Littérature scientifique sur le sujet « Maladies de la vessie – thérapie »
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Articles de revues sur le sujet "Maladies de la vessie – thérapie"
Fahmy, Nader, Armen Aprikian, Mohammed Al-Otaibi, Simon Tanguay, Jordan Steinberg, Suganthiny Jeyaganth, Moamen Amin et Wassim Kassouf. « Impact of treatment delay in patients with bladder cancer managed with partial cystectomy in Quebec : a population-based study ». Canadian Urological Association Journal 3, no 2 (25 avril 2013) : 131. http://dx.doi.org/10.5489/cuaj.1045.
Texte intégralGiménez y Ribotta, Minerva, et Alain Privat. « Maladies neurodégénératives : thérapie génique ». Annales de l'Institut Pasteur / Actualités 11, no 2 (avril 2000) : 79–96. http://dx.doi.org/10.1016/s0924-4204(00)80012-8.
Texte intégralGiménez y Ribotta, Minerva, et Alain Privat. « Maladies neurodégénératives : thérapie génique ». Journal of Engineering and Technology Management 14, no 2 (juin 1997) : 79–96. http://dx.doi.org/10.1016/s0923-4748(97)80012-4.
Texte intégralPoenaru, L. « Thérapie génique des maladies lysosomales ». médecine/sciences 12, no 1 (1996) : 3535–46. http://dx.doi.org/10.4267/10608/601.
Texte intégralTeiger, E., M. Eloit, I. Déprez, C. Partovian, JL Dubois-Randé, P. Lemarchand et S. Adnot. « Thérapie génique et maladies cardiovasculaires. » médecine/sciences 15, no 5 (1999) : 615. http://dx.doi.org/10.4267/10608/1400.
Texte intégralVilquin, Jean-Thomas, et Serge Braun. « Thérapie cellulaire des maladies musculaires ». médecine/sciences 35 (novembre 2019) : 7–10. http://dx.doi.org/10.1051/medsci/2019188.
Texte intégralFarge-Bancel, D. « Thérapie cellulaire et maladies autoimmunes ». La Revue de Médecine Interne 32 (décembre 2011) : S204—S207. http://dx.doi.org/10.1016/j.revmed.2011.09.004.
Texte intégralCohen-Haguenauer, O. « Thérapie génique des maladies rares ». La Revue de Médecine Interne 32 (décembre 2011) : S210—S212. http://dx.doi.org/10.1016/j.revmed.2011.09.015.
Texte intégralMoullier, P., A. Salvetti, D. Bohl, O. Danos et JM Heard. « Thérapie génique des maladies lysosomales ». Archives de Pédiatrie 3 (janvier 1996) : S65—S68. http://dx.doi.org/10.1016/0929-693x(96)85996-3.
Texte intégralZekre, Franck. « Thérapie ciblée dans les maladies dysimmunitaires ». Perfectionnement en Pédiatrie 7, no 2 (juin 2024) : 2S31–2S32. http://dx.doi.org/10.1016/s2588-932x(24)00123-2.
Texte intégralThèses sur le sujet "Maladies de la vessie – thérapie"
Biardeau, Xavier. « Optimisation des thérapies de stimulation/modulation électrique dans le traitement des troubles vésico-sphinctériens neurogènes et non-neurogènes ». Electronic Thesis or Diss., Université de Lille (2022-....), 2024. http://www.theses.fr/2024ULILS014.
