43 research outputs found

    Regulation and Repair of the Alveolar-Capillary Barrier in Acute Lung Injury

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    Considerable progress has been made in understanding the basic mechanisms that regulate fluid and protein exchange across the endothelial and epithelial barriers of the lung under both normal and pathological conditions. Clinically relevant lung injury occurs most commonly from severe viral and bacterial infections, aspiration syndromes, and severe shock. The mechanisms of lung injury have been identified in both experimental and clinical studies. Recovery from lung injury requires the reestablishment of an intact endothelial barrier and a functional alveolar epithelial barrier capable of secreting surfactant and removing alveolar edema fluid. Repair mechanisms include the participation of endogenous progenitor cells in strategically located niches in the lung. Novel treatment strategies include the possibility of cell-based therapy that may reduce the severity of lung injury and enhance lung repair

    Pulmonary surface film stability and composition

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    Surfactant release in excised rat lung is stimulated by air inflation

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    Analysis of single-joint rapid movements in patients with sporadic olivopontocerebellar atrophy

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    Patients with pure cerebellar cortical atrophy (CCA) present isolated cerebellar signs, whereas patients with sporadic olivopontocerebellar atrophy (sOPCA) present various combinations of cerebellar and extracerebellar signs. However, the differential diagnosis between these two forms of cerebellar degeneration is often a challenge for the clinician. Therefore, any test helping in this differential diagnosis might have a potential clinical interest. In this study, our goal was to investigate the adaptation to increased inertia in patients with sOPCA exhibiting combined cerebellar and pyramidal signs, during the performance of fast wrist flexions. We found that these patients exhibited a hypermetria which remained unchanged after addition of inertia, because they were unable to increase neither their agonist activity (launching force), nor their antagonist activity (braking force). This contrasts with our previous findings in patients with CCA. In these latter, the hypermetria worsened when the inertial load of the hand increased because those patients were able to increase their agonist activity, but not their antagonist activity. The adaptation to inertia might thus help to differentiate CCA and sOPCA.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

    Vascular regulation of type II cell exocytosis

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