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Lippi G.,U.O. Diagnostica Ematochimica | Lippi G.,Laboratory of Clinical Chemistry and Hematology | Salvagno G.L.,Laboratory of Clinical Chemistry and Hematology | Da Rin G.,Service of Laboratory Medicine | Giavarina D.,Laboratory of Clinical Chemistry and Hematology
Rivista Italiana della Medicina di Laboratorio | Year: 2014

Background. Standardization of cardiac troponin I (cTnI) immunoassays remains an unmet target and comparability of current commercial methods is modest. We hence planned a study to investigate whether realignment of cTnI data by means of reference samples may improve comparability among different cTnI methods. Methods. Seventy six routine serum samples were collected in one center, centrifuged, aliquoted and shipped to participant centers, along with four additional reference serum samples with defined cTnI concentrations. The centers performed blind measurement of thawed aliquots and reference samples using four widespread contemporary-sensitive immunoassays (Ortho-Clinical Diagnostics Vitros cTnI ES, Beckman Coulter DXI 800 AccuTnI, Siemens Healthcare Diagnostics Dimension Vista cTnI and Abbott Diagnostics Architect STAT cTnI). Test results were analyzed as provided by the centers, and also after data alignment by means of polynomial regression parameters obtained on reference sera. Results. In five out of six circumstances the Deming fit improved after harmonization. The median inter-assay variability increased from 22% to 53% after alignment with polynomial regression parameters. A reduction of bias was observed in half of the circumstances, whereas in the remaining the bias increased. After harmonization, the agreement at diagnostic thresholds decreased in 4 out of 6 circumstances. Conclusions. These results show that calibration may only be a minor contributor of inter-assay variability of commercial cTnI immunoassays. Harmonization by means of reference sera was also counterproductive for improving methods agreement around a diagnostic threshold. © Springer-Verlag 2014. Source


Santaularia N.,Althaia Xarxa Assistencial Universitaria de Manresa | Santaularia N.,Autonomous University of Barcelona | Caminal J.,Autonomous University of Barcelona | Arnau A.,Clinical Research Unit | And 7 more authors.
BMC Cardiovascular Disorders | Year: 2013

Background: In recent decades, several studies have assessed the value of cardiac rehabilitation as secondary prevention and have reported substantial reductions in readmissions. However, conclusive evidence is scarce. The present study aims to evaluate the efficacy of a supervised exercise training program for improving percentages of hospital readmission for cardiac causes in patients with myocardial ischemia in the first year after a cardiac event. The effect on all-cause readmission, all-cause mortality, functional capacity, quality of life and adherence to regular exercise is also discussed.Methods/Design: This study will be conducted as a randomized controlled trial. Eligible patients will be randomly assigned to a control group receiving standard care or to an intervention group which, in addition to standard care, will take part in a supervised exercise training program consisting of three hours a week (spread over three alternate days) of supervised exercise training for 10 weeks. Both groups will perform an exercise stress test and a blood test during the first and third month after hospital discharge. The follow-up period will be 12 months after hospital discharge. The primary outcome measures will be the percentage of patients readmitted, total number of readmissions and length of hospitalization for cardiac disease during the first year after hospital discharge, and time to first hospital admission for cardiac disease.Discussion: A representative group of hospitalized patients after myocardial ischemia will be studied in order to provide comprehensive data on the potential impact of a supervised exercise training program on hospital readmission rates.Trial registration: Current Controlled Trials ISRCTN57634424. © 2013 Santaularia et al.; licensee BioMed Central Ltd. Source


Renna L.V.,University of Milan | Cardani R.,Laboratory of Muscle Histopathology and Molecular Biology | Botta A.,University of Rome Tor Vergata | Rossi G.,University of Rome Tor Vergata | And 5 more authors.
European Journal of Histochemistry | Year: 2014

