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Roy, Sébastien. "Rôle de la signalisation des Bmp au sein des cellules mésenchymateuses dans le maintien de l'homéostasie gastrique." Thèse, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/11429.
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Les bones morphogenetic protein (Bmp) sont des morphogènes qui jouent des rôles sur la prolifération et la différenciation cellulaire. La perte de signalisation dans cette voie est associée à la polypose juvénile familiale et à un risque accru de cancer gastrique. Elle est aussi associée avec l’inflammation et la guérison des tissus. Il est montré qu’au niveau de l’estomac, les ligands et les récepteurs de la signalisation des Bmp sont exprimés dans les compartiments épithéliaux et mésenchymateux. Les différents modèles animaux développés ont confirmé l’importance de cette signalisation dans la carcinogenèse gastrique. Cependant, ces modèles causent une perte de signalisation dans l’ensemble de la muqueuse gastrique et ne réussissent pas à montrer un mécanisme. Parallèlement, notre laboratoire a montré qu’une perte de signalisation de la voie des Bmp, exclusivement dans le compartiment épithélial, ne développe pas les phénotypes associés à la progression du cancer gastrique. Ce résultat suggère que les cellules mésenchymateuses pourraient être la clé de l’importance de la signalisation des Bmp dans l’estomac. Afin de mettre en lumière le rôle de la signalisation des Bmp dans le compartiment mésenchymateux, des souris qui perdent de façon spécifique le récepteur de type 1a des Bmp dans ce compartiment ont été généré (Bmpr1aMES). Il semble que la perte de signalisation des Bmp induit au niveau du mésenchyme une modification du comportement et une activation des fibroblastes en myofibroblastes. Cette modification produit également un microenvironnement (matrices, facteurs de croissance, cytokines, interleukines) propice au développement du cancer et induire des modifications importantes de l’épithélium et un appel de cellules immunitaires. Cet environnement semble être suffisant pour réduire de façon importante le nombre de cellules endocriniennes et de cellules pariétales dans l’épithélium gastrique. Il semble que la perte mésenchymateuse de signalisation des Bmp au niveau gastrique entraîne le développement d’une métaplasie au niveau de l’estomac des souris, une hyperplasie atypique qui évolue jusqu'à une dysplasie accompagnée d’une desmoplasie importante. Mes travaux ont également démontré que, dans ce contexte, une mutation oncogénique, comme la perte de Trp53, pourrait devenir maligne. En conclusion, au sein du mésenchyme, la signalisation des Bmp est importante pour le maintien de celui-ci dans un état sain. Il est probable qu’elle joue un rôle important dans le retour à l’état normal suivant les gastrites. Sa perte rend l’estomac des souris fragile au développement d’adénomes.Abstract : Bone morphogenetic proteins (Bmp) play roles in the proliferation and differentiation. It is also associated with inflammation and tissue repair. Disruption of signaling in this pathway is associated with familial juvenile polyposis and an increase risk of gastric cancer. It has been shown that in the stomach, Bmp signaling is bidirectional. Meaning that ligands and receptors are expressed in both the epithelial and stromal compartments. Gastric abrogation animal models of the Bmp signaling pathway have confirmed the importance of this signaling in gastric carcinogenesis. However these models cause a loss of signaling in both compartments of the gastric mucosa, and the mechanism of action for this has yet been undefined. Previous work by a student in our laboratory provided a model of loss of the Bmp signaling pathway exclusively in the epithelial compartment. This model does not develop phenotypes associated with the progression of gastric cancer, suggesting, that the stromal compartment is the key in tumorigenesis by Bmp signaling in the stomach. To further test this hypothesis, we generated mice with a stromal compartment-specific loss of type1a BMP receptor (Bmpr1aMES). It appears that this deletion in the stroma induced behavior alteration with activation of fibroblasts into myofibroblasts. This change also produces a microenvironment (matrix, growth factors, cytokines, and interleukins) that is conducive to the development of cancer and induces significant modifications of the epithelium as well as a recruitment of immune cells. This microenvironment seems to be sufficient to significantly reduce the number of endocrine cells and parietal cells in the gastric epithelium. It seems that the loss of stromal Bmp signaling in the mice’s stomachs causes development of metaplasia; atypical hyperplasia that progresses to dysplasia accompanied by a significant desmoplasia. My work also shows that in this environment an oncogenic mutation such as the loss of Trp53 may become malignant. In conclusion, in the stromal compartment, Bmp signaling is important for maintaining a healthy state. It is probably involved in the return to the normal state following gastritis, and its loss makes the mouse stomach susceptible to adenoma development.
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Dahllöf, Göran. "Phenytoin-induced gingival overgrowth in epileptic children a clinical, histological and biochemical study /." Stockholm : [Karolinska Institutet], 1986. http://catalog.hathitrust.org/api/volumes/oclc/13674550.html.
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Sadaghianloo, Nirvana. "Rôle de l’hypoxie et du métabolisme dans la maturation des fistules artério-veineuses pour hémodialyse." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4017.
