Relevant bibliographies by topics / Intimal hyperplasia

Academic literature on the topic 'Intimal hyperplasia'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "Intimal hyperplasia"

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Yan, Huifang, Xiwei Peng, Hao Xu, Jiahuan Zhu, and Changqing Deng. "Inhibition of Aortic Intimal Hyperplasia and Vascular Smooth Muscle Proliferation and Extracellular Matrix Protein Expressions by Astragalus–Angelica Combination." Evidence-Based Complementary and Alternative Medicine 2018 (August 13, 2018): 1–15. http://dx.doi.org/10.1155/2018/1508637.

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VSMC proliferation and ECM deposition always resulted in intimal hyperplasia. Astragalus–Angelica combination has a protective effect on the cardiovascular system. The inhibition effect of different Astragalus–Angelica combination on the hyperplastic intima after vascular balloon injury in rats was investigated in this study. Astragalus–Angelica combination can inhibit the intima hyperplasia after balloon injury, in which a 1:1 ratio shows excellent results. Astragalus–Angelica combination can enhance the expression of smooth muscleα-actin (SMа-actin) and inhibit the expression of proliferating cell nuclear antigen (PCNA), cyclin D1, cyclin E, collagen I (Col-I), fibronectin (FN), and matrix metallopeptidase-9 (MMP-9) in hyperplastic intima, suggesting that Astragalus–Angelica combination can inhibit the intimal hyperplasia of blood vessels in rats. The mechanism is related to the inhibition of PI3K/Akt signaling pathway activation and thereby inhibits the phenotypic transformation and cell proliferation of VSMCs and thus inhibits the extracellular matrix (ECM) deposition of vascular wall during intimal hyperplasia.
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O'Malley, M. K. "Intimal hyperplasia." European Journal of Vascular Surgery 6, no. 4 (July 1992): 343–45. http://dx.doi.org/10.1016/s0950-821x(05)80277-4.

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Koshy, Prakash, Amanda Self, Philip J. Kadowitz, Vivian A. Fonseca, and Dennis B. McNamara. "Effects of low-dose candesartan on the rate of re-endothelialisation following vascular wound healing." Journal of the Renin-Angiotensin-Aldosterone System 2, no. 1_suppl (March 2001): S81—S83. http://dx.doi.org/10.1177/14703203010020011401.

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The wound healing response of the vascular wall to injury involves re-endothelialisation of the denuded luminal surface and thickening of the intimal area (intimal hyperplasia), as expressed by the intimal-to-medial area ratio (I/M). Candesartan, at doses of 1 mg/kg/day or higher, has been reported to attenuate the intimal hyperplastic response. We tested the hypothesis that candesartan, at doses lower than those associated with attenuation of intimal hyperplasia, may affect re-endothelialisation. New Zealand White rabbits were subjected to balloon catheter injury to the thoracic aorta. Candesartan, at doses of 50, 100, and 500 µg/kg/day, was delivered via an Alzet pump placed in the abdomen one week prior to aortic injury. There was no attenuation of the hyperplastic response of the aortic wall. However, at 50 µg/kg/day the rate of reendothelialisation was significantly increased. These data suggest that candesartan may exhibit pleiotropic effects on vascular wound healing, in addition to the well-known effect of attenuating the development of intimal hyperplasia.
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Hirai, T., Y. Korogi, M. Harada, and M. Takahashi. "Prevention of Intimal Hyperplasia by Irradiation." Acta Radiologica 37, no. 1P1 (January 1996): 229–33. http://dx.doi.org/10.1177/02841851960371p147.

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Purpose: This experimental study was designed to investigate the effect of irradiation in prevention of intimal hyperplasia. Material and Methods: Twenty rabbits were divided into 4 groups, which were irradiated with 2, 5, 10, and 20 Gy, respectively. The intima of both femoral arteries was injured by air-drying, and irradiation was performed on the unilateral side. The contralateral femoral artery served as a control. Angiograms as well as histologic specimens were obtained 1 month later. Results: Marked intimal hyperplasia was observed in all control sites. There were no significant differences in thickness of intimal hyperplasia between irradiated and control sites in groups irradiated with 2 and 5 Gy. However, in the 10-Gy- and 20-Gy-irradiated groups, intimal hyperplasia of the irradiated site was significantly suppressed. Medial thinning and dilation of the lumen were observed in the 20-Gy-irradiated group. Conclusion: Radiation may prevent intimal hyperplasia. Further investigation of the optimal dose, timing of irradiation, and long-term patency of irradiated vessels may be needed.
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ARPA, Abdurrahman, and Pınar AYDIN OZTURK. "Histopathological effects of nimodipine and pentoxifylline on the vessel wall in end-to-end anastomoses in rat carotid arteries." Journal of Experimental and Clinical Medicine 39, no. 3 (August 30, 2022): 879–83. http://dx.doi.org/10.52142/omujecm.39.3.54.

