appearance to those known to be responsible for lymphocyte recirculation described in lymphoid tissues and chronic inflammatory sites. In the course of performing this survey, a perivascular hyaline material was noted surrounding capillaries close to the bacterial plaque irritant. The incidence, distribution, extent, ultrastructre and immuo-histochemistry of this material was more closely investigated, and the possible pathogenesis and significance of the material discussed in Chapter 4. In Chapter 5, the ultrastructural, histochemical and functional properties of gingival HECs are described, and compared with the well characterised HECs of rat lymph nodes. It was found that periodontal vessels were very similar to those in rat lymph nodes, with the exception however, that the gingival vessels appeared to exchange polymorphonuclear leukocytes almost exclusively, while vessels with HECs in lymph nodes and other locations are known as sites of lymphocyte recirculation. This observation indicated that the function of HECs requires further investigation, with particular regard to the synthetic activity of the cells. HECs were consistently alkaline phosphatise (AP) negative. The negative association between leukocyte emigration and AP activity (APA), as well as evidence in the literature illustrating both the wide substrate specificity of this enzyme and the importance of phosphorylation in the control of protein activation, suggested that AP could play a role in regulating leukocyte emigration. A pre-requisite for the investigation of this possibility, is the identification of a rich source of the identical iso-enzyme of AP to what is present in ECs. In Chapter 6, the sensitivity of endothelial AP to a panel of inhibitors is compared with that of a number of tissues for which isoenzyme has been identified. Endothelial AP was identified as the liver/bone/kidney isoenzyme. This allows the use of kidney tissue as a relevant source of AP for use in further study of the role of this enzyme in EC biology. It was clear that in order to study both the synthetic activity of HECs, as well as the role of AP in the control of leukocyte emigration, a method for obtaining high density primary cultures of HECs had to be established. Chapter 7 describes work done towards the development of such a culture system. The availability in the latter phase of the work of suitable probe for the technique of the in-situ hybridization allowed the possibility of testing the hypothesis that HECs are important cytokine producers. It was felt that this would provide some basis for the further study of those cells in-virtro. This work is described in the appendix. The general discussion in Chapter 8, summarises the work, and develops potential areas of study arising from the finding of this thesis.
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Huijbers, Elisabeth J. M. "Development of a Cancer Vaccine Targeting Tumor Blood Vessels." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-170887.
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A treatment strategy for cancer is the suppression of tumor growth by directing an immune response to the tumor vessels, which will destroy the tissue. In this thesis we describe the development of a vaccine that targets antigens expressed around angiogenic vasculature in most solid tumors. These antigens are alternative spliced extra domains of glycoproteins present in the extracellular matrix; e.g. the extra domain-B (ED-B) and extra domain-A (ED-A) of fibronectin and the C-domain of tenascin-C (TNCC). We show that it is possible to break self-tolerance and induce a strong antibody response against ED-B by vaccination. Furthermore, tumor growth was inhibited and the changes observed in the tumor tissue were consistent with an attack of the tumor vasculature by the immune system. For clinical development of therapeutic vaccines, targeting self-molecules like ED-B, a potent but non-toxic biodegradable adjuvant is required. The squalene-based Montanide ISA 720 (M720) in combination with CpG DNA fulfilled these requirements and induced an equally strong anti-self immune response as the preclinical golden standard Freund’s adjuvant. We have further characterized the immune response against ED-B generated with the adjuvant M720/GpG. The ED-B vaccine also inhibited tumor growth in a therapeutic setting in a transgenic mouse model of pancreatic insulinoma in which tumorigenesis was already initiated. Furthermore, antibodies against ED-A and TNCC could be induced in mice and rabbits. We analyzed the expression of ED-A in breast tumors of transgenic MMTV-PyMT mice, a metastatic breast cancer model, with the aim to use this model to study the effect of an ED-A vaccine on metastasis. We also detected ED-B in canine mammary tumor tissue. Therefore vascular antigens might also represent potential therapeutic targets in dogs. All together our preclinical data demonstrate that a vaccine targeting tumor blood vessels is a promising new approach for cancer treatment.