Texte intégralEven if it involves alternating between a filling phase and an emptying phase, the normal micturition cycle cannot be summed up as a binary operation but involves the constant consideration of multiple factors: the filling level of the bladder reservoir, the safety of the environment in which we live, the emotional context in which we evolve and the social constraints to which we are subjected.We now know that there are alterations and/or modifications in brain activity and connectivity, as well as changes in the regulation of the autonomic nervous system, in certain types of lower urinary tract dysfunction - notably in overactive bladder or urge urinary incontinence and in certain types of voiding dysfunctions. Among the therapies available today, electrical modulation/stimulation therapies (tibial neurostimulation and sacral neuromodulation) appear able to normalize and/or modify brain activity and connectivity, as well as ANS balance. They could thus provide at least a partial response to some of the etiopathogenies underlying these lower urinary tract dysfunctions. However, the deployment and positioning of these electrical modulation/stimulation therapies are still limited by an incomplete understanding of their mechanisms of action, imperfect identification of the indications and populations most likely to benefit from these therapies, a lack of consensus on the setting of the electrical current delivered, and a lack of medium and long-term evaluation. In the first part, we questioned the indications for these therapies, and particularly their place as a preventive approach for lower urinary tract dysfunctions due to spinal cord injury. We also questioned the relation, in terms of efficacy, between transcutaneous tibial neurostimulation and sacral neuromodulation, to better support patients in shared medical decision-making processe. Finally, we developed the first tool to predict the success of sacral neuromodulation as a treatment for voiding dysfunction. In the second part, we questioned the mechanisms of action, and more specifically the changes in the balance of the autonomic nervous system in response to an acute S3 sacral root stimulation.In the third part, we questioned the mid-term follow-up (5 years) after definitive implantation of sacral neuromodulation in a geographic population pool, looking for risk factors for discontinuation of follow-up. These data, although still to be supplemented by future research projects, will enable us to further optimize electrical modulation/stimulation therapies in the management of neurogenic and non-neurogenic lower urinary tract dysfunctions
Berrahmoune, Saoussen. « Étude des mécanismes régissant l’efficacité photodynamique sélective de l’Héxylaminolévulinate-Protoporphyrine IX dans le traitement du cancer de la vessie : Application dans le cadre de la prévention de ses récidives ». Thesis, Nancy 1, 2009. http://www.theses.fr/2009NAN10012/document.
Texte intégralPhotodynamic therapy (PDT) is a treatment modality based on the cytotoxic effect occurring on target tissues by interaction of a photosensitizer with light in the presence of oxygen. The aim of this study was to optimise PDT for treatment and prevention of recurrence of bladder cancer. The study was performed in vivo. PDT was performed with Hexvix® a precursor of the photosentitizer protoporphyrin IX (PpIX). First, we executed a mechanistic analysis of differential PDT effects according to Hexvix® concentration. 8 or 16 mM induced diametrically opposed photodynamic effects. PDT efficacy is depends on the mitochondrial localization of PpIX and its concentration and leads to pro-apoptotic damages. Second, PDT was performed in a rat model mimicking post fluorescence guided TUR. The amount of viable tumor cell within the bladder lumen significantly decreased with PDT and resulted in a significant reduction of tumor implantation
Latourette, Solange. « La thérapie génique ». Paris 5, 1994. http://www.theses.fr/1994PA05P100.
Texte intégralCosserat-Gérardin, Isabelle. « Evaluation expérimentale de la Protoporphyrine IX (PpIX) induite par l'hexylester d'acide 5-aminolévulinique(hALA), et de l'hypéricine pour le traitement photodynamique de tumeurs de vessie ». Nancy 1, 2001. http://www.theses.fr/2001NAN11308.
Texte intégralPhilippe, Catherine. « Le lavage vésical : un exemple d'application de pharmacie clinique ». Paris 5, 1991. http://www.theses.fr/1991PA05P124.
Texte intégralLe, Bacquer Anne-Véronique. « Les complications de la BCG-thérapie endovésicale dans le traitement des cancers superficiels de "la vessie" : revue générale à propos d'un cas ». Montpellier 1, 1995. http://www.theses.fr/1995MON11047.
Texte intégralLe, Souder Cosette. « Maladies à prions : vers le développement d'une thérapie génique et cellulaire ». Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT051.