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When reperfusion following ischemia occurs, oxygen returns to the ischemic tissue, increasing free oxygen radicals and inducing paradox secondary damage. Before infarction, revascularization may influence the morbidity rate. Successful revascularization is not always achieved due to stenosis incidence, proliferation of smooth muscle cells, and intimal hyperplasia. This study compares the effects of nimodipine that prevents vasospasm and pentoxifylline, which stimulates growth factors and reduces collagen synthesis on intimal hyperplasia. Eighteen randomly selected Sprague-Dawley rats were divided into three groups: Group 1, the control group; Group 2, intraperitoneally administered nimodipine; Group 3, orally administered pentoxifylline. Their right-sided carotid arteries were used for anastomosis and the left-sided ones for the control. After a 7-day treatment, both the right and left carotid arteries were removed. In the biopsy, the lumen’s area and diameter, thickness of tunica media thickness, thrombus, edema, intimal hyperplasia, vessel wall injury, and inflammation were analyzed. Pentoxifylline was effective in preventing intimal hyperplasia and tunica intima was similar to that in untreated carotid arteries. However, nimodipine inhibited intimal hyperplasia, but it was not as effective as pentoxifylline. The effects of pentoxifylline after anastomosis should be further assessed in vasoprotective treatment taking into account its efficacy against intimal hyperplasia.
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Mesfin, G. M., M. J. Higgins, W. P. Brown, and D. Rosnick. "Cardiovascular Complications of Chronic Catheterization of the Jugular Vein in the Dog." Veterinary Pathology 25, no. 6 (November 1988): 492–502. http://dx.doi.org/10.1177/030098588802500613.

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Cardiovascular changes associated with indwelling catheters were evaluated in 51 adult beagle dogs catheterized for 4 to 9 weeks. Pathologic changes consistent with traumatic injury were in the vena cava and endocardium of the right atrium of 88% of cannulated dogs. Lesions were characterized by surface denudation and diffuse intimal thickening due to myointimal hyperplasia and deposition of extracellular matrix. Affected intima was lined by hyperplastic, poorly differentiated endothelial cells and contained round to oval cells with characteristics of smooth muscle cells. After 9 weeks, thickened intima was vascularized and composed of spindle-shaped cells and fibrillar stroma. Intimal sclerosis and localized proliferative papillary projections in the vena cava cranial to areas of myointimal hyperplasia occurred infrequently. Traumatic lesions, regardless of location or severity, did not extend below the internal elastic membrane. Inflammatory cellular responses, when present, were minimal. The location, distribution, and morphogenesis of catheter-related cardiovascular lesions distinguishes them from those induced by chemical toxicity or pharmacotoxicity.
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Bledsoe, Shelly L., Aliza T. Brown, Joseph A. Davis, Hongjiang Chen, John F. Eidt, and Mohammed M. Moursi. "Effect of Clopidogrel on Platelet Aggregation and Intimal Hyperplasia following Carotid Endarterectomy in the Rat." Vascular 13, no. 1 (January 2005): 43–49. http://dx.doi.org/10.1258/rsmvasc.13.1.43.

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Intimal hyperplasia results in significant morbidity and mortality following vascular intervention. Both platelets and elevated homocysteine have been implicated in the development of intimal hyperplasia. We previously demonstrated that a locally applied antiplatelet agent decreases the development of intimal hyperplasia. We were therefore interested in a systemic antiplatelet agent, clopidogrel. We hypothesized that clopidogrel would decrease platelet aggregation and activity and intimal hyperplasia. Male Sprague-Dawley rats underwent carotid endarterectomy (CEA) and treatment with either placebo or varying regimens of clopidogrel, including chronic, pre-CEA bolus, chronic plus pre-CEA bolus, and chronic plus post-CEA bolus; a homocystine diet was used to elevate both plasma homocysteine and the degree of intimal hyperplasia. Platelet aggregation, platelet activity, and intimal hyperplasia were then assessed. Platelet aggregation was not decreased with chronic clopidogrel; however, it was decreased with pre-CEA bolus clopidogrel. Similarly, platelet activity was not inhibited by chronic clopidogrel but was inhibited by pre-CEA and chronic plus pre-CEA bolus clopidogrel. Neither chronic, pre-CEA bolus, chronic plus pre-CEA bolus, nor chronic plus post-CEA bolus clopidogrel resulted in a decrease in intimal hyperplasia. Although pre-CEA bolus clopidogrel resulted in a decrease in both platelet aggregation and activity, it was unable to decrease the development of intimal hyperplasia at any dose. Additional factors must therefore contribute to the pathologic development of intimal hyperplasia.
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Aydin, Unal, Murat Ugurlucan, Funda Gungor, Sedat Ziyade, Bekir Inan, Maciej Banach, Yusuf Kalko, and Tahsin Yasar. "Effects of Atorvastatin on Vascular Intimal Hyperplasia: An Experimental Rodent Model." Angiology 60, no. 3 (September 15, 2008): 370–77. http://dx.doi.org/10.1177/0003319708321102.

