Literatura científica selecionada sobre o tema "Stress de sécrétion"
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Artigos de revistas sobre o assunto "Stress de sécrétion"
Nabi, H. "Place du stress dans le risque cardiovasculaire". European Psychiatry 28, S2 (novembro de 2013): 38–39. http://dx.doi.org/10.1016/j.eurpsy.2013.09.097.
Texto completo da fonteBesseiche, A., G. Guillemain, E. Ramond, J. Riveline, P. Ferre, J. Gautier, B. Breant e B. Blondeau. "O83 PGC-1a inhibe la sécrétion d’insuline en déclenchant un stress oxydant et un stress énergétique". Diabetes & Metabolism 40 (março de 2014): A20. http://dx.doi.org/10.1016/s1262-3636(14)72257-8.
Texto completo da fonteFarre, C., M. Bayle, J. L. Bosson, P. Faure e O. Chabre. "P022 - La sécrétion de prolactine n’est pas stimulée par le stress de la ponction veineuse". Annales d'Endocrinologie 65, n.º 4 (setembro de 2004): 285. http://dx.doi.org/10.1016/s0003-4266(04)95733-2.
Texto completo da fonteTorrisi, R. "Réponses neuroendocriniennes au stress chez des jeunes adultes nés grands prématurés : interactions entre le système HPA et le système ocytocinergique". European Psychiatry 28, S2 (novembro de 2013): 15–16. http://dx.doi.org/10.1016/j.eurpsy.2013.09.037.
Texto completo da fonteBerger, M., C. Castellani, K. Ninoreille, T. Basset, D. Frere-Meusnier e C. Rigaud. "Stress dus aux traumatismes relationnels précoces : conséquences cérébrales de la perturbation de la sécrétion du cortisol sanguin chez les nourrissons". Neuropsychiatrie de l'Enfance et de l'Adolescence 58, n.º 5 (agosto de 2010): 282–92. http://dx.doi.org/10.1016/j.neurenf.2009.09.003.
Texto completo da fonteRabhi, N., P. Denechaud, E. Salas, A. Bonnefond, C. De Bettignies, P. Froguel e J. Annicotte. "O5 La lysine acetyl-transferase P300/CBP-associated factor (PCAF) contrôle la sécrétion d’insuline et la réponse au stress du reticulum". Diabetes & Metabolism 40 (março de 2014): A2. http://dx.doi.org/10.1016/s1262-3636(14)72179-2.
Texto completo da fonteAUROUSSEAU, B., D. DURAND e D. GRUFFAT. "Contrôle des phénomènes oxydatifs pendant la gestation chez les monogastriques et les ruminants". INRAE Productions Animales 17, n.º 5 (5 de outubro de 2004): 339–54. http://dx.doi.org/10.20870/productions-animales.2004.17.5.3607.
Texto completo da fonteYoul, E., G. Bardy, R. Magous, G. Cros, P. Petit, D. Bataille e C. Oiry. "P217 La quercétine potentialise la sécrétion d’insuline et protège la fonctionnalité des cellules INS-1 soumises à un stress oxydant exogène en sur-activant ERK1/2". Diabetes & Metabolism 36 (março de 2010): A90. http://dx.doi.org/10.1016/s1262-3636(10)70365-7.
Texto completo da fontePerron, H. "La voie des rétrovirus humain endogènes, un espoir thérapeutique dans la schizophrénie". European Psychiatry 30, S2 (novembro de 2015): S25. http://dx.doi.org/10.1016/j.eurpsy.2015.09.077.
Texto completo da fonteROUSSEL, S., E. MERLOT, A. BOISSY e C. DUVAUX-PONTER. "Le stress prénatal : état des connaissances et conséquences potentielles en élevage". INRAE Productions Animales 20, n.º 1 (7 de março de 2007): 81–86. http://dx.doi.org/10.20870/productions-animales.2007.20.1.3439.
