Traitement de la maladie de Vogt-Koyanagi-Harada : Une revue narrative de la littérature: Treatment of Vogt-Koyanagi-Harada disease: A narrative literature review

Non-traumatic, exudative, bilateral panuveitis associated with extraocular manifestations, Vogt-Koyanagi-Harada disease (VKH) is an autoimmune disease mediated by Th1 lymphocytes reacting against melanocytes. It is a rare disease with female predominance. VKH disease is a diagnostic and therapeutic emergency. Treatment is based mainly on early and aggressive corticosteroid therapy to shorten the duration of the disease, prevent progression to chronicity, and reduce the incidence of extraocular manifestations. It is a corticosteroid-responsive disease, but unfortunately, relapses in the form of anterior uveitis are not rare, mainly at the time or at the end of tapering of corticosteroids. In these situations, or in case of intolerance to prolonged corticosteroid therapy, the use of conventional immunosuppressive agents or immunomodulatory drugs able to suppress the lymphocyte response is recommended. Intravenous immunoglobulins may also be used in patients with relapse or attack of the disease. In the present study, we performed a narrative literature review to summarize the different therapeutic aspects of VKH in the form of treatment algorithm. Panuvéite bilatérale non traumatique, exsudative, associée à des manifestations extraoculaires, la maladie de Vogt-Koyanagi-Harada (VKH) est une maladie auto-immune médiée par les lymphocytes Th1 réagissant contre les mélanocytes. C’est une maladie rare à prédominance féminine. La maladie de VKH est une urgence diagnostique et thérapeutique. Le traitement repose essentiellement sur une corticothérapie précoce et agressive avec possibilité de dégression progressive lente sur plusieurs mois, afin deraccourcir la durée de la maladie, d’empêcher la progression vers la chronicité, et de réduire l’incidence des manifestations extraoculaires. C’est une maladie corticosensible, mais malheureusement des rechutes sous forme d’uvéite antérieure ne sont pas rares, principalement au moment ou en fin de dégression de la corticothérapie. Dans ces situations ou en cas d’intolérance à la corticothérapie prolongée, le recours aux immunosuppresseurs conventionnels ou médicaments immunomodulateurs capables de supprimer la réponse lymphocytaire est de règle. Les immunoglobulines intraveineuses peuvent également être proposées chez les patients présentant une rechute ou une poussée de la maladie. Dans la présente étude, nous réalisons une revue narrative de la littérature en décrivant les différents aspects thérapeutiques de la maladie de VKH afin de les résumer sous forme d’un algorithme thérapeutique

Cyclic Naphthalene Diimide with a Ferrocene Moiety as a Redox-Active Tetraplex-DNA Ligand

Cyclic naphthalene diimides (cNDIs), with a ferrocene moiety (cFNDs) and different linker lengths between the ferrocene and cNDI moieties, were designed and synthesized as redox‐active, tetraplex‐DNA ligands. Intramolecular stacking was observed between ferrocene and the NDI planes, which could affect the binding properties for G‐quadruplexes. Interestingly, the circular dichroism spectrum of one of these compounds clearly shows new Cotton effects around 320–380 and 240 nm, which can be considered a direct evidence of intramolecular stacking of ferrocene and the NDI. Regarding recognition of hybrid G‐quadruplexes, the less rigid structures (longer linkers) show higher binding affinity (106 M−1 order of magnitude). All new compounds show higher selectivity for G4 during electrochemical detection than noncyclic FND derivatives, which further identifies the redox‐active potentiality of the cFNDs. Two of the three compounds tested even show preferential inhibition of cell growth in cancer cells over normal cells in a low concentration range, highlighting the potential for bioapplications of these cFNDs

K-ras mutation in the endometrium of tamoxifen-treated breast cancer patients, with a comparison of tamoxifen and toremifene

The putative presence of a mutation in codon 12 of the K-ras gene was investigated in the endometrium of tamoxifen (TAM) and toremifene (TOR)-treated breast cancer patients. DNA was extracted from fresh cytologic samples of the endometrium in 86 TAM and 21 TOR-treated breast cancer patients. Mutations were detected by enriched PCR and an enzyme-linked mini-sequence assay (ELMA). K-ras mutation was found in 35 TAM-treated endometrial samples, and in only one TOR-treated endometrium (P<0.003). In 24 premenopausal patients, K-ras mutation was found in seven (43.8%) of 16 patients with less than 47 months of TAM treatment, while none was found in eight patients with more than 48 months of TAM treatment (P<0.03). In 62 postmenopausal-amenorrheic patients, K-ras mutation was found in three (15.8%) of 19 patients with less than 23 months of TAM treatment, while it was found in 16 (61.5%) of 26 patients with 24–47 months of TAM treatment and nine (52.9%) of 17 patients with more than 48 months of TAM treatment (P=0.002). The presence of K-ras mutation is significantly influenced by the duration of TAM treatment and menstrual status of the patients. TOR may have a lower potential genotoxicity than TAM

C-jun Inhibits Mammary Apoptosis In Vivo

c-Jun mediates ROS production and apoptosis