1,721,028 research outputs found
Role of transcription factors in the pathogenesis of asthma and COPD
No full textInflammation is a central feature of asthma and chronic obstructive pulmonary disease (COPD). Despite recent advances in the knowledge of the pathogenesis of asthma and COPD, much more research on the molecular mechanisms of asthma and COPD are needed to aid the logical development of new therapies for these common and important diseases, particularly in COPD where no effective treatments currently exist. In the future the role of the activation/repression of different transcription factors and the genetic regulation of their expression in asthma and COPD may be an increasingly important aspect of research, as this may be one of the critical mechanisms regulating the expression of different clinical phenotypes and their responsiveness to therapy, particularly to anti-inflammatory drugs
Pathophysiology of viral-induced exacerbations of COPD
No full textInflammation of the lower airways is a central feature of chronic obstructive pulmonary disease (COPD). Inflammatory responses are associated with an increased expression of a cascade of proteins including cytokines, chemokines, growth factors, enzymes, adhesion molecules and receptors. In most cases the increased expression of these proteins is the result of enhanced gene transcription: many of these genes are not expressed in normal cells under resting conditions but they are induced in the inflammatory process in a cell-specific manner. Transcriptions factors regulate the expression of many pro-inflammatory genes and play a key role in the pathogenesis of airway inflammation. Many studies have suggested a role for viral infections as a causative agent of COPD exacerbations. In this review we will focus our attention on the relationship between common respiratory viral infections and the molecular and inflammatory mechanisms that lead to COPD exacerbations
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
COPD pathology in the small airways
No full textIn the last quarter of century, the analysis of small airways specimens obtained from chronic obstructive pulmonary disease (COPD) patients compared with those from a control group of age-matched smokers with normal lung function has provided novel insights on the potential role of the different inflammatory and structural cells, pro/anti-inflammatory mediators and intracellular signalling pathways, contributing to a better knowledge of the pathogenesis of stable COPD. This also has provided a scientific rationale for new drugs discovery and targeting to the small airways. This review summarizes and discusses the pathology of small airways of stable COPD patients, of different severity, compared with control smokers with normal lung function
Mechanisms involved in lung cancer development in COPD
No full textLung cancer and chronic obstructive pulmonary disease (COPD) are leading causes of morbidity and mortality worldwide. They share a common environmental risk factor in cigarette smoke exposure and a genetic predisposition represented by the incidence of these diseases in only a fraction of smokers. COPD is also a major independent risk factor for lung carcinoma, among long-term smokers. Smokers with COPD also have a higher risk of developing a specific histological subtype of non-small cell lung cancer termed squamous cell carcinoma. For these reasons the focus of this review is on the potential pathogenic molecular links between tobacco smoking-related COPD and squamous cell carcinoma. We believe that we need to promote more studies on the molecular and cellular pathobiology of smokers with premalignant bronchial lesions of the squamous cell lung carcinoma compared with a control group of smokers with and without COPD to unravel the complex molecular interactions between COPD and early squamous cell lung carcinoma. These studies should also look at younger healthy smokers in combination with risk models of lung cancer and COPD. Overall these studies may allow the discovery of new molecular targets of the early carcinogenesis process that in the foreseeable future may render the early diagnosis and treatment, and may be even the prevention, of invasive squamous cell lung carcinoma a reality
Ruolo dello stress ossidativo nella patogenesi delle broncopneumopatie croniche ostruttive in fase stabile.
No full textLa broncopneumopatia cronica ostruttiva (BPCO) in fase stabile si associa ad un significativo stress ossidativo nelle vie aeree inferiori ed a livello sistemico. Il fumo di sigaretta costituisce la principale fonte di ossidanti/nitrosanti per i polmoni dei pazienti con BPCO in fase stabile, ma lo stress ossidativo può derivare anche da altre fonti esogene come l’inquinamento atmosferico o l’ossigenoterapia, e da numerose fonti endogene. Numerosi studi clinici hanno dimostrato un aumento dello stress ossidativo nei liquidi biologici (sangue, urine, aria espirata, espettorato, lavaggio broncoalveolare) e nei tessuti polmonari dei pazienti con BPCO in fase di stabilità clinica, rispetto a gruppi di controllo di soggetti fumatori e non fumatori con normale funzionalità respiratoria
COPD immunopathology
No full textThe immunopathology of chronic obstructive pulmonary disease (COPD) is based on the innate and adaptive inflammatory immune responses to the chronic inhalation of cigarette smoking. In the last quarter of the century, the analysis of specimens obtained from the lower airways of COPD patients compared with those from a control group of age-matched smokers with normal lung function has provided novel insights on the potential pathogenetic role of the different cells of the innate and acquired immune responses and their pro/anti-inflammatory mediators and intracellular signalling pathways, contributing to a better knowledge of the immunopathology of COPD both during its stable phase and during its exacerbations. This also has provided a scientific rationale for new drugs discovery and targeting to the lower airways. This review summarises and discusses the immunopathology of COPD patients, of different severity, compared with control smokers with normal lung function
Role of stem cells in the pathogenesis of chronic obstructive pulmonary disease and of pulmonary emphysema
No full textThere are only few human translational studies performed in the area of stem cell research in patients with chronic obstructive pulmonary disease (COPD) and/or pulmonary emphysema. Before progress to clinical trials with stem cells we believe that more human translational studies are necessaries, otherwise the clinical rationale would be solely based on limited in vitro and animal studies. In the future, stem cell therapy could be a treatment for this disease. Currently, stem cell therapy is still to be considered as an area of active research, lacking a strong rationale for performing clinical trials in COPD. Although stem cells would be likely to represent a heterogeneous population of cells, the different cell subsets and their importance in the pathogenesis of the different clinical phenotypes need to be fully characterised before progressing to clinical trials. Moreover, the potential side effects of the stem cell therapy are often underestimated. We should not ignore that some of the most deadly neoplasms are arising from stem cells
Trattamento personalizzato dei pazienti con BPCO in fase stabile
No full textIn clinical practice there are no more justifications for the therapeutic nihilism because nowadays the personalised pharmacologic and non-pharmacologic treatment of the patients with stable chronic obstructive pulmonary disease (COPD), according to current Global initiative for chronic Obstructive Lung Disease (GOLD) guidelines is effective in decreasing respiratory symptoms, in increasing exercise tolerance and capacity, improving quality of life, preventing many COPD exacerbations (even the most severe) and decrease the mortality. However, smoking cessation and long-term oxygen therapy (in patients with advanced COPD and severe chronic hypoxemia refractory to maximal treatment with bronchodilator and anti-inflammatory drugs) are the only two interventions that have unequivocally shown to reduce COPD mortality. At the opposite the current pharmacologic personalised treatment of stable COPD is mainly symptomatic and modify only partially the natural history of the disease. This conclusion should reinforce the necessity of further human translational medicine research in order to promote a better understanding of the pathogenesis of COPD and also we need more long term controlled clinical studies of new drugs using as primary measures of clinical efficacy their effects on the lung function decline and the mortality. To accelerate research in this field, substantial investments are required at all levels, including the public and private sectors, with the ambitious aim of making in the near future COPD a preventable and fully treatable disease
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