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L’accès vasculaire pour hémodialyse est à la fois la ligne de vie et le talon d’Achille des malades souffrant d’insuffisance rénale terminale. La fistule artério-veineuse (FAV), accès vasculaire pourtant recommandé en premier intention, présente des résultats loin d’être optimaux : 50% des FAV crées présenteront une dysfonction la 1ère année. Lors de la création d’une FAV, la paroi de la veine doit s’adapter à de nouveaux paramètres. D’une part, des modifications hémodynamiques sont responsables de modifications de la matrice extracellulaire et de lésions endothéliales. D’autre part, la dissection et la manipulation de la veine par le chirurgien, impliquant la rupture des vasa vasorum, causent une ischémie de la paroi et un stress oxydatif. In fine, la migration et la prolifération des cellules vasculaires participent à l’épaississement de la paroi par une hyperplasie néointimale (HNI) excessive, entraînant une sténose et un dysfonctionnement de la FAV. Mon projet de thèse s’articulait autour de 3 objectifs: 1) Montrer que la non-dissection de la veine évite l’apparition d’HNI, 2) Cibler l’hypoxie cellulaire pour inhiber l’HNI et 3) Evaluer la régulation par l’hypoxie d’une protéine de la matrice extracellulaire, l’ostéopontine (OPN), dans l’HNI.Résultats : 1) Nous avons développé la technique RADAR (Radial Artery Deviation And Reimplantation) de création de FAV, dont le concept est d’éviter la dissection chirurgicale de la veine en détournant l’artère, et ainsi limiter l’HNI. Les résultats de la première cohorte de malades ont montré une quasi-disparition de la sténose veineuse par HNI. Afin d’étudier l’hémodynamique de RADAR, en collaboration avec l’Université Yale, nous avons créé chez le rat un modèle de FAV avec détournement de l’artère (mimant RADAR). Grâce à des mesures moléculaires, histologiques, et d’imagerie, associées aux résultats à long terme de la cohorte RADAR, nous avons confirmé que l’HNI veineuse est inhibée et montré le rôle du flux laminaire dans ce montage. 2) Nous avons cherché une substance pharmacologique qui, appliquée dès la chirurgie, ciblerait HIF pour inhiber l’INH. In vitro, nous avons étudié la réponse des différents types de cellules vasculaires (endothéliales, musculaires lisses, fibroblastes), sous l’action de l’hypoxie, de 5 médicaments (Desferrioxamine, Everolimus, Metformine, N-Acetylcystéine, Topotecan) influençant HIF et le métabolisme cellulaire, et de 3 invalidations géniques (siRNA HIF1alpha, siRNA HIF2alpha, siRNA, HIF1/2alpha). Trois de ces substances et 1 invalidation génique agissaient sur le métabolisme et la prolifération de nos cellules. Nous les avons donc testé sur un modèle murin de FAV: 2 substances et l’invalidation de HIF1/2 ont montré une inhibition significative de l’HNI. 3) Nous avons étudié l’expression d’OPN dans les cellules vasculaires sous l’effet de l’hypoxie. Si les cellules vasculaires veineuses en monoculture n’exprimaient ni ne sécrétaient d’OPN sous l’effet de l’hypoxie, la co-culture de ces trois lignées permettaient la sécrétion d’OPN induite par l’hypoxie. Nous avons ainsi montré que l’hypoxie, le métabolisme et les paramètres du flux sont impliqués dans le développement de l’HNI lors de la maturation de la FAVFor hemodialysis patients, their vascular access is both their life line and their Achille’s heel. Despite being recommended as a primary vascular access, the arteriovenous fistula (AVF) shows sub-optimal results, with about 50% of patients needing a revision during the year following creation. As the AVF is created, the venous wall must adapt to new environment. While hemodynamic changes are responsible for the adaptation of the extracellular matrix and activation of the endothelium, surgical dissection and mobilization of the vein disrupt the vasa vasorum, causing wall ischemia and oxidative stress. As a consequence, migration and proliferation of vascular cells participate in venous wall thickening by a mechanism of neointimal hyperplasia (NH). When aggressive, NH causes stenosis and AVF dysfunction. I had 3 aims during my thesis : 1) To show that minimal dissection of the vein inhibits NH, 2) to target the Hypoxia Inducible Factor (HIF) pathway to inhibit NH, and 3) to understand the hypoxic regulation of an adhesion molecule, osteopontin (OPN), in NH. Results: 1) We developed the Radial Artery Deviation And Reimplantation (RADAR) technique of AVF creation, where we avoid venous dissection to prevent NH. The first cohort of patients showed only 2% of venous stenosis. To study RADAR hemodynamics, in collaboration with Yale University, we created a rat model of artery-to-vein AVF that mimics RADAR geometry. By means of molecular, histological and imaging analysis, associated to the long-term outcome of the RADAR cohort, we confirmed that this configuration shows laminar flow and limits NH.2) We looked for a way to inhibit HIF during surgery by local delivery of a small molecule. In vitro, we analyzed the behavior of vascular cells (endothelial, smooth muscle and fibroblasts) in response to hypoxia, to 1 of 5 compounds regulating HIF or metabolism (Desferrioxamine, Everolimus, Metformine, N-Acetylcysteine, Topotecan), and to HIF silencing. Three of these compounds and HIF silencing had a significant impact on the metabolism and/or proliferation of our cells. We therefore tested them in a mouse model of AVF, to show that 2 compounds and HIF silencing inhibited NH. 3) We analyzed the expression of OPN in our cells in hypoxia. While in monoculture, they did not express or secrete OPN in response to hypoxia, co-culture of the same cell lines induced OPN secretion in hypoxia. We could show that hypoxia, metabolism and flow parameters are intricate mechanisms responsible for the development of NH during AVF maturation
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Ashton, R. E. "Retinoid induced epidermal hyperplasia." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596189.
