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  • 1
    Online Resource
    Online Resource
    SAGE Publications ; 2002
    In:  The International Journal of Biological Markers Vol. 17, No. 2 ( 2002), p. 141-145
    In: The International Journal of Biological Markers, SAGE Publications, Vol. 17, No. 2 ( 2002), p. 141-145
    Type of Medium: Online Resource
    ISSN: 0393-6155
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2002
    detail.hit.zdb_id: 1475778-3
    SSG: 12
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  • 2
    In: Rhinology journal, Stichting Nase, Vol. 49, No. 2 ( 2011-06-01), p. 232-237
    Abstract: BACKGROUND: Obstructive sleep apnea syndrome (OSAS) has been shown to be associated to upper and lower airways inflammation. Continuous positive airway pressure (CPAP) is the elective treatment of OSAS. The aim of the present study was to assess the effect of CPAP-therapy on airway and nasal inflammation. METHODS: In 13 non-smoking subjects affected by untreated OSAS and in 11 non-smoking normal volunteers, airway inflammation was detected by analyses of the induced sputum. In the OSAS group measurements were repeated after 1, 10 and 60 days of the appropriate CPAP treatment. In addition, in 12 subjects of the OSAS group, nasal inflammation was detected by the analysis of induced nasal secretions at baseline, and after 1, 10 and 60 days of CPAP treatment. RESULTS: OSAS patients, compared to normal controls, showed at baseline a higher percentage of neutrophils and a lower percentage of macrophages in the induced sputum. One, 10 and 60 days of appropriate CPAP-therapy did not change the cellular profile of the induced sputum. In addition, in the OSAS patients, the high neutrophilic nasal inflammation present under baseline conditions was not significantly modified by CPAP-therapy. Finally, no patients developed airway hyper-responsiveness after CPAP therapy. CONCLUSIONS: In OSAS subjects, the appropriate CPAP-therapy, while correcting the oxygen desaturation, does not modify the bronchial and nasal inflammatory profile.
    Type of Medium: Online Resource
    ISSN: 0300-0729
    Language: Unknown
    Publisher: Stichting Nase
    Publication Date: 2011
    detail.hit.zdb_id: 2120704-5
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  • 3
    In: Respiratory Medicine, Elsevier BV, Vol. 94, No. 3 ( 2000-03), p. 240-246
    Type of Medium: Online Resource
    ISSN: 0954-6111
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2000
    detail.hit.zdb_id: 2002557-9
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  • 4
    Online Resource
    Online Resource
    Elsevier BV ; 2013
    In:  Respiratory Medicine Vol. 107, No. 2 ( 2013-02), p. 310-316
    In: Respiratory Medicine, Elsevier BV, Vol. 107, No. 2 ( 2013-02), p. 310-316
    Type of Medium: Online Resource
    ISSN: 0954-6111
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2013
    detail.hit.zdb_id: 2002557-9
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  • 5
    Online Resource
    Online Resource
    PAGEPress Publications ; 2016
    In:  Monaldi Archives for Chest Disease Vol. 73, No. 1 ( 2016-01-19)
    In: Monaldi Archives for Chest Disease, PAGEPress Publications, Vol. 73, No. 1 ( 2016-01-19)
    Abstract: Background. An altered balance of oxidants/anti-oxidants is one of the pathological mechanisms of many agedependent disorders. We aimed to investigate the age-related airways oxidative stress, using non invasive, safe and repeatable techniques; to evaluate the correspondence between systemic and local oxidative stress in healthy subjects of different age ranges; to analyse the correlation between systemic and local oxidative stress with lung function and with cognitive impairment. Methods. Thirty consecutive healthy high school graduated subjects (8 M, 22 F), divided in three ranges of age (60 years) were enrolled. All subjects underwent oxygen free radicals and exhaled nitric oxide measurement (by the diacron reactive oxygen metabolites test and by a rapid-response chemiluminescence nitric oxide analyzer), lung function tests, and cognitive impairment scales (Mini Mental State Examination and Geriatric Depression Scale). Results. A significant increase of oxygen free radicals, exhaled nitric oxide, and Geriatric Depression Scale score and a significant decrease of forced expiratory volume in 1 second and forced expiratory vital capacity from younger to older subjects were identified. Moreover, the significant positive correlation between oxygen free radicals and exhaled nitric oxide, and between oxygen free radicals and exhaled nitric oxide with Geriatric Depression Scale score were found. The significant negative correlation between forced expiratory volume in 1 second and oxygen free radicals or exhaled nitric oxide was also demonstrated. Conclusions. Our data supports the role of progressive local oxidative stress in damaging the lung function and in inducing depression symptoms.