Texto completo da fonteTeses / dissertações sobre o assunto "Stress de sécrétion"
Broquet, Alexis Marcel Henri. "Sécrétion de la protéine Hsp70 dans les cellules intestinales : un marqueur de stress ?" Paris 6, 2005. http://www.theses.fr/2005PA066274.
Texto completo da fonteVerchier, Yann. "Microanalyse dynamique des phénomènes de sécrétion cellulaire : études de l'exocytose vésiculaire et du stress oxydant". Paris 6, 2007. http://www.theses.fr/2007PA066121.
Texto completo da fonteWang, Yidan. "Mécanismes de sécrétion d'ATP et d'exposition de la calréticuline au cours d'une chimiothérapie immunogène". Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T045/document.
Texto completo da fonteCytotoxic anti-neoplastic agents were considered for a long time to mediate their therapeutic effects via their capacity to directly kill malignant cells. Nevertheless, this high cytotoxicity is non-targeted and will eventually diminish immune cells. During the last years, it has been shown that radiotherapy and some anticancer agents, such as anthracyclines and oxaliplatin, can stimulate actively anti-tumor immune responses. In fact, they can induce an immunogenic type of apoptosis, which we termed immunogenic cell death (ICD). Thereby, dying cells can act as therapeutic vaccine against residual cancer cells that overcame the initial treatment.ICD is characterized by three major hallmarks: a pre-mortem stress of the endoplasmic reticulum (ER), which triggers the translocation of the ER chaperone protein called calreticulin (CRT) to the cell surface, the secretion of ATP from apoptotic cells, which acts as a signal for the recruitment of dendritic cells and for the activation of the NLRP3 inflammasome via its receptor P2RX7, and the release of HMGB1 into the extracellular space, allowing it to interact with TLR4 and thus stimulate the antigen-presenting functions of the DCs.The first part of my work focused on the precise molecular mechanisms by which ATP is actively secreted during ICD. Using a large panel of techniques, including chemical compounds screens and monitoring the subcellular localization of ATP, we showed that following treatment of various tumor cells with ICD inducers, ATP is redistributed from lysosomes to autolysosomes and the lysosomal protein LAMP1 is required for active ATP secretion. We also showed that Rho and pannexin 1 (PANX1) are indispensable for efficient ATP release in response to ICD inducers. Surprisingly, we observed an unexpected link between PANX1 and the exposure of LAMP1 at the cell surface. These results will help to understand the mechanisms necessary for ATP secretion during ICD.In the second part of this work we further studied the surface exposure of CRT during ICD. We observed that mitoxantrone (MTX), which belongs to the group of anthracyclines, can induce a peripheral relocalisation of CRT, both in human cells and yeast cells. In addition, we showed that pheromones can act as a physiological inducer of CRT translocation in yeast. Focused siRNA screening combined with transcriptome analyses revealed that human CXCL8 (also called interleukin-8) and its mouse ortholog Cxcl2 play an essential role in the translocation of CRT to the cell surface. Interestingly, MTX-treated human cancer cells displayed an elevated production of CXCL8 in vitro. These results were confirmed in vivo, with MTX treated murine tumors, which also displayed elevated Cxcl2 levels. The MTX-induced CRT exposure was significantly reduced when we performed a knockdown of CXCL8/Cxcl2 receptors. Altogether, these results showed the importance of chemokine signaling circuitries in immunogenic CRT exposure.This work allows for the detailed understanding of the mechanisms of ICD and might thus be useful for further targeted drug development
Meunier, Anne. "Méthodes analytiques pour la détection de phénomènes biologiques de sécrétion à l'échelle de la cellule unique". Phd thesis, Université Pierre et Marie Curie - Paris VI, 2011. http://tel.archives-ouvertes.fr/tel-00858915.
Texto completo da fonteBenayoun, Sandra. "Glandes corticosurrénales : régulation de l'activité de l'axe corticotrope". Paris 5, 1996. http://www.theses.fr/1996PA05P048.
