Evaluation of the rate,location, and morphology of perforations in surgical gloves worn in urological operations

Surgical perforation or intrinsic defects within the polymer membranes of surgical gloves are responsible for an increased exposure, and consequently infection risk, to HIV and HCV or other infectious diseases for the medical healthcare professional. A prospective field study was undertaken to evaluate the number and location of glove perforations, tested by the waterfill test. The morphology of these perforations was then inspected by stereo light and scanning electron microscopy. By comparing in-use defects to simulated defects created by medical instruments in unused gloves it was possible to categorize perforations caused by intrinsic defects or extrinsic mechanical stress. In six different types of surgical gloves collected from 720 urological operations the waterfill test revealed leakage rates of 6.6 percent to 12.3 percent. Further assessment of these gloves revealed intrinsic polymer material defect rates of 0.2 percent to 3.3 percent. The in-use acquired instrumental and mechanical perforation rate ranged from 4.6 percent to 12.15 percent. Perforations were mostly located at the index finger (left > right) or the thumbs. The morphology of the intrinsic defects was visualized as either incorporated membranous air bubbles or granular areas. The simulation of defects by surgical instruments in unused gloves resulted in the production of a catalog for comparison with defects seen in used gloves. This knowledge of the location and cause of these perforations highlights the need for a better avoidance strategy and/or establishment of a schedule for routine glove change by surgeons. In addition, the intrinsic polymer film quality of gloves can be improved by a lower incidence of air bubbles together with less granular sites.     

Biochemische Marker bei isch?mischen und nicht isch?mischen Myokardsch?digungen

Zusammenfassung Hintergrund: Biochemische Marker sind seit fast 50 Jahren integrativer Bestandteil der nicht invasiven kardialen Diagnostik und haben mit den kardialen Troponinen angesichts ihres prognostischen Potentials bei akutem Koronarsyndrom eine Renaissance erfahren. Diagnostik: Nach den Empfehlungen der National Acadamy of Clinical Biochemistry und der International Federatuion of Clinical Chemistry stellen das kardiale Troponin T und das kardiale Troponin I den neuen Goldstandard in der biochemischen kardialen Ischämiediagnostik dar. Charakteristikum dieser neuen Marker ist zum einen das verbesserte diagnostische Potential, das sich in der Wahl zweier Grenzwerte zur Differenzierung einer minimalen Myokardschädigung vom definitiven akuten Myokardinfarkt widerspiegelt. Zum anderen erlauben die neuen kardiospezifischen Marker eine Risikostratifizierung in dem klinisch bedeutsamen Szenario des akuten Koronarsyndroms (zwei- bis dreifach erhöhte Mortalitätsrate für Patienten mit ST-Strecken-Hebung oder Ruhe-Angina pectoris und kardialer Troponinerhöhung zum Zeitpunkt der Aufnahme). Eine weitere Indikation für die Bestimmung karidaler Marker liegt in der Beurteilung des Therapieerfolgs invasiver und nicht invasiver Reperfusionsstrategien und in der nicht invasiven Diagnostik von nicht ischämischen Myokardschädigungen (Myokarditis, Herzkontusion und Chemotherapie). Schlussfolgerung: Biochemische kardiale Marker sind zur Diagnostik ischämischer und nicht ischämischer Myokardschädigungen einsetzbar. Die kardialen Troponine scheinen sich dabei als Goldstandard für das neue Millennium zu etablieren. Abstract Background: Biochemical markers have been an integrative part of non-invasive diagnostic strategies in cardiology for nearly 50 years, experiencing a renascence by the recently acknowledged prognostic potential of cardiac troponins in acute coronary syndromes. Diagnosis: According to the guidelines of the National Academy of Clinical Biochemistry and the International Federation of Clinical Chemistry cardiac troponin T and cardiac troponin I should be considered as the new "gold markers" of ischemic myocardial injury. One characteristic feature of these new markers is the improved diagnostic potential, reflected by the choice of two cut-off values to distinguish minor myocardial injury from acute myocardial infarction. In addition, cardiac troponins allow risk stratification in the clinical setting of acute coronary syndromes: approximately threefold higher mortaligy rate for patients with rest angina or ST segment elevation and cardiac troponin elevation on admission. Other indications for cardiac marker analysis are monitoring of therapeutic success in case of invasive and non-invasive reperfusion strategies and non-invasive diagnosis of non-ischemic myocardial injury (myocarditis, cardiac contusion and chemotherapy). Conclusion: Biochemical cardiac markers are a useful tool in the diagnosis of both ischemic and non-ischemic myocardial injury. Among these, cardiac troponins seem to become the gold markers for the new millennium.     

