Genetic analysis on growth and carcass traits in Nelore cattle.

In this study, the objective was to estimate genetic parameters of body weight at 210 (BW210) and 365 (BW365) days of age in relation to rib eye area (REA), subcutaneous back fat thickness (BF) and rump fat (RF), and their respective genetic trends, in Nelore beef cattle. Estimates of genetic parameters and breeding values for the studied traits were obtained using the REML method. The direct and maternal heritability estimates were respectively: 0.

IL-32, a novel proinflammatory cytokine in chronic obstructive pulmonary disease.

Rationale: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder of the lung, yet the mechanisms that regulate this immune-inflammatory response are not fully understood.

Objectives: We investigated whether IL-32, a newly discovered cytokine, was related to markers of inflammation and clinical progression in COPD.

Methods: Using immunohistochemistry, expression of IL-32 was examined in surgically resected specimens from 40 smokers with COPD (FEV(1) = 39 +/- 4% predicted), 11 smokers with normal lung function, and 9 nonsmoking control subjects.

Nonatopic children with multitrigger wheezing have airway pathology comparable to atopic asthma.

Rationale: Epidemiologic studies have shown that, in atopic children, wheezing is more likely to persist into adulthood, eventually becoming asthma, whereas it appears to resolve by adolescence in nonatopic children.

Objectives: To investigate whether among children with multitrigger wheeze responsive to bronchodilators the airway pathology would be different in nonatopic wheezers, who are often considered nonasthmatic, compared with atopic wheezers, who are more frequently diagnosed as having asthma.

Methods: Bronchial biopsies were obtained from 55 children undergoing bronchoscopy for appropriate clinical indications: 18 nonatopic children with multitrigger wheeze (median age, 5 yr; range, 2-10 yr), 20 atopic children with multitrigger wheeze (medan age, 5 yr; range, 2-15 yr), and 17 control children with no atopy or wheeze (median age, 4; range, 2-14 yr).

Out-patient high-dose-rate endobronchial brachytherapy for palliation of lung cancer: an observational study.

Background And Aim: Out-patient high-dose-rate endobronchial brachytherapy (HDREB) is a possible option in the palliation of symptoms in patients with advanced lung cancer, but literature data is limited and the technique is still under development in Italy. Our aim was to evaluate safety and effectiveness of out-patient HDREB for palliation of malignant endobronchial tumours in the context of a multidisciplinary approach.

Methods: Out-patient HDREB sessions were scheduled at weekly intervals (500-1000 cGy per session) with prior Diodi-laser resection in some cases.

Increased activation of p38 MAPK in COPD.

Inflammation, oxidative stress and apoptosis, which are involved in chronic obstructive pulmonary disease (COPD) pathogenesis, may activate the p38 subgroup of mitogen-activated protein kinases (MAPKs). Therefore, the aim of the present study was to evaluate the expression of the phosphorylated, active form of p38 MAPK (phospho-p38) in the lungs of COPD patients. Surgical specimens were obtained from 18 smokers with COPD at different stages of disease severity, plus nine smoking and eight nonsmoking subjects with normal lung function.

The Role of Lymphocytes in the Pathogenesis of Asthma and COPD.

Asthma and chronic obstructive pulmonary disease (COPD) are two different inflammatory disorders of the lungs which share a common functional abnormality, i.e. airflow limitation [1,2].

Matrix metalloproteinase-2 protein in lung periphery is related to COPD progression.

Background: There is increasing evidence that matrix metalloproteinases (MMPs) may contribute to the pathogenesis of COPD, but their role in humans is not completely understood. We performed this study to quantify the expression of MMP-2 in a population of COPD patients at different stages of severity.

Methods: We collected surgical specimens from 46 subjects, as follows: 10 smokers with severe COPD (Global Initiative for Chronic Obstructive Lung Disease [GOLD] stage III-IV); 13 smokers with mild/moderate COPD (GOLD stage I-II); 12 control smokers; and 11 nonsmoking control subjects.

