Vito Brusasco
University of Genoa
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Publication
Featured researches published by Vito Brusasco.
European Respiratory Journal | 2005
M.R. Miller; John L. Hankinson; Vito Brusasco; Felip Burgos; Richard Casaburi; Allan L. Coates; Robert O. Crapo; Paul L. Enright; C.P.M. van der Grinten; P. Gustafsson; Robert L. Jensen; D.C. Johnson; Neil R. MacIntyre; Roy T. McKay; Daniel Navajas; O.F. Pedersen; R. Pellegrino; G. Viegi; Jack Wanger
[⇓][1] SERIES “ATS/ERS TASK FORCE: STANDARDISATION OF LUNG FUNCTION TESTING” Edited by V. Brusasco, R. Crapo and G. Viegi Number 2 in this Series [1]: #F13
European Respiratory Journal | 2005
Jack Wanger; J.L. Clausen; Allan L. Coates; O.F. Pedersen; Vito Brusasco; Felip Burgos; Richard Casaburi; Robert O. Crapo; Paul L. Enright; C.P.M. van der Grinten; P. Gustafsson; John L. Hankinson; Robert L. Jensen; D.C. Johnson; Neil R. MacIntyre; Roy T. McKay; M.R. Miller; Daniel Navajas; R. Pellegrino; G. Viegi
[⇓][1] SERIES “ATS/ERS TASK FORCE: STANDARDISATION OF LUNG FUNCTION TESTING” Edited by V. Brusasco, R. Crapo and G. Viegi Number 3 in this Series [1]: #F7
European Respiratory Journal | 2005
M.R. Miller; Robert O. Crapo; John L. Hankinson; Vito Brusasco; Felip Burgos; Richard Casaburi; Allan L. Coates; Paul L. Enright; C.P.M. van der Grinten; P. Gustafsson; Robert L. Jensen; D.C. Johnson; Neil R. MacIntyre; Roy T. McKay; Daniel Navajas; O.F. Pedersen; R. Pellegrino; G. Viegi; Jack Wanger
SERIES “ATS/ERS TASK FORCE: STANDARDISATION OF LUNG FUNCTION TESTING” Edited by V. Brusasco, R. Crapo and G. Viegi Number 1 in this Series ⇓In preparing the joint statements on lung function testing for the American Thoracic Society (ATS) and the European Respiratory Society (ERS), it was agreed by the working party that the format of the statements should be modified so that they were easier to use by both technical and clinical staff. This statement contains details about procedures that are common for many methods of lung function testing and, hence, are presented on their own. A list of abbreviations used in all the documents is also included as part of this statement. All terms and abbreviations used here are based on a report of the American College of Chest Physicians/ATS Joint Committee on Pulmonary Nomenclature 1. The metrology definitions agreed by the International Standards Organization (ISO) are recommended 2 and some important terms are defined as follows. Accuracy is the closeness of agreement between the result of a measurement and the conventional true value. Repeatability is the closeness of agreement between the results of successive measurements of the same item carried out, subject to all of the following conditions: same method, same observer, same instrument, same location, same condition of use, and repeated over a short space of time. In previous documents, the term reproducibility was used in this context, and this represents a change towards bringing this document in line with the ISO. Reproducibility is the closeness of agreement of the results of successive measurements of the same item where the individual measurements are carried out with changed conditions, such as: method of measurement, observer, instrument, location, conditions of use, and time. Thus, if a technician tests a subject several times, this is looking at the …
European Respiratory Journal | 2008
Mario Cazzola; William MacNee; Fernando J. Martinez; Klaus F. Rabe; L.G. Franciosi; P J Barnes; Vito Brusasco; P.S. Burge; Peter M. Calverley; Bartolome R. Celli; Paul W. Jones; Donald A. Mahler; Barry J. Make; Marc Miravitlles; Clive P. Page; Paolo Palange; David Parr; Massimo Pistolesi; S. Rennard; Mp Rutten-van Mölken; Robert A. Stockley; Sean D. Sullivan; Jadwiga A. Wedzicha; Emiel F.M. Wouters
The American Thoracic Society/European Respiratory Society jointly created a Task Force on “Outcomes for COPD pharmacological trials: from lung function to biomarkers” to inform the chronic obstructive pulmonary disease research community about the possible use and limitations of current outcomes and markers when evaluating the impact of a pharmacological therapy. Based on their review of the published literature, the following document has been prepared with individual sections that address specific outcomes and markers, and a final section that summarises their recommendations.
