1,721,016 research outputs found
Protocols for the preoperative selection of palpable thyroid nodules. Review and progress
No full textMolecular markers of hemostasis activation in nephrotic syndrome
No full textFibrinopeptide A (FPA), a sensitive index of in vivo thrombin activity, beta-thromboglobulin (beta TG) and platelet factor 4 (PF4), specific markers of platelet intravascular activation, have been measured in plasma by radioimmunoassays in 23 patients with nephrotic syndrome and in 32 normal subjects. FPA concentration was 2.40 +/- 1.42 ng/ml (mean +/- SD) in nephrotic patients and 1.16 +/- 0.58 ng/ml in normal controls (p less than 0.001); beta TG concentration was 57.9 +/- 33.2 ng/ml in nephrotic patients and 25.7 +/- 7.4 ng/ml in controls (p less than 0.001); PF4 level was not different from controls. These data indicate in vivo blood hypercoagulability and platelet hyperfunction in nephrotic syndrome. Moreover, we have documented a slow in vitro FPA generation pattern (delta FPA): 0.97 +/- 0.51 ng/ml/10 min; this suggests that thrombin activity is predominantly local
In vivo measurements of fibrin formation and degradation in nephrotic patients
No full textIntraglomerular fibrin deposition has been implicated as an important pathogenetic mechanism in patients with glomerular diseases and the nephrotic syndrome. To investigate fibrin formation and degradation in nephrosis, we measured fibrinopeptide A by radioimmunoassay and D-dimer by enzyme-linked immunosorbent assay in the plasma of 30 consecutive adult patients with the nephrotic syndrome; in 10 the serum creatinine was more than 2 mg/dl. Both fibrinopeptide A and D-dimer were abnormally elevated in the majority of nephrotics (P < 0.001 vs. healthy controls), providing evidence of increased fibrin generation and lysis "in vivo." A positive correlation was found between fibrinopeptide A and D-dimer (correlation coefficient 0.64, P < 0.001), suggesting a close relationship between fibrin formation and degradation. Calcium heparin, administered to 12 nephrotics, caused a marked decrease in plasma fibrinopeptide A, due to a reduction of in vivo thrombin activity. As enhanced thrombin activity can favor fibrin deposition within the renal parenchyma, as well as vascular complications, it is reasonable to assume that an antithrombotic treatment aimed at controlling thrombin generation may ameliorate the natural history of nephrosis
Serum concentration of five markers (TATI, TPA, TPS, CYFRA 21-1, SCC) and renal function in man
No full textGoing Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Expression of tissue-type plasminogen activator, plasminogen activator inhibitor and von Willebrand factor in the supernatant of endothelial cell cultures in response to the seeding of adenocarcinoma cell line HRT-18
No full textPlasminogen activator inhibitor (PAI-1), tissue type plasminogen activator (tPA) and von Willebrand factor (vWF) concentrations were measured by ELISA in the supernatant of the following cultures: endothelial cells from human umbilical vein (HUVEC); human colon cancer cells (HRT-18); and co-culture cells of HUVEC + HRT-18. No measurable amount of the three substances was found in the supernatant of HRT-18 cell culture. Compared to the value in the HUVEC supernatant, in the UVEC/HRT-18 co-cultures, tPA concentration was significantly lower (P = 0.0047), PAI-1 significantly higher (P = 0.026) and vWF also significantly higher (P = 0.0048). These data indicate that HRT-18 tumor cells do not produce tPA, PAI-1 and vWF; however, these tumor cells induce endothelial cells to change the production of these substances. As a consequence, the interaction between tumor and endothelial cells in vivo may lead to depression of fibrinolysis and enhancement of platelet adhesio
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