    Type of Medium: Online Resource
    ISSN: 1122-0643
    Language: Unknown
    Publisher: PAGEPress Publications
    Publication Date: 2016
    detail.hit.zdb_id: 2375904-5
    detail.hit.zdb_id: 2375907-0
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  • 6
    Online Resource
    Online Resource
    PAGEPress Publications ; 2016
    In:  Monaldi Archives for Chest Disease Vol. 65, No. 2 ( 2016-02-15)
    In: Monaldi Archives for Chest Disease, PAGEPress Publications, Vol. 65, No. 2 ( 2016-02-15)
    Abstract: Obstructive sleep apnea (OSA) is characterised by repetitive episodes of upper airway occlusion during sleep. OSA has been shown to be associated with a variable degree of nasal inflammation, uvula mucosal congestion and airway hyperreactivity. The upper airway inflammation, whose clinical importance is uncertain, is characterised by leukocytes infiltration and interstitial oedema. In addition, recent data has shown the presence of neutrophilic inflammation in the lower airways. The current opinion is that airway inflammation is caused by the local, repeated mechanical trauma related to the intermittent airway occlusion typical of the disease. Another potential mechanism involves the intermittent nocturnal hypoxemia that through the phenomenon of the ischemia- reperfusion injury may induce the production of oxygen free radicals and therefore cause local and systemic inflammation. Finally, a state of low-grade systemic inflammation may be related to obesity per se with the pro-inflammatory mediators synthesised in the visceral adipose cells. Several authors stress the role of circulating and local inflammatory mediators, such as proinflammatory cytokines, exhaled nitric oxide, pentane and 8-isoprostane as the determinants of inflammation in OSA.
    Type of Medium: Online Resource
    ISSN: 2532-5264 , 1122-0643
    Language: Unknown
    Publisher: PAGEPress Publications
    Publication Date: 2016
    detail.hit.zdb_id: 2375904-5
    detail.hit.zdb_id: 2375907-0
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  • 7
    Online Resource
    Online Resource
    PAGEPress Publications ; 2004
    In:  Monaldi Archives for Chest Disease Vol. 61, No. 4 ( 2004-12-30)
    In: Monaldi Archives for Chest Disease, PAGEPress Publications, Vol. 61, No. 4 ( 2004-12-30)
    Abstract: The lung parenchyma is anatomically and mechanically connected to the intraparenchymal airways. Due to forces of interdependence the lung parenchyma represents a mechanical load that opposes bronchial narrowing during airway smooth muscle activation. The mechanical load caused by the parenchyma is a function of the number of the alveolar attachments to the airways, and of the mechanical properties of the parenchyma. The extracellular matrix is a major component of the lung parenchyma responsible of most of its mechanical properties. The excessive airway narrowing observed in the asthmatic population may be the consequence of the altered mechanical properties of the extracellular matrix reducing the mechanical load that opposes airway smooth muscle contraction.
