How to run a heart surgical unit: experiences during the first year of the Department of Cardiothoracic and Vascular Surgery, University Clinic of Regensburg.

The heart surgery unit in Regensburg was opened in June 1992. A cost analysis was done for the first year, thru May 1993 with respect to facilities, output and wages. Facilities were divided into rooms, beds and personnel. The number of rooms was constant throughout the reporting period whereas beds and personnel increased continuously. Particularly the nursing staff was expanded to meet the rising demand. A direct consequence of this progressive personnel policy was that the personnel costs also increased continuously. 644 operations were done, 542 with and 102 without a heart-lung-machine. The number of operations using a heart-lung-machine rose from 18 per month in June 1992 to 59 in May 1993. The average length of hospitalization was 13.6 days. The cost of wages per month rose from DM 166,000 initially to DM 378,000. The cost of wages per hospitalization day, however, sank from DM 740 to DM 393. Distributing non-assigned costs to the cost objects in the same relationship as assigned costs, costs per hospitalization day were as follows: Intensive care unit DM 1,233 and care unit S43 DM 193. The cost of wages per operation was estimated at DM 1,553.

Beta-defensin-2 genomic copy number variation and chronic periodontitis.

Chronic periodontitis (ChP) is a multifactorial disease influenced by microbial and host genetic variability; however, the role of beta-defensin-2 genomic (DEFB4) copy number (CN) variation (V) in ChP remains unknown. The association of the occurrence and severity of ChP and DEFB4 CNV was analyzed. Our study included 227 unrelated Caucasians, that is, 136 ChP patients (combined ChP) and 91 control individuals. The combined ChP group was subdivided into the severe ChP and slight-to-moderate ChP subgroups. To determine DEFB4 CNV, we isolated genomic DNA samples and analyzed them by relative quantitation using the comparative CT method. The serum beta-defensin-2 (hBD-2) level was determined via ELISA. The distribution pattern and mean DEFB4 CN did not differ significantly in combined ChP cases vs. the controls; however, the mean DEFB4 CN in the severe ChP group differed significantly from those for the control and slight-to-moderate ChP groups. Low DEFB4 CN increased the risk of severe ChP by about 3-fold. DEFB4 CN was inversely associated with average attachment loss. Mean serum hBD-2 levels were highest in the controls, followed by the slight-to-moderate ChP group and the severe ChP group. The results suggested an association between decreased DEFB4 CN and serum hBD-2 levels and periodontitis severity.

Histamine modulates γδ-T lymphocyte migration and cytotoxicity, via Gi and Gs protein-coupled signalling pathways.

BACKGROUND AND PURPOSE: The biogenic amine, histamine plays a pathophysiological regulatory role in cellular processes of a variety of immune cells. This work analyses the actions of histamine on γδ-T lymphocytes, isolated from human peripheral blood, which are critically involved in immunological surveillance of tumours. EXPERIMENTAL APPROACH: We have analysed effects of histamine on the intracellular calcium, actin reorganization, migratory response and the interaction of human γδ T cells with tumour cells such as the A2058 human melanoma cell line, the human Burkitt's Non-Hodgkin lymphoma cell line Raji, the T-lymphoblastic lymphoma cell line Jurkat and the natural killer cell-sensitive erythroleukaemia cell line, K562. KEY RESULTS: γδ T lymphocytes express mRNA for different histamine receptor subtypes. In human peripheral blood γδ T cells, histamine stimulated Pertussis toxin-sensitive intracellular calcium increase, actin polymerization and chemotaxis. However, histamine inhibited the spontaneous cytolytic activity of γδ T cells towards several tumour cell lines in a cholera toxin-sensitive manner. A histamine H(4) receptor antagonist abolished the histamine induced γδ T cell migratory response. A histamine H(2) receptor agonist inhibited γδ T cell-mediated cytotoxicity. CONCLUSIONS AND IMPLICATIONS: Histamine activated signalling pathways typical of chemotaxis (G(i) protein-dependent actin reorganization, increase of intracellular calcium) and induced migratory responses in γδ T lymphocytes, via the H(4) receptor, whereas it down-regulated γδ T cell mediated cytotoxicity through H(2) receptors and G(s) protein-coupled signalling. Our data suggest that histamine activated γδ T cells could modulate immunological surveillance of tumour tissue.