Enhanced magneto-optical Kerr effect in oxidized Co thin films

We have studied the structural and magneto-optical properties of postdeposition oxidized Co thin films. The oxidization process leads to the formation of a double-layered structure of fcc Co3O4 on top of metallic Co. The magneto-optical Kerr effect (MOKE), measured in the range 0.8 eV ⩽ EPh ⩽ 5.5 eV reveals characteristic dependencies of the MOKE spectra on annealing temperature and time. In particular, we observe resonance-type enhancements of the Kerr effects by up to a factor of 10 compared with unannealed metallic Co. The experimental data are quantitatively reproduced by bilayer optical stack calculations.One of the authors ~B.R.! has been gratefully supported by means of the Deutsche Forschungsgemeinschaft. One of the authors ~G.A.! thanks the Ministerio De Educacion y Ciencia ~Spain! for financial support.Peer reviewe

Plasmatic parameters of fibrin formation and degredation in cancer patients: correlation between fibrinopeptide A and D-dimer

This investigation was carried out to evaluate fibrin formation and degradation in various types of solid neoplasms by measuring fibrinopeptide A (fpA) in the plasma with a radioimmunoassay and D-dimer (DD) with an enzyme-linked immunosorbent assay in 176 cancer patients; 77 of them showed signs of distant metastasis (M1). FpA and DD were abnormally elevated in 81 and 143 patients respectively. FpA and DD were significantly correlated and unrelated to plasma fibrinogen. Both fpA and DD levels were more elevated in M1 than M0 patients. Coumarin anticoagulants, administered to 32 patients of our series with the aim of preventing cancer growth and dissemination, caused a significant decrease both in fpA and DD levels. Our data provide evidence of increased in vivo fibrin formation and degradation in solid neoplasms: oral anticoagulants can modulate cancer-related hypercoagulatio

The association of myeloproliferative and lymphoproliferative diseases.

No abstract availabl

In vivo measurements of fibrin formation and degradation in nephrotic patients.

Intraglomerular 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

In vivo measurements of fibrin formation and degradation in nephrotic patients

Intraglomerular 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