The laws of attraction: chemokines, neutrophils and eosinophils in severe exacerbations of asthma.

A possible new therapeutic strategy for preventing exacerbations

High-dose N-acetylcysteine in patients with exacerbations of chronic obstructive pulmonary disease.

Objective: To investigate the efficacy and tolerability of high-dose N-acetylcysteine (NAC) in the treatment of patients with exacerbations of chronic obstructive pulmonary disease (COPD).

Design And Patients: Randomised, double-blind, double-dummy, placebo-controlled study in 123 patients experiencing an acute exacerbation of COPD.

Interventions: NAC 1200 mg/day, 600 mg/day or placebo administered once daily for 10 days.

Epithelial damage and angiogenesis in the airways of children with asthma.

Rationale: Airway remodeling and inflammation are characteristic features of adult asthma that are still poorly investigated in childhood asthma.

Objectives: To examine epithelial and vascular changes as well as the inflammatory response in airways of children with asthma.

Methods: We analyzed bronchial biopsies obtained from 44 children undergoing bronchoscopy for appropriate clinical indications other than asthma: 17 with mild/moderate asthma (aged 2-15 yr), 12 with atopy without asthma (1-11 yr), and 15 control children without atopy or asthma (1-14 yr).

Transforming growth factor-beta type II receptor in pulmonary arteries of patients with very severe COPD.

A mild-to-moderate increase in pulmonary arterial pressure is often associated with severe chronic obstructive pulmonary disease (COPD). Transforming growth factor (TGF)-beta is a cytokine involved in the maintenance of integrity of vasculature. The aim of the study was to investigate whether the TGF-beta pathway might be involved in the development of pulmonary hypertension associated with COPD.

Upregulation of basic fibroblast growth factor in smokers with chronic bronchitis.

The aim of the study was to investigate the expression of basic fibroblast growth factor (bFGF) and its receptor, fibroblast growth factor receptor (FGFR)-1, in the central airways of smokers with chronic bronchitis. The lobar bronchi from 17 subjects undergoing thoracotomy for solitary nodules were examined. All had a history of cigarette smoking, nine had symptoms of chronic bronchitis and airflow limitation, and eight were asymptomatic with normal lung function.

Decreased expression of TGF-beta type II receptor in bronchial glands of smokers with COPD.

Background: The role of transforming growth factor-beta1 (TGF-beta1) in chronic obstructive pulmonary disease is still controversial, but it has been proposed that it may protect from mucus hypersecretion since it is able to downregulate mucin production. A study was undertaken to investigate the expression of TGF-beta1 and its type II receptor (TGF-beta RII) in the bronchial glands of smokers with COPD.

Methods: The expression of TGF-beta(1) and TGF-beta RII were examined immunohistochemically in the bronchial glands of 24 smokers undergoing lung resection for solitary peripheral nodules: 12 with airflow limitation (smokers with COPD) and 12 with normal lung function.

Marked alveolar apoptosis/proliferation imbalance in end-stage emphysema.

Background: Apoptosis has recently been proposed to contribute to the pathogenesis of emphysema.

Methods: In order to establish if cell fate plays a role even in end-stage disease we studied 16 lungs (9 smoking-associated and 7 alpha1antitrypsin (AAT)-deficiency emphysema) from patients who had undergone lung transplantations. Six unused donor lungs served as controls.

[Pathology of chronic obstructive pulmonary disease].

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder of the lung characterized by poorly reversible airflow limitation. It is not a unique disease entity but rather a complex of conditions which include emphysema, chronic bronchitis and, sometimes, asthma. Moreover, COPD is a progressive disease often associated with exacerbations.

Neutrophilic infiltration within the airway smooth muscle in patients with COPD.

Background: COPD is an inflammatory disorder characterised by chronic airflow limitation, but the extent to which airway inflammation is related to functional abnormalities is still uncertain. The interaction between inflammatory cells and airway smooth muscle may have a crucial role.