Texto completo da fonteAlharake, Jawad. "Study of genetic factors involved in enzyme secretion in hyperproductive strains of Trichoderma reesei". Electronic Thesis or Diss., université Paris-Saclay, 2023. http://www.theses.fr/2023UPASB061.
Texto completo da fonteFossil fuels are a major contributor to global warming, and their non-renewable nature is an impediment for building sustainable societies. In this context, second generation biofuels represent an attractive and more environmentally friendly alternative. The process of second-generation biofuel production consists of several steps including a physicochemical pretreatment of lignocellulosic (non-edible) biomass, the enzymatic hydrolysis of cellulose into glucose and the fermentation of simple sugars into biofuels, such as bioethanol. One of the main bottlenecks for a large implementation of this process is, however, the relatively high cost of hydrolytic enzymes, namely cellulases, used to deconstruct the pretreated lignocellulosic biomass into fermentable sugars.The filamentous fungus Trichoderma reesei is the preferred choice for industrial production of cellulases since it has hyperproduction and hypersecretion capacities. Industrial strains of T. reesei can secrete up to 100 g/L of cellulases in controlled industrial fermenters. In particular, the mutant strain Rut- C30 is a reference hyperproducer strain, but our incomplete understanding of its enhanced secretion system complicates further improvement of its hypersecretion capacity by genetic engineering. Therefore, this work aimed at unravelling the regulatory pathways controlling secretion and the secretion stress response in order to identify bottlenecks and to develop new strains with enhanced secretion capacity in the future.To this end, transcriptomic data were generated from cultivations of T. reesei Rut-C30 in different secretion stress conditions which allowed to identify potential components of secretion regulation that were targeted for deletion. As a complementary approach, mining of transcriptomic data obtained with other filamentous fungi in secretion stress conditions revealed further target genes potentially involved in the regulation of the secretion pathway. Finally, nine genes were deleted in the Rut-C30 strain, and the resulting strains phenotypically characterized. All of them displayed reduced growth and showed altered protein secretion behavior. RNA sequencing was performed on ∆res2, ∆rpn4 and ∆snd1 mutant strains and compared to that of Rut-C30 in the same culture conditions. Neither of the three transcription factors impacts transcription of genes involved in secretion or the secretion stress response in our conditions. However, in all three mutants, genes encoding enzymes of lipid metabolism are differentially expressed which could affect secretion in an indirect way. The results represent first clues to alleviate bottlenecks in secretion in T. reesei Rut-C30 and pave the way to develop strains with still improved secretion capacity
Youl, Estelle. "Syndrome métabolique, stress oxydant et insulino-sécrétion : étude in vivo et in vitro du mécanisme d’action des polyphénols". Montpellier 1, 2009. http://www.theses.fr/2009MON13519.
Texto completo da fonteOxidative stress (OS) induced by hyperglycaemia favors the progressive deficiency of insulin secretion through gluco-toxicity of endocrine pancreatic ß cells. OS can also occur in the absence of hyperglycaemia during metabolic syndrome (MS), or pre-diabetes, and favor the occurrence of cardiovascular complications and insulin secretion impairment. It is also known that the natural anti-oxidants polyphenols are susceptible to prevent cardiovascular complications and ß-cell apoptosis. In our work, we studied the effect of pure polyphenolic molecules from various families on a nutritionallyinduced MS model (the fructose-fed rat). We showed that the various polyphenols had differential effects on the various expressions of MS, and displayed similar effects on the prevention or cardiac fibrosis in relation with their anti-oxidant properties. The mechanism of two polyphenols, quercetine (Q) and resveratrol (R), as well as that of a synthetic antioxidant, N-acetyl cystein (NAC), were studied on a ß-cell model, the INS1 cell line, in the absence or presence of H2O2-induced OS. Q, but not R or NAC, potentiated glucose-induced insulin secretion and overactivated p42/44 MAPKinase (ERK1/2), a signaling pathways involved in the regulation of insulin secretion and ß-cell survival. Moreover, Q, but not R or NAC, protected ß-cell function against OS via ERK1/2 overactivation. This effect could possibly occur through the inhibition of JNK, a pathway activated by OS and a promoter of ERK1/2 dephosphorylation
Payet, Laurie-Anne. "Effets des acides gras saturés sur la voie de sécrétion. Relation avec la mucoviscidose". Thesis, Poitiers, 2013. http://www.theses.fr/2013POIT2299/document.