Regulation of CC chemokine receptor 5 in hepatitis G virus infection

INTRODUCTION: Epidemiological data demonstrate an association between hepatitis G virus (HGV) co-infection and improved survival of HIV-positive individuals. However, the mechanism by which HGV affects progression of HIV disease remains unclear. As down-regulation of CC chemokine receptor 5 (CCR5) delays HIV progression, we investigated whether CCR5 expression is altered by exposure of lymphocytes to HGV proteins. METHODS: A cross-sectional analysis of CCR5 expression was carried out on CD4 and CD8 T lymphocytes of 11 HGV-positive and 12 HGV-negative persons, who were homozygous for the CCR5 wild-type gene. Binding of the HGV E2 protein to CD81 was analysed by flow cytometry. Lymphocytes were stimulated with immobilized HGV E2, anti-CD81 or serum proteins from HGV-infected subjects and changes in CCR5 expression and CC chemokine secretion were determined. RESULTS: We demonstrate that the HGV envelope protein E2 specifically binds to CD81 on T lymphocytes. This interaction induces a dose-dependent release of RANTES and down-regulation of CCR5 surface expression with concomitant intra-cellular accumulation of CCR5 proteins. This effect of HGV E2 on CCR5 expression was confirmed when lymphocytes were incubated with serum proteins from HGV-infected subjects. Finally, our cross-sectional analysis revealed CCR5 expression to be reduced by 53% and 36% on CD4 and CD8 lymphocytes of HGV-infected subjects, respectively (P < 0.01). CONCLUSIONS: Our results demonstrate that an interaction of HGV E2 with CD81 leads to increased RANTES secretion and decreased CCR5 surface expression. This mechanism might contribute to the delayed progression of HIV-infection in HGV-coinfected patients.     

Thrombin generation in severe haemophilia A and B: the endogenous thrombin potential in platelet-rich plasma

Thrombin generation was investigated in platelet-rich plasma (PRP) from 11 healthy controls, 17 patients with severe haemophilia A and 7 patients with severe haemophilia B. Mean endogenous thrombin potential (ETP) in arbitrary fluorescence units (FU) was 226.9 +/- 44.6, 186.4 +/- 22.5, 154.2 +/- 41.3 in controls, haemophilia A and B, respectively, all at a platelet count of 200 x 10(9)/l (p = 0.004 for controls vs. haemophilia A, p = 0.003 for controls vs. haemophilia B, no significant difference between haemophilia A and B). The contribution of FVIII to thrombin generation in haemophilia A was 1.31 +/- 0.16 FU/% of FVIII:C activity, while for FIX in haemophilia B this was 0.80 +/- 0.21 FU/% of FIX activity. There was an almost linear relationship between increasing platelet count and thrombin generation up to a mean platelet count of 100 x 10(9)/l. Further increase in platelet count has only a marginal influence on thrombin generation. Platelets increase ETP in haemophilia A by 0.184 +/- 0.022 FU/10(9) platelets/l and in haemophilia B by 0.319 +/- 0.085 FU/10(9) platelets/l, and this was significantly different between the two groups (p = 0.0002). This influence of plate-lets diminishes with increasing concentration of either FVIII or FIX. In conclusion, there is a difference in thrombin generation between haemophilia A and B, and this may be attributed to the role of platelets in the assembly of the tenase complex on their surface.     

Preoperative plasma fibrinogen levels predict mortality after coronary artery bypass grafting

This study was designed to investigate whether plasma fibrinogen levels as well as the beta-fibrinogen -455 G/A genotype are associated with outcome after coronary artery bypass graft (CABG) operation. We enrolled 249 consecutive CAD patients one day before they underwent a CABG operation. Data from 220 patients with available plasma fibrinogen levels were analyzed. The primary end-point was total mortality, the secondary end-point mortality from cardiac causes or the need for myocardial revascularization. The 2-year total mortality was 9.1% in the entire cohort. Multivariable analysis revealed an independent relationship between the primary end-point and preoperative plasma fibrinogen levels but not the beta-fibrinogen -455 G/A genotype. Neither preoperative plasma fibrinogen levels nor the beta-fibrinogen -455 G/A genotype could predict the secondary end-point. We conclude, that elevated preoperative plasma fibrinogen levels, but not the beta-fibrinogen -455 G/A genotype predict the total mortality after CABG operation.     

Loss of nicotinic acetylcholine receptor subunits alpha4 and alpha7 in the cerebral cortex of Parkinson patients

Cerebral cortical cholinergic deficits, represented by a decrease in choline acetyltransferase activity, severe losses of nicotinic binding sites as well as cell degeneration in the basal forebrain can be observed in neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease. The potential role of nicotinic acetylcholine receptor subunits as pharmacological targets for the treatment of cognitive deficits raises the question as to what extent these subunits are affected in neurodegenerative diseases. We here report on a significant decrease of the alpha4 and the alpha7 nicotinic acetylcholine receptor subunit in cortices of Parkinson patients which turns out to be similar to recent findings in Alzheimer patients.