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 HIF1a and 2a, 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 HIF1a (or HIF2a) 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.

Continuous infusion of 2% propofol at large doses for the sedation of rabbits undergoing prolonged mechanical ventilation induced fatal multiorgan dysfunction syndrome similar to the propofol infusion syndrome seen in humans. Our novel findings including lung, liver, gallbladder, and urinary bladder injury were also noted. The role of propofol's lipid vehicle in the manifestation of the syndrome was minor. Sevoflurane proved to be a safe alternative medication for prolonged sedation.

Evacuation of subglottic secretions using the Evac ETT is often ineffective due to prolapse of tracheal mucosa into the subglottic suction port.

No abstract

The minimized extracorporeal circulation system (MECC) is being used to reduce priming volume and blood/polymer contact during cardiac procedures. In this study, we evaluated the efficacy and potential advantages of the system in coronary artery bypass graft (CABG) patients. We included two groups of patients destined for CABG in a prospective, randomized study: Group A was operated on the usual pump (n = 30) while Group B was operated using the MECC (n = 50). Pre-operative demographics, intra-operative times and values as well as a series of post-operative outcome data (blood loss, transfusion requirements, ventilation time, ICU and hospital stay) were recorded. CK, CK-MB, troponin-T, IL-6 and IL-8 were measured. Pre-operative and post-operative lung function were assessed. In the MECC-operated group, patients developed less post-operative troponin-T (0.2 +/- 0.3 vs. 0.5 +/- 0.5 ng/mL, p=0.031) and less IL-8 (13.8 +/- 5 vs. 22.5 +/- 0.5 microg/L, p = 0.05). While blood loss was comparable in both groups, packed red blood cells and fresh frozen plasma were given less frequently in the MECC group (p = 0.015 resp. 0.022). The one-tailed Student's t-test revealed shorter bypass time in the MECC group (74 +/- 17 vs. 82 +/- 24 min). There was no difference in ventilation and ICU-time (patients were not treated in a fast-track fashion). The FEV1 was better in the MECC group (relative values: 70.1 +/- 18.2% vs. 61.1 +/- 12.3%, p = 0.02). Utilization of the MECC may cause less cytokine (IL-8) liberation, owing to less blood/tubing contact, as well as less red blood cell and fresh frozen plasma demand. It may also be the circuit in patients with chronic obstructive pulmonary disease (COPD).