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Razavi, Habib M. "Conduit versus resistance blood vessels, adrenoceptors and nitric oxide." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0011/MQ40846.pdf.
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Lohsiriwat, Varut. "characterisation of receptors on blood vessels in haemorrhoid tissue." Thesis, University of Nottingham, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.537691.
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Caldwell, Mark Alexander. "Modeling blood vessels and oxygen diffusion into brain tissue." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1565276066111476.
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Norotte, Cyrille Forgács G. "From developmental biology to tissue-engineering printing blood vessels /." Diss., Columbia, Mo. : University of Missouri--Columbia, 2009. http://hdl.handle.net/10355/6188.
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Title from PDF of title page (University of Missouri--Columbia, viewed on Feb 15, 2010). The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file. Dissertation advisor: Dr. Gabor Forgacs. Vita. Includes bibliographical references.
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Zdanowski, Zbigniew. "Synthetic vascular graft infection an experimental study with special reference to host mechanisms affecting bacterial graft colonization /." Lund : Dept. of Surgery, Lund University, 1993. http://catalog.hathitrust.org/api/volumes/oclc/39798633.html.
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Keung, Wen-yee Wendy, and 姜韻兒. "Mechanisms of acute actions of 17B-estradiol in the vascular system." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B29697487.
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Chan, Yap-hang, and 陳熠恆. "Role of phytoestrogen in vascular function and dysfunction." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40733725.
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黃鉦沅 and Ching-yuen Wong. "Impact of diet on vascular function in patients with type II diabetes mellitus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42904936.
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Zhao, Yingzi, and 趙瑩子. "Acute and chronic impact of pressure on vascular responsiveness." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/207185.
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Hypertension leads to vascular complications including endothelial dysfunction, heart failure and stroke. The purpose of the present studies was to investigate the chronic and acute impact of high pressure on vascular responsiveness.
In Study I, isometric tension measurements demonstrated that contractions to phenylephrine, in the presence of indomethacin (inhibitor of cyclooxygenase), were smaller in aortae of spontaneously hypertensive rats (SHR) with, than in those without, endothelium, while they were comparable in such preparations of normotensive Wistar-Kyoto rat (WKY); the difference in SHR aortae was not affected by L-NAME [inhibitor of nitric oxide synthase (NOS)]. This endothelium-dependent, NOS-independent inhibition of phenylephrine-induced contraction was greater in older SHR (36 versus 18 weeks), and abolished by NO scavengers and ODQ (inhibitor of soluble guanylyl cyclase). It was observed not only in the presence of indomethacin but also apocynin (antioxidant), but inhibited by diphenyleneiodonium (inhibitor of cytochrome P450 reductase). These results suggest that the endothelium-dependent, eNOS-independent inhibition is caused by NO produced by cytochrome P450 reductase in the endothelium of the SHR aorta.
Study II investigated the mechanisms underlying the reduced contractions to prostaglandin E2 [agonist of prostaglandin E2 and thromboxane-prostanoid (TP) receptors] by a previous exposure to phenylephrine (agonist of α1-adrenoceptor) in the aortic smooth muscle of the SHR. This inhibition induced by the pre-activation of α1-adrenoceptor was augmented in aortae of older SHR (36 versus 18 weeks) and was not present in WKY preparations. Pre-exposure to the protein kinase C (PKC) activator, phorbol 12,13-dibutyrate, also inhibited subsequent contractions to prostaglandin E2 in SHR aortae. Inhibition of PKC by calphostin C abolished the effect of pre-exposure to phenylephrine. The mRNA expressions of PKC isoforms differed in WKY and SHR smooth muscle. These experiments suggest that in the SHR but not the WKY aorta, α1-adrenergic activation causes heterologous desensitization of TP receptor through activation of a specific PKC isoform(s).