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Introduction Vascular intimal hyperplasia is associated with increased mortality and morbidity. The authors investigated the effects of atorvastatin on vascular intimal hyperplasia. Materials and methods Rats were divided into 4 groups. Groups 1, 2, and 3 had experimental aortic injury and received intraperitoneal injection of atorvastatin, solvent, or 0.9% NaCl, respectively. Group 4 was a nonintervention (laparotomy only) control group. Animals were sacrificed after 3 weeks. Blood samples and injured aortic segment were analyzed. Results Atorvastatin administration significantly lowered total and low-density lipoprotein cholesterol levels ( P = .012 and P = .001, respectively), intima—media ratio ( P = .002), and intimal smooth muscle cell accumulation ( P < .05) in group 1. Luminal narrowing in animals in group 1 was significantly lower than that in animals in groups 2 and 3, but was higher than in animals in group 4 ( P = .009). Conclusions Atorvastatin suppresses intimal hyerplasia and aids in intimal regeneration by lowering blood lipids and intimal smooth muscle cell accumulation.
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Brody, Jerome I., and Nancy J. Pickering. "Pathobiology of intimal hyperplasia." Journal of Vascular Surgery 10, no. 5 (November 1989): 585–87. http://dx.doi.org/10.1016/0741-5214(89)90154-7.

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Haudenschild, Christian C. "Morphology of intimal hyperplasia." Journal of Vascular Surgery 10, no. 5 (November 1989): 591–92. http://dx.doi.org/10.1016/0741-5214(89)90157-2.

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Dissertations / Theses on the topic "Intimal hyperplasia"

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Chen, Changyi. "Intimal hyperplasia in endarterectomized arteries." Diss., Georgia Institute of Technology, 1996. http://hdl.handle.net/1853/25393.

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Jackson, Andrew John. "Cellular aspects of intimal hyperplasia formation." Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/2417/.

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Introduction: 12,000 infrainguinal bypass grafts are performed annually in the UK. Despite improvements in surgical technique, outcomes remain suboptimal: 20% of above knee grafts require intervention to maintain patency by 3 years. Only antiplatelet agents have been demonstrated thus far to improve graft survival. 80% of graft failure is as a result of intimal hyperplasia, an inflammatory process characterised by the proliferation and migration of vascular smooth muscle cells. Toll Like Receptors (TLR), part of the innate immune system, have been implicated in atherosclerosis formation but not investigated in a model of infrainguinal graft failure. When a vein is used as a conduit for infrainguinal bypass graft it has been exposed to ischaemic and hypoxic conditions: preliminary data has demonstrated that ischaemic vascular smooth muscle cell explants are hyperproliferative. Phospholipase C γ (PLC γ) is a signalling pathway with potential links to innate immune pathways and pathways induced by hypoxia and ischaemia. Methods: Human vein tissue was obtained from patients undergoing amputation and coronary artery bypass surgery and used for immunohistochemistry and to obtain vascular smooth muscle cells by explant method. Immunohistochemistry was used to determine the presence of TLR4 and PLC γ in human vein tissue. Specific TLR Ligands were used to determine the functional response of TLR’s in vascular smooth muscle cells as measured by Interleukin 8 ELISA. Radiolabelled Thymidine incorporation was used to measure proliferation of vascular smooth muscle cells in response to TLR4 activation, hypoxia and PLC γ inhibition. Results: TLR4 was demonstrated to be present in human vein tissue, and functionally active in human vascular smooth muscle cells. Furthermore stimulation with the specific ligand of TLR4 caused enhanced proliferation of vascular smooth muscle cells. Hypoxia (5% and 10% Oxygen) significantly enhanced proliferative responses of vascular smooth muscle cells. PLC γ was demonstrated to be present in human vein tissue, and inhibition, using U73122 in vascular smooth muscle cells reduced proliferation. Conclusion: TLR activation and hypoxia appear to enhance the proliferative responses of human vascular smooth muscle cells, a key cellular pathway of intimal hyperplasia formation and infrainguinal graft failure. Inhibition of PLC γ reduces proliferative responses. Further research is required to confirm that PLC γ is a key common pathway mediating enhances of proliferation caused by TLR activation and hypoxia.
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Religa, Piotr. "Development of intimal hyperplasia in transplant arteriosclerosis /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-448-8/.

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Porter, Karen Elizabeth. "An investigation into human vein graft intimal hyperplasia." Thesis, University of Leicester, 1995. http://hdl.handle.net/2381/34203.

