Reduction of monocyte-platelet interaction and monocyte activation in patients receiving antiplatelet therapy after coronary stent implantation

BACKGROUND: Monocyte activation induces different procoagulant and proadhesiveinflammatory responses and thus may play a role in thromboticcomplications after coronary interventions. Monocyte-plateletinteraction may trigger these effects inducing monocyte activation. AIMS: To characterize the effect of antiplatelet vs anticoagulationtherapy on monocyte-platelet interaction and monocyte functionafter intracoronary stenting. METHODS AND RESULTS: Immediately before, and during the first 12 days after successfulcoronary stenting, monocyteplatelet conjugates and monocytefunction were assessed by flow cytometric detection of GPIIb/IIIa(CD41) on monocytes and by monocyte surface exposure of Mac-1(CD11b/ CD18) and L-selectin (CD62L). Twenty patients receivingcombined antiplatelet therapy (ticlopidine, aspirin) were comparedto 20 patients with standard anticoagulation (phenprocoumon,overlapping heparin, aspirin). Before stenting, monocyte-plateletconjugates and Mac-1 surface expression in both groups weresignificantly increased, while L-selectin was significantlydiminished. Anticoagulation did not change these variables significantlyduring the subsequent 12 days. In contrast, antiplatelet therapyreduced platelet-monocyte conjugates by 46±9·3%(mean±SEM, P=0·0019) within 4 days, which wasassociated with a decrease in Mac-1 expression (28±6·7%,P=0·0013) and an increase in L-selectin (56±15·0%,P=0·0061). CONCLUSION: After intracoronary stenting, combined antiplatelet therapy,but not anticoagulation, causes reduction of monocyte-plateletinteraction, which is associated with monocyte deactivation.This may contribute to a decreased risk for thrombotic events.     

Staphylococcus aureus bacteremia and endocarditis

The prevalence of Stapylococcus bacteriaemia is increasing worldwide, because of the increasing use of invasive procedures leading to nosocomial infections, but also of a changing way of life (increasing fashion for tattoos or piercing, use of intravenous drugs). Infective endocarditis develops in 10-30% of the cases of staphylococcus bacteriaemia. Staphylococcus aureus endocarditis must be suspected when it develops in the year following heart surgery or implantation of permanent devices. In drug users, it usually involves the tricuspid valve. According to the resistance of the germ to meticillin, antibiotic therapy uses a combination of intravenous penicillin or glycopeptide and an aminoside. Other antibiotics such as fosfomycin, rifampicin, fusidic acid, or clindamycin can be used when aminosides are contra-indicated. The role of newer antibiotic agents, such as daptomycin or linezolide, remains to be established.     

Human vascular endothelial cells with extended life spans: in vitro cell response,protein expression,and angiogenesis

An in vitro angiogenesis system was designed for screening angiogenic agonists and antagonists. In order to obtain large quantities of cells and reproducibility, human endothelial cells with extended life spans were developed by retroviral transfection. The resulting cells grown in a serum-free medium containing endothelial cell growth supplement (ECGS) have a telomerase activity, extended life spans of at least 21 passages, and an endothelial cell phenotype (diI-acetylated-LDL upake, factor VIII-related antigen, VEGFR-1 and R-2, and tissue-type plasminogen activator (tPA)) that resembled that of unaltered primary endothelial cells. Exceptions were (i) a higher expression of tPA, and (ii) a non-significant growth response to FGF-2 or VEGF stimulation. Within three-dimensional fibrin gels, specific cell clones rapidly formed tubular structures in a more reproducible manner than those observed with low-passage primary cells. Tube formation by primary endothelial cells and those with extended life spans was dependent upon FGF-2 and ECGS, respectively. Both cell types produced FGF-2 and VEGF cytokines. Increasing doses of suramin significantly decreased the size of microvessels formed by both cell lines. These functional results indicate that a vascular matrix system containing human cells with extended life spans can be successfully utilized as an in vitro assay for antiangiogenic compounds.     

Drug-associated deaths of medical inpatients.

Of 7,423 medical inpatients, 16 (0.22%) died of drug-associated causes. The overall mortality for all medical inpatients was 6.5%. Eleven of the 16 patients who died of drug-associated causes had been terminally ill; the rest had been seriously ill before the fatal drug reaction occurred. Half of the patients had had either hematologic malignant changes or lupus nephritis. Antineoplastic drugs, azathioprine, prednisone, and heparin sodium were the most frequently implicated drugs. In other studies, we have found widely differing incidences of fatal drug reactions, due to a number of different drugs; these disparities are probably related to variations in the types of illnesses amoung different hospital populations and to varying interpretations of the term "drug-associated death." Extrapolation from the available data to a national incidence of drug-associated deaths is not possible. Drug-associated deaths are relatively uncommon and usually occur in the cases of severely or terminally ill patients treated with potentially highly toxic drugs.     

Rapid adrenocorticotropic hormone test in practice. Retrospective review

Retrospective analysis of the rapid adrenocorticotropic hormone (ACTH) test in a large adult population shows a marked interdependence of the basal cortisol concentration, peak cortisol concentration, and increase in cortisol concentration. Repetition of the rapid ACTH test in the same patient does not improve diagnostic accuracy. A significant number of falsely abnormal rapid ACTH test results were observed (in comparison to continuous ACTH infusion as a reference test). This supports the use of the rapid ACTH test as a screening test, but not as a diagnostic test for adrenocortical failure. It is proposed that a peak cortisol level greater than or equal to 20 micrograms/dl (550 nmol/liter) is a sufficient single criterion for normal adrenal function as assessed by the rapid ACTH test.     

Extended glaze firings for porcelain-veneered zirconia: Effects on the mechanical and optical behavior

ObjectiveThis study evaluated the effect of dwell time (conventional or extended) and cooling protocol (fast or slow) of self-glaze firings on the mechanical (flexural strength and crack propagation) and optical (color and translucency) properties of a porcelain-veneered zirconia system.MethodsBilayer disc-shaped samples were prepared (Vita VM9 + In-Ceram YZ) and divided according to the final thermal treatment: glaze firing followed by slow cooling (furnace opening at 200 °C) (G-S) or fast cooling (furnace opening at 600 °C) (G-F, manufacturer-recommended protocol), extended glaze firing (15 min of dwell time) followed by slow cooling (EG-S) or fast cooling (EG-F), or no thermal treatment (CTRL). Porcelain roughness (Ra and Rz) was measured before and after glaze firings. Color (ΔE₀₀) and translucency (TP₀₀) alteration were also evaluated. Flexural strength was measured with the piston-on-three-ball test and crack propagation analysis was performed after Vickers indentations. Complementary analyzes of crystalline phase and scanning electron microscopy were carried out.ResultsSignificant effect of dwell time was observed, with extended glaze leading to higher flexural strength and shorter crack lengths. Cracks of EG groups were observed to end in clusters of crystals. Color and translucency changed below perceptibility thresholds. All treatments led to a smoother surface and EG groups reached the lowest Rz values. An extra SiO₂ peak was revealed in control and EG groups. No effect of cooling protocol was found.SignificanceExtended glaze firing was able to improve the resistance to crack initiation and propagation of porcelain-veneered zirconia without clinically perceptible changes in optical properties.