1,721,092 research outputs found

    Deconditioning in COVID-19 survivors with reduced exercise performance: A role for endothelial dysfunction?

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    Recent studies have reported an impaired exercise response at cardiopulmonary exercise testing (CPET) during convalescence from coronavirus disease 2019 (COVID-19). In detail, these previous reports suggest the presence of functional limitations in a consistent proportion of COVID-19 survivors, in the absence of relevant alterations of ventilatory and gas exchange parameters at CPET. Therefore, deconditioning has been proposed as the main mechanism of the reduced peak oxygen uptake in this clinical setting. This interpretation of the results is supported by the evidence that deconditioning is a recognized aspect of the post-intensive care syndrome, with acute sarcopenia being frequently observed among COVID-19 survivors. Here, we hypothesized the role of endothelial dysfunction as a key pathogenic mechanism of the functional limitations of COVID-19, including multisystem deconditioning and subsequent exercise intolerance

    Recent advances on nitric oxide in the upper airways

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    Exhaled nitric oxide (NO) originates from the upper airways, and takes action, to varying extents, in regulation, protection and defense, as well as in noxious processes. Nitric oxide retains important functions in a wide range of physiological and pathophysiological processes of the human body, including vaso-regulation, antimicrobial activity, neurotransmission and respiration. This review article reports the ongoing investigations regarding the source, biology and relevance of NO within upper respiratory tract. In addition, we discuss the role of NO, originating from nasal and paranasal sinuses, in inflammatory disorders such as allergic rhinitis, sinusitis, primary ciliary dyskinesia, and cystic fibrosis

    Chronic obstructive pulmonary disease's eosinophilic phenotype: Clinical characteristics, biomarkers and biotherapy

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    COPD is a chronic, heterogeneous inflammatory disorder of the airways with persistent and poorly reversible airflow limitation, causing symptoms such as cough, shortness of breath, and sputum production. Despite optimal treatment, some patients remain symptomatic due to the disease's heterogeneity, manifesting in various phenotypes. One notable phenotype involves eosinophilic inflammation, with a variable prevalence. Identifying eosinophilic phenotypes is crucial for tailored therapeutic strategies, as they respond favorably to corticosteroids and potentially biologics. Recent advances in both clinical trials and spontaneous research have helped understand the biological and clinical characteristics of this phenotype, although no universal consensus has been reached yet on the definition of the cut-off values of the eosinophil peripheral blood count. Moreover, there is evidence of novel emerging biomarkers which might go beyond the sole eosinophil count, while significant advancements in terms of pharmacological treatment have been made, with dupilumab being the first biological drug being licensed for COPD patients with elevated circulating eosinophils in the stable phase. In light of the above, although several papers have been written on the relationship between eosinophils and COPD, in the present work we endeavored to summarize and discuss the pivotal literature findings regarding the eosinophilic COPD in order to help define the biological and clinical features of this peculiar phenotype, with particular attention to the use of established and emerging biomarkers, as well as current and future therapeutic perspectives
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