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Bonfig, Walter, Friedhelm Roehl, Stefan Riedl, Jürgen Brämswig, Annette Richter-Unruh, Angela Hübner, Susanne Fricke-Otto, et al. "Sodium Chloride Supplementation Is Not Routinely Performed in the Majority of German and Austrian Infants with Classic Salt-Wasting Congenital Adrenal Hyperplasia and Has No Effect on Linear Growth and Hydrocortisone or Fludrocortisone Dose." Karger, 2018. https://tud.qucosa.de/id/qucosa%3A70638.
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Introduction: Sodium chloride supplementation in saltwasting congenital adrenal hyperplasia (CAH) is generally recommended in infants, but its implementation in routine care is very heterogeneous. Objective: To evaluate oral sodium chloride supplementation, growth, and hydrocortisone and fludrocortisone dose in infants with salt-wasting CAH due to 21-hydroxylase in 311 infants from the AQUAPE CAH database. Results: Of 358 patients with classic CAH born between 1999 and 2015, 311 patients had salt-wasting CAH (133 females, 178 males). Of these, 86 patients (27.7%) received oral sodium chloride supplementation in a mean dose of 0.9 ± 1.4 mmol/kg/day (excluding nutritional sodium content) during the first year of life. 225 patients (72.3%) were not treated with sodium chloride. The percentage of sodium chloride-supplemented patients rose from 15.2% in children born 1999–2004 to 37.5% in children born 2011–2015. Sodium chloride-supplemented and -unsupplemented infants did not significantly differ in hydrocortisone and fludrocortisone dose, target height-corrected height-SDS, and BMI-SDS during the first 2 years of life. Conclusion: In the AQUAPE CAH database, approximately one-third of infants with salt-wasting CAH receive sodium chloride supplementation. Sodium chloride supplementation is performed more frequently in recent years. However, salt supplementation had no influence on growth, daily fludrocortisone and hydrocortisone dose, and frequency of adrenal crisis.
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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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Gallos, Ioannis D. "Management & prognosis of endometrial hyperplasia." Thesis, University of Birmingham, 2014. http://etheses.bham.ac.uk//id/eprint/5157/.
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This thesis investigates the management and prognosis of endometrial hyperplasia. The literature on conservative therapies for endometrial hyperplasia is systematically reviewed and a meta-analysis is performed to identify the most effective treatment. Further meta-analysis is performed for young women with severe endometrial hyperplasia or cancer to explore the effectiveness of fertility-sparing treatment. A national survey of Gynaecologists is performed to evaluate current and the need for further research. A large cohort study is included that defines the regression and relapse of endometrial hyperplasia with two popular conservative therapies, the Levonorgestrel-releasing intrauterine system (LNG-IUS) and oral progestogens. The LNG-IUS is found to induce regression more often with fewer events of relapse than oral progestogens. A prediction model based on clinical characteristics and biomarkers finds that morbid obesity is an independent predictor for relapse. This research has major implications for clinical practice and a national guideline in process is based on its findings.
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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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Clarke, Michael Joseph. "Clinical and laboratory aspects of myointimal hyperplasia." Thesis, University of Newcastle Upon Tyne, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366584.
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Robert, Grégoire. "Rôle de l'inflammation prostatique chronique dans le développement de l'hyperplasie bénigne de la prostate." Thesis, Paris Est, 2011. http://www.theses.fr/2011PEST0099.
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Eedes, Christopher Robert, and Christopher Robert Eedes. "Atypical reactive lymphoid hyperplasia : a 5 year study with analysis of 10 cases for latent Epstein-Barr virus infection by in situ hybridization and immunohistochemistry." Master's thesis, University of Cape Town, 1994. http://hdl.handle.net/11427/25581.
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AIMS OF THE STUDY: 1. To perform a retrospective, epidemiological analysis of cases of reactive lymphadenopathy and atypical reactive lymphoid hyperplasia (ARLH) received in the Department of Anatomical Pathology, UCT and GSH, over a 5 year period, in order to determine the number of cases of ARLH, and the frequency of the various subtypes of reactive lymphoid. hyperplasia, so as to provide base-line information for further studies. 2. To set up IN SITU HYBRIDIZATION (ISH) for detection of Epstein-Barr virus (EBV)-encoded RNA's (EBERs) in latently infected cells in selected cases, to determine if virus is present in ARLH. 3. To perform immunohistochemical analysis for the detection of EBY-derived latent membrane protein (LMP) in those cases subjected to ISH.
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Jia, Guang. "MR imaging biomarkers for benign prostatic hyperplasia pharmacotherapy." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1164686290.
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Swords, Francesca. "Activation of the adrenocorticotropin pathway in adrenal hyperplasia." Thesis, Queen Mary, University of London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411793.
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Sivridis, E. "An immunohistochemical study of endometrial hyperplasia and neoplasia." Thesis, University of Manchester, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374781.
