78 research outputs found

    Régime pauvre en hydrates de carbone et douleurs articulaires: quel rapport? [Low-carb diet and joint pain: how are they related?]

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    We report the case of a 69-year-old male who presented with acute bilateral ankle pain treated as acute gouty arthritis but resistant to colchicine and NSAIDs. In view of very high inflammatory parameters, septic arthritis was initially suspected but ruled out by joint aspiration; the final diagnosis was gouty arthritis. He finally responded well to a short course of oral prednisone. We found this case interesting in view of the initial differential diagnosis and association with a low-carb diet, known to be associated with many metabolic complications among which gout is frequent. [Authors]]]> Diet, Carbohydrate-Restricted ; Arthritis, Gouty fre oai:serval.unil.ch:BIB_F31B6FE6921F 2022-05-07T01:30:01Z openaire documents urnserval <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> https://serval.unil.ch/notice/serval:BIB_F31B6FE6921F The 1925 Opium Purchasing Campaign in Laos: The Anatomy of a Colonial Scandal Rapin, A.-J. info:eu-repo/semantics/other misc 2014 <![CDATA[Opium purchasing campaigns, initiated in 1915, were abruptly interrupted ten years later following the discovery that the Douanes &amp; Régies of the General Government of Indochina had been victim of a gigantic fraud. Various inquiries expedited with a view to establishing responsibility for the fiasco, involving purchases made at Luang Prabang in 1925, highlight the dysfunctions affecting the colonial civil service. The 1925 scandal revealed not only the difficulties encountered by the French in their attempts to control the drug trade, but also the prevailing circumstantial inefficiency of the colonial bureaucracy

    Electron-Microscopy Investigations of the Warping Effect in Pigmented High Density Polyethylene

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    The warping effect of high-density polyethylene (HDPE) articles produced by organic pigmentation has been studied by scanning electron microscopy. A warping pigment and its warp-free analogue obtained by surface treatment have been observed and compared to an inorganic warp-free pigment. The results indicate that the generally accepted nucleation theory is not sufficient to describe fully the warping effect. An attempt is made to describe this effect in terms of pigment-polymer compatibility

    Physical activity and energy expenditure in rheumatoid arthritis patients and matched controls

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    Objectives. To compare daily energy expenditure between RA patients and matched controls, and to explore the relationship between daily energy expenditure or sedentariness and disease-related scores. Methods. One hundred and ten patients with RA and 440 age- and sex-matched controls were included in this study. Energy expenditure was assessed using the validated physical activity (PA) frequency questionnaire. Disease-related scores included disease activity (DAS-28), functional status (HAQ), pain visual analogue scale (VAS) and fatigue VAS. Total energy expenditure (TEE) and the amount of energy spent in low- (TEE-low), moderate- (TEE-mod) and high-intensity (TEE-high) PAs were calculated. Sedentariness was defined as expending <10% of TEE in TEE-mod or TEE-high activities. Between-group comparisons were computed using conditional logistic regression. The effect of disease-related scores on TEE was investigated using linear regression. Results. TEE was significantly lower for RA patients compared with controls [2392 kcal/day (95% CI 2295, 2490) and 2494 kcal/day (2446, 2543), respectively, P = 0.003]. A significant difference was found between groups in TEE-mod (P = 0.015), but not TEE-low (P = 0.242) and TEE-high (P = 0.146). All disease-related scores were significantly poorer in sedentary compared with active patients. TEE was inversely associated with age (P < 0.001), DAS-28 (P = 0.032) and fatigue VAS (P = 0.029), but not with HAQ and pain VAS. Conclusion. Daily energy expenditure is significantly lower in RA patients compared with matched controls, mainly due to less moderate-intensity PAs performed. Disease activity and fatigue are important contributing factors. These points need to be addressed if promoting PA in RA patients is a health goal. Trial registration. ClinicalTrials.gov, http://clinicaltrials.gov, NCT0122881

    Evaluation of the Interaction Between TGF β and Nitric Oxide in the Mechanisms of Progression of Colon Carcinoma

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    It is recognised that stromal cells determine cancer progression. We have previously shown that active TGFβ produced by rat colon carcinoma cells modulated NO production in rat endothelial cells. To elucidate the role of TGFβ and NO in the mechanisms of interaction of colon carcinoma cells with stromal cells and in cancer progression, we transfected REGb cells, a regressive colon carcinoma clone secreting latent TGFβ, with a cDNA encoding for a constitutively-secreted active TGFβ. Out of 20 injected rats only one tumour progressed, which was resected and sub-cultured (ReBeta cells). ReBeta cells secreted high levels of active TGFβ. The adhesive properties of REGb and Rebeta cells to endothelial cells were similar, showing that the secretion of active TGFβ is not involved in tumour cell adhesion to endothelial cells. ReBeta, but not REGb, cell culture supernatants inhibited cytokine-dependent NO secretion by endothelial cells, but inhibition of NO production was similar in co-cultures of REGb or ReBeta cells with endothelial cells. Therefore, secretion of active TGFβ regulated endothelial NO synthase activity when tumour cells were distant from, but not in direct contact with, endothelial cells. However, only ReBeta cells inhibited cytokine-dependent secretion of NO in coculture with macrophages, indicating that the active-TGFβ-NO axis confers an advantage for tumour cells in their interaction with macrophages rather than endothelial cells in cancer progressio

    Helper-dependent adenovirus vectors devoid of all viral genes cause less myocardial inflammation compared with first-generation adenovirus vectors