Texte intégralTransmissible spongiform encephalopathies are neurodegenerative diseases characterized by a strong vacuolization, a neuronal lost and deposits of prion pathologic protein: PrPSc. This PrPSc accumulation is the result of the conformational conversion of the host encoded endogenous PrPC protein. Although the incidence of these diseases in humans remains low (about one to two cases per million inhabitants per year), these diseases remain a public health problem. Indeed, because of their long and silent incubation period, patients with prion disease may expose people through blood transfusion or organ transplantation with a risk of iatrogenic contamination. In addition, when the diagnosis occurs, brain damage is often massive, and the outcome is always fatal and rapidly occurs. Until now, there is no treatment that could be proposed to patients.The alternative developed by our laboratory for several years, is a strategy of cell therapy coupled with gene therapy. The general objective is to use pluripotent embryonic stem cells (ESC) and graft them as a “medicine” not only to orchestrate a functional recovery of the damaged zones and protect the grafted cells from prion propagation but also to deliver anti-prion molecules.For the anti-prion molecules, we have chosen dominant negative PrP mutants (PrP-DN). Our choice is based on studies showing that a lysine at codon 219 of the human PrP or an arginine at codon 171 of the ovine PrP protect against the development of a TSE. Study of these mutants in infected cells or in transgenic mice showed that the mutated PrPC were not converted into PrPSc. Moreover, they exibit a so-called "dominant negative" protective effect on the conformational conversion of their wild-type PrPC counterparts. A first approach of gene and cell therapy was initiated in the laboratory and has shown encouraging results. Indeed, the graft of murine neural stem cells (NSC) derived from murine embryonic stem cells and expressing anti-prion molecules, has allowed, for some of the mice, to an increase the incubation time of the diseaseas well as to a decrease of astrogliosis and vacuolization.In this context, the first objective of my thesis was to validate the therapeutic approach by showing that the grafted cells were able to inhibit prion replication trough the dominant negative effect of the PrP-DN. To address this point, we have chosen to use an organotypic culture model infected with murine prions (22L strain). In addition to fill the ethical requirements under the European Directive 2010/63 and the 3Rs, organotypic culture models offer the advantage to perform and repeat experiments, kinetic tests, and PrPres analysis. This model also allows to visualize the fate of the grafted cells. Finally, by choosing this strategy, it will be possible to transpose into a humanized model the work previously performed on mouse organotypic cultures.To achieve this task, it was necessary to establish an ex vivo prion model of organotypic culture brain slices, in which it was possible to perform grafts and to evaluate the inhibitory effect of PrP-DN mutants on the prion replication.In addition, as our group is included in the team "Stem cell biology and regenerative medicine" (led by Pr Jorgensen) in which several stem cells are studied (liver stem cells and mesenchymal stem cells (MSC)) and because MSC have been shown to provide protective effects when grafted in the brain of mice with neurological diseases, it was therefore relevant to evaluate the effect of MSC on prion pathology in our prion models and in particular to evaluate the impact of concomitant MSC grafts on NSC-PrP-DN.In a last step, our goal was to transpose the mouse tools (NSC from ES and expressing the PrP-DN mutants) to "human" tools by producing human NSCs derived from human ESC and expressing human PrP-DN, and to characterized the resulted cells
Delmouly, Karine. « Cellules Souches Neurales : modélisation et thérapie cellulaire des maladies à prions ». Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20134/document.