In Study III, experiments were performed in a pressure myograph to determine whether or not acute elevation of transmural pressure in the isolated carotid artery of adult mouse (10-12 weeks) impairs endothelium-dependent dilatation by increasing angiotensin II expression or by directly activating AT1 receptors. Transient exposure of arteries to increased pressure (150 mmHg, three hours) inhibited endothelium-dependent, NO-mediated dilatations to acetylcholine, but did not affect responses to the NO donor DETA-NONOate. Inhibiting angiotensin II signaling or angiotensin converting enzyme prevented the impairment of endothelium-dependent dilatation by elevated pressure. Elevated pressure increased the expression of angiotensinogen [precursor of angiotensin II]. Thus, exposure of carotid arteries to elevated pressure leads to local release of angiotensin II, which activates AT1 receptors to cause endothelial dysfunction.
In summary, chronic increased pressure increased the endothelial NO release produced by cytochrome P450 reductase from nitrate and developed the heterologous desensitization of TP receptor caused by PKC in SHR aorta. Acute increased pressure impaired endothelium-dependent NO-mediated vasodilatation by activation of local angiotensin system in adult mouse carotid artery. These processes likely contribute to the pathogenesis of hypertension-induced vascular dysfunction and organ injury.published_or_final_version
Pharmacology and Pharmacy
Doctoral
Doctor of Philosophy
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Burbridge, Michael Frank. "The rat aortic ring model of angiogenesis in vitro as an assay for angiogenic modulators, the role of the matrix metalloproteinases in vessel formation." Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367795.
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Chan, Yap-hang. "Role of phytoestrogen in vascular function and dysfunction." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40733725.
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Johnson, Lynelle. "Effects of exercise training on pulmonary vasomotor responses in the pig /." free to MU campus, to others for purchase, 2000. http://wwwlib.umi.com/cr/mo/fullcit?p9974642.
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Wong, Ching-yuen. "Impact of diet on vascular function in patients with type II diabetes mellitus." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B42904936.
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Schindelhauer, Nancy Lynn. "Trophic interactions between rat thigh blood vessels and their innervation." Thesis, University of British Columbia, 1986. http://hdl.handle.net/2429/26069.
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Much less work has been done on the denervation of smooth muscle compared with the extensive studies carried out on skeletal muscle. It was thought that denervation of smooth muscle produced few alterations in its morphology or physiology, especially since many blood vessels have virtually no innervation, and therefore, they can survive without it. Simple severing or excising a section of nerve trunk is sufficient to denervate skeletal muscle, but this does not apply to smooth muscle. Therefore, denervation methods for smooth muscle have included those with widespread effects such as chemical and immunological sympathectomies, and superior cervical ganglionectomy. In this study, I have developed a a semi-permanent, localized denervation method for rat thigh vessels and have used this method to study the trophic interactions between blood vessels and their innervation.
Female Wistar rats were denervated at 1-3 or 12 days of age, and examined at 30, 60, 90 and 120 days of age. The femoral nerve, which carries the vasomotor innervation to the thigh vessels, was severed in the thigh and brought inside the abdominal cavity. This method was necessary since preliminary experiments showed rapid re-innervation of the vessels if any part of the proximal root remained in the thigh. Inside the abdominal cavity, the nerve was slipped into a plastic tube and heat sealed. The tubing further inhibited re-innervation by preventing collateral sprouting from the proximal stump. Samples of the distal nerve stump, the proximal nerve stump, and from the femoral vein and saphenous artery were taken. In every animal, the contralateral side acted as a control.
The distal and proximal nerve stumps showed marked evidence of degeneration. Fluorescence microscopy (specific for catecholamines) showed a significant decrease in the number of fluorescing dots around both the artery and vein. The presence of some fluorescencing dots around the denervated vessels may be from the nerves that were seen re-innervating the vessels at the time of sampling. These nerves came from aberrant areas. Arteries sampled at 90 days showed a significant decrease in the cross-sectional area of the tunica media on the denervated side.
The denervated femoral vein, in situ, was seen to be grossly dilated compared to the control side. Measurements of the luminal perimeter of sections of the vein showed that the denervated vein had a luminal area up to three times that of the controls. The difference in wall thickness in the femoral vein was not significant at the p<0.05 level. My results indicate that adrenergic nerves may not only have a trophic influence on arteries, but may influence veins as well. Therefore, in this study, trophic influences of nerves on blood vessels have been suggested by denervation causing 1) a thinner arterial wall and by producing 2) a reproducible dilation of the femoral vein. Also, trophic influences of blood vessels on nerves is suggested by the presence of re-innervation from aberrant areas.Medicine, Faculty of
Graduate
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Elliot, Jonathan. "Semicarbazide-sensitive amine oxidase of blood vessels : a functional study." Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316733.