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May, Brenda. "Psychosocial outcome in women with congenital adrenal hyperplasia." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287994.
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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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DOUVIZY, ISABELLE. "Lymphomes cutanes et hyperplasie pseudo-epitheliomateuse." Clermont-Ferrand 1, 1993. http://www.theses.fr/1993CLF1M012.
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MOURET, SYLVIE. "Hyperplasie angiolymphoide avec eosinophilie et nephropathie." Amiens, 1989. http://www.theses.fr/1989AMIEM138.
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Haider, Ursula G. B. "Resveratrol Attenuates Vascular Smooth Muscle Cell Hypertrophy and Hyperplasia." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-8688.
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三井, 伸二, Masahide Takahashi, Masatoshi Ichihara, Sayaka Sobue, Kaori Ushida, Atsushi Enomoto, Masato Asai, et al. "Epidermal Hyperplasia and Appendage Abnormalities in Mice Lacking CD109." Thesis, Elsevier, 2012. http://hdl.handle.net/2237/17140.
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Ortova, Gut Marta. "Gastric hyperplasia in MN, carbonic anhydrase IX deficient mice." [S.l.] : [s.n.], 2001. http://www.diss.fu-berlin.de/2002/35/index.html.
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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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Lajić, Svetlana. "Molecular analysis of mutated P450c21 in congenital adrenal hyperplasia /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980604laji.
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Nordenström, Anna. "Congenital adrenal hyperplasia, CYP21 deficiency, screening and clinical aspects /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4670-1/.
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Chan, Siew-luen, and 陳兆麟. "A cephalometric study of dentoalveolar hyperplasia in dentofacial deformities." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1994. http://hub.hku.hk/bib/B31953979.
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Chan, Siew-luen. "A cephalometric study of dentoalveolar hyperplasia in dentofacial deformities." [Hong Kong] : University of Hong Kong, 1994. http://sunzi.lib.hku.hk/hkuto/record.jsp?B14019930.
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Nguyen, Trang Nguyen. "Localized Juvenile Spongiotic Gingival Hyperplasia: Clinicopathologic and Microbiologic Correlations." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1498257896007226.
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STREBELLE, DANIEL. "Cystadenome pancretique associe a nodule thyroidien froid, hyperplasie nodulaire parathyroidienne, hyperplasie des surrenales : a propos d'un cas." Lille 2, 1991. http://www.theses.fr/1991LIL2M003.
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MONNIER, BEAUVIR LAURENCE. "Hyperplasie lymphoide du tube digestif chez l'enfant." Lyon 1, 1993. http://www.theses.fr/1993LYO1M018.
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Fernandes, Ancilla W. "Evaluating diagnostic and treatment modalities in the management of benign prostatic hyperplasia in the Veterans Administration population." Morgantown, W. Va. : [West Virginia University Libraries], 2000. http://etd.wvu.edu/templates/showETD.cfm?recnum=1543.
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Thesis (M.S.)--West Virginia University, 2000.Title from document title page. Document formatted into pages; contains ix, 154 p. : ill. Includes abstract. Includes bibliographical references (p. 137-143).
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Ambrosini, Gina L. "Dietary risk factors for prostate cancer and benign prostatic hyperplasia." University of Western Australia. School of Population Health, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0135.
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[Truncated abstract] This thesis examines the potential role of dietary intake in the development of two common conditions affecting the prostate gland; prostate cancer and benign prostatic hyperplasia (BPH). Diet is of interest as a potential risk factor for prostate cancer because of geographical variations in prostate cancer incidence and increased prostate cancer risks associated with migration from Asian to western countries. Some geographical variation has been suggested for BPH, but this is less certain. However, both prostate cancer and BPH have potential links with diet through their positive associations with sex hormone levels, metabolic syndrome, increased insulin levels and chronic inflammation. In addition, zinc is an essential dietary micronutrient required for semen production in the prostate gland. The original work for this thesis is presented in six manuscripts of which, four have been published in peer-reviewed journals (at the time of thesis completion). BPH investigated in this thesis is defined as surgically-treated BPH. The following hypotheses were investigated. Regarding foods, nutrients and the risk of prostate cancer and BPH: 1. Increasing intakes of fruits, vegetables and zinc are inversely associated with the risk of prostate cancer and BPH 2. Increasing intakes of total fat and calcium are positively associated with the risk of prostate cancer and BPH. 3. Dietary patterns characterised by high meat, processed meat, calcium and fat content are positively associated with the risk of prostate cancer and BPH. 4. Dietary patterns characterised by high fruit and vegetable and low meat content are inversely associated with the risk of prostate cancer and BPH. v Regarding methodological issues related to the study of diet-disease relationships: 5. Dietary patterns (overall diet) elicited from principal components analysis yield stronger diet-disease associations than when studying isolated nutrients. 6. Remotely recalled dietary intake is reliable enough to be used in studies of chronic disease with long latency periods, such as prostate cancer and BPH. Methods: Data from two studies was used to address the hypotheses above. ... Based on the literature reviewed and the original work for this thesis, the most important dietary risk factors for prostate cancer and BPH appear to be those common to western style diets, i.e. diets high in red meat, processed meat, refined grains, dairy products, and low in fruit and vegetables. This type of diet is likely to result in marginal intakes of antioxidants and fibre, excess intakes of fat and possibly, moderate intakes of carcinogens associated with processed meat and meat cooked at high temperatures. These dietary factors have been linked with biomarkers of inflammation, and they support the hypotheses that chronic inflammation is involved in the development of both prostate cancer and BPH. In addition, this work builds on evidence that zinc is an important factor in prostate health. There is scope for more investigation into the reliability of dietary patterns and the use of nutrient patterns as an alternative to focussing on single food components. Further studies on the reliability of remote dietary intake would also be useful. Because of the latency of chronic disease, it can be theorised that remote dietary recall may uncover more robust diet-disease relationships.