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The most common cause of vein bypass graft failure in the postoperative period of 1 month to 1 year is stenosis, which occurs in up to 30% of arterial reconstructions. This thesis investigates the intimal hyperplasia underlying such lesions using a laboratory model. The first chapter reviews the current literature regarding vein graft stenoses and is followed in Chapter 2 by a brief introduction to tissue and organ culture and their usefulness as investigative research tools. Before embarking on a study of a pathological condition, Chapter 3 studies the structure of the "normal" long saphenous vein in patients undergoing arterial surgery. A degree of intimal thickening was identified in the majority of the veins in this population, the possible causes of which are discussed. The fourth chapter describes and validates an organ culture of human saphenous vein to study the vascular biology of vein graft intimal hyperplasia. Since smooth muscle cell proliferation is a pivotal event in the development of such lesions, a reliable and reproducible method of assessing proliferation was required and is described in Chapter 5. Chapter 6 investigates the effect of endothelial denudation on the development of intimal thickening, and an organ coculture study described in Chapter 7 positively identifies a soluble paracrine mediator produced by the endothelium which can promote intimal hyperplasia. The following chapters utilise variations of the coculture method to further define the precise role played by the endothelium. Chapter 8 demonstrates that isolated, cultured endothelial cells do not promote intimal thickening in denuded veins, suggesting that the normal anatomical location of endothelial cells overlying smooth muscle cells in the vein wall may be important. Chapter 9 therefore describes the development of a method to reseed endothelial cells onto denuded vein segments in order to observe whether the development of intimal hyperplasia can be restored. This proved not to be the case, possibly because the process of culturing had phenotypically altered the endothelial cells, thereby rendering them incapable of producing their paracrine factor. However, a number of other hypotheses and methods by which they could be investigated, are also discussed. The main drawback of human saphenous vein organ culture is that it is a no-flow system. There is considerable evidence in the literature to show that haemodynamics modify the normal and pathological structure and function of blood vessels. Chapter 10 therefore describes the development of an in vitro flow model of saphenous vein graft intimal hyperplasia in an attempt to model the in vivo situation more closely. The final chapter summarises the data presented in this thesis, draws conclusions, and examines prospects for future research in this field.
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Mellander, Stefan. "On cellular sources for intimal hyperplasia after vascular interventions /." Göteborg : Sahlgrenska Academy at Göteborg University, 2007. http://hdl.handle.net/2077/4440.

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Kanjickal, Deenu George. "Perivascular Drug Delivery Systems for the Inhibition of Intimal Hyperplasia." University of Akron / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=akron1133715441.

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Sivanesan, Sharmila. "Correlating geometry, haemodynamics and intimal hyperplasia in radiocephalic arteriovenous fistulae." Thesis, University of Liverpool, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337127.

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Favreau, John T. "Oscillatory wall strain reduction precedes arterial intimal hyperplasia in a murine model." Digital WPI, 2014. https://digitalcommons.wpi.edu/etd-dissertations/172.

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Cardiovascular diseases (CVD) remain the most common cause of death in the United States. Additionally, peripheral artery disease affects thousands of people each year. A major underlying cause of these diseases is the occlusion of the coronary or peripheral arteries due to arteriosclerosis. To overcome this, a number of vascular interventions have been developed including angioplasty, stenting, endarterectomies and bypass grafts. Although all of these methods are capable of restoring blood flow to the distal organ after occlusion, they are all plagued by unacceptably high restenosis rates. While the biological reactions that occur as a result of each of these methods differ, the initiating factor of both the primary atherosclerosis and subsequent failure of vascular interventions appears to be intimal hyperplasia (IH). Intimal hyperplasia is most simply defined as the expansion of multiple layers of cells internally to the internal elastic lamina of the blood vessel. This excessive cellular growth leads to arterial stenosis, plaque formation and inflammatory reactions. Despite extensive research the underlying factors that cause IH remain unclear. A quantity of research to date has implicated endothelial cell mechanosensation as the mechanism by which IH is initiated with evidence positively correlating wall shear stress with IH. Others, however, have demonstrated that changes in the stresses applied to the wall in vitro can modulate IH independent of hemodynamic shear stress. Thus, relations between wall tensile stress and IH in vivo may shed light on the underlying mechanisms of IH. Since noninvasive measurement of wall tensile stress in vivo is difficult, it is most feasible to measure oscillatory wall strain which is intimately related to wall tensile stress through the mechanical properties of the arterial wall. In this dissertation, we hypothesize that reductions in oscillatory wall strain precede the formation of intimal hyperplasia in a murine model. To test our hypothesis, we first developed a novel, high spatial and temporal resolution method to measure oscillatory wall strains in the murine common carotid artery. We validated this method both in vitro using an arterial phantom and in vivo using a murine model of abdominal aortic aneurysms. To assess relationships between strain and IH, we applied our strain measurement technique to a recently developed mouse model of IH. In this model, a suture is used to create a focal stenosis and reduce flow through the common carotid artery by 85%; resulting in proximal IH formation. Using this approach, we identified a relationship between oscillatory strain reductions and IH. Subsequent analysis demonstrated that early reductions in mechanical strain just 4 days after focal stenosis creation correlate with IH formation nearly 1 month later. Since IH is not expected to form by day 4 in this model, we went on to assess changes in gross vascular morphology at day 4. We discovered that, although strains are significantly reduced by day 4, no significant IH can be observed, suggesting that changes in wall structure are resulting in strain reductions. At day 4 post-op, we observed cellular proliferation and leukocyte recruitment to the wall without intimal hyperplasia. These studies suggest that early reductions in mechanical strain may be an important predictor of IH formation. Clinically, this relation could be important for the development of novel techniques for predicting IH formation before it becomes hemodynamically significant.
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Bastijanic, Jennifer M. "Multifunctional Biomimetic Modifications to Address Endothelialization and Intimal Hyperplasia in Vascular Grafts." Case Western Reserve University School of Graduate Studies / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=case1428065969.

