[The fate of children who have undergone correction of Fallot's tetralogy. Report of fifty long term assessments (author's transl)].
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Biomedical subjects
Publications and source records attributed to M Nicoli.
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In evaluation of annoyance level due to road traffic, many criterions of noise exposure and degrees of basic adverse effect have been proposed through composite numerical values. In the present study procedures and units proposed by various AA. are recognizded and mathematical prediction models which correlate the influence of traffic density, composition, speed and geometry of road on emitted noise level are evaluated. At last limits of noise exposure levels set up in many countries or promulgated by Authorities with respect to the health and well being of man and in function of zoning urban areas, are referred.
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BACKGROUND: The aim of this study was to investigate some physical changes (volume, conductivity and scatter) in human polymorphonuclear leukocytes (PMN) activated with phorbol myristate acetate (PMA). METHODS: Volume changes in PMA-activated neutrophils were assayed by both STKR and STKS, two Coulter hematological analyzers. Scatter changes in PMN activated by PMA in suspensions containing nitro-blue tetrazolium (NBT) were investigated on STKS scattergrams. RESULTS: PMA activation induced PMN volumetric increases that could be assayed with STKR and displayed with STKS. The activation of PMN in suspension containing NBT induced cellular scatter changes on STKS scattergrams. The differences in scatter between resting and PMA-activated neutrophils may thus provide a semiquantitative assay of NBT reduction and superoxide production. Volume changes in PMA-activated neutrophils were due to cellular swelling through water uptake, induced by Na+/H+ antiport activation and Na+ influx. Since volume changes in PMA-activated neutrophils might occur without O2- production and vice versa, in the cases in which PMA activation of protein kinase C cannot be demonstrated by O2- production, the effect of PMA on protein kinase C- mediated Na+/H+ antiport activation, and in turn on PMA volume changes, reflects protein kinase C activation. CONCLUSIONS: A screening of neutrophils unresponsive to volumetric changes from PMA activation may be easily performed using both Coulter STKR and STKS analyzers, whereas expected or defective PMA-induced production of O2- may be semi-quantitatively evaluated by STKS.
In vitro EDTA-induced platelet aggregation is a fairly rare event but can have serious clinical consequences producing pseudothrombocytopenia and pseudoleukocytosis. Sixteen specimens with previously recognized EDTA-induced platelet aggregation were collected in a new anticoagulant-antiaggregant mixture containing trisodium citrate 17 mmol/l, pyridoxal 5'-phosphate 11.3 mmol/l and Tris 24.76 mmol/l (CPT mixture) and analyzed at various times after venepuncture with four hematological instruments: Coulter Counter S-Plus STKR, Technicon H6000, Technicon H1 and Ortho ELT-8. In CPT-anticoagulated specimens the signals and instrumental flags of platelet clumping were absent, and the platelet number correlated very well with a microscopic count from a finger stick drawn into Unopette. The complete blood count was very similar in "normal" hematological specimens either collected in K3. EDTA or in CPT, although Technicon H1 and Ortho3 ELT-8 required a suitable calibration for MCV and hematocrit in the latter mixture. Mean platelet volume was stable for up to 24 h only in CPT-collected specimens, if it was measured on a Coulter Counter S-Plus STKR. In routine hematological practice CPT can be an alternative anticoagulant to K3. EDTA, most suitable for automated complete blood count and useful in avoiding EDTA-induced platelet clumping.
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BACKGROUND: The aim of this study was to investigate a case of EDTA-induced polymorphonuclear leukocyte (PMN) agglutination in vitro on Bayer Technicon H*1. Coulter Counter STKS and STKR analyzers. METHODS: Venous whole blood was anticoagulated with K3.EDTA, sodium citrate, lithius heparinate, acid citrate dextrose (ACD) and with two other anticoagulant mixtures containing citric acid-theophylline-adenosine-dipyridamole (CTAD) or citrate-pyridoxal 5'-phosphate-tris (CPT). RESULTS: PMN agglutination, EDTA--but not temperature--dependent, was found by mere chance in an asymptomatic 48-year-old Caucasian male who did not show detectable PMN antibodies. Pseudoneutropenia without pseudoleukopenia was registered on H*1 exclusively in EDTA anticoagulated blood with a characteristic higher density PMN population on the BASO cytogram. Spuriously low white blood cell (WBC) counts and pseudoneutropenia appeared on STKR and STKS in EDTA anticoagulated blood, but signals on PMN agglutination were unsatisfactory. Accurate total and differential WBC counts were obtained in CTAD or CPT anticoagulated samples on the three analyzers. Heparin was the worst choice because it induced pseudothrombocytopenia and pseudoleukocytosis on STKR and STKS. CONCLUSIONS: Since PMN agglutination was not observed on peripheral smears and was undetected on EDTA anticoagulated samples processed immediately by H*1, the presence in vivo of PMN clumps should be excluded. Further hematological investigations will demonstrate in the long run whether the observed PMN agglutination in vitro is a transient occurrence in an apparently healthy subject not taking drugs at the time of observation.