[Current issues in pulmonary pathology. Report of the working group on pulmonary pathology of the German Society of Pathology]. / Aktuelles zur Pneumopathologie. Bericht der Arbeitsgemeinschaft Pneumopathologie der Deutschen Gesellschaft für Pathologie.

The working group on pulmonary pathology of the German Society of Pathology (Deutsche Gesellschaft für Pathologie, DGP) developed very actively in the last year. Apart from the autumn meeting in Heidelberg in 2011 and the sessions at the annual DGP meeting in Berlin it was possible to realize a first publication with support and coauthorship of several members of the working group dealing with the classification of lung adenocarcinoma. In this report the key aspects of the activity related to the following issues are summarized including non-small cell lung carcinoma, neuroendocrine tumors of the lungs, interstitial pulmonary diseases, cell blocks in cytology and banking in thoracic pathology.

Interstitial fibrosis in the heart: differences in extracellular matrix proteins and matrix metalloproteinases in end-stage dilated, ischaemic and valvular cardiomyopathy.

AIMS: To investigate whether or not there are differences in the distribution of extracellular matrix (ECM) proteins and matrix metalloproteinases (MMPs) in end-stage heart failure underlying different cardiomyopathies. METHODS AND RESULTS: Thirty-nine explanted human hearts were investigated: 15 with dilated cardiomyopathy (DCM), 17 with ischaemic cardiomyopathy (ICM) and seven with valvular cardiomyopathy (VCM). Transmural samples from four different sites were investigated. Frozen sections were processed for immunohistochemistry for collagens type I, III, IV, laminin and fibronectin, as well as MMP-1, -2 and -9. Volume densities were determined. All ECM components were expressed more frequently in DCM than in ICM. Comparing ICM with VCM, all proteins were found more frequently in VCM than in ICM except for type III collagen, which was significantly more frequent in ICM. Comparing DCM and VCM, VCM showed significantly higher volume densities for type III collagen and laminin. MMPs showed only slight variations between the cardiomyopathies. CONCLUSION: The distribution of ECM proteins differs between DCM, ICM and VCM, which suggests that they can be morphologically discriminated by interstitial fibrosis, especially by their expression of matrix proteins.

Different preservation of myocardial capillary endothelial cells and cardiomyocytes during and after cardioplegic ischemia (25 degrees C) of canine hearts.

Complete resumption of cardiac function after cardioplegic arrest presupposes a well-preserved myocardial ultrastructure during and after ischemia. Therefore, we determined ischemia-induced ultrastructural alterations in the myocardium during and after reversible cardioplegic ischemia using stereological methods. Cardiac arrest was induced with St. Thomas' Hospital- or Custodiol (HTK) solution. Reperfusion with Tyrode's solution followed after reversible cardioplegic ischemia in situ. Samples were taken 1) from beating hearts, 2) from cardioplegically arrested hearts immediately after the end of coronary perfusion, 3) from ischemic hearts incubated in the cardioplegic solution at 25 degrees C, and 4) from reperfused beating hearts after ischemia in situ at 22 degrees C. Cellular swelling was determined as the barrier thickness of capillary endothelium and as the sum of cardiomyocyte volume fractions of free sarcoplasm and mitochondria. In St. Thomas'-arrested hearts, intraischemic volume increase was significantly more pronounced in endothelial cells than in cardiomyocytes. Reperfusion at the intraischemic practical limit of resuscitability (ATP levels of 4 micromol/gww) significantly reduced intraischemic swelling of cardiomyocytes, but not of capillary endothelial cells. Mitochondrial damage was more pronounced in capillary endothelial cells during ischemia and after reperfusion. Thus, after reversible cardioplegic arrest, structural recovery of cardiomyocytes is better than that of capillary endothelial cells. An incomplete structural protection of capillary endothelial cells may predominantly contribute to postischemic dysfunction in the reperfused heart.