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Dunlop, Paul. "Clincial and laboratory aspects of intimal hyperplasia in lower limb bypass grafts." Thesis, University of Leicester, 1995. http://hdl.handle.net/2381/34332.

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This thesis examines aspects of intimal hyperplasia in infrainguinal bypass grafts. There are 3 introductory chapters. Chapter 1 describes the aetiology and treatment of lower limb vascular disease, with particular reference to atherosclerosis. Chapter 2 is a review of the literature regarding the vascular biology of intimal hyperplasia. Chapter 3 is a review of the techniques of cell and organ culture used in the study of vascular disorders. Chapter 4 is composed of four clinical studies of infrainguinal grafts performed at the Leicester Royal Infirmary. There is a prospective study of the long-term benefit of vein graft surveillance. This is followed by a study of the long-term results of percutaneous transluminal angioplasty of vein graft stenoses. A retrospective review of the outcome of polytetrafluoroethylene (PTFE) grafts used in lower limb bypass surgery forms the 3rd part of the chapter. This is followed by a prospective study of the benefits of graft surveillance for synthetic grafts. The next 3 chapters are laboratory based. Chapter 5 looks at the effect of various growth factors on the proliferation of human saphenous vein smooth muscle cells, the ceils involved in the intimal hyperplasia of vein graft stenoses. Chapter 6 looks at aspects of platelet- derived growth factor on the proliferation seen in an organ culture model of human saphenous vein. Chapter 7 examines 2 different ways of incorporating flow in an organ culture of human saphenous vein and compares the effects of high and low shear rates on the development of intimal hyperplasia in the model. In the final chapter, the experimental results are summarised and possible future work relating to the thesis is discussed.
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Books on the topic "Intimal hyperplasia"

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B, Dobrin Philip, ed. Intimal hyperplasia. Austin: R.G. Landes Co., 1994.

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Davenport, Kathryn. Drug delivery coatings for nitinol stents to prevent intimal hyperplasia. Birmingham: University of Birmingham, 2002.

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Oskar, Klotz. Concerning compensatory hyperplasia of the intima. [S.l: s.n., 1995.

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Pharmacologic suppression of intimal hyperplasia. Austin, Tex: R.G. Landes, 1993.

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Lamuraglia, G. Photodynamic Therapy of Intimal Hyperplasia. Chapman & Hall, 1997.

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Cheema, Asim N. Arterial repair after balloon angioplasty and stenting: Role of extracellular matrix and adventitial microvessels in the development of intimal hyperplasia and restenosis. 2004.

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Alchi, Bassam, and David Jayne. The patient with antiphospholipid syndrome with or without lupus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0164.

