9 research outputs found

    Emergency left colon resection for acute perforation: primary anastomosis or Hartmann's procedure? A case-matched control study.

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    BACKGROUND: The optimal treatment remains controversial for acute left-sided colon perforation. Therefore, the effectiveness and safety of primary anastomosis versus Hartmann's operation (HP) was compared in a case-matched control study. METHODS: Thirty consecutive patients with primary anastomosis and protective ileostomy (PAS) were matched to 30 HP patients, controlling for age, gender, American Society of Anesthesiologists (ASA) score, body mass index (BMI), and peritonitis severity (Hinchey). In a second analysis, PAS patients with purulent peritonitis (Hinchey 3) were matched to patients with primary anastomosis without ileostomy (PA). RESULTS: Hospital mortality was similar between HP (17%) and PAS (10%). Complication frequency and severity (requiring re-intervention or admission to the Intensive Care Unit [ICU]) were comparable for the first operation (60% versus 56% and 30% versus 32%). The stoma reversal rate was higher in PAS than in HP (96% versus 60%, p = 0.001), with significantly fewer complications (23% versus 66%, p = 0.02), and lower severity (7% versus 33%, p = 0.02). Additional analysis of PAS versus PA showed similar morbidity (52% versus 41%, p = 0.45) and complication severity (18% versus 24%, p = 0.51), whereas overall operation time and hospital stay were significantly shorter in PA (169 versus 320 min, p = 0.003, 17 versus 28 days, p < 0.001). CONCLUSIONS: Primary anastomosis and protective ileostomy is a superior treatment to HP in acute left-sided colon perforation. In the absence of feculent peritonitis an ileostomy appears unnecessary

    Alteration of blood clot structures by interleukin-1 beta in association with bone defects healing

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    The quality of hematomas are crucial for successful early bone defect healing, as the structure of fibrin clots can significantly influence the infiltration of cells, necessary for bone regeneration, from adjacent tissues into the fibrin network. This study investigated if there were structural differences between hematomas from normal and delayed healing bone defects and whether such differences were linked to changes in the expression of IL-1β. Using a bone defect model in rats, we found that the hematomas in the delayed healing model had thinner fibers and denser clot structures. Moreover, IL-1β protein levels were significantly higher in the delayed healing hematomas. The effects of IL-1β on the structural properties of human whole blood clots were evaluated by thrombelastograph (TEG), scanning electronic microscopy (SEM), compressive study, and thrombolytic assays. S-nitrosoglutathione (GSNO) was applied to modulate de novo hematoma structure and the impact on bone healing was evaluated in the delayed healing model. We found that GSNO produced more porous hematomas with thicker fibers and resulted in significantly enhanced bone healing. This study demonstrated that IL-1β and GSNO had opposing effects on clot architecture, the structure of which plays a pivotal role in early bone healing

    The role of the acquired immune response in systemic sclerosis

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    Profound alterations characterize the adaptive immune response in systemic sclerosis, and several layers of evidence support a prominent role exerted by immune cellular effectors and humoral mediators in the pathogenesis of this disease. These include (i) the presence of oligoclonal T cells in tissues undergoing fibrosis consistent with (auto)antigen-specific recruitment, (ii) the preferential expansion of polarized CD4+ and CD8+ T cells producing pro-fibrotic cytokines such as IL-4 and IL-13, (iii) the presence of increased number of cells producing mediators belonging to the IL-17 family, including IL-22, which may drive and participate in inflammatory pathways involving epithelial cells as well as fibroblasts, (iv) the deficient or redirected function of T regulatory cells favoring fibrosis, and (v) the enhanced expression of CD19 and CD21 on naïve B cells, and the upregulation of co-stimulatory molecules in mature B cells, which together with the increased levels of B cell activating factor (BAFF) underlie the propensity to an exaggerated humoral response possibly favoring fibrogenesis. Despite all the progress made in understanding the features of the aberrant immune response in scleroderma, it remains unclear whether the activation of immune effector pathways ultimately drives the disease pathogenesis or rather represents a defective attempt to limit or even reverse excessive extracellular matrix deposition and progressive vasculopathy, the main hallmarks of this disease

    Inflammation and immunity

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    Fermente

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