11 research outputs found

    Lactate dehydrogenase-5 (LDH-5) overexpression in non-small-cell lung cancer tissues is linked to tumour hypoxia, angiogenic factor production and poor prognosis

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    Lactate dehydrogenase-5 (LDH-5) catalyses the reversible transformation of pyruvate to lactate, having a principal position in the anaerobic cellular metabolism. Induction of LDH-5 occurs during hypoxia and LDH-5 transcription is directly regulated by the hypoxia-inducible factor 1 (HIF1). Serum LDH levels have been correlated with poor prognosis and resistance to chemotherapy and radiotherapy in various neoplastic diseases. The expression, however, of LDH in tumours has never been investigated in the past. In the present study, we established an immunohistochemical method to evaluate the LDH-5 overexpression in tumours, using two novel antibodies raised against the rat muscle LDH-5 and the human LDH-5 (Abcam, UK). The subcellular patterns of expression in cancer cells were mixed nuclear and cytoplasmic. In direct contrast to cancer cells, stromal fibroblasts were reactive for LDH-5 only in a minority of cases. Serum LDH, although positively correlated with, does not reliably reflect the intratumoral LDH-5 status. Lactate dehydrogenase-5 overexpression was directly related to HIF1alpha and 2alpha, but not with the carbonic anhydrase 9 expression. Patients with tumours bearing high LDH-5 expression had a poor prognosis. Tumours with simultaneous LDH-5 and HIF1alpha (or HIF2alpha) overexpression, indicative of a functional HIF pathway, had a particularly aggressive behaviour. It is concluded that overexpression of LDH-5 is a common event in non-small-cell lung cancer, can be easily assessed in paraffin-embedded material and provides important prognostic information, particularly when combined with other endogenous markers of hypoxia and acidity

    Factors affecting post minimally invasive direct coronary artery bypass grafting incidence of myocardial infarction, percutaneous transluminal coronary angioplasty, coronary artery bypass grafting and mortality of cardiac origin

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    In the present study we identify parameters which influence the incidence of myocardial infarction (MI), need for percutaneous coronary intervention (PCI), coronary artery bypass grafting (CABG) and cardiac mortality after minimal invasive coronary artery bypass grafting (MIDCABG). With a mean follow-up of 30+/-11.2 months, 390 patients were assessed with Wald test-corrected chi(2) analysis to identify preoperative factors which correlate with a higher incidence of post-MIDCABG MI, PCI, CABG and mortality from cardiac causes. We found an increased incidence of postoperative MI in patients with 2-vessel (8.7%) and 3-vessel (7.7%) vs. 1.3% 1-vessel coronary artery disease (CAD) (P=0.023), and in patients with preceding cardiac procedure (CABG and PCI: 8.4% vs. 2.0% without, P=0.023). Also diabetes was associated with higher post-MIDCABG frequency of MI (P=0.035). Severity of angina was associated with lesser post-MIDCAB-PCI (P=0.011) while preceding CABG predicted a higher incidence (P=0.012). Preoperative low ejection fraction (EF) (multivariate, P<0.001), preoperative MI (P=0.007) and extent of CAD (P=0.001) were associated with a higher post-MIDCABG mortality. None of the parameters correlated with subsequent CABG MIDCABG. The extent and history of CAD, history of cardiac interventions and low EF seem to influence the outcome adversely and should be considered deciding pro or against the MIDCAB-option

    Aortic prosthesis re-replacement due to concealed stenosing subvalvular pannus ring

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    10.1055/s-2006-924710Thoracic and Cardiovascular Surgeon555331-33
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