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Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent arterial or venous thrombosis and/or pregnancy loss, accompanied by laboratory evidence of antiphospholipid antibodies (aPL), namely anticardiolipin antibodies (aCL), lupus anticoagulant (LA), and antibodies directed against beta-2 glycoprotein 1 (β‎‎‎2GP1). APS may occur as a ‘primary’ form, ‘antiphospholipid syndrome,’ without any known systemic disease or may occur in the context of systemic lupus erythematosus (SLE), ‘SLE-related APS’. APS may affect any organ system and displays a broad spectrum of thrombotic manifestations, ranging from isolated lower extremity deep vein thrombosis to the ‘thrombotic storm’ observed in catastrophic antiphospholipid syndrome. Less frequently, patients present with non-thrombotic manifestations (e.g. thrombocytopaenia, livedo reticularis, pulmonary hypertension, valvular heart disease, chorea, and recurrent fetal loss).The kidney is a major target organ in both primary and SLE-related APS. Renal involvement is typically caused by thrombosis occurring at any location within the renal vasculature, leading to diverse effects, depending on the size, type, and site of vessel involved. The renal manifestations of APS include renal artery stenosis and/or renovascular hypertension, renal infarction, APS nephropathy (APSN), renal vein thrombosis, allograft vasculopathy and vascular thrombosis, and thrombosis of dialysis access.Typical vascular lesions of APSN may be acute, the so-called thrombotic microangiopathy, and/or chronic, such as arteriosclerosis, fibrous intimal hyperplasia, tubular thyroidization, and focal cortical atrophy. The spectrum of renal lesions includes non-thrombotic conditions, such as glomerulonephritis. Furthermore, renal manifestations of APS may coexist with other pathologies, especially proliferative lupus nephritis.Early diagnosis of APS requires a high degree of clinical suspicion. The diagnosis requires one clinical (vascular thrombosis or pregnancy morbidity) and at least one laboratory (LA, aCL, and/or anti-β‎‎‎2GP1) criterion, positive on repeated testing.The aetiology of APS is not known. Although aPL are diagnostic of, and pathogenic in, APS, a ‘second hit’ (usually an inflammatory event) may trigger thrombosis in APS. The pathogenesis of the thrombotic tendency in APS remains to be elucidated, but may involve a combination of autoantibody-mediated dysregulation of coagulation, platelet activation, and endothelial injury.Treatment of APS remains centred on anticoagulation; however, it has also included the use of corticosteroids and other immunosuppressive therapy. The prognosis of patients with primary APS is variable and unpredictable. The presence of APS increases morbidity (renal and cerebral) and mortality of SLE patients.
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Dasgupta, Bhaskar. Polymyalgia rheumatica. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0134.

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This chapter reviews advances in pathogenesis; European League Against Rheumatism/American College of Rheumatology (EULAR/ACR) classification criteria with clinical, laboratory, and ultrasound criteria for classification as polymyalgia rheumatica (PMR); the heterogeneity and overlap between PMR, inflammatory arthritis, and large-vessel vasculitis as illustrated by representative cases; recent guidelines on early and correct recognition, investigations, and management of PMR; the scope of disease-modifying agents; socio-economic impact, outcomes, and patient experience in PMR. It also discusses areas for future research including clinical trials with biological agents and newer steroid formulations, standardized outcome assessments, and the search for better biomarkers in PMR. PMR is one of the common inflammatory rheumatic diseases of older people and represents a frequent indication for long-term glucocorticoid (GC) therapy. It is characterized by abrupt-onset pain and stiffness of the shoulder and pelvic girdle muscles. Its management is subject to wide variations of clinical practice and it is managed in primary or secondary care by general practitioners (GPs), rheumatologists, and non-rheumatologists. The evaluation of PMR can be challenging, as many clinical and laboratory features may also be present in other conditions, including other rheumatological diseases, infection, and neoplasia. PMR is usually diagnosed in the primary care setting, but standard clinical investigations and referral pathways for suspected PMR are unclear. The response to standardized therapy is heterogeneous, and a significant proportion of patients do not respond completely. There is also an overlap with inflammatory arthritis and large-vessel vasculitis for which adjuvant disease-modifying medications are often used. Prolonged corticosteroid therapy is associated with a variety of side effects, especially when high-dose glucocorticoid therapy is employed. Giant cell arteritis (GCA) is also often linked to PMR. It is a vasculitis of large- and medium-sized vessels causing critical ischaemia. GCA is a medical emergency because of the high incidence of neuro-ophthalmic complications. Both conditions are associated with a systemic inflammatory response and constitutional symptoms. The pathogenesis is unclear. The initiating step may be the recognition of an infectious agent by aberrantly activated dendritic cells. The key cell types involved are CD4+ T cells and macrophages giving rise to key cytokines such as interferon-γ‎ (implicated in granuloma formation), PDGF (intimal hyperplasia), and interleukin (IL)-6 (key to the systemic response). The pathogenesis of PMR may be similar to that of GCA, although PMR exhibits less clinical vascular involvement. The mainstay of therapy is corticosteroids, and disease-modifying therapy is currently indicated in relapsing disease.
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Book chapters on the topic "Intimal hyperplasia"

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Tanner, Felix C., and Thomas F. Lüscher. "Pathophysiology of Intimal Hyperplasia." In Radiology of Peripheral Vascular Diseases, 29–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-56956-2_4.

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Purcell, Seth T., Shruti Rao, and Ruth L. Bush. "Understanding Intimal Hyperplasia Biology in Hemodialysis Access." In Hemodialysis Access, 245–48. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-40061-7_28.

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Sheng, Neha, and Brittany Mead. "Hemodynamics, Atherosclerosis, Intimal Hyperplasia, and Wound Healing." In The Vascular Surgery In-Training Examination Review (VSITE), 59–73. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-24121-5_5.

