Literatura científica selecionada sobre o tema "Charbon (maladie) – Thérapeutique"
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Artigos de revistas sobre o assunto "Charbon (maladie) – Thérapeutique"
Desoubeaux, Guillaume, e Mireia Pelegrin. "Anticorps monoclonaux en infectiologie". médecine/sciences 35, n.º 12 (dezembro de 2019): 1008–13. http://dx.doi.org/10.1051/medsci/2019200.
Texto completo da fonteClavere, Albane. "Un espoir thérapeutique contre la maladie de Charcot ?" Cerveau & Psycho N° 164, n.º 4 (25 de março de 2024): 11. http://dx.doi.org/10.3917/cerpsy.164.0011.
Texto completo da fonteM, J. M. "Maladie de Charcot-Marie-Tooth : l’essai thérapeutique se poursuit". Revue Francophone des Laboratoires 2017, n.º 490 (março de 2017): 13. http://dx.doi.org/10.1016/s1773-035x(17)30063-1.
Texto completo da fonteZamoum, Radia, e Salma Kaddour. "Methemoglobinemia and Dapsone overdose : A Literature review". Batna Journal of Medical Sciences (BJMS) 7, n.º 2 (9 de novembro de 2020): 167–70. http://dx.doi.org/10.48087/bjmsra.2020.7222.
Texto completo da fonteMignot, T., L. Maillard, V. Laprevote, R. Schwan e C. Hingray. "Crises psychogènes non épileptiques : une maladie émotionnelle ?" European Psychiatry 30, S2 (novembro de 2015): S117. http://dx.doi.org/10.1016/j.eurpsy.2015.09.224.
Texto completo da fonteYOUAN, Bi-Botti Celestin. "Systèmes nanoparticulaires : Applications phytopharmaceutiques et cosmétiques". Journal Africain de Technologie Pharmaceutique et Biopharmacie (JATPB) 2, n.º 3 (20 de dezembro de 2023). http://dx.doi.org/10.57220/jatpb.v2i3.116.
Texto completo da fonteTeses / dissertações sobre o assunto "Charbon (maladie) – Thérapeutique"
Golicki, Isabelle. "Les propriétés hépatoprotectrices du chardon Marie (Silybum Marianum L. )". Paris 5, 1998. http://www.theses.fr/1998PA05P099.
Texto completo da fonteBelin, Sophie. "Acide ascorbique et pathologies humaines : de la maladie rare à la maladie fréquente". Aix-Marseille 2, 2009. http://www.theses.fr/2009AIX20703.
Texto completo da fontePitard, Irène. "Analyse du mécanisme d'action d'inhibiteurs ciblant l'activation allostérique du facteur œdématogène de Bacillus anthracis". Electronic Thesis or Diss., Sorbonne université, 2020. http://www.theses.fr/2020SORUS420.
Texto completo da fonteEdema factor (EF), a major Bacillus anthracis toxin, is activated by host calmodulin (CaM) to produce supraphysiological concentrations of cyclic AMP (cAMP) thus perturbing intracellular signaling. The EF-CaM interaction induces conformational changes in an allosteric switch region of EF that lead to the formation of the catalytic site. Previous in silico studies targeting this switch region, complemented with experimental data, showed that thiophen ureidoacids (TUA) inhibit the enzyme catalytic activity. However, knowledge of the binding site and inhibition mode of TUA compounds are still lacking. Here, we characterize the interaction of the most active TUA compound (TUA-diCl) with EF, CaM and EF-CaM using biochemical assays coupled to biophysical methods and molecular modeling. We show that TUA-diCl interacts with EF, EF-CaM and unexpectedly with CaM. Mapping of the binding site by NMR, showed that TUA-diCl binds to the exposed hydrophobic patches of calcium loaded CaM, causing the compaction and changes in internal dynamics of the protein. Importantly, enzymatic, fluorescence and NMR data show that EF inhibition is due to the interaction of the compound with EF and is CaM-independent. Furthermore, competition experiments between TUA-diCl and the EF catalytic-site inhibitor 2’-MANT-3’-dATP, indicate that TUA-diCl is an allosteric inhibitor of EF. HDX-MS identifies a putative binding site of TUA-diCl on the helical domain of EF, a critical region for CaM insertion. Several possible binding pockets in the helical domain are analyzed in silico. TUA-diCl represents a new class of EF inhibitors with an allosteric mechanism, opening the way towards the design of innovative therapeutic compounds
Charvin, Delphine. "Dopamine et dégénérescence des neurones striataux dans la maladie de Huntington : vers l'identification de nouvelles cibles thérapeutiques". Phd thesis, Université Pierre et Marie Curie - Paris VI, 2005. http://tel.archives-ouvertes.fr/tel-00069699.
