108 research outputs found

    L’incompatibilité entre le mandat parlementaire et l'exercice de fonctions de direction et d'administration

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    International audienceno

    Les conséquences de la diffusion d'un message télévisé en faveur d'un candidat le jour du scrutin

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    International audienceno

    Il y a 180 ans : l'acte additionnel aux constitutions de l'Empire ou l'éphémère retour de Napoléon Bonaparte

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    International audienceno

    Ouverture de l’université sportive d’été

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    Photo 1 – À la tribune, de gauche à droite, le président Ernest Gibert, le conférencier Jean Durry et Jean-Marc Michel pour l’UJSF. Photo 2 – Jean-François Renault pendant sa communication. Photo 3 – Thierry Buffalon, animateur de la 4e séquence. Photo 4 – Le groupe des stagiaires. Daniel BONZOMSMontpellier Université Club Monsieur le Président de l’Université de Montpellier 1, Monsieur le Président de l’Union nationale des clubs universitaires, Chers amis, J’avais préparé cette ouverture ..

    Characterization and Validation of a Chronic Model of Cyclophosphamide-Induced Interstitial Cystitis/Bladder Pain Syndrome in Rats

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    Interstitial cystitis/Bladder Pain Syndrome (IC/BPS) is a chronic inflammatory disease characterized by visceral pain and voiding symptoms. IC/BPS is still an unsolved enigma with ineffective diagnosis criteria and treatment. A main limitation in IC/BPS understanding is the lack of appropriate preclinical model. Cyclophosphamide (CYP) is commonly used as an experimental model for IC/BPS in rodent. However, the proposed models are very aggressive, contrasting with what occurs in clinic, and often associated with severe toxicity and high mortality rate. In addition, visceral pain, the hallmark symptom of IC/BPS, has been validated in only few of them. In this study, we developed a chronic model of CYP-induced IC/BPS in female rat. In our protocol, no severe weight loss occurred and the survival rate was 100%. In accordance to human pathology, chronic CYP-injected rats developed severe painful behavior whereas only sparse inflammation was observed. Inflammatory response was characterized by bladder edema and focal urothelial damage but absence of massive infiltrate. This chronic model showed persistent symptoms indicative for a central sensitization mechanism. We further demonstrate that CYP-induced chronic visceral pain was significantly reduced by curative treatment with clinically relevant compounds (gabapentin, ibuprofen, and Ialuril ®). We therefore developed and validated a rat model of chronic cystitis that shares strong similarity with human non-ulcerative IC/BPS features without overtly affecting the animal health. This model will thus provide mechanistic insights of the disease and help to evaluate therapeutic agents for IC/BPS

    Experimental in vivo model to evaluate the impact of Cernitin™ on pain response on induced chronic bladder inflammation

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    Objective: Inflammation of the urinary bladder may cause burdensome pain also called bladder pain syndrome (BPS). A limitation in understanding BPS pathophysiology is the lack of appropriate preclinical model. Previously published clinical and preclinical studies revealed positive impact of Cernitin™ on pain relief in chronic prostatitis. The objective of this study was to evaluate the effects of Cernitin™ on induced inflammation of the urinary bladder in rats. We also sought to identify biomarkers which might play a role in the management of BPS. Materials and methods: Cystitis was induced by injection of cyclophosphamide (CYP) in female rats. Thereafter, animals were randomly divided into four treatment groups and two control groups. Evaluation of pain scores was assessed by von Frey assay. Expression of pain- and pro-inflammatory biomarkers was determined by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry. Results: Treatments with Cernitin™ displayed significant anti-nociceptive effects on CYP-induced visceral pain (p <.01). In contrast, vehicle-treated animals showed high pain score even at the lowest force. Furthermore, results of ELISA showed that Cernitin™-treated animals had significantly reduced levels of COX-2 (T60, p <.01; GBX, p <.05) in bladder tissue homogenate. Immunohistochemical (IHC) staining of bladder tissues showed that Cernitin™-treated animals exhibited less CD45-positive cells, while massive CD45-positive cells infiltration was detected in vehicle-treated animals. IHC also revealed lower SP and PGD2 expression levels in Cernitin™-treated tissues. Conclusions: Cernitin™ components reduced pain score and inflammatory marker COX-2. Our findings suggest a potential therapeutic role for Cernitin™ in the management of BPS
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