Texte intégralTransmissible Spongiform Encephalopathies (TSE) are neurodegenerative disorders with long asymptomatic incubation periods and fatal issue. They are induced by accumulation of the pathogen isoform of the prion protein (PrPSc) in the central nervous system (CNS) resulting in neuronal degeneration and astrogliosis. PrPSc, produced by the conversion of the physiological form of the prion protein (PrPC), plays a key role in the disease transmission. The mechanisms underlying the conversion of PrPC and the propagation of PrPSc are uncertain just as the molecular mechanisms giving rise to prion diseases. In the aim of creating or improving cell culture models, it has been shown that CNS Neural Stem Cells (NSC) could support PrPC conversion into PrPSc in vitro. In this project, we used NSC to improve and characterize cellular infection and hypothesized that modification of culture conditions could modulate PrPSc production in NSC. Hence, we used factors known to influence cellular identity in our culture model and showed that higher amount of prions were produced. These models also allow molecular mechanisms studies that could be at infection origin. During the course of this study, we also demonstrated that HEPES added to our culture medium could stop prion propagation in a dose-dependant manner. Moreover, to date no therapy aimed at stopping disease progression has been established in humans. We therefore used NSC with the ultimate goal to elaborate a therapeutic strategy based on the delivery of antibodies into the CNS to block prion replication. These cells will also able to repair damaged brain area thus combining cell and gene therapy
Guttin, Audrey. « Développement d’une bithérapie antitumorale basée sur une approche théranostique : applications aux cancers du cerveau et de la vessie ». Thesis, Paris, EPHE, 2016. http://www.theses.fr/2016EPHE3018/document.
Texte intégralSolid malignant tumors have molecular characteristics that clearly distinguish them from healthy tissue. The project is to develop a new therapeutic strategy based on these molecular characteristics. We set up a new therapeutic approach so as to customize treatment by connecting it directly to the diagnosis of the tumor (theranostic approach).Brain tumours and bladder tumours are two examples of particularly aggressive solid tumours. These two types of tumors are classified into several subgroups that have their own molecular profiles. The microRNAs (miR) are molecules naturally synthesized by cells. These molecules may have a role of oncogene or tumour suppressors whose expression is strongly deregulated in tumours. So the assessment of the expression levels of few microRNA allows the distinction of gliomas of high grade compared to low grade.To set up the new therapy we needed to modulate the expression of microRNAs deregulated in tumors. The proposed approach was to counter the expression of oncogenic microRNAs overexpressed using an antimicroARN (antimiR). This type of molecule is chemically similar to the naturally occurring RNA molecules in the cells. For a better efficiency of this new therapeutic strategy, we tried to optimize the transport of the antimiR to increase the therapeutic effect. To vectorize the therapeitic antimiR to the heart of the tumor, we envisioned to chemically combine the antimiR to a cell-penetrating antitumoral compound. Chalcones derivatives which are hydrophobic have this capability. A combination of the two molecules (antimicroARN and chalcone) was evaluated and the results appeared promising
Toupet, Karine. « Stratégies thérapeutiques des maladies à prions ». Montpellier 2, 2009. http://www.theses.fr/2009MON20128.
Texte intégralPrion diseases are fatal neurodegenerative disorders that affect both humans and animals. These diseases are induced by the accumulation in the brain of the misfolded isoform of the normal cellular prion protein: PrPSc. The emergence of new risks of transmission for these diseases and the lack of efficient treatments, prompt us to search for new therapeutic strategies and targets. We developed two innovative therapeutic approaches. The first one consisted in searching for molecules able to trap preamyloid forms of PrPSc (dimers and trimers), known as key elements in the replication cycle of prions. A drugs screening approach, in silico and in cellulo, allowed us to discover thienyl pyrimidine and thienyl azine compounds able to specifically oligomerize PrPSc molecules. These PrPSc oligomers decrease prions infectivity in vivo, highlighting the therapeutic potential of these compounds. Our second strategie is a gene therapy approach using the dominant negative properties of certain polymorphisms of the prion protein, such as the Q218K and Q167R mutants. Our objective was to evaluate the therapeutic potential of lentiviral vectors carrying the PrPQ218K and PrPQ167R mutants, in mice, at the terminal stage of the disease. We succeeded in significantly prolonging the survival time of mice of 20%, with two intracerebrally chronic injections of lentiviral vectors carrying the PrPQ167R mutant. All our results not only open the way for new therapeutic strategies against prion diseases but also will benefit for therapies of other neurodegenerative disorders
Livres sur le sujet "Maladies de la vessie – thérapie"
recherche, Canada Bibliothèque du Parlement Service de. La thérapie génétique humaine. Ottawa, Ont : Bibliothèque du Parlement, Service de recherche, 1988.