Methods: To investigate the microlocalisation of inflammatory cells within the airway smooth muscle in COPD, surgical specimens obtained from 26 subjects undergoing thoracotomy (eight smokers with COPD, 10 smokers with normal lung function, and eight non-smoking controls) were examined.

Airway inflammation in childhood asthma.

Airway pathology has been extensively investigated in adulthood asthma, whereas only few studies examined bronchial biopsies in childhood asthma. To evaluate the airway pathology in children with asthma, we analyzed bronchial biopsies obtained from 23 children undergoing bronchoscopy for clinical indications other than asthma. Nine had mild/moderate asthma.

Increased proportion of CD8+ T-lymphocytes in the paratracheal lymph nodes of smokers with mild COPD.

Previous studies have shown an increased number of inflammatory cells and, in particular, of CD8+ T lymphocytes, in central airways, peripheral airways, lung parenchyma and pulmonary arteries of smokers with COPD. In this study we investigated whether this inflammatory process is restricted to the lung tissue or whether a similar process is also present in the lymph nodes of these subjects. We examined paratracheal lymph nodes obtained from 6 smokers with COPD (FEV1/VC < 88% predicted and FEV1/FVC < 70% both before and after 200 microg of inhaled salbutamol) and 6 smokers without COPD (FEV1/VC > 88% predicted and FEV1/FVC > 70%) undergoing lung resection for localised pulmonary lesions.

Airway inflammation in severe chronic obstructive pulmonary disease: relationship with lung function and radiologic emphysema.

The lung pathology of severe chronic obstructive pulmonary disease (COPD) has been poorly investigated. We examined surgical specimens obtained from patients with severe (forced expiratory volume in 1 second [FEV(1)] = 29 +/- 3% predicted, n = 9) or mild/no airflow limitation (FEV(1) = 86 +/- 5% predicted, n = 9) and similar smoking history. With histochemical and immunohistochemical methods we quantified the structural changes and the inflammatory cells in small airways and in muscular pulmonary arteries.

Increased expression of the chemokine receptor CXCR3 and its ligand CXCL10 in peripheral airways of smokers with chronic obstructive pulmonary disease.

CXCR3 is a chemokine receptor preferentially expressed on lymphocytes, particularly on type-1 T-lymphocytes. Smokers who develop chronic obstructive pulmonary disease (COPD) have a chronic bronchopulmonary inflammation that is characterized by an increased infiltration of T-lymphocytes, particularly CD8(+), in the airways and lung parenchyma. To investigate the expression of CXCR3 and its ligand interferon-induced protein 10/CXCL10 in COPD, we counted the number of CXCR3(+) cells and analyzed the expression of CXCL10 in the peripheral airways of 19 patients undergoing lung resection for localized pulmonary lesions.

[Current knowledge on pathogenesis and pathologic anatomy of chronic obstructive pulmonary disease].

In smokers with chronic obstructive pulmonary disease (COPD), pathological changes can be found in the central airways, peripheral airways, lung parenchyma and pulmonary arteries. Interestingly, some of these changes can be already present in the lungs of smokers with normal lung function indicating that smoking itself is able to damage the lung even before airflow limitation occurs. The purpose of this paper is to describe the structural changes present in the lungs of smokers with normal lung function and those present in the lungs of smokers with COPD, in an attempt to underline the possible mechanisms contributing to airflow limitation in these patients.

Pathogenesis and pathology of COPD.

Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation. Since flow is the result of a driving pressure that promotes flow and of an opposing resistance that contradicts it, the reduction in flow observed in COPD has two main components: increased resistance, which is due to airway obstruction, and a loss of the elastic recoil pressure of the lung, which is due to parenchymal destruction. Although it has long been known that the major site of increased resistance in COPD is the peripheral airways, recent studies have shown that central airways are involved in the disease as well.