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Bradley, Jane Louise. "Quantitative aspects of blood vessels and perineurium in diabetic neuropathy." Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307586.
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Lee, Carol Hsiu-Yueh. "Electrospun Polycaprolactone Scaffolds for Small-Diameter Tissue Engineered Blood Vessels." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1376924954.
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Strobel, Hannah A. "Engineered blood vessels with spatially distinct regions for disease modeling." Digital WPI, 2018. https://digitalcommons.wpi.edu/etd-dissertations/541.
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Tissue engineered blood vessels (TEBVs) have great potential as tools for disease modeling and drug screening. However, existing methods for fabricating TEBVs create homogenous tissue tubes, which may not be conducive to modeling focal vascular diseases such as intimal hyperplasia or aneurysm. In contrast, our lab has a unique modular system for fabricating TEBVs. Smooth muscle cells (SMCs) are seeded into an annular agarose mold, where they aggregate into vascular tissue rings, which can be stacked and fused into small diameter TEBVs. Our goal is to create a platform technology that may be used for fabricating focal vascular disease models, such as intimal hyperplasia. Because tubes are fabricated from individual ring units, each ring can potentially be customized, enabling the creation of focal changes or regions of disease along the tube length. In these studies, we first demonstrated our ability to modulate cell phenotype within individual SMC ring units using incorporated growth factor-loaded degradable gelatin microspheres. Next, we evaluated fusion of ring subunits to form composite tissue tubes, and demonstrated that cells retain their spatial positioning within individual rings during fusion. By incorporating electrospun polycaprolactone cannulation cuffs at each end, tubes were mounted on bioreactors after only 7 days of fusion to impart luminal medium flow for 7 days at a physiological shear stress of 12 dyne/cm2. We then created focal heterogeneities along the tube length by fusing microsphere-containing rings in the central region of the tube between rings without microspheres. In the future, microspheres may be used to deliver growth factors to this localized region of microsphere incorporation and induce disease phenotypes. Due to the challenges of working with primary human SMCs, we next evaluated human mesenchymal stem cells (hMSCs) as an alternative cell source to generate vascular SMCs. We evaluated the effects of microsphere-mediated platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), and transforming growth factor beta-1 (TGF-β1) delivery on ring thickness, proliferation, and contractile protein expression over a 14 day period. Finally, we created a structurally distinct region of smooth muscle within tissue tubes by fusing human aortic SMCs in a central region between hMSC rings. In summary, we developed a platform technology for creating modular tubular tissues that may be further developed into an in vitro intimal hyperplasia model. It may also be modified to model other focal vascular diseases, such as aneurysm, or to create other types of multi-tissue tubular structures, such as trachea.
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Law, Wai Kong. "Segmentation of vessels using weighted local variances and an active contour model /." View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?COMP%202006%20LAW.
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Huang, Min, and 黃民. "Modulation of low density lipoprotein oxidation and its effects on vascular function." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B3123706X.
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Cheung, Ka-hei, and 張嘉熹. "Adaptive clutter filter design for micro-ultrasound color flow imagingof small blood vessels." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45517873.
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Nicholls, Juliet A. "Ca'2'+ mobilisation in cultured human vascular smooth muscle cells." Thesis, University of Newcastle Upon Tyne, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295537.
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Hanzlik, Josa A. "Effects of complex vessel geometrics on neutrophil margination and adhesion in post-capillary vessels /." Online version of thesis, 2008. http://hdl.handle.net/1850/9990.
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Huang, Min. "Modulation of low density lipoprotein oxidation and its effects on vascular function /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19905038.
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Bosch, Rué Èlia. "Strategies to induce vascularization: angiogenesis stimulation and tissue engineering blood vessels." Doctoral thesis, Universitat Internacional de Catalunya, 2021. http://hdl.handle.net/10803/670474.
