An interleukin-1 polymorphism additionally intensified by atopy as prognostic factor for aseptic non-mechanical complications in metal knee and hip arthroplasty.

Background: In contrast to infection or mechanical issues joint replacement failure following inflammatory adverse reactions is poorly understood. Objective: To assess the association of IL-1ß polymorphisms and history of allergy with aseptic non-mechanical complications following arthroplasty. Methods: In 102 patients with aseptic non-mechanically caused symptomatic knee or hip arthroplasty (SA) and 93 patients with asymptomatic arthroplasty (AA) questionnaire-based history, patch test with at least standard series, lymphocyte transformation test (LTT) with nickel, cobalt and chromium and interleukin-1 polymorphism analysis were done. Three polymorphisms of the IL1B gene [IL-1b -3954 (rs1143634), IL-1b -511 (rs16944) and IL-1b -31 (rs1143627)] and one polymorphism of the IL1RN gene [IL1RN intron 2, variable number of tandem repeats, VNTR (rs2234663)] were assessed by PCR and gel electrophoresis. Results: We found no significant difference in smoking history and atopy but 25% versus 10% of self-reported metal allergy in SA versus AA; the patch test (respective, LTT) for metal sensitivity was more often positive in SA patients. The allele 498 bp of the IL1RN polymorphism occurred significantly more often in the SA group (37% versus 11%; p < 0.0001). Upon additional presence of atopy, the difference was even greater (60% vs 10%) (p < 0.000001). There was no association of IL-1 polymorphisms with metal allergy. Conclusion: The IL1RN VNTR allele 498 bp was strongly associated with SA. In patients with a history of atopy, presence of the IL1RN VNTR allele 498 bp led to a four-fold higher SA prevalence compared to patients without this allele.

Spatio-temporal Aspects of Ca2+ Signalling: Lessons from Guard Cells and Pollen Tubes.

Changes in cytosolic Ca2+ concentration ([Ca2+]cyt) serve to transmit information in eukaryotic cells. The involvement of this second messenger in plant cell growth as well as osmotic- and water relations is well established. After almost 40 years of intense research on the coding and decoding of plant Ca2+ signals, numerous proteins involved in Ca2+ action have been identified. However, we are still far from understanding the complexity of Ca2+ networks. New in vivo Ca2+ imaging techniques combined with molecular genetics allow visualisation of spatio-temporal aspects of Ca2+ signalling. In parallel, cell biology together with protein biochemistry and electrophysiology are able to dissect information processing by this second messenger in space and time. Here we focus on the time-resolved changes in cellular events upon Ca2+ signals, concentrating on the two best-studied cell types, pollen tubes and guard cells. We put their signalling networks side by side, compare them with those of other cell types and discuss rapid signalling in the context of Ca2+ transients and oscillations to regulate ion homeostasis.

[Cost analysis as a tool for assessing the efficacy of intensive care units]. / Kosten als Instrument zur Effizienzbeurteilung intensivmedizinischer Funktionseinheiten.

BACKGROUND: The German "Hospital Structure Act" intends to align the state hospital planning on quality criteria. Within this process cost-utility analyses (CUAs) shall be used to assess the efficacy of medical care. To be objective, CUAs of intensive care units (ICUs) require standardization (adjustment) of costs. The present study analyzed the extent to which treatment costs are related to patient-specific baseline variables (such as type and severity of the primary disease). METHODS: From 2000-2004, a bottom-up procedure was used to quantify total costs on 14 ICUs in nine German university hospitals. Results were combined with demographic data, and data indicating type (ICD-10 codes) and severity (ICU scoring systems) of the primary disease at ICU admission. Various statistical models were tested to identify that which best described the associations between baseline variables and costs. RESULTS: In all, 3803 critically ill patients could be examined. The median of treatment costs per patient was 3199 € (IQR 1768-6659 €). No model allowed an acceptably precise adjustment of costs; the estimated mean absolute prognostic error was at least 3860 € (mean relative prognostic error 66%), when we tested an Extreme Gradient Boosting Model. CONCLUSION: Instruments which are currently available (cost adjustment based on patient-specific baseline variables) do not allow a standardization of costs, and an objective CUA of ICUs. Factors unknown at baseline may cause a large portion of treatment costs.