A pulmonary mass with invasion into the heart.

We describe the case of a 58 year old woman who presented with bronchial atypical carcinoid found at surgery to invade the left atrium along the pulmonary veins. A right pneumonectomy and removal of a portion of the left atrium was performed. The patient made an excellent post operative recovery. Three years later she presented in acute respiratory failure secondary to local recurrence. This is first case described in which recurrence after resection of bronchial carcinoid metastatic to the heart is described.

Expression of genes involved in oxidative stress responses in airway epithelial cells of smokers with chronic obstructive pulmonary disease.

RATIONALE: The molecular mechanisms involved in airway oxidative stress responses reported in healthy smokers and in those with chronic obstructive pulmonary disease (COPD) are poorly understood. OBJECTIVES: To assess the expression of genes involved in oxidative stress responses in the bronchial epithelium of smokers with or without COPD and in relation to disease severity. METHODS: Global gene expression was assessed in bronchial brushings in 38 subjects with COPD, 14 healthy nonsmokers, and 18 healthy smokers. RESULTS: Gene expression analysis using Affymetrix arrays revealed mRNAs representing 341 out of 642 oxidative stress genes from two predefined gene sets to be differentially expressed in healthy nonsmokers when compared with healthy smokers, and 200 differentially expressed oxidative genes in subjects with COPD when compared with healthy smokers. Gene set enrichment analysis showed that pathways involved in oxidant/antioxidant responses were among the most differentially expressed gene pathways in smoking individuals, with further differences seen in COPD. Distinct, nonlinear gene expression patterns were identified across the severity spectrum of COPD, which correlated with the presence of certain transcription factor binding sites in their promoters. Significant changes in oxidant response genes observed in vivo were reproduced in vitro using primary bronchial epithelial cells from the same donors cultured at an air-liquid interface and exposed to cigarette smoke extract. CONCLUSIONS: Cigarette smoke induces significant changes in oxidant defense responses; some of these are further amplified, but not in a linear fashion, in individuals who develop COPD.

Extensively drug-resistant tuberculosis (XDR-TB) - a potential threat in Ireland.

We describe a case of a 25 year old female from Lithuania who presented with a productive cough. Chest radiograph demonstrated an infiltrate in the left upper lobe and a cavitating lesion in the right middle lobe. Sensitivity testing of her sputum led to a diagnosis of extensively drug-resistant tuberculosis (XDR-TB). This is the first case in Ireland and highlights the need for physicians to be aware of the possibility of XDR-TB. Moreover it underlines the need for improvement in service provision in terms of a TB reference laboratory and TB clinics.

Autocrine ligands for the epidermal growth factor receptor mediate interleukin-8 release from bronchial epithelial cells in response to cigarette smoke.

Airway neutrophilia is a prominent feature of chronic obstructive pulmonary disease. As cigarette smoke (CS) and epidermal growth factor (EGF) both cause release of interleukin-8 (IL-8) from epithelial cells in vitro, we investigated whether autocrine ligands for the EGF receptor (EGFR) are involved in this proinflammatory response to CS. NCI-H292 or primary bronchial epithelial cells were cultured with or without cigarette smoke extract (CSE) or EGF for 6-48 h. We then tested culture supernatants for lactate dehydrogenase activity to assess cell viability, and for IL-8 and EGFR ligands by ELISA; quantitative RT-PCR was used to measure IL-8 and EGFR ligand mRNA. EGF and low concentrations of CSE both promoted cell survival and caused enhanced transcription and release of IL-8. Similarly, levels of mRNA encoding transforming growth factor alpha (TGF-alpha), heparin-binding EGF-like growth factor, and amphiregulin (AR) were increased, as was shedding of TGF-alpha and AR protein into the culture medium. With the exception of AR gene transcription, the CS-induced responses were blocked by the EGFR-selective kinase inhibitor AG1478. Furthermore, ~ 45% of CS-induced IL-8 release was inhibited by a neutralising anti-EGFR. Our data indicate that secretion of IL-8 in response to CSE is dependent on EGFR activation and that autocrine production of TGF-alpha makes a substantial contribution to this response.