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McNamara, Dennis B., Harmeet Aurora, Brenda Bedi, Thomas Osgood, Raphael Santiago, I.-L. Chen, Philip J. Kadowitz, and Donald L. Akers. "Nitric Oxide: An Endogenous Inhibitor of Balloon Catheter-Induced Intimal Hyperplasia." In Biochemical, Pharmacological, and Clinical Aspects of Nitric Oxide, 175–80. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1903-4_21.

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Wu, Jiacheng, and Kevin W. Cassel. "Observer-Based Feedback Control of a Mathematical Model of Intimal Hyperplasia." In 2013 Proceedings of the Conference on Control and its Applications, 184–90. Philadelphia, PA: Society for Industrial and Applied Mathematics, 2013. http://dx.doi.org/10.1137/1.9781611973273.25.

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Geary, Randolph L., and Stephen M. Schwartz. "Intimal Hyperplasia is the Wrong Target: Restenosis as a Failure of Remodeling." In Arterial Remodeling: A Critical Factor in Restenosis, 199–230. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-6079-1_11.

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Landymore, R. W., M. A. MacAulay, B. Sheridan, and C. Cameron. "Eicosapentaenoic Acid, Persantine, and Aspirin for the Prevention of Vein Graft Intimal Hyperplasia." In Coronary Artery Surgery in the Nineties, 179. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-45622-0_35.

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Choi, Eric T., Niraj Sehgal, Shaping Sun, Jeffrey Trachtenberg, Una S. Ryan, and Allan D. Callow. "A Novel Approach to Preventing Intimal Hyperplasia: Inhibition of Smooth Muscle Cell Migration with Enalapril." In Modern Vascular Surgery, 28–40. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4612-2632-1_3.

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Thankam, Finosh G., Victoria E. D. Wilson, and Devendra K. Agrawal. "Preclinical Models of Intimal Hyperplasia and Restenosis to Predict Clinical Events and Develop Novel Therapies." In Biomedical Translational Research, 427–45. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-4345-3_26.

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Esato, Kensuke, Nobuya Zempo, Masaki O-hara, Kentaroh Fujioka, Takayuki Kuga, and Hiroaki Takenaka. "Effects of Morphology of Distal Anastomosis Immediately After Surgery on Intimal Hyperplasia in Femoropopliteal Bypass Graft." In Modern Vascular Surgery, 314–21. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2946-9_26.

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Conference papers on the topic "Intimal hyperplasia"

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Berceli, Scott A., and Alexander W. Clowes. "Intimal Hyperplasia — Development and Regression in Response to Fluid Shear." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0381.

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Abstract The long-term success of autogenous and prosthetic bypass grafts is dictated by the development and subsequent progression of intimal hyperplasia. While recent advances in vascular biology continue to improve our understanding of the mechanisms which control this process, available clinical therapies which treat or slow its progression have yet to be identified. Among the factors which influence the development of intimal hyperplasia are the physical forces exposed to bypass conduits. As initially described by Glagov et al. (1988) and confirmed by multiple other investigators, the biology of the hyperplastic response is modulated by the imposed fluid shearing forces While our ability to modulate the local hemodynamics of bypass conduits is limited, an understanding of how these forces govern the healing response can serve as a basis for future pharmacological therapies. In our laboratory we have employed a primate model to understand the influence of shear stress on the development of intimal hyperplasia in PTFE grafts.
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Tran-Son-Tay, Roger, Minki Hwang, Scott A. Berceli, C. Keith Ozaki, and Marc Garbey. "A Model of Vein Graft Intimal Hyperplasia." In 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4353667.

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Harper, R. A., I. F. Lane, C. M. Backhouse, C. N. McCollum, and A. C. Meek. "PLATELET DEPOSITION AND PSEUDO-INTIMAL HYPERPLASIA IN PROSTHETIC VASCULAR GRAFTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643088.

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Platelet and fibrin accumulation in arterial grafts may cause pseudo-intimal hyperplasia and graft occlusion. The relationship between the rate of post-operative platelet accumulation and subsequent pseudo-intimal hyperplasia has been studied in prosthetic grafts implanted in greyhounds.The femoral artery in 30 greyhounds was replaced by a 6cm length of 6mm PTFE. Autologous 111In-platelet deposition over the graft was measured by probe and ratemeter for 7 days and radioactivity compared to the contralateral thigh. The daily increase in this ratio graft over reference was calculated as the Thrombogenicity Index (TI). Grafts were removed at 8 weeks and sectioned at 5, 30 and 55mm for measurement of pseudo-intimal thickening by grid microscopy.The animals subsequently developing occlusion or pseudo-intimal harrowing of greater than 50% of the lumen had a markedly greater TI of 0.22±0.027 compared to 0.03±0.019 in the 23 grafts maintaining wide patency (p<0.05). TI was highest in the 4 grafts which occluded at 0.3110.09 compared to 0.04±0.02 in the 26 that remained patent (p<0.01). There was a highly significant correlation (r=0.69) between post-operative TI and subsequent pseudo-intimal hyperplasia (p<0.001).Platelet deposition in the early post-operative period appears to promote the development of progressive pseudo-intimal thickening and ultimate occlusion
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Kopacz, Adrian M., Brandon J. Tefft, Shu Q. Liu, and Wing K. Liu. "Modeling of Endothelial Cell Adhesion Dynamics Modulated by Molecular Engineering." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13269.