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Charmandari, Evangelia. "Congenital adrenal hyperplasia : the influence of puberty on cortisol pharmacokinetics." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395379.
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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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Kraft, Kathryn A. "Supporting Families with Congenital Adrenal Hyperplasia: Encouraging Whole Family Health." Antioch University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=antioch1405512617.
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Chalmers, R. T. A. "A new approach to the prevention of anastomotic neointimal hyperplasia." Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/20905.
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The need for an effective means of limiting the development of anastomic neointimal hyperplasia forms the basis of this thesis. Endovascular stents were developed for use in native arteries after balloon angioplasty to overcome vessel elastic recoil as well as to rescue immediate angioplasty failures and intimal dissections. The work presented in this thesis was performed in order to investigate the effect on the site and development of anastomotic neointimal hyperplasia of placing such a device across the distal anastomosis of an animal model of an arterial bypass graft. A canine model of an aorto-bi-iliac bypass graft was developed and two separate distal anastomotic patterns investigated in separate experiments, namely the end-to-end and the end-to-side configurations. The early and late effects of stenting the distal anastomoses were examined for both models. In the following Sections, an overview of anastomotic neointimal hyperplasia is presented. After outlining basic histological and pathophysiological considerations, a review of a variety of operative and pharmacological approaches to anastomotic neointimal hyperplasia that have been described in the literature is presented. There follows a general review of the use of endovascular stents prior to a description of my own experimental work on endovascular anastomotic stenting and the results obtained. These results are then analysed with particular focus on possible future refinements and modifications of the experimental model as well as the clinical applicability of anastomotic stenting. The work presented in this thesis represents a novel approach to the problem of anastomotic neointimal hyperplasia in lower limb arterial bypass grafts.
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Ferrer, Lucas Manuel. "ROLE OF CKD AND CASPASE-1 IN NEOINTIMAL HYPERPLASIA DEVELOPMENT." Master's thesis, Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/300901.
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Public HealthM.S.
Vascular access dysfunction is a cause of morbidity and mortality in chronic kidney disease (CKD) patients that require hemodialysis. The major cause of vascular access failure is venous stenosis due to neointimal hyperplasia (NH). Vascular smooth muscle cells (VSMC) are critical for the development of NH lesions, as they have the ability to modulate their phenotype from a "contractile" to a "synthetic" phenotype in the presence of uremia, through the regulation of sensor genes for uremia danger signals and VSMC-specific differentiation genes. Recent research indicates that Caspase-1 (casp-1) activation plays an essential role in sensing metabolic danger signal-associated molecular patterns and initiating vascular inflammation. Carbamylated LDL, a uremic toxin that has been shown to be found in higher levels in patients with CKD and in CKD murine models when compared to controls, and could play a role in casp-1 activation. Therefore, the goal of this project is to examine the role of cLDL/CKD-driven casp-1 activation in VSMC and CKD-related NH. We have established a CKD mouse model and published on CKD-associated vascular remodeling. We exposed wild type and caspase-1 knockout mice to our CKD model, analyzed and quantified the NH lesion formed. We also examined in vitro and ex-vivo changes in VSMC-specific differentiation genes when exposed to uremic serum and cLDL, in the presence or absence of caspase-1 inhibitor. We found that CKD serum induces with casp-1 activation and phenotypic changes in VSMCs from a "contractile" to a "synthetic" phenotype, which are reversed with casp-1 inhibition. In an ex-vivo model using relative quantification we found that VSMC contractile markers α -Actin, Calponin, SM-22, and Smoothelin gene expression of CKD mouse carotid VSMC were higher in casp-1 knockout mice when compared to wild-type (1.40, 1.28, 1.22, 1.41 respectively). Also using an in-vivo model, relative quantification of α-actin decreased from 1.0 to 0.329 when VSMCs were exposed to uremic serum and but increased back to 0.588 when Caspase-1 inhibitor is added. The relative quantification of Calponin also decreased from 1.0 to 0.394 when exposed to uremic serum and increased back to 0.601 with caspase-1 inhibitor. We also found that caspase-1 deficiency significantly reversed CKD-related vascular remodeling in casp-1 knockout mice and reduced NH volume by 50% from 1,440,023in wild-type mice to 71,069 µm2 in casp-1 knockouts (p-value 0.002). This evidence provides evidence that casp-1 plays a critical role in NH formation. Furthermore our results provide a novel insight over the therapeutic potential of casp-1 inhibitors for CKD induced NH and other inflammation induced vascular remodeling.
