Platelet lumiaggregation testing: Reference intervals and the effect of acetylsalicylic acid in healthy adults

BackgroundLight transmission aggregometry with lumiaggregometry are methods commonly recommended as a first-line test in platelet dysfunction diagnostic work-up. They are poorly standardized and usually performed in specialized laboratories. For proper interpretation, each laboratory should establish its own diagnostic approach in order to recognize abnormal aggregation patterns. The aim of this study was to measure plasma lumiaggregometry with basic agonists to establish the analyzer-reagent reference intervals (RI) for adults and to test the method response to aspirin.MethodsThe Chrono-Log Model 700 lumiaggregometer using Chrono-Par and Chrono-lume reagents (Chrono-Log Corp., Havertown, PA, USA) was used to measure the maximal aggregation and adenosine triphosphate release using adenosine diphosphate (2 μmol/L), collagen (2 μg/mL), arachidonic acid (1 μmol/L), epinephrine (5.5 μmol/L) and ristocetin (1.25 mg/mL), and thrombin (1 U/mL). The effect of aspirin on platelet aggregation and granule release was inspected.ResultsRIs derived from 40 healthy adults were calculated using the non-parametric approach. Wider intervals and low lower limits were determined for weak agonist as well as absence or impaired aggregation in up to one of 7 healthy controls. The response of platelets to aspirin shows response comparable to previously reported study.ConclusionsLocally established RI in our study enable us to investigate platelet function in patients with a high probability of bleeding disorders. Values are agonist and equipment specific. The variability of the method can be reduced by considering standardized preanalytical and analytical variables. Pathological results must be interpreted in the context of other hemostasis test results and clinical findings.     

Jurassic neptunian dikes at Mt Mangart (Julian Alps,NW Slovenia)

Jurassic neptunian dikes are common within Upper Triassic to Lower Jurassic platform limestone of the Julian Alps. At Mt Mangart, the following geometries were observed: irregular dissolution cavities, thin penetrative fractures, larger fractures with sharp sidewalls, and laterally confined breccia bodies. Inside a complex neptunian dike system two main generations of infillings were differentiated. The first generation is heterogeneous and consists of bioclastic limestones, representing uniquely preserved sediments subdivided into five different microfacies. The second generation is more common and typically consists of coarse-grained breccias with host-rock clasts and marly limestone matrix containing echinoderms. Fracture formation and void filling of the first generation of neptunian dikes is dated as Pliensbachian and is interpreted to be caused by the Julian carbonate platform dissection due to widely recognized Lower Jurassic Tethyan rifting. The timing of formation for the second generation is only broadly constrained, ranging from the Pliensbachian to the Late Cretaceous.     

Therapy effect of antiulcer agents on new chronic cysteamine colon lesion in rat

After demonstration that cysteamine induced duodenal lesions in gastrectomized rats, while a number of antiulcer drugs mitigated these lesions, it was shown that one single intrarectal (i.r.) cysteamine application produced severe colon lesions in acute studies in rats. Thus, the further focus was on the protracted effect of cysteamine challenge (400 mg/kg b.w. i.r.) and therapy influence in chronic experiments in female rats. Regularly, cysteamine colon lesions were markedly mitigated by ranitidine (10), omeprazole (10), atropine (10), methylprednisolone (1), sulphasalazine (50; mg/kg), pentadecapeptide BPC 157 (PL-10, PLD-116; 10 microg or 10 ng/kg). Specifically, after 1 or 3 months following initial challenge (cysteamine 400 mg/kg i.r.) in female rat, the therapy [BPC 157 (PL-10, PLD-116 (10.0 microg or 10.0 ng/kg; i.g., i.p., i.r.), ranitidine, omeprazole, atropine, methylprednisolone, sulphasalazine (i.p.)] reversed the protracted cysteamine colon injury: the 1 week-regimen (once daily application) started after 1 month post-cysteamine, as well as the 2 weeks-regimen (once daily application), which started after 3 months. The effect on recidive lesion was also tested. These cysteamine lesions may reappear after stopping therapy (after stopping therapy for 3 weeks at the end of 2-weeks regimen started in 3 months-cysteamine female rats) in sulphasalazine group, while this reappearance is markedly antagonized in pentadecapeptide BPC 157 (PL-10, PLD-116)-rats (cysteamine-colon lesion still substantially low).