Most studies of idiopathic nonspecific interstitial pneumonia (NSIP) have primarily studied mortality. In order to clarify the detailed outcome and prognostic markers in idiopathic NSIP, the clinical course with initial radiological and clinical features was analysed.The clinical course of 83 patients who were classified with idiopathic NSIP (72 fibrotic, 11 cellular; 27 males and 56 females; mean¡SD age 54.4¡10.1 yrs) was retrospectively analysed.In fibrotic NSIP, 16 (22%) patients died of NSIP-related causes with a median (range) follow-up of 53 (0.3-181) months. Despite the favourable survival (5-yr 74%), patients with fibrotic NSIP were frequently hospitalised with recurrence rate of 36%. Reduced forced vital capacity at 12 months was a predictor of mortality. On follow-up, lung function was improved or stable in ,80% of the patients. The extent of consolidation and ground-glass opacity on initial highresolution computed tomography correlated significantly with serial changes of lung function, and the presence of honeycombing was a predictor of poor prognosis. During follow-up, eight (10%) patients developed collagen vascular disease.In conclusion, the overall prognosis of fibrotic nonspecific interstitial pneumonia was good; however, there were significant recurrences despite initial improvement and a subset of the patients did not respond to therapy. Some patients developed collagen vascular diseases at a later date.

Our results emphasize the importance of being aware of synovial sarcoma as a possible primary pleural malignancy, especially in a young patient with a localized mass. In addition, the presence of bcl-2 protein perhaps represents a useful marker in distinguishing synovial sarcoma, especially monophasic variants, from mesothelioma within a panel of antibodies.

Chlamydia pneumoniae, Chlamydia trachomatis and Chlamydia psittaci were detected at low frequencies (o20%) among 69 pulmonary mucosa-associated lymphoid tissue (MALT) lymphomas, 30 other lymphoproliferative disorders (LPD) and 44 non-LPD. The incidence of individual Chlamydiae was generally higher in MALT lymphoma than non-LPD, although not reaching statistical significance. Mycoplasma pneumoniae DNA was not detected.

Objective: Our aim is to determine whether mitochondrial dysfunction is a contributing factor to the increased risk of non-small cell lung carcinoma (NSCLC) in COPD patients. Methods:The clinical relevance of mitochondrial-related gene expression in lung cancer was determined using transcriptomic data from more than 1000 human NSCLC samples. Immunohistochemistry was then used to study cell type specific expression of the relevant mitochondrial-related protein in normal and cancerous lung tissue. Gene set variation analysis (GSVA) was applied in NSCLC datasets to determine the relative expression of specific macrophage transcriptomic signatures. Results:The expression of 33 mitochondrial-related genes was correlated with NSCLC patient survival. We studied further the expression of PGAM5 and FUNDC1, which are regulators of mitochondrial degradation (mitophagy). In background lung tissue, PGAM5 and FUNDC1 were only expressed in alveolar macrophages, with highest expression in smokers with emphysema compared to healthy smokers and non-smokers. In cancerous tissue, only the malignant epithelial cells and associated macrophages at the periphery of the cancer, expressed PGAM5 and FUNDC1. PGAM5 was also expressed in pre-neoplastic epithelium (squamous dysplasia and carcinoma in situ). There was no difference in expression in cancer tissue between the emphysema, healthy smokers and non-smokers group. Macrophages at the edge of the cancer from emphysema patients had a trend towards higher expression of PGAM5 and FUNDC1 compared to those from the other groups. There was a significant correlation between PGAM5 expression in cancer tissue and 9 out of 49 previously defined macrophage transcriptomic signatures with one (module 22) associated with patient survival (p<0.05). Conclusion:PGAM5 is expressed in pre-neoplastic tissue and NSCLC, but not in normal epithelium. The association between PGAM5 expression and lung cancer outcome may be mediated by the induction of specific macrophage phenotypes.

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