Heparin-releasable platelet factor 4 in patients with coronary artery disease

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Value of thrombin-antithrombin III complexes in major orthopedic surgery: relation to the onset of venous thromboembolism.

This study evaluated (a) the possible changes of plasma levels of thrombin-antithrombin III complexes during hospitalization to predict venous thromboembolism in patients undergoing elective total hip replacement and (b) the sensitivity and specificity of thrombin-antithrombin III complexes in the late incidence of deep vein thrombosis when these patients are discharged from the hospital. In 50 consecutive patients (18 men, mean age = 63 ± 8 years) a venous blood sample was obtained from each patient before surgery and postsurgery on days 5 ± 2, 9 ± 2, and 45 to evaluate the thrombin-antithrombin III complexes by the enzyme-linked immunosorbent assay as a part of a larger surveillance program. Six of 50 patients devel oped deep vein thrombosis, diagnosed by phlebography on the 45th day postsurgery. From the day before until the ninth day after surgery, mean values of the thrombin-antithrombin III complexes increased to a greater extent in patients with deep vein thrombosis than in those without, although the differences were not significant (from 14.8 ± 11.2 ng/mL to 36.2 ± 19.1 ng/mL in the former group and from 13.6 ± 3.3 ng/mL to 22.4 ± 5.1 ng/mL in the latter, p = NS). On the 45th day after surgery the mean value of the thrombin-antithrombin III com plexes reduced less in patients with deep vein thrombosis (up to 9.9 ± 1.9 ng/mL and to 25.2 ± 17.2 ng/mL, respectively, p = NS). In addition, thrombin-antithrombin III complexes re mained over the level reached on the fifth day only in the patients who developed deep vein thrombosis. On the 45th day after surgery, thrombin-antithrombin III complexes exhibited a sensitivity of 17%, a specificity of 86%, and an accuracy of 78% in differentiating the presence and absence of deep vein thrombosis as compared with phlebography. We conclude that after total hip replacement (a) serial measurement of the throm bin-antithrombin III complexes does not appear helpful in pre dicting venous thromboembolism during hospitalization, and (b) measurement of thrombin-antithrombin III complexes has a low diagnostic accuracy in diagnosing delayed deep vein thrombosis. However, the greater and persistent increase of thrombin-antithrombin III complexes level in patients who de veloped deep vein thrombosis may deserve further investiga tions

Thrombocytosis in Malignancy: A Paraneoplastic Syndrome?

An increased platelet number may be secondary to many conditions. Malignancies are known to induce thrombocytosis in some cases. We report data of paraneoplastic thrombocytosis recognized in 54 out of 159 patient (33.9%) with reactive thrombocytosis diagnosed in our department over the last 10 years. In most of our patients increased platelet count was observed at the time of diagnosis (33.7%) or during the first year thereafter (35.2%). Evidence of other causes for reactive thrombocytosis including iron deficiency, anemia, inflammatory diseases, surgical procedures including splenectomy, and drugs were observed in 74% of our patients. 35% of our subjects had non fatal hemorrhagic or thrombotic accidents. In about one half of our patients, increased levels of fibrinogen, ESR and plasma alpha2 globulins were observed while 5 hydroxytryptamine (5HT) intraplatelet level was normal in about all these patients. The diagnosis of paraneoplastic thrombocytosis must be postulated only after exclusion of all other reactive conditions. Often an increased platelet count in patients with cancer may be considered a reactive phenomenon

The b -> s gamma decay revisited

In this work we compute the leading logarithmic corrections to the b -> s gamma decay in a dimensional scheme which does not require any definition of the gamma5 matrix. The scheme does not exhibit unconsistencies and it is therefore a viable alternative to the t'Hooft Veltman scheme, particularly in view of the next-to-leading computation. We confirm the recent results of Ciuchini et al.Comment: 11 pages RevTeX + 2 EPSF figures, report IFUP-TH 2/94, HUTP-93/A038. PostScript file or hardcopy available from the authors upon reques

Lattice energy-momentum tensor with Symanzik improved actions

We define the energy-momentum tensor on lattice for the $\lambda \phi^4$ and for the nonlinear $\sigma$-model Symanzik tree-improved actions, using Ward identities or an explicit matching procedure. The resulting operators give the correct one loop scale anomaly, and in the case of the sigma model they can have applications in Monte Carlo simulations.Comment: Self extracting archive fil

"Nanoscopium Nominare Libuit": Approaches Towards Optical Nanoscopy and Individual Molecule Localization Microscopy Improvements

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Soluble plasma thrombomodulin levels in patients with chronic myeloproliferative disorder.