Trouver le texte intégral1958-, Atala Anthony, et Slade Debra, dir. Bladder disease : Research concepts and clinical applications. New York : Kluwer Academic/Plenum Publishers, 2004.
Trouver le texte intégral1958-, Atala Anthony, et Slade Debra, dir. Bladder disease : Research concepts and clinical applications. New York : Kluwer Academic/Plenum Publishers, 2003.
Trouver le texte intégralLes maladies de l'oreille et de l'audition en 200 questions. Paris : De Vecchi, 2002.
Trouver le texte intégralGuimón, J. Art et psychiatrie : Mécanismes psycho-biologiques de la créativité. Genève : Georg éditeur, 2004.
Trouver le texte intégralReynaud, Michel. Addictions et psychiatrie. Issy-les-Moulineaux : Masson, 2005.
Trouver le texte intégralNochomovitz, Lucien E. Bladder biopsy interpretation. New York : Raven Press, 1992.
Trouver le texte intégralDavid, Rampton, dir. Inflammatory bowel disease : Clinical diagnosis and management. London : Martin Dunitz, 2000.
Trouver le texte intégrald'Encausse, Marina Carrère. Le Gène sacralisé. Paris : Editions Julliard, 1994.
Trouver le texte intégralLes douleurs rhumatologiques en pratique quotidienne. Montrouge : J. Libbey Eurotext, 2008.
Trouver le texte intégralChapitres de livres sur le sujet "Maladies de la vessie – thérapie"
Diana, Jean-Sébastien, et Marina Cavazzana. « Thérapie génique des déficits immunitaires primitifs ». Dans Maladies Immunitaires de L'enfant, 281–84. Elsevier, 2022. http://dx.doi.org/10.1016/b978-2-294-77580-2.00041-4.
Texte intégralLéglise, Audrey, et Clément Thiebaut. « Méthodologie des ateliers thérapeutiques auprès des patients atteints de la maladie d'Alzheimer et maladies apparentées ». Dans Méthodologie des ateliers thérapeutiques auprès des patients atteints de la maladie d'Alzheimer et maladies apparentées, 109–17. In Press, 2016. http://dx.doi.org/10.3917/pres.engas.2016.01.0110.
Texte intégralBoulogne, Jacques. « L’intempérance verbale. L’imaginaire de Plutarque dans la thérapie des maladies de l’âme ». Dans Les passions antiques et médiévales, 161. Presses Universitaires de France, 2003. http://dx.doi.org/10.3917/puf.bedou.2003.01.0161.
Texte intégralSillou, Jean-Marie. « Méthodologie des ateliers thérapeutiques auprès des patients atteints de la maladie d'Alzheimer et maladies apparentées ». Dans Méthodologie des ateliers thérapeutiques auprès des patients atteints de la maladie d'Alzheimer et maladies apparentées, 31–40. In Press, 2016. http://dx.doi.org/10.3917/pres.engas.2016.01.0032.
Texte intégralFoulquet, Amélie. « Méthodologie des ateliers thérapeutiques auprès des patients atteints de la maladie d'Alzheimer et maladies apparentées ». Dans Méthodologie des ateliers thérapeutiques auprès des patients atteints de la maladie d'Alzheimer et maladies apparentées, 41–48. In Press, 2016. http://dx.doi.org/10.3917/pres.engas.2016.01.0042.
Texte intégralURBANOWICZ, Agata, Aurélie GAUCHET, Jaynie RANCE, Paul BENNETT et Rebecca SHANKLAND. « Comment prévenir et réduire le burnout parental grâce à des interventions psychologiques de groupe ? » Dans Le patient et son entourage, 131–42. Editions des archives contemporaines, 2023. http://dx.doi.org/10.17184/eac.7248.
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