Extracellular matrix remodeling in idiopathic pulmonary fibrosis. It is the 'bed' that counts and not 'the sleepers'.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease characterized by irreversible fibrosis. Current disease pathogenesis assumes an aberrant wound healing process in response to repetitive injurious stimuli leading to apoptosis of epithelial cells, activation of fibroblasts and accumulation of extracellular matrix (ECM). Particularly, lung ECM is a highly dynamic structure that lies at the core of several physiological and developmental pathways.

Diagnostic and prognostic challenges in Idiopathic Pulmonary Fibrosis: A patient's "Q and A" approach.

Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive, debilitating disease of unknown etiology that leads to death nearly half of the patients within 3-3.5 years. The past 15 years, the scientific community has made tremendous progress towards standardized diagnostic and prognostic algorithms that led to the generation of the 2011 ATS/ERS/JRS/ALAT guidelines.

Association Study for 26 Candidate Loci in Idiopathic Pulmonary Fibrosis Patients from Four European Populations.

Idiopathic pulmonary fibrosis (IPF) affects lung parenchyma with progressing fibrosis. In this study, we aimed to replicate MUC5B rs35705950 variants and determine new plausible candidate variants for IPF among four different European populations. We genotyped 26 IPF candidate loci in 165 IPF patients from four European countries, such as Czech Republic (n = 41), Germany (n = 33), Greece (n = 40), France (n = 51), and performed association study comparing observed variant distribution with that obtained in a genetically similar Czech healthy control population (n = 96) described in our earlier data report.

Toll-like receptors in the pathogenesis of pulmonary fibrosis.

Pulmonary fibrosis (PF) constitutes the end stage of a broad range of heterogeneous interstitial lung diseases, characterized by the destruction of the pulmonary parenchyma, deposition of extracellular matrix and dramatic changes in the phenotype of both fibroblasts and alveolar epithelial cells. More than 200 causes of pulmonary fibrosis have been identified so far, yet the most common form is idiopathic pulmonary fibrosis (IPF). IPF is a lethal lung disorder of unknown etiology with a gradually increasing worldwide incidence and a median survival of 3-5 years from the time of diagnosis.

Asthma-COPD Overlap Syndrome (ACOS): Single disease entity or not? Could exhaled nitric oxide be a useful biomarker for the differentiation of ACOS, asthma and COPD?

Asthma and chronic obstructive pulmonary disease (COPD) represent two major public health problems. However, there is a significant proportion of patients with a mixed asthma-COPD phenotype. This condition is defined as asthma-COPD overlap syndrome (ACOS).

Attitudes towards euthanasia among Greek intensive care unit physicians and nurses.

Objectives: To investigate the attitudes of Greek intensive care unit (ICU) medical and nursing staff towards euthanasia.

Background: ICU physicians and nurses deal with end-of-life dilemmas on a daily basis. Therefore, the exploration of their stances on euthanasia is worthwhile.

Dyspnea and respiratory muscle strength in end-stage liver disease.

Aim: To investigate the prevalence of chronic dyspnea and its relationship to respiratory muscle function in end-stage liver disease.

Methods: Sixty-eight consecutive, ambulatory, Caucasian patients with end-stage liver disease, candidates for liver transplantation, were referred for preoperative respiratory function assessment. Forty of these (29 men) were included in this preliminary study after applying strict inclusion and exclusion criteria.

Pulmonary function tests, sputum induction, and bronchial provocation tests: diagnostic tools in the challenge of distinguishing asthma and COPD phenotypes in clinical practice.

Background: despite a number of important differences in the pathogenesis, course, and prognosis, asthma and chronic obstructive pulmonary disease (COPD) have many features in common. Furthermore, smoking induces considerable overlap in pathogenesis and clinical features between these conditions. This study aimed to reveal what inflammatory patterns prevail in clinically established diagnosis groups, including overlap phenotypes of asthma and COPD, and to evaluate the correlation with airway reversibility and hyperreactivity in these overlapping conditions.

IL-18 in induced sputum and airway hyperresponsiveness in mild asthmatics: effect of smoking.

Interleukin 18 (IL-18) is a pro-inflammatory cytokine, which has been shown to be implicated in the induction of airway hyperresponsiveness (AHR) in murine asthma models. The association of IL-18 with AHR in human bronchial asthma is not clear as yet. As cigarette smoking modifies airway inflammation we aimed to assess the relationship of IL-18 with airway hyperresponsiveness (AHR) in non-smoking versus smoking asthmatics.

Non-invasive measurement of the mean alveolar O(2) tension from the oxygen uptake versus tidal volume curve.

Aims: The classical equations for measuring the mean and the ideal alveolar O(2) tension are based on assumptions, which are shown to be invalid. So we thought to develop a new, non-invasive method for measuring the mean alveolar P,O(2) within the volume domain (PA,O(2(Bohr))). This method is based on the oxygen uptake vs.

Unevenness of ventilation assessed by the expired CO(2) gas volume versus V(T) curve in asthmatic patients.

Recently, we have shown that the expired CO2 gas volume versus tidal volume (VCO2-VT) curve is a useful tool for assessing unevenness of ventilation because it allows the separation of tidal volume into three functional compartments: (a) the CO2-free expired air (V0), (b) the transitional volume (Vtr), (c) the alveolar volume (VA) and the measurement of alveolar FCO2 during resting breathing in normal subjects and patients with COPD. In this paper, we have investigated whether changes pertaining to unevenness of ventilation taking place immediately after the administration of methacholine can be assessed using the VCO2-VT curve in asthmatic patients. The VCO2-VT curve was obtained during tidal breathing from 16 stable asthmatic patients who underwent a methacholine challenge test.

Negative expiratory pressure: a new tool.

The term expiratory flow limitation is used to indicate that maximal expiratory flow is achieved during tidal breathing and is characteristic of intra-thoracic airflow obstruction. Despite the severe consequences of expiratory flow limitation, the prevalence and clinical significance of this phenomenon have not been adequately studied in chronic obstructive pulmonary disease (COPD), asthma, and patients with other pulmonary and non-pulmonary disease. This is due to the fact that the conventional method to detect expiratory flow limitation, i.

Noninvasive measurement of mean alveolar carbon dioxide tension and Bohr's dead space during tidal breathing.

The lack of methodology for measuring the alveolar carbon dioxide tension (PA,CO2) has forced investigators to make several assumptions, such as that PA,CO2 is equal to end-tidal (PET,CO2) and arterial CO2 tension (Pa,CO2). The present study measured the mean PA,CO2 and Bohr's dead space ratio (Bohr's dead space/tidal volume (VD,Bohr/VT)) during tidal breathing. The method used is a new, simple and noninvasive technique, based on the analysis of the expired CO2 volume per breath (VCO2) versus the exhaled VT.