Texto completo da fonteSaturated fatty acids (SFA) have been reported to alter organelle integrity in many cell types. This process, also known as lipotoxicity, has been proposed to be responsible for several human pathologies such as type 2 diabetes.At the cellular level, SFA accumulation is associated with an increase of the saturation rate of membrane phospholipids (PL), the major components of organelle membranes, and an increase of ceramides levels, implicated in apoptosis induction.In the first part of this work, we took advantage of a simple yeast-based model to study the relative contributions of saturated PL and ceramides to SFA cytotoxicity. We demonstrated that ceramides act early in the secretory pathway, while saturated PL impact the later steps, and particularly the formation of secretory vesicles.In parallel, we observed that SFA amounts were significantly increased in the membrane PL of cystic fibrosis (CF) patient cells. The most common mutation responsible for this genetic disease results in the retention of the corresponding protein in the endoplasmic reticulum. Pharmacological agents, which correct the mistrafficking of the protein, have been isolated in vitro, but they did not show significant improvements in clinical trials. We propose in the present manuscript, that SFA-related lipointoxication could be an important bottleneck for the use of these pharmacological agents in clinical trials
Bussières, Ève-Line. "Stress maternel prénatal et développement précoce : données de naissance, attention et sécrétion cortisolaire à trois mois : association entre le stress maternel prénatal, l'âge gestationnel et le poids de naissance du bébé : une méta-analyse d'études prospectives : association entre le stress maternel prénatal, l'attention/éveil et la sécrétion cortisolaire de l'enfant à trois mois". Thesis, Université Laval, 2012. http://www.theses.ulaval.ca/2012/29070/29070.pdf.
Texto completo da fonteGoulaouic, Stéphane. "Effets des particules fines atmosphériques sur la sécrétion des cytokines pro-inflammatoires par les cellules THP-1 et mesures de marqueurs du stress oxydant". Thesis, Metz, 2009. http://www.theses.fr/2009METZ018S/document.
Texto completo da fonteParticles are concerning constituent of the atmospheric pollution, in particular the PM2,5 fraction (aerodynamic diameter lower than 2,5 µm) which is capable of penetrating into lungs up to alveoli. It can be the cause of inflammation processes leading to respiratory diseases. Studies have shown that alveolar macrophages exposed to PM2,5 secrete inflammatory cytokines. Identification of PM2,5 compounds responsible for observed effects, is not clarified yet. Factors such as the composition in metals and organic compounds, as well as the physical characteristics of particles have all been proposed as being involved in the induction of the inflammatory response. The aim of this thesis is to study in vitro effects of particles on the immune response of macrophages, specifically of the cell line THP-1. The parameters measured are the secretion of inflammatory and oxidative stress markers, in order to give a mechanistic explanation of observed phenomena. It was shown that PM2,5 induce in a significant way the secretion of cytokines IL-1[bêta] and IL-8. Black carbon particles (fine and ultrafine) coated with metals do not (or very slightly induce) a secretion of cytokines superior to that induced by uncoated particles. On the contrary, effect of polycyclic aromatic hydrocarbons (PAHs) adsorbed on particles surface depends on its size. Comparison between the effects of PAHs alone and those adsorbed on particles, showed that ultrafine particles potentiate PAH effects. Particle size appears to be the most determining parameter in the modulation of cytokines secretion. Ultrafine particles, characterized by a strong oxidizing potential, also induce an oxidative stress in vitro. They lead to the formation of a lipid peroxidation product, the HNE which is a mediator of the oxidative stress. However, HNE does not mime the oxidative stress induced by ultrafine particles