Literatura científica selecionada sobre o tema "Lésions tubulaires"
Crie uma referência precisa em APA, MLA, Chicago, Harvard, e outros estilos
Consulte a lista de atuais artigos, livros, teses, anais de congressos e outras fontes científicas relevantes para o tema "Lésions tubulaires".
Ao lado de cada fonte na lista de referências, há um botão "Adicionar à bibliografia". Clique e geraremos automaticamente a citação bibliográfica do trabalho escolhido no estilo de citação de que você precisa: APA, MLA, Harvard, Chicago, Vancouver, etc.
Você também pode baixar o texto completo da publicação científica em formato .pdf e ler o resumo do trabalho online se estiver presente nos metadados.
Artigos de revistas sobre o assunto "Lésions tubulaires"
Luque, Y. "Toxicité rénale des immunoglobulines intraveineuses". Médecine Intensive Réanimation 27, n.º 4 (julho de 2018): 324–30. http://dx.doi.org/10.3166/rea-2018-0059.
Texto completo da fonteAudard, V., S. Moutereau, A. Habibi, M. Khellaf, P. Grimbert, Y. Levy, S. Loric et al. "Lésions tubulaires infra-cliniques au cours des crises vaso-occlusives drépanocytaires". Néphrologie & Thérapeutique 10, n.º 5 (setembro de 2014): 357. http://dx.doi.org/10.1016/j.nephro.2014.07.204.
Texto completo da fonteGirshovich, A., C. Vinsonneau, J. Perez, S. Vandermeersch, S. Placier, E. Letavernier, L. Baud e J. P. Haymann. "Effet protecteur du FGF7 dans un modèle d’insuffisance rénale aiguë ischémique : prévention des lésions tubulaires et accélération de la régénération". Néphrologie & Thérapeutique 8, n.º 5 (setembro de 2012): 289–90. http://dx.doi.org/10.1016/j.nephro.2012.07.347.
Texto completo da fonteKormann, R., N. Prakoura, S. Placier, S. Vandermeersch, M. C. Verpont, J. C. Dussaule, C. Chadjichristos e C. Chatziantoniou. "La délétion du gène de la periostine augmente les lésions tubulaires, réduit l’infiltrat inflammatoire macrophagique, et augmente la fibrose rénale dans le modèle murin d’ischémie-reperfusion rénale". Néphrologie & Thérapeutique 14, n.º 5 (setembro de 2018): 268. http://dx.doi.org/10.1016/j.nephro.2018.07.045.
Texto completo da fonteOgunleye, A. O., A. T. P. Ajuwape, A. I. Adetosoye e O. G. Ohore. "Pathogénicité de Salmonella Paratyphi A chez des poulettes". Revue d’élevage et de médecine vétérinaire des pays tropicaux 59, n.º 1-4 (1 de janeiro de 2006): 5. http://dx.doi.org/10.19182/remvt.9954.
Texto completo da fonteGabarre, Paul, Guillaume Dumas e Lara Zafrani. "Insuffisance rénale aiguë chez les patients COVID-19 en soins intensifs". Médecine Intensive Réanimation 30, Hors-série 1 (16 de junho de 2021): 43–52. http://dx.doi.org/10.37051/mir-00069.
Texto completo da fonteMarchiset, Antoine, e Matthieu Jamme. "Répercussions rénales au cours du SDRA". Médecine Intensive Réanimation 33, n.º 2 (7 de junho de 2024): 205–16. http://dx.doi.org/10.37051/mir-00220.
Texto completo da fonteIyeghe-Erakpotobor, G. T., J. O. Omirinde, A. E. Enaohwo e P. P. Barje. "Semen Characteristics and Testiculo-Epididymal Histology of Red Sokoto Bucks Fed Whole Cottonseed and Cottonseed Cake". Nigerian Journal of Animal Production 49, n.º 5 (26 de maio de 2023): 75–86. http://dx.doi.org/10.51791/njap.v49i5.3766.
Texto completo da fonteTeses / dissertações sobre o assunto "Lésions tubulaires"
Dewitte, Antoine. "Plaquettes sanguines et insuffisance rénale aiguë : rôle du couple CD154/CD40 dans la constitution des lésions tubulaires". Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0906.
Texto completo da fonteAcute kidney injury (AKI) is a common complication in critically ill patients and is associated with increased morbidity and mortality. Sepsis is the most common cause of AKI. The understanding of sepsis pathophysiology and its complications has progressed significantly in recent years but has not yet been translated into significant therapeutic advances in clinical practice. The traditional paradigm that sepsis-induced AKI is linked to renal hypoperfusion has been challenged by recent evidences showing that renal blood flow is not universally impaired during sepsis,and that AKI can develop in the presence of normal or even increased renal bloodflow. Sepsis is characterized by profound alterations of the immune response and adisproportionate inflammatory response. Inflammation and microcirculatorydysfunction are now considered as fundamental pathophysiological mechanisms atthe origin of renal injuries. Beyond haemostasis, the contribution of platelets ininflammation, tissue integrity and defence against infections has considerablywidened the spectrum of their role and made them potential physiopathologicalactors in sepsis. Platelets fulfil most of these functions through the expression ofmembrane-bound or soluble mediators. Among them, CD154 holds a peculiarposition, as platelets represent a major source of CD154 and as CD154 is a centralregulator of inflammation. Here, we provide an overview of these recentpathophysiological advances and discuss the platelets and CD154 contribution tomicrocirculatory alterations in multi-organ dysfunction in sepsis. We investigated thepro-inflammatory role of CD154 under hypoxic conditions in the renal tubularepithelium as recent data highlight the importance of hypoxia in the inflammatoryreaction. We studied the control of interleukin (IL)-6 production, a key cytokineinvolved in inflammation, by CD154 in oxygen deprivation conditions using a kidneytubular epithelial (TEC) cell line model. We also studied a murine model of kidneyinjury after ischemia/reperfusion, a model that was applied in CD154 and CD40deficient mice. We found that CD154 is a potent inducer of IL-6 secretion by TEC inhypoxia and that CD154-deficient mice regenerate earlier the tubular epithelium afterischemia/reperfusion injury. These findings may provide potential avenues for septicAKI management and therapy
Pillebout, Evangéline. "Progression des lésions rénales après réduction néphronique : rôle de la prolifération tubulaire et de l'angiogenèse". Paris 7, 2003. http://www.theses.fr/2003PA077177.
Texto completo da fonte