Publications by authors named "Agnes Bellocq"

The physiotherapist's practice involves taking care of patients with various chronic pathologies: neurological, rheumatic, respiratory, etc. The physiotherapist must carry out an educational approach in these patients, at the same time as the physical work of re-education, in order to induce behavioural changes beneficial to their physical and psychological health and to empower them in the best possible way in the management of their pathology.

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The benefit of exercise has been demonstrated in asthma, but the role of pulmonary rehabilitation (PR) in people with severe asthma, especially with airway obstruction, has been less investigated. The activity limitation mechanisms differ in asthma and COPD, so the effect of a PR program not specific to asthma is unclear. We retrospectively compared the effect of an ambulatory PR program in nonsmoking patients with severe asthma and airway obstruction (FEV1/FVC ratio <70% and FEV1 < 80% measured twice, not under an exacerbation) and sex-, age-, FEV1-, and BMI-matched COPD controls.

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The use of a mouthpiece to measure ventilatory flow with a pneumotachograph (PNT) introduces a major perturbation to breathing ("instrumental/observer effect") and suffices to modify the respiratory behavior. Structured light plethysmography (SLP) is a non-contact method of assessment of breathing pattern during tidal breathing. Firstly, we validated the SLP measurements by comparing timing components of the ventilatory pattern obtained by SLP vs.

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Background: Reduced exercise capacity severely impacts quality of life in pulmonary Langerhans cell histiocytosis. Ascertaining mechanisms that impair exercise capacity is necessary to identify targets for symptomatic treatments.

Methods: Dyspnea, pulmonary function tests and cardiopulmonary exercise test were analysed in 62 study participants.

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Objective: Calpains, calcium-activated proteases, mediate the angiogenic signals of vascular endothelial growth factor. However, their involvement in vascular repair has not been investigated and the underlying mechanisms remain to be fully elucidated.

Methods And Results: A rapidly progressive form of glomerulonephritis in wild type and transgenic mice expressing high levels of calpastatin, a calpain-specific inhibitor, was studied.

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Rejection of solid organ allograft involves alloreactive T-cell expansion. The importance of NF-κB and NFAT in this process is underscored by the therapeutic efficacy of immunosuppressive agents, which target the two transcription factors. Since calpains, calcium-activated proteases, are involved in the activation of NF-κB and NFAT, we investigated the role of calpains in allograft rejection.

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In hypertension, angiotensin (Ang) II is a critical mediator of cardiovascular remodeling, whose prominent features include myocardial and vascular media hypertrophy, perivascular inflammation, and fibrosis. The signaling pathways responsible for these alterations are not completely understood. Here, we investigated the importance of calpains, calcium-dependent cysteine proteases.

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Glomerular injury and albuminuria in acute glomerulonephritis are related to the severity of inflammatory process. Calpain, a calcium-activated cysteine protease, has been shown to participate in the development of the inflammatory process. Therefore, for determination of the role of calpain in the pathophysiology of acute glomerulonephritis, transgenic mice that constitutively express high levels of calpastatin, a calpain-specific inhibitor protein, were generated.

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Repair of inflammatory and/or ischemic renal injury involves endothelial, mesangial and epithelial regeneration. These structures may be rebuilt by resident progenitor cells and bone marrow-derived stem cells. Resident progenitor cells in adult kidney have not yet been conclusively identified.

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Ischemic acute renal failure is characterized by damages to the proximal straight tubule in the outer medulla. Lesions include loss of polarity, shedding into the tubule lumen, and eventually necrotic or apoptotic death of epithelial cells. It was recently shown that peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta) increases keratinocyte survival after an inflammatory reaction.

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15-deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)) is involved in the control of inflammatory reaction. We tested the hypothesis that 15d-PGJ(2) would exert this control in part by modulating the sensitivity of inflammatory cells to glucocorticoids. Human U937cells and mouse RAW 264.

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Calpains are cysteine proteases first identified 50 years ago. Because they are present in the cytosol of mammalian cells and because they are activated in response to Ca2+ mobilization, they are thought to be involved mainly in cell signalling pathways. They could participate in cellular responses such as apoptosis, proliferation, extracellular matrix adhesion and motility, that have relevance to pathophysiological issues in ischemia, inflammation, repair and tumor progression.

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Background: Although the possibility of reversing hepatopulmonary syndrome (HPS) after liver transplantation is now well established, the proportion of patients in whom reversibility is observed and the time to resolution of HPS remain uncertain.

Methods: We analyzed the outcome of all adult patients with HPS who underwent orthotopic liver transplantation in all the liver transplant centers in Paris, during a 10-year period.

Results: Twenty-three adult patients (median age, 47 years; range, 14-64) underwent transplantation in four institutions.

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Background: Renal inflammation is regulated by a network of local and systemic mediators. Of them, transforming growth factor-beta1 (TGF-beta 1) and glucocorticoids play an important role in deactivating monocytes/macrophages. We examined the hypothesis that TGF-beta 1 effects may be partially achieved through modulation of the sensitivity of these cells to glucocorticoids.

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NF-kappa B comprises a family of transcription factors. These are thought to have a central role in the expression of genes involved in cell mobilization, cell proliferation and cell differentiation, and, hence, in inflammation, repair and fibrosis processes. In particular, NF-kappa B activation appears to drive a number of inflammatory diseases of the kidney and their progression to end-stage renal failure.

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