Myotonic dystrophy type 1 (DM1) and type 2 (DM2) are multisystemic disorders linked to two different genetic loci and characterized by several features including myotonia, muscle weakness and atrophy, cardiac dysfunctions, cataracts and insulin-resistance. In both forms, expanded nucleotide sequences cause the accumulation of mutant transcripts in the nucleus deregulating the activity of some RNAbinding proteins and providing an explanation for the multisystemic phenotype of DM patients. However this pathogenetic mechanism does not explain some histopathological features of DM skeletal muscle like muscle atrophy. It has been observed that DM muscle shares similarities with the ageing muscle, where the progressive muscle weakness and atrophy is accompanied by a lower regenerative capacity possibly due to the failure in satellite cells activation. The aim of our study is to investigate if DM2 satellite cell derived myoblasts exhibit a premature senescence as reported for DM1 and if alterations in their proliferation potential and differentiation capabilities might contribute to some of the histopathological features observed in DM2 muscles. Our results indicate that DM myoblasts have lower proliferative capability than control myoblasts and reach in vitro senescence earlier than controls. Differentely from DM1, the p16 pathway is not responsible for the premature growth arrest observed in DM2 myoblasts which stop dividing with telomeres shorter than controls. During in vitro senescence, a progressive decrease in fusion index is observable in both DM and control myotubes with no significant differences between groups. Moreover, myotubes obtained from senescent myoblasts appear to be smaller than those from young myoblasts. Taken together, our data indicate a possible role of DM2 premature myoblast senescence in skeletal muscle histopathological alterations i.e., dystrophic changes and type 2 fibre atrophy. © L.V. Renna et al., 2014. Source


Valaperta R.,Research Laboratories Molecular Biology | Sansone V.,Stroke Unit and Center for Neuromuscular Disease | Lombardi F.,Research Laboratories Molecular Biology | Verdelli C.,Research Laboratories Molecular Biology | And 6 more authors.
BioMed Research International | Year: 2013

The expansion of the specific trinucleotide sequence, [CTG], is the molecular pathological mechanism responsible for the clinical manifestations of DM1. Many studies have described different molecular genetic techniques to detect DM1, but as yet there is no data on the analytical performances of techniques used so far in this disease. We therefore developed and validated a molecular method, "Myotonic Dystrophy SB kit," to better characterize our DM1 population. 113 patients were examined: 20 DM1-positive, 11 DM1/DM2-negative, and13 DM1-negative/DM2-positive, who had a previous molecular diagnosis, while 69 were new cases. This assay correctly identified 113/113 patients, and all were confirmed by different homemade assays. Comparative analysis revealed that the sensitivity and the specificity of the new kit were very high (>99%). Same results were obtained using several extraction procedures and different concentrations of DNA. The distribution of pathologic alleles showed a prevalence of the "classical" form, while of the 96 nonexpanded alleles 19 different allelic types were observed. Cardiac and neuromuscular parameters were used to clinically characterize our patients and support the new genetic analysis. Our findings suggest that this assay appears to be a very robust and reliable molecular test, showing high reproducibility and giving an unambiguous interpretation of results. © 2013 Rea Valaperta et al. Source


Gessoni G.,Transfusional Service | Gessoni G.,Service of Laboratory Medicine | Valverde S.,Service of Laboratory Medicine | Canistro R.,Onco Hematology Unit | And 3 more authors.
Biochimica Clinica | Year: 2013

Acquired hemophilia A (AHA) is a rare, but often life-threatening hemorrhagic disorder characterized by antibodies directed against coagulation factor VIII. We report clinical and laboratory investigations of two cases with AHA observed in our hospital. These patients were two elderly women (73 and 62 years old), who presented with subcutaneous bleeding, intramuscular hematoma and a prolonged activated partial thromboplastin time (aPTT). On the basis of these findings as well as decreased factor VIII activities and the presence of factor VIII inhibitors, we made a diagnosis of AHA. Both patients were referred to a specialized hospital for treatment. The diagnosis of AHA should be considered in any elderly patient who presents with bleeding and prolonged aPTT. Moreover, the coexistence of a series of underlying diseases associated with AHA should be always searched for. Source

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