Texto completo da fonteCaillaud, Martial. "Etude des effets thérapeutiques de la curcumine dans des modèles in vitro et in vivo de neuropathies périphériques". Thesis, Limoges, 2018. http://www.theses.fr/2018LIMO0047/document.
Texto completo da fontePeripheral nerves are subject to many pathologies and the etiology of peripheral neuropathies (PN) is vast (metabolic disorders, infections, toxins, physical injuries and genetic mutations, etc.). For example, PN of traumatic origin are common and are characterized by a called Wallerian degeneration of nerve fibres. Another example is Charcot-Marie-Tooth disease 1A (CMT1A), which is the most common hereditary genetic PN. It is characterized by an overexpression of the PMP22 protein involved in maintaining the myelin sheath. Currently, there is no pharmacological treatment for these two nerve disorders. Recently, interest in the role of dietary antioxidants, such as curcumin, has led to much research. This molecule has long been used in Asian medicine for its therapeutic properties. However, it has a very low bioavailability and therefore requires the use of very high doses to obtain beneficial effects. In a first study, our results showed that low doses of curcumin administered locally and continuously improve functional recovery, electrophysiological and histological parameters, and expression of major myelin proteins in a rat sciatic nerve crush model. These beneficial effects have been attributed to the antioxidant properties of curcumin. In a second study, our results showed that a low dose of curcumin nanocrystals (Nano-Cur), injected in IP, improves phenotype, electrophysiological and histological parameters in a transgenic model of CMT1A rats. In this study, the positive effects were attributed to the antioxidant properties of the Nano-cur, coupled with the activation of the endoplasmic reticulum associated degradation pathway, allowing the reduction of harmful overexpression of PMP22 in CMT1A rats. All these results show that the administration of low doses of curcumin is a promising treatment for peripheral nerve repair
Kauntz, Henriette. "Cellular and molecular targets of silibinin, a natural flavonoid, in colorectal cancer prevention and therapy". Thesis, Strasbourg, 2012. http://www.theses.fr/2012STRAJ052/document.
Texto completo da fonteColorectal cancer (CRC) is the second most common cause for cancer-related deaths in Europe and in the USA. Because of the limited efficacy and considerable toxicity of chemotherapeutic agents, new approaches are needed. The hepatoprotective flavonolignan silibinin is the major biologically active compound of the milk thistle (Silybum marianum).The molecular mechanisms of the anticancer properties of silibinin in CRC were studied in an in vitro model of cancer progression consisting of the adenocarcinoma cell line SW480 and its derived metastatic cell line SW620. Its chemopreventive effects were assessed in an in vivo model of azoxymethane-induced colon carcinogenesis in the rat. Silibinin induced apoptotic cell death with activation of caspase-3 in both cell lines. The expression of death receptors was upregulated, and caspase-8 was activated. The potential of the mitochondrial membrane was perturbed permitting the release of cytochrome c and the activation of caspase-9. Besides the activation of the extrinsic and the intrinsic apoptotic pathway, silibinin induced an autophagic response. Combination of silibinin and TRAIL, a promising anticancer agent selectively inducing apoptosis in cancer cells, induced synergistic cell death in both cell lines. Synergy in cell death induction was also observed by the combination of silibinin and the histone deacetylase (HDAC) inhibitors TSA and SAHA. In the preclinical model in the rat, silibinin administration was able to reduce by half the number of preneoplastic lesions present in the colon. In conclusion, silibinin is a promising natural agent for colon cancer chemoprevention and for combination therapy with TRAIL/HDAC inhibitors