The plasma levels of soluble thrombomodulin (TM) were measured in 44 patients with chronic myeloprolif erative disorder, 15 with polycythemia vera (PV), 29 with es sential thrombocythemia (ET), and a group of 62 matched healthy controls. The younger patients had significantly lower TM levels (mean: 15.6 ± 4.8 ng/mL) than the older patients (mean: 28.6 ± 8.2 ng/mL, p < .001). Moreover, a significant negative correlation between platelet counts and plasma TM levels in healthy persons was noted (r = 0.317, p < .05). The only significant difference we found in plasma TM levels be tween patients and controls or among patients was between the young patients with ET (mean: 29.0 ± 19.2 ng/mL) and young healthy controls (mean: 15.6 ± 4.8 ng/mL). It is possible that younger ET patients with more active platelets are more sus ceptible to earlier vascular damage. The lack of any significant difference compared with the older patient population supports this hypothesis. Key Words: Thrombomodulin—Essential thrombocythemia—Polycythemia vera

PACE: A Probabilistic Atlas for Normal Tissue Complication Estimation in Radiation Oncology

In radiation oncology, the need for a modern Normal Tissue Complication Probability (NTCP) philosophy to include voxel-based evidence on organ radio-sensitivity (RS) has been acknowledged. Here a new formalism (Probabilistic Atlas for Complication Estimation, PACE) to predict radiation-induced morbidity (RIM) is presented. The adopted strategy basically consists in keeping the structure of a classical, phenomenological NTCP model, such as the Lyman-Kutcher-Burman (LKB), and replacing the dose distribution with a collection of RIM odds, including also significant non-dosimetric covariates, as input of the model framework. The theory was first demonstrated in silico on synthetic dose maps, classified according to synthetic outcomes. PACE was then applied to a clinical dataset of thoracic cancer patients classified for lung fibrosis. LKB models were trained for comparison. Overall, the obtained learning curves showed that the PACE model outperformed the LKB and predicted synthetic outcomes with an accuracy &gt;0.8. On the real patients, PACE performance, evaluated by both discrimination and calibration, was significantly higher than LKB. This trend was confirmed by cross-validation. Furthermore, the capability to infer the spatial pattern of underlying RS map for the analyzed RIM was successfully demonstrated, thus paving the way to new perspectives of NTCP models as learning tools

The Release of Tissue Factor Pathway Inhibitor and Platelet Factor 4 After Heparin Injection in Patients with Thrombocytosis.

Platelet factor 4 (PF4) and tissue factor pathway inhibitor (TFPI) are two proteins with high affinity for heparin. They are each stored in platelets, as well as on endothelial cell surfaces, from where both are displaced or released following an injection of heparin with a rapid and marked increase in serum levels. Prior work has demonstrated that the platelet count is one of the factors affecting the levels of heparin-releasable PF4. We therefore characterized the response to a dose of intravenous heparin previously demonstrated to completely displace PF4 from the non-platelet pool in subjects with normal or increased platelet counts. Seventeen patients with essential thrombocytosis (ET), 10 patients with polycythemia vera and high platelet counts (PV-H), 7 patients with polycythemia vera and normal platelet counts (PV-N) and 10 controls received an initial bolus of 40 I.U./kg of unfractionated heparin, followed 2 hours later by a 2nd bolus of a fixed dose of 1000 I.U. TFPI activity did not show any variation among the different groups, either before (TFPI) or after (HR-TFPI) the first bolus of heparin: ET, TFPI 92.6 ± 21.5%, HR-TFPI 298.3 ± 165.8; PV-H, TFPI 91.5 ± 32.0, HR-TFPI 210 ± 1.0; PV-N, TFPI 69.4 ± 24.0, HR-TFPI 203.0 ± 79.0; C, TFPI 109.5 ± 33.5, HR-TFPI 234.0 ± 60.4. TFPI activity returned to basal values prior to the 2nd injection of heparin, which again elicited a rise in TFPI, albeit smaller due to the lower level of heparin injected. In contrast to the lack of any difference between groups with respect to TFPI, the level of heparin-releasable PF4 (HR-PF4) was significantly higher in ET and PV-H patients compared to PV-N patients or controls. However when normalized for platelet count, both PV-H and PV-N had HR-PF4 levels after the 1st heparin injection that were significantly higher than observed in ET patients (PV-H 1.163 + 0.108, PV-N 1.411 + 0.019, ET 0.737 + 0.086 ng/10/3 platelets) supporting an increased platelet activation in PV. Thus, although platelets contain approximately 5-10% of the total amount of TFPI in plasma, they do not affect the major intravascular pool of TFPI mobilizable by heparin. However, since the concentration at the site of vessel wall injury is enhanced several-fold, TFPI could play a role in competing with PF4 to limit thrombus formation in patients with high platelet count