Temple University--Theses
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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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Heindl, Mario. "Die Rolle des PTEN/PI3K/AKT-Signalweges für die intestinale Immunregulation beim Menschen." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-77393.
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Der PTEN/PI3K/AKT-Signalweg spielt eine entscheidende Rolle bei der Regulation von Proliferation, Migration und Apoptose. Mäuse mit Defekten innerhalb dieses Signalweges weisen multiple Veränderungen in B- und T-Zell- Homöostase auf, welche zu Thymushyperplasie, Lymphadenopathie, Auto- immunität und Lymphomen führen können. Die Entwicklung und der Erhalt von Foxp3+ regulatorischen T-Zellen ist vom PTEN/PI3K/AKT-Signalweg abhängig. Die immunologischen Konsequenzen von PTEN-Defekten beim Menschen sind bisher nicht verstanden. Aufgrund dieser Tatsache wurden sechs Patienten mit PTEN-Hamartom-Tumor-Syndrom auf immunologische Veränderungen unter- sucht. Die gefundenen Dysregulationen beinhalteten Thymushyperplasie, Tonsillenhypertrophie und ausgedehnte lymphoide Hyperplasien des oberen und unteren Gastrointestinaltraktes. Eine erhöhte Anzahl von naiven Lymphozyten zirkuliert im peripheren Blut und akkumuliert in lymphoiden Organen. Intestinale lymphoide Hyperplasien waren mit einer gesteigerten Phosphorylierung von AKT assoziiert, zeigten jedoch normale Proliferation in T-Zell-Zonen sowie eine normale Verteilung CD3+Foxp3+ T-Zellen. Foxp3+ T-Zellen zeigten jedoch eine gesteigerte Proliferation und Aktivierung des mTORC1-Pfades in situ, was auf einen Schwelleneffekt für PTEN-Aktivität hinweisen könnte. Auffällig war eine reduzierte Apoptose bei gleichzeitig gesteigerter Proliferation und erhöhter mTOR- Aktivität bei CD20+CD10+ B-Zellen des Keimzentrums. Diese Daten zeigen, dass ein Verlust von PTEN-Aktivität auch beim Menschen mit Defekten in B- und T-Zell- Homöostase assoziiert ist. Dies führt zur Akkumulation von Lymphozyten und intestinaler lymphoider Hyperplasie bei weitgehend erhaltener Immunkompetenz.
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Calmon, Hamaty Flavia. "Etude des réponses cellulaires induites par LT alpha, TRAIL et FASL dans les Synoviocytes fibroblastiques de la polyarthrite rhumatoïde." Thesis, Montpellier 1, 2011. http://www.theses.fr/2011MON1T003.
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La polyarthrite rhumatoïde (PR) est une maladie inflammatoire chronique qui touche les articulations synoviales. La PR se caractérise par une expansion pseudo-tumorale des cellules synoviales de types fibroblastiques (FLS) qui envahissent et détruisent les articulations. Le Facteur de Necrose Tumorale (TNF) alpha joue un rôle primordial dans cette pathologie et le blocage de son action constitue une thérapie efficace contre la PR. Il existe néanmoins des patients non-répondeurs aux anti-TNFs ce qui suggére la participation d'autres cytokines dans la PR. La Lymphotoxine (LT) alpha est le plus proche homologue du TNFalpha, mais son rôle dans la PR reste peu étudié et le potentiel thérapeutique de son blocage pour traiter la maladie doit encore être établi. La déplétion des FLS hyperprolifératives constitue une autre stratégie pour le traitement de la PR. L'utilisation des membres de la Famille du TNF, TRAIL et Fas ligand (FasL), a été proposée pour induire la mort cellulaire pa r apoptose des FLS dans les articulations synoviales. Toutefois, ces cytokines sont pleiotropiques et peuvent causer des effets secondaires. Nous avons caractérisé les effets de la LTalpha, de TRAIL et FasL dans les FLS pour mieux comprendre ses rôles dans la PR. Nos résultas montrent que les niveaux sériques de la LTalpha sont augmentés dans la PR comparés aux patients sains ou atteints d'arthrose. Toute comme le TNFalpha, la LTalpha induit la prolifération et l'activation des FLS. Ainsi, l'inhibition simultanée de la LTalpha et du TNFalpha pourrait fournir un avantage thérapeutique dans le cadre des traitements contre la PR. Nous avons par ailleurs démontré que TRAIL est un facteur protecteur en début de la PR mais a un rôle promoteur au cours de la maladie. Le double rôle de TRAIL est corrélé à l'expression de TRAIL récepteur 1. Enfin, nous avons montré que FasL joue un rôle non-apoptotique dans les FLS, en modulant leur prolifération. Pour cette raison, une thérapie basée sur TRAIL ou FasL demande une sensibilisation à l'apoptose des FLSRheumatoid arthritis (RA) is a chronic inflammatory disease affecting synovial joints. A hallmark of RA is the pseudo-tumoral expansion of fibroblast-like synoviocytes (FLS), which invade and destroy the joint. Blocking of Tumor Necrosis Factor (TNF) alpha is effective to treat RA. However, some patients are nonresponsive to anti-TNF therapies, suggesting the participation of other cytokines in RA. Lymphotoxin (LT) alpha is the closest homologous to TNFalpha, but little is known about its role in RA and therapeutic potential of blocking this cytokine to treat RA. Another strategy to treat RA is the depletion of hyperproliferative FLS. The TNF family members TNF-related apoptosis-inducing ligand (TRAIL) and Fas ligand (FasL) have been proposed for targeting FLS in arthritic joints. However, these cytokines are pleiotropic and can thus cause unwanted effects. We aimed to characterize the effects of LTalpha, TRAIL and FasL in RA FLS and better understand their role in the pathog enesis of RA. Our results show that serum levels of LTalpha are increased in RA compared to osteoarthritis and healthy controls and LTalpha induces proliferation and activation of RA FLS to the same extent that TNFalpha. Thus, simultaneous blocking of LTalpha and TNFalpha appears to be of benefit for RA patients. Additionally, we demonstrated that TRAIL could be a protective factor in the initial phase of RA but subsequently has a disease-promoting role. The dual role of TRAIL is correlated to TRAIL receptor 1 expression of RA FLS. Moreover, we showed that FasL induces non-apoptotic effects in RA FLS, such as proliferation. Therefore, a TRAIL or FasL based therapeutic strategy in RA requires sensitization for apoptosis of FLS
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Doyle, Peter J. "A study of the chemical interaction between thyroxine and the sulphonamides." Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238849.