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Vascular thrombosis, intimal hyperplasia, and atherosclerosis are common disorders affecting a very large portion of the human population. A potential reduction in these disorders will elicit a significant impact. It has been shown that endothelial cells play a critical role in protecting blood vessels against the formation of thrombosis and atherosclerosis. Hence, a successful endothelial cell lining of arterial constructs will prevent intimal hyperplasia in reconstructed arteries. However, in practice endothelial cells often detach from reconstructed arteries due to weak adhesion strength, hindering the effectiveness of endothelial cell lining.
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Ballyk, Peter D., Matadial Ojha, and Colin Walsh. "Comparing the Influence of Graft Angle on Peri-Anastomotic Wall and Fluid Mechanics." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0248.

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Abstract Distal anastomotic intimal hyperplasia (DAIH) can lead to outflow stenosis of vascular bypass grafts. In end-to-side graft-artery anastomoses, two separate regions of DAIH have been identified: (i) the suture line and (ii) the floor of the anastomosis across from the suture line (Bassiouny et al., 1992). Suture-line intimal thickening seems to be associated with post-surgical healing and influenced by graft-artery compliance mismatch (Trubel et al., 1994), while floor hyperplasia appears to be linked to fluid mechanical phenomena, such as temporal variations in wall shear stress (Ojha, 1994).
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Chesler, Naomi C., Nathan Brewton, and David N. Ku. "Alterations in Endothelial Permeability After Intravascular Intervention." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0178.

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Abstract Intravascular interventions such as balloon embolectomy are effective in removing arterial and venous thrombi and emboli but lead to endothelial injury. The clinical sequelae of this injury include intimal hyperplasia and renewed clot formation. Changes in endothelial permeability after intravascular intervention may influence the development of intimal hyperplasia. To assess the extent and type of injury engendered by the Fogarty embolectomy catheter, the permeability of the endothelium after sham embolectomy (catheter withdrawal in the absence of a thrombus or thrombus model) was measured in porcine carotid arteries. The maximum shear force required for catheter withdrawal was also measured. The changes in permeability resulting from a prototype textured balloon catheter (Applied Medical, Laguna Hills, CA) were measured for comparison to the Fogarty catheter. While the textured balloon showed a distinct pattern of increased permeability and required significantly more force to withdraw at a set balloon pressure than a Fogarty balloon catheter (p &lt; 0.02), there was no difference in permeability after three balloon inflation and removal cycles. This study demonstrates useful techniques for comparing catheter designs which may be clinically relevant to intimal hyperplasia and rethrombosis after intravascular intervention.
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Gabeler, Edward E., Richard van Hillegersberg, R. G. Statius van Eps, Wim Sluiter, D. Hayes, and Hero van Urk. "Endovascular photodynamic therapy inhibits intimal hyperplasia PTA in a rat model." In EOS/SPIE European Biomedical Optics Week, edited by Patrick Brouwer. SPIE, 2001. http://dx.doi.org/10.1117/12.413698.

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Lucas, Alexandra, Masis Perk, Yue Wen, Fermin O. Tio, and Wolfgang Schneider. "Laser-induced fluorescence identification of intimal hyperplasia after intravascular stent implantation." In OE/LASE '92, edited by George S. Abela. SPIE, 1992. http://dx.doi.org/10.1117/12.137302.

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Ortu, Paolo, Glenn M. LaMuraglia, Walter G. Roberts, Kevin T. Schomacker, Thomas F. Deutsch, Thomas J. Flotte, and Tayyaba Hasan. "Photochemical effects of chloroaluminum-sulfonated phthalocyanine in arteries with intimal hyperplasia." In OE/LASE '92, edited by Steven L. Jacques. SPIE, 1992. http://dx.doi.org/10.1117/12.137458.

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LaMuraglia, Glenn M., N. R. ChandraSekar, Thomas J. Flotte, and Tayyaba Hasan. "Long-term healing of photodynamic therapy: treatment of experimental intimal hyperplasia." In OE/LASE '94, edited by George S. Abela. SPIE, 1994. http://dx.doi.org/10.1117/12.179926.

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