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    Abstract. : Background: : First-generation, E1-deleted (ΔE1) adenovirus vectors currently used in cardiovascular gene therapy trials are limited by tissue inflammation, mainly due to immune responses to viral gene products. Recently, helper-dependent (HD; also referred to as "gutless”) adenovirus vectors devoid of all viral coding sequences have been shown to cause low inflammation when injected intravenously or into skeletal muscles. However, HD vectors have not been evaluated in cardiovascular tissues. Methods and results: : HD and ΔE1 vectors containing a cytomegalovirus-driven expression cassette for the green fluorescent protein (GFP) gene were administered intramyocardially to adult rats (n = 54). GFP expression was measured by ELISA at varying time intervals after gene transfer. HD and ΔE1 vectors were equally efficient at transducing the myocardium. Tissue inflammation was assessed by immunostaining for leukocytes and quantitative real-time RT-PCR for cytokine mRNA expression. Monocyte/macrophages, CD4+ and CD8+ lymphocytes infiltrating the myocardium were less abundant with HD than ΔE1 vectors. Transcripts levels for pro-inflammatory cytokines such as IL-1β, tumor necrosis factor-α, and RANTES were decreased with HD vectors. However, both vectors were associated with a decline in GFP expression over time, although low-level expression was occasionally detectable 10 weeks after HD vector administration. The two vectors transduced endothelial cells in rat arteries (n = 11) with comparable efficiencies. Vascular GFP expression was not detectable at 10 weeks. Conclusions: : HD vectors are as efficient as ΔE1 vectors at transducing the myocardium and vascular endothelium, while causing less myocardial inflammation. Thus, HD vectors may be superior to earlier-generation adenovirus vectors for cardiovascular gene therapy application

    Gene transfer of soluble interleukin-17 receptor prolongs cardiac allograft survival in a rat model

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    Objective: Interleukin-17 (IL-17), a potent proinflammatory cytokine, has been implicated in allograft rejection. We analyzed the efficacy of an adenoviral vector expressing an IL-17 inhibitor in delaying acute allograft rejection in a rat model of heart transplantation, and the biological mechanisms underlying the protective effect. Methods: We constructed an adenoviral vector expressing a soluble IL-17 receptor-immunoglobulin (IL-17R-Ig) fusion protein. IL-17R-Ig activity was assessed by inhibition of IL-17-induced IL-6 release in HeLa cells preincubated with the vector. Intracoronary vector administration was performed in F344 donor hearts that were placed as vascularized grafts into Lewis hosts. Inflammatory cells infiltrating the graft were analyzed by immunohistology. Cytokine transcripts in the graft were determined by real-time RT-PCR. Results: IL-17R-Ig gene transfer resulted in prolonged allograft survival (16.1 ± 3.1 days vs 10.3 ± 2.5 days with control virus and 10.1 ± 2.1 days with virus dilution buffer alone; p ≪ 0.001). IL-17R-Ig gene transfer reduced inflammatory cell infiltrates, especially monocytes/macrophages and CD4+ T cells (p ≪ 0.05). It also reduced intragraft cytokine transcripts for interferon-γ and transforming growth factor-β (p ≪ 0.05) and, to a lesser extent, IL-1β and tumor necrosis factor-α (p = 0.083). Conclusions: Local expression of soluble IL-17 receptor-immunoglobulin attenuates T helper type 1 (Th1) cytokine responses and leukocyte infiltration in rat cardiac allografts, thereby mediating prolonged graft survival. Intragraft IL-17 inhibition may be useful as an adjuvant therapy to systemic immunosuppression in heart transplantatio

    Gene transfer of a soluble IL-1 type 2 receptor-Ig fusion protein improves cardiac allograft survival in rats

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    Objective: Interleukin-1 (IL-1) mediates ischemia-reperfusion injury and graft inflammation after heart transplantation. IL-1 affects target cells through two distinct types of transmembrane receptors, type-1 receptor (IL-1R1), which transduces the signal, and the non-signaling type-2 receptor (IL-1R2), which acts as a ligand sink that subtracts IL-1β from IL-1R1. We analyzed the efficacy of adenovirus (Ad)-mediated gene transfer of a soluble IL-1R2-Ig fusion protein in delaying cardiac allograft rejection and the mechanisms underlying the protective effect. Methods: IL-1 inhibition by IL-1R2-Ig was tested using an in vitro functional assay whereby endothelial cells preincubated with AdIL-1R2-Ig or control virus were stimulated with recombinant IL-1β or tumor necrosis factor-α (TNF-α), and urokinase-type plasminogen activator (u-PA) induction was measured by zymography. AdIL-1R2-Ig was delivered to F344 rat donor hearts ex vivo, which were placed in the abdominal position in LEW hosts. Intragraft inflammatory cell infiltrates and proinflammatory cytokine expression were analyzed by immunohistochemistry and real-time reverse transcriptase-polymerase chain reaction (RT-PCR), respectively. Results: IL-1R2-Ig specifically inhibited IL-1β-induced u-PA responses in vitro. IL-1R2-Ig gene transfer reduced intragraft monocytes/macrophages and CD4+ cell infiltrates (p≪0.05), TNF-α and transforming growth factor-β (TGF-β) expression (p≪0.05), and prolonged graft survival (15.6±5.7 vs 10.3±2.5 days with control vector and 10.1±2.1 days with buffer alone; p≪0.01). AdIL-1R2-Ig combined with a subtherapeutic regimen of cyclosporin A (CsA) was superior to CsA alone (19.4±3.0 vs 15.9±1.8 days; p≪0.05). Conclusions: Soluble IL-1 type-2 receptor gene transfer attenuates cardiac allograft rejection in a rat model. IL-1 inhibition may be useful as an adjuvant therapy in heart transplantatio
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