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      Fourteen days of smoking cessation improves muscle fatigue resistance and reverses markers of systemic inflammation

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          Abstract

          Cigarette smoking has a negative effect on respiratory and skeletal muscle function and is a risk factor for various chronic diseases. To assess the effects of 14 days of smoking cessation on respiratory and skeletal muscle function, markers of inflammation and oxidative stress in humans. Spirometry, skeletal muscle function, circulating carboxyhaemoglobin levels, advanced glycation end products (AGEs), markers of oxidative stress and serum cytokines were measured in 38 non-smokers, and in 48 cigarette smokers at baseline and after 14 days of smoking cessation. Peak expiratory flow ( p = 0.004) and forced expiratory volume in 1 s/forced vital capacity ( p = 0.037) were lower in smokers compared to non-smokers but did not change significantly after smoking cessation. Smoking cessation increased skeletal muscle fatigue resistance ( p < 0.001). Haemoglobin content, haematocrit, carboxyhaemoglobin, total AGEs, malondialdehyde, TNF-α, IL-2, IL-4, IL-6 and IL-10 ( p < 0.05) levels were higher, and total antioxidant status (TAS), IL-12p70 and eosinophil numbers were lower ( p < 0.05) in smokers. IL-4, IL-6, IL-10 and IL-12p70 had returned towards levels seen in non-smokers after 14 days smoking cessation ( p < 0.05), and IL-2 and TNF-α showed a similar pattern but had not yet fully returned to levels seen in non-smokers. Haemoglobin, haematocrit, eosinophil count, AGEs, MDA and TAS did not significantly change with smoking cessation. Two weeks of smoking cessation was accompanied with an improved muscle fatigue resistance and a reduction in low-grade systemic inflammation in smokers.

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          Standardisation of spirometry.

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            Association between chronic obstructive pulmonary disease and systemic inflammation: a systematic review and a meta-analysis.

            Individuals with chronic obstructive pulmonary disease (COPD) are at increased risk of cardiovascular diseases, osteoporosis, and muscle wasting. Systemic inflammation may be involved in the pathogenesis of these disorders. A study was undertaken to determine whether systemic inflammation is present in stable COPD. A systematic review was conducted of studies which reported on the relationship between COPD, forced expiratory volume in 1 second (FEV(1)) or forced vital capacity (FVC), and levels of various systemic inflammatory markers: C-reactive protein (CRP), fibrinogen, leucocytes, tumour necrosis factor-alpha (TNF-alpha), and interleukins 6 and 8. Where possible the results were pooled together to produce a summary estimate using a random or fixed effects model. Fourteen original studies were identified. Overall, the standardised mean difference in the CRP level between COPD and control subjects was 0.53 units (95% confidence interval (CI) 0.34 to 0.72). The standardised mean difference in the fibrinogen level was 0.47 units (95% CI 0.29 to 0.65). Circulating leucocytes were also higher in COPD than in control subjects (standardised mean difference 0.44 units (95% CI 0.20 to 0.67)), as were serum TNF-alpha levels (standardised mean difference 0.59 units (95% CI 0.29 to 0.89)). Reduced lung function is associated with increased levels of systemic inflammatory markers which may have important pathophysiological and therapeutic implications for subjects with stable COPD.
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              Advanced glycation end products: sparking the development of diabetic vascular injury.

              Advanced glycation end products (AGEs) are proteins or lipids that become glycated after exposure to sugars. AGEs are prevalent in the diabetic vasculature and contribute to the development of atherosclerosis. The presence and accumulation of AGEs in many different cell types affect extracellular and intracellular structure and function. AGEs contribute to a variety of microvascular and macrovascular complications through the formation of cross-links between molecules in the basement membrane of the extracellular matrix and by engaging the receptor for advanced glycation end products (RAGE). Activation of RAGE by AGEs causes upregulation of the transcription factor nuclear factor-kappaB and its target genes. Soluble AGEs activate monocytes, and AGEs in the basement membrane inhibit monocyte migration. AGE-bound RAGE increases endothelial permeability to macromolecules. AGEs block nitric oxide activity in the endothelium and cause the production of reactive oxygen species. Because of the emerging evidence about the adverse effects of AGEs on the vasculature of patients with diabetes, a number of different therapies to inhibit AGEs are under investigation.
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                Author and article information

                Contributors
                darabseh.moh@gmail.com
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                10 June 2021
                10 June 2021
                2021
                : 11
                : 12286
                Affiliations
                [1 ]GRID grid.25627.34, ISNI 0000 0001 0790 5329, Department of Life Sciences, Centre of Musculoskeletal Sciences and Sport Medicine, , Manchester Metropolitan University, ; John Dalton Building; Chester Street, Manchester, M1 5GD UK
                [2 ]GRID grid.5884.1, ISNI 0000 0001 0303 540X, Academy of Sport and Physical Activity, Faculty of Health and Wellbeing, Collegiate Campus, , Sheffield Hallam University, ; Sheffield, UK
                [3 ]GRID grid.12380.38, ISNI 0000 0004 1754 9227, Laboratory for Myology, Faculty of Behavioural and Movement Sciences, Amsterdam Movement Sciences, , Vrije Universiteit Amsterdam, ; Amsterdam, The Netherlands
                [4 ]GRID grid.25627.34, ISNI 0000 0001 0790 5329, Department of Life Sciences, Centre for Bioscience, , Manchester Metropolitan University, ; John Dalton Building; Chester Street, Manchester, M1 5GD UK
                [5 ]GRID grid.269741.f, ISNI 0000 0004 0421 1585, Virology Department, , Royal Liverpool and Broadgreen University Hospitals NHS Trust, ; Liverpool, UK
                [6 ]GRID grid.25627.34, ISNI 0000 0001 0790 5329, Department of Health Professions, Faculty of Health, Psychology and Social Care, , Manchester Metropolitan University, ; Brooks Building; 53 Bonsall Street, Manchester, M15 6GX UK
                [7 ]GRID grid.25627.34, ISNI 0000 0001 0790 5329, Department of Sport and Exercise Sciences, Centre of Musculoskeletal Sciences and Sport Medicine, , Manchester Metropolitan University, ; All Saints Building; Oxford Street, Manchester, M15 6BH UK
                [8 ]GRID grid.419313.d, ISNI 0000 0000 9487 602X, Institute of Sport Science and Innovations, , Lithuanian Sports University, ; Kaunas, Lithuania
                Author information
                http://orcid.org/0000-0002-0535-0195
                http://orcid.org/0000-0003-3781-5177
                Article
                91510
                10.1038/s41598-021-91510-x
                8192509
                34112815
                92282de8-3ba9-4b6f-87d6-0ee24637b7ac
                © The Author(s) 2021

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 20 February 2021
                : 20 May 2021
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                © The Author(s) 2021

                Uncategorized
                respiratory tract diseases,physiology
                Uncategorized
                respiratory tract diseases, physiology

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