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Angiogenesis, which results in a capillary network formation, is one of the crucial events that take place when there is tissue damage, being critical for successful tissue regeneration. It does not only allow the arrival of oxygen, nutrients and waste removal, but it also allows the arrival of progenitor cells necessary to induce tissue restoration. However, when there is an excessive damage, tissues are unable to regenerate by themselves. During the last decades, tissue engineering emerged as an alternative to improve tissue regeneration, with the combination of biomaterials (which serves as scaffolds), cells and/or stimulatory molecules. Therefore, one of the aims of tissue engineering is to incorporate stimulatory molecules within scaffolds to promote blood vessel formation for successful tissue regeneration and integration. Alternatively, there are some clinical situations in which high caliber vessels are needed instead of capillary network formation. An example would be with cardiovascular diseases (CVD), such as atherosclerosis or aneurysms, in which blood vessel replacement is needed. Autologous and xenogeneic grafts present some limitations, mainly risk of disease transmission and shortage of donors. Therefore, tissue engineered blood vessels (TEBVs) emerged as a promising alternative.
Regarding angiogenesis, generally, growth factors have been incorporated within scaffolds as molecules of choice to stimulate blood vessel formation. Although they have demonstrated a proper angiogenic response, they present some limitations, such as delicate handling properties and short half-life. As naturally found in human body, ions have demonstrated to be a promising alternative, being able to stimulate cellular functions, such as blood vessel formation. However, sometimes there is no consensus about the appropriate non-toxic and therapeutic doses, due to a lack of concentration screening studies before introducing them into the scaffolds. Regarding TEBVs, different approaches have been described for their development. However, they usually include several manufacturing steps and additional biomaterial patterning or additional stimulus to acquire native vascular cell alignment.
This thesis is focused on angiogenesis stimulation and TEBVs, divided in two main blocks: i) development of a drug delivery system (DDS) with the incorporation of ions to stimulate early phases of bone regeneration, including angiogenesis; ii) development of TEBVs through extrusion-based approach.
In the first part, an initial screening of different concentrations of therapeutic ions was performed to assess non-toxic and therapeutic concentrations in angiogenesis and osteogenesis, with endothelial cells (ECs) and human mesenchymal stem cells (hMSCs), respectively. Results allowed establishing therapeutic doses of both ions for blood vessel formation, although they showed impairment when tested for osteogenic differentiation. These ions were then incorporated within a biomaterial to allow forming a DDS, showing that the incorporated therapeutic ions could have antibacterial and angiogenic potential, allowing a sequential delivery of both ions. The designed DDS consisted of a fiber like structure incorporating hydroxyapatite based microparticles which could potentially be used for bone tissue regeneration.
In the second part, TEBVs were successfully developed with extrusion-based approach in one single step procedure. Moreover, specific vascular cell types were incorporated, with high cell survival and presenting native cell alignment and some vasoactive functionality. Furthermore, we could improve their mechanical properties by extruding TEBVs with high concentrations of collagen, allowing their perfusion with arterial shear stress. Further studies are required to prove their functionality and maturation, with the potential to be used as blood vessel replacement or even vascular disease modelingL’angiogènesis, que dona lloc a la formació de xarxes capil·lars, és un dels esdeveniments més importants que té lloc quan hi ha dany als teixits, sent fonamental per aconseguir la regeneració dels teixits. No només permet l’arribada d’oxigen, nutrients i eliminació de residus, sinó que també permet l’arribada de cèl·lules progenitores necessàries per induir la restauració dels teixits. Tot i així, quan es produeix un dany gran, els teixits no poden regenerar-se per si mateixos. En les darreres dècades, l’enginyeria