    Type of Medium: Online Resource
    ISSN: 2465-1028 , 1122-0643
    Language: Unknown
    Publisher: PAGEPress Publications
    Publication Date: 2004
    detail.hit.zdb_id: 2375904-5
    detail.hit.zdb_id: 2375907-0
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  • 8
    Online Resource
    Online Resource
    PAGEPress Publications ; 2016
    In:  Monaldi Archives for Chest Disease Vol. 73, No. 4 ( 2016-01-19)
    In: Monaldi Archives for Chest Disease, PAGEPress Publications, Vol. 73, No. 4 ( 2016-01-19)
    Abstract: -
    Type of Medium: Online Resource
    ISSN: 1122-0643
    Language: Unknown
    Publisher: PAGEPress Publications
    Publication Date: 2016
    detail.hit.zdb_id: 2375904-5
    detail.hit.zdb_id: 2375907-0
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  • 9
    Online Resource
    Online Resource
    PAGEPress Publications ; 2016
    In:  Monaldi Archives for Chest Disease Vol. 71, No. 1 ( 2016-01-25)
    In: Monaldi Archives for Chest Disease, PAGEPress Publications, Vol. 71, No. 1 ( 2016-01-25)
    Abstract: The extracellular matrix is the main determinant of the structure and of mechanical behaviour of the lung. The extracellular matrix is also responsible for the mechanical interdependence between airway and parenchyma due to the alveolar attachments to the airways. Asthma is characterized by bronchial hyperresponsiveness, airway remodelling and inflammation, and an altered extracellular matrix may play a role in all these functional and structural abnormalities. The excessive airway narrowing observed in asthma may be related to the altered viscoelastic properties of lung parenchyma and airway wall, determining a decrease in the mechanical load opposing the airways’ smooth muscle contraction. Indeed, an altered extracellular matrix deposition in asthma in humans, has been demonstrated. In addition, in the asthmatic lung, the matrix seems to contribute to airway inflammation, airway remodelling, and to those alterations of the smooth muscle function of the airway and morphology typical of asthma.
    Type of Medium: Online Resource
    ISSN: 2465-1028 , 1122-0643
    Language: Unknown
    Publisher: PAGEPress Publications
    Publication Date: 2016
    detail.hit.zdb_id: 2375904-5
    detail.hit.zdb_id: 2375907-0
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  • 10
    Online Resource
    Online Resource
    PAGEPress Publications ; 2016
    In:  Monaldi Archives for Chest Disease Vol. 67, No. 2 ( 2016-02-03)
    In: Monaldi Archives for Chest Disease, PAGEPress Publications, Vol. 67, No. 2 ( 2016-02-03)
    Abstract: Brittle asthma is a clinical phenotype of the disease at the severe end of the spectrum. Type 1 brittle asthma is characterised by a maintained wide PEF variability ( 〉 40% diurnal variation for 〉 50% of the time over a period of at least 150 days) despite considerable medical therapy including a dose of inhaled steroids of at least 1500 μg of beclomethasone or equivalent. Type 2 brittle asthma is characterised by sudden acute attacks occurring in less than three hours without an obvious trigger on a background of apparent normal airway function or well controlled asthma. Mechanisms behind the development of brittle asthma include smooth muscle contraction and edema of the airways, which are supported by chronic airway inflammation. Allergy reactions, impairment of local immunity, respiratory infections, psycho-social disorders and reduced perception of worsening airway function are the risk factors for brittle asthma. The diagnosis is based on the analysis of specific symptoms, role of triggers, personal or family history, measurement of lung function and PEF monitoring. Pharmacological treatment of type 1 brittle asthma in addition to the high doses of inhaled and/or oral steroids and bronchodilators includes subcutaneous injections of β2 agonist and inhalation of long acting β2 agonist. The treatment of patients with type 2 brittle asthma includes exclusion of allergen exposure, identification of triggers, self management and management of acute attacks.
    Type of Medium: Online Resource
    ISSN: 2532-5264 , 1122-0643
    Language: Unknown
    Publisher: PAGEPress Publications
    Publication Date: 2016
    detail.hit.zdb_id: 2375904-5
    detail.hit.zdb_id: 2375907-0
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