Thorax | 2003
Vito Brusasco; R Hodder; M Miravitlles; L Korducki; L Towse; S Kesten
We wish to clarify issues raised by your recent letter regarding the abovementioned paper published in May 2003 in Thorax (2003; 58 :399–404). Our intention was to notify the editors and to reference the paper by Donohue et al appearing in Chest . We believe this is evidenced by our declaring in the cover letter that the data from one of the two trials were under review. However, we wish to apologise that we did not follow this up and did …
European Respiratory Journal | 2007
Steven S. An; Tony R. Bai; Jason H. T. Bates; Judith L. Black; Robert H. Brown; Vito Brusasco; Pasquale Chitano; Linhong Deng; Maria L. Dowell; David H. Eidelman; Ben Fabry; Nigel J. Fairbank; Lincoln E. Ford; Jeffrey J. Fredberg; William T. Gerthoffer; Susan H. Gilbert; Reinoud Gosens; Susan J. Gunst; Andrew J. Halayko; R. H. Ingram; Charles G. Irvin; Alan James; Luke J. Janssen; Gregory G. King; Darryl A. Knight; Anne-Marie Lauzon; Oren Lakser; Mara S. Ludwig; Kenneth R. Lutchen; Geoff Maksym
Excessive airway obstruction is the cause of symptoms and abnormal lung function in asthma. As airway smooth muscle (ASM) is the effecter controlling airway calibre, it is suspected that dysfunction of ASM contributes to the pathophysiology of asthma. However, the precise role of ASM in the series of events leading to asthmatic symptoms is not clear. It is not certain whether, in asthma, there is a change in the intrinsic properties of ASM, a change in the structure and mechanical properties of the noncontractile components of the airway wall, or a change in the interdependence of the airway wall with the surrounding lung parenchyma. All these potential changes could result from acute or chronic airway inflammation and associated tissue repair and remodelling. Anti-inflammatory therapy, however, does not “cure” asthma, and airway hyperresponsiveness can persist in asthmatics, even in the absence of airway inflammation. This is perhaps because the therapy does not directly address a fundamental abnormality of asthma, that of exaggerated airway narrowing due to excessive shortening of ASM. In the present study, a central role for airway smooth muscle in the pathogenesis of airway hyperresponsiveness in asthma is explored.
European Respiratory Journal | 2005
Vito Brusasco; Robert O. Crapo; G. Viegi
Since 1979, guidelines for standardising pulmonary function tests have been published and updated by both the American Thoracic Society (ATS) 1–6 and the European Respiratory Society (ERS) 7–9. In addition, several joint ATS/ERS workshops on pulmonary function testing have been held and the resulting reports published 10, 11. In 1995, European scientists participated in the ATS updates of standards for spirometry and single-breath carbon monoxide diffusing capacity of the lung ( D L,CO), but no joint statement has been published by the two societies. Although generally concordant, the spirometry and D L,CO guidelines published separately by the ATS and the ERS differed in some aspects that were of appreciable importance. Official guidelines for the measurement of lung volumes were made available by the ERS 7, 10, but not the ATS. In recent years, global initiatives were undertaken for the diagnosis and treatment of pulmonary diseases, and the worldwide market for instruments to test lung function widened considerably. This increased the pressure for more uniform pulmonary function testing across the world, and prompted the ATS and the ERS to appoint a joint Task Force to provide new combined standards for clinical pulmonary function testing, with the hope that they will be accepted by other respiratory societies. A new Task Force on pulmonary function testing, implemented by the Forum of International Respiratory Societies (FIRS), has recently started its work based on the ATS/ERS documents. Our Task Force consisted of 19 scientists with recognised expertise in pulmonary function testing. The group worked on a “one-draft” system, in which each of five sections was assigned to a small subgroup and eventually discussed by the whole committee. There …
Thorax | 1998
Vito Brusasco; Emanuele Crimi; Riccardo Pellegrino