tissular va sorgir com una alternativa per millorar la regeneració de teixits, amb la combinació de biomaterials (que serveixen com a bastides), cèl·lules i/o molècules estimuladores. Així doncs, un dels objectius de l’enginyeria de teixits és la incorporació de molècules estimuladores en els biomaterials per promoure la formació de vasos sanguinis per aconseguir amb èxit la regeneració de teixits i la seva integració en l’hòspeda. Alternativament, hi ha algunes situacions clíniques en les que es necessita vasos sanguinis grans en comptes de xarxes capil·lars. Un exemple el trobem amb les malalties cardiovasculars, com l’arterioescleròsi o aneurismes, en els quals és necessari un recanvi del vas sanguini. Els empèlts autòlegs i xenogènics s’han usat com a material substitutori, però presenten algunes limitacions, principalment el risc de transmissió de malalties i escassetat de material o donants. Així doncs, l’enginyeria tissular de vasos sanguinis va sorgir com una alternativa prometedora. Generalment, pel que fa l’angiogènesis, els factors de creixement s’han incorporat en els biomaterials com a molècules d’elecció per estimular la formació de vasos sanguinis. Tot i que han demostrat induir una resposta angiogènica adequada, presenten algunes limitacions, com ara propietats delicades per la seva manipulació i una vida de curta durada. Per altra banda, els ions, que es troben de manera natural en el cos humà, han demostrat ser una alternativa prometedora, ja que són capaços d’estimular funcions cel·lulars com seria la formació de vasos sanguinis. Tanmateix, no hi ha un ampli consens respecte les concentracions apropiades que no siguin tòxiques i que indueixin un efecte terapèutic, degut a la falta d’estudis previs on es faci un cribatge abans d’introduir-los en els biomaterials. Pel que fa a l’enginyeria tissular de vasos sanguinis, s’han descrit diferents metodologies per desenvolupar-los. Tot i així, aquests mètodes inclouen diversos passos i l’addició de patrons addicionals en els biomaterials o estímuls addicionals per induir l’alineament cel·lular similar als vasos nadius. Aquesta tesi es centra en l’estimulació de l’angiogènesi i l’enginyeria tissular de vasos sanguinis, dividida en dos blocs principals: i) el desenvolupament d’un sistema d’alliberació de fàrmacs amb la incorporació de ions per estimular fases primerenques de la regeneració de l’ós, incloent l’angiogènesi; ii) el desenvolupament de vasos sanguinis per enginyeria tissular mitjançant un mètode basat en l’extrusió. En la primer part, es va fer inicialment un cribatge amb diferents concentracions de dos tipus de ions terapeutics per determinar quin rang de concentracions no eren tòxiques i tenien un efecte terapèutic en l’angiogenesi i l’osteogènesis, usant cèl·lules endotelials i cèl·lules mesenquimals humanes, respectivament. Els resultats obtinguts van permetre establir un rang de concentracions terapèutiques dels dos ions per la formació de vasos sanguinis, però van mostrar un efecte deleteri quan es van usar per induir la diferenciació òssia. Posteriorment, es va desenvolupar un sistema d’alliberació de fàrmacs on es van incorporar aquests ions, demostrant que els ions terapèutics incorporats poden tenir un potencial antimicrobià i angiogènic, permetent l’alliberació seqüencial d’ambdós ions. El sistema d’alliberació de fàrmacs dissenyat consistia en una estructura similar a una fibra incorporant micropartícules amb contingut d’hidroxiapatita que potencialment es podria utilitzar per la regeneració de teixit ossi. En la segona part, els vasos sanguinis desenvolupats per enginyeria tissular van ser creats satisfactoriament mitjançant el mètode d’extrusió, involucrant un sol pas. A més a més, es va poder incorporar els tipus cel·lulars vasculars específics, amb una alta taxa de viabilitat i presentant l’alineament cel·lular nadiu i certa functionalitat vasoactiva. Posteriorment, es va poder millorar les propietats mecàniques extruint aquests vasos amb concentracions altes de col·lagen, permetent la seva perfusió amb un shear stress arterial. Es requereixen estudis addicionals per demostrar la seva funcionalitat i maduració, amb el potencial de ser usats com a reemplaçament de vasos sanguinis o, fins i tot, com a model de malalties vasculars.
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Mani, Mohammad H. "Ultrasonic instrument for accurate measurements of spatial parameters in blood vessels." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/33355/.