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Riemen, Anna Helene Katrin. "Does synovial hyperplasia after traumatic joint surface injury affect the development of secondary osteoarthritis?" Thesis, University of Aberdeen, 2018. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=239453.
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The burden of osteoarthritis continuous to increase. While joint replacement surgery provides a cost effective and efficacious treatment for end stage osteoarthritis, no treatment exists to prevent or slow the progression of the disease. Understanding the cellular and molecular changes in the synovium following trauma and in early osteoarthritis could facilitate the identification of novel therapeutic targets. Previous studies identified synovial hyperplasia following intra-articular fractures, cartilage injury and in osteoarthritis. In mice, proliferation of synovial mesenchymal stromal/stem cells (MSCs) leads to synovial hyperplasia following joint surface injury. The driver for this expansion of MSCs in the synovium is unknown. Recently, YAP, a key downstream effector of the Hippo pathway, has been shown to causes tissue overgrowth due to modulation of MSC proliferation. The joint surface injury model of osteoarthritis was used to investigate whether YAP may play a role in synovial hyperplasia following joint surface injury. This work shows that synovial hyperplasia is common to both healer and non-healer mouse strains after joint injury and that Yap expression is up regulated on a protein and mRNA level. Using the same injury model in a mouse with a conditional knockout of Yap in Gdf5 lineage cells, showed that a Yap knockout in Gdf5 progeny cells prevented hyperplasia of synovial lining after joint surface injury, suggesting that YAP is required for MSCs in the synovium to proliferate. In patient synovial samples, YAP expression was up regulated in activated synovium, including a subset of CD55 positive fibroblast-like synoviocytes in the synovial lining. Proliferating cells were positive for active YAP. This suggests that findings in our mouse model are clinically relevant. Furthermore, modulation of YAP and synovial MSC proliferation after JSI provides a means to study the role of synovial hyperplasia after trauma. This could lead to a potential novel therapeutic target for the treatment of posttraumatic osteoarthritis.
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Menassa, Rita. "Études fonctionnelles et structurales des mutants du gène CYP21A2 dans l’hyperplasie congénitale des surrénales." Thesis, Lyon 1, 2009. http://www.theses.fr/2009LYO10160/document.
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Le déficit en 21-hydroxylase est la cause la plus fréquente des hyperplasies congénitales des surrénales. Un grand nombre de nouvelles mutations a été trouvé dans le laboratoire qui centralise la plus grande cohorte de familles au niveau international et l’évaluation de leur sévérité était primordiale pour optimiser la prise en charge des patients (thérapeutique, conseil génétique). Grâce à l’analyse approfondie du phénotype des patients et au développement d’études fonctionnelles (in vitro, in silico), nous avons pu évaluer le retentissement de la plupart des 85 nouvelles mutations ; nous avons choisi comme témoins des mutations fréquentes de sévérité connue et nous avons comparé nos résultats avec ceux de la littérature. L’analyse plus approfondie d’une quinzaine de mutations rares a confirmé l’existence de bonnes corrélations phénotype-génotype comme ceci est décrit dans cette pathologie. Par ailleurs, les études structurales que nous avons développées ont permis d’améliorer les connaissances sur les relations structure-fonction des cytochromes P450 en généralSteroid 21-hydroxylase deficiency is the most common enzymatic defect causing congenita ladrenal hyperplasia. A large number of new mutations has been detected in the laboratory, which centralizes the biggest cohort of families in the world, and evaluation of their severity wasessential to optimize the care of the patients (treatment, genetic counselling). Thanks to detailed analysis of the patients phenotype and to the development of functional studies (in vitro, in silico), we were able to evaluate the severity of most of the 85 novel mutations; we decided touse as controls frequent known mutations and to compare our results with those of literature. Themore detailed analysis of about fifteen rare mutations confirmed the existence of goodcorrelations phenotype-genotype as this is described in this pathology. Moreover, the structural studies we developed led to improve the knowledge on structure-function relationship of theP450 cytochromes family
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Robins, Tiina. "Functional and structural studies on CYP21 mutants in congenital adrenal hyperplasia /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-529-1/.