According to the most recent definition, bronchial asthma is a chronic inflammatory disorder of the airways associated with reversible airway obstruction and increased airway responsiveness to a variety of stimuli.1 An intuitive inference from this definition is that a causal relationship may exist between airway inflammation and airway hyperresponsiveness. Along this line of reasoning, most of the research in the last two decades in this field was aimed at identifying inflammatory cell products possibly responsible for the pathogenesis of bronchial asthma and airway hyperresponsiveness.2 However, the common observation that the asthmatic airways are equally hyperresponsive to a variety of different stimuli does challenge the idea that a single inflammatory cell or mediator may be central to the pathogenesis of asthma and airway hyperresponsiveness and focuses on the importance of an altered mechanical response of the target organ. This view has been recently corroborated by the finding that airway responsiveness of normal individuals may become similar to that of asthmatics by simply changing the pattern of breathing during the bronchial challenge.3It is therefore legitimate to wonder how much of airway hyperresponsiveness is due to inflammation or to inherent predisposing factors. The aims of the present review are to show that airway narrowing in asthma is the ultimate result of an interaction between complex and multiple mechanisms not necessarily and uniquely related to airway inflammation, and to revisit the evidence on which the theorem “airway inflammation equal to airway hyperresponsiveness” has been constructed. Airway calibre in vivo is the result of a delicate balance between the force generated by the airway smooth muscle (ASM) and a number of opposing factors.4 The latter are mainly represented by autonomic mechanisms that tend to limit the ASM tone and by mechanical forces that oppose ASM shortening. ### AIRWAY SMOOTH MUSCLE (ASM) Although it is widely …
European Respiratory Journal | 1998
Riccardo Pellegrino; Peter J. Sterk; J.K. Sont; Vito Brusasco
Bronchoconstriction in bronchial asthma and chronic obstructive pulmonary disease (COPD) may be due to decreased airway calibre and/or to the inability of the airways to distend after a deep inhalation (DI). The purpose of this review is to discuss the physiological and clinical relevance of this latter mechanism. During induced constriction, DI shows remarkable bronchodilatation in normal subjects, but a blunted or null effect in asthmatics. In contrast, during spontaneous bronchospasm DI tends to decrease airway calibre. From a functional point of view, airway inflammation, remodelling, and peripheral bronchoconstriction could prevent airway smooth muscle from stretching. Therapeutic intervention improving lung function may change the response to DI. For example, bronchodilators allow expiratory airflow before DI to increase more than after DI, because of decreased bronchial hysteresis. This suggest that bronchodilation might be systematically underestimated from parameters derived from maximal expiratory manoeuvres. Inhaled corticosteroids tend to increase the dilator effect of DI, likely due to decreased bronchial and peribronchial oedema. In conclusion, measuring the effects of deep inhalation on lung function is an easy and simple test able to evaluate the structural changes occurring in the airways and to monitor the effectiveness of therapy.
Thorax | 2000
Michela Silvestri; Daniela Spallarossa; Elena Battistini; Vito Brusasco; Giovanni A. Rossi
BACKGROUND Bronchial hyperresponsiveness and airway inflammation are distinctive features of asthma. Evaluation of nitric oxide (NO) levels in expired air have been proposed as a reliable method for assessing the airway inflammatory events in asthmatic subjects. A study was undertaken to evaluate whether airway hyperresponsiveness is related to levels of exhaled NO. METHODS Thirty two steroid-naive atopic children with mild intermittent asthma of mean (SD) age 11.8 (2.3) years and 28 age matched healthy controls were studied to investigate whether baseline lung function or airway hyperresponsiveness is related to levels of exhaled NO. Airway responsiveness was assessed as the dose of methacholine causing a 20% decrease in forced expiratory volume in one second (FEV1) from control (PD20 methacholine) and exhaled NO levels were measured by chemiluminescence analysis of exhaled air. RESULTS At baseline asthmatic children had significantly higher NO levels than controls (mean difference 25.87 ppb (95% CI 18.91 to 32.83); p<0.0001) but there were no significant differences in lung function parameters (forced vital capacity (FVC), FEV1 (% pred), and forced expiratory flows at 25–75% of vital capacity (FEF25–75%)). In the asthmatic group exhaled NO levels were not significantly correlated with baseline lung function values or PD20 methacholine. CONCLUSIONS These results suggest that levels of exhaled NO are not accurate predictors of the degree of airway responsiveness to inhaled methacholine in children with mild intermittent asthma.