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The present research is aimed at the development of an ultrasonic medical instrument capable of measuring the intima-media thicknesses (IMT) of artery walls that are considered by medical practitioners as good indicators of the risk of atherosclerosis. This overcomes two notable limitations of the instruments available at present – insufficient axial resolution and lack of synchronisation to the heart cycle that make the measurements difficult to use, e.g., for annual screening of patients and like-for-like comparisons. These limitations were addressed by using a combination of on-the-fly averaging and interleaved sampling for acquiring echo waveforms, and triggering the scans at a particular instant of the heart cycle. The developed electronic instrumentation consisted of a battery powered electrocardiogram (ECG) monitor that transmitted the ECG data using an infrared link to the ECG processor that triggered the scans. Such architecture eliminated any possibility of accidentally connecting the patient to a source of voltage capable of causing serious injury and of causing radio frequency interference to medical equipment located in a close proximity. The algorithm for detecting the R-waves from noisy ECGs was fully verified with simulated and experimental ECG records, and implemented in firmware on board the ECG processor. The rate of R-wave detection of the developed algorithm is 88.24% out of 204 heartbeats recorded. In order to ease the interpretation of the recorded echoes, both mathematical and physical simulations of tubular objects were carried out. The calculated resolution of the system was estimated 2.5um. Spatial resolution of 15um was achieved during the in-vivo experiments. Some of the factors that might have caused this difference have been discussed with suggestions on possible methods of improvements. The set of experimental waveforms recorded in vivo demonstrated the correct operation of the developed instrument, appropriate consistency and some features that were expected and described in the literature. The developed instrument seems ready for application to a broader group of subjects.
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Bai, Ni. "Impact of diesel exhaust inhalation on the heart and blood vessels." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/35864.
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Numerous epidemiological studies have shown that exposure to ambient particulate matter (PM) is implicated in increased cardiovascular morbidity and mortality; however, the biological mechanisms are not fully understood. Diesel exhaust (DE) is the single biggest contributor to the urban ambient PM, and accounts for up to 90% of the total mass of fine particulate mass in ambient air of many major cities, such as London.
In this dissertation, I evaluated the effects of DE inhalation at an environmentally relevant level in a mouse model of atherosclerosis, the apolipoprotein E deficient (apoE knockout) mouse. I hypothesized that exposure to DE causes progression of atherosclerosis and vascular dysfunction, which leads to cardiovascular morbidity and mortality. I used a morphometric analysis to determine the compositional changes in atherosclerotic plaques, and showed that DE inhalation increased lipid accumulation, foam cell formation and smooth muscle cell recruitment in plaques, whereby suggesting a progression of atherogenesis. The magnitude of DE deposition in the lung correlates with foam cell formation suggesting a strong link between DE inhalation and atherogenesis. Oxidative stress markers, including CD36 and nitrotyrosine, were all increased after exposure to DE, suggesting that reactive oxygen species played an important role in this vascular effect. In addition, I showed that exposure to DE up-regulated iNOS and COX2 expression at both protein and mRNA levels in blood vessel and heart tissue. A functional study of blood vessels showed no impairment of acetylcholine (ACh) relaxation, but the sodium nitroprusside-stimulated endothelium-independent relaxation was enhanced following DE exposure. This could be partly explained by an increase in soluble guanylate cyclase expression in blood vessels. However, there was attenuated phenylephrine (PE)-stimulated vasoconstriction induced by DE exposure. An increased iNOS-derived NO production and up-regulation of COX2 could contribute to this attenuated constriction.
In conclusion, I demonstrate that DE inhalation alters the composition of atherosclerotic plaque resulting in unstable plaques that are vulnerable to rupture. Oxidative stress and iNOS up-regulation contribute to these DE exposure-induced vascular effects. We postulate that compensatory effects are activated to minimize the deleterious impact of DE exposure on vascular function.
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Keen, John A. "Investigation of the structure and function of equine laminar blood vessels." Thesis, Glasgow Caledonian University, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517934.
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Stone, Oliver Andrew. "On the origin of blood vessels : mechanisms of post-natal neovascularisation." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.520634.
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