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Fays, Ségolène Schmutz Jean-Luc. "Maladie de Kimura et hyperplasie angiolymphoïde avec éosinophilie." [S.l.] : [s.n.], 2003. http://www.scd.uhp-nancy.fr/docnum/SCDMED_T_2003_FAYS_SEGOLENE.pdf.
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GALEY, ISABELLE. "Hyperplasie congenitale des surrenales : devenir a long terme." Toulouse 3, 1994. http://www.theses.fr/1994TOU31020.
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MERIAUX, DELANNOY VERONIQUE. "Hyperplasie nodulaire focale hepatique : a propos d'un cas." Lille 2, 1988. http://www.theses.fr/1988LIL2M042.
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Rösler, Stefan K. "Die Hämodynamik von femoro-cruralen Bypasanastomosen." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2007. http://dx.doi.org/10.18452/15739.
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Die moderne Gefäßchirurgie bedient sich bei hohen Stadien der pAVK, spezieller Gefäßrekonstruktionen in Form von distalen End-zu-Seit-Gefäßanastomosen. Das langfristige Versagen der Gefäßanastomose hängt primär von der Entstehung einer subendothelialen Intimahyperplasie (IH) ab. Diese IH-Gebiete befinden sich je nach Anastomosengeometrie im Gebiet der Hauben- und Fersenzone sowie am Boden der Anastomose. // Mit Hilfe der Particle Image Velocimetry-Technik wird eine Taylor-Patch-, eine Miller-Cuff-Anastomose und eine femoro-crurale Patch-Prothese bezüglich ihrer Flussmuster sowie ihrer hämodynamischen Eigenschaften wie Geschwindigkeit, Scherstress und Rotation in z-Richtung (Vorticity) untersucht. // In einem hydrodynamischen Kreislaufmodell werden elastische, transparente Silikonmodelle der Anastomosen hergestellt und mit einem blutanalogen Newtonschen Fluid (Glycerol-Wasser-Gemisch) unter Simulation der femorocruralen Druckkurve, pulsatil bei Variation der Strömungsbedingung perfundiert. Der periphere Widerstand beträgt 0,5 mmHg/ml/min (PRU) und die Phasenverschiebung -12 Grad (zwischen Druck- und Flusskurve). // Die Flussmuster variieren zwischen den unterschiedlichen Ausstromverhältnissen erheblich. Bei den unterschiedlichen Flussstärken hingegen ähneln sich die Flussmuster. Alle drei Modelle zeigen ausgeprägte Flussseparationszonen im Hauben- und Fersengebiet sowie geometrieabhängig auch eine Stagnationszone am Boden. Diese Bereiche wiesen die geringsten Fluidgeschwindigkeiten, deutlich unter normalem Wandscherstressniveau liegende Scherstressverhältnisse sowie geringe Vorticitywerte auf. Im Bereich der Übergangszonen finden sich hohe Scherstress- sowie Vorticitywerte. Geschwindigkeitsunterschiede des Fluids zeigten sich im Bereich der Ausstromsegmente. Variable Stressverteilungen zeigen sich auch innerhalb der Separationszonen. Eine Erklärung für die unterschiedlich beschriebenen Offenheitsraten der drei Anastomosenformen wird durch diese Arbeit nicht gefunden.Modern vascular surgery uses special termino-lateral anastomoses for treating high levels of peripheral arterial disease (PAD). Long term stenoses and occlusions of vascular anastomoses mostly depend on the development of subendothelial myointimal hyperplasia (MIH). There are characteristic areas within the anastomoses, where this process can be examined: The heel, the tow and the floor zone. // This examination observes local hemodynamics like velocity, shear stress and vorticity (rotation in z-direction) and flow patterns of a Taylor-Patch-, a Miller-Cuff-Anastomosis and a feroro-crural patch prothesis (FCPP) with the usage of a Particle Image Velocimetry. In a hydrodynamic circulation model various elastic, transparent silicon phantoms of termino-lateral anastomoses are perfused with a Newton fluid blood analogon (glycerol-water mixture) while simulating the femorocrural pressure curve in a pulsatile manner under variation of the flow conditions. The outflow resistance is 0.5 mmHg/ml/min (PRU, peripheral resistance units) and a phase shift of -12° between flow and pressure curve is simulated. // The flow patterns differed extremely in accordance of the various outflow ratios. Using different flow intensity, the flow patterns are very similar. // All three anastomoses show characteristic heel and toe separation zones. In the FCPP centre a stagnation zone on the floor can not be examined. Shear stress inside the flow separations was significantly lower than normal wall shear stress. High shear stress levels were found inside the transition zones between flow separation and high velocity mainstream. An explanation for the different stenoses and occlusions time of the three different anastomoses can not be found.
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Hallin, Anders. "Transurethral microwave thermotherapy of benign prostatic hyperplasia : a clinical and methodological evaluation /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2727-8.
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Zhou, Baixue [Verfasser]. "Role of endothelial CXCR4 in neointimal hyperplasia after wire injury / Baixue Zhou." Aachen : Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen, 2015. http://d-nb.info/1071001884/34.
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