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H Nishikado

Publications and source records attributed to H Nishikado.

11 recordsLinked to original sources
PubMed1991

[Factor XIa-alpha 1 antitrypsin complex].

We developed a new rapid assay for the factor XIa-alpha 1 antitrypsin complex (FXIa-alpha 1AT) in plasma using an anti FXI monoclonal antibody (KMXI-1). In 20-fold diluted plasma samples, this assay was not affected by co-existing FXI or non specific color development of the plasma. Normal level of FXIa-alpha 1AT (11 +/- 4.1 ng/ml plasma) increased with the aging of healthy adults. The FXIa-alpha 1AT levels of patients with disseminated intravascular coagulation (DIC) rose along with the progression of the disease, and the appearance of high levels and the peak of FXIa-alpha 1AT developed faster than FDP-E or alpha 2plasmin inhibitor-plasmin complex (alpha 2PI-PmC) in most patients. These results indicate that, in addition of FDP and alpha 2PI-PmC, FXIa-alpha 1AT is a useful molecular marker for DIC.

Adult↗
PubMed1989

Accumulation of 125I-factor XI in atheroma of rabbit with hereditary hyperlipidemia (WHHL-rabbit).

We have studied the turnover and accumulation of rabbit factor XI (F.XI) in atherosclerotic lesion in Watanabe-hereditable hyperlipidemic rabbit (WHHL rabbit) to reveal the participation of blood coagulation in atherosclerotic lesion. Rabbit F.XI was iodinated and administered intravenously to WHHL rabbits and Japanese white rabbits. The turnover of 125I-rabbit F.XI was significantly faster in WHHL rabbits (T1/2 = 2.84 +/- 0.44 days) than in normal rabbits (T1/2 = 4.44 +/- 0.42 days). The thoracic aorta of WHHL rabbit was strongly labelled with 125I-rabbit F.XI, in sections obtained after 5 days by en-face autoradiography, whereas no radioactivity was detected in normal aorta. By an immunohistochemical study of WHHL rabbit aorta, we confirmed that many F.XI- and fibrin-related compounds existed in the atheroma, whereas albumin did not in these area. These results suggest that the activation of F.XI proceeds on the atherosclerotic lesions of WHHL rabbits.

Animals↗
PubMed1989

New rapid assay for factor XIa-alpha 1 antitrypsin complex--application to DIC.

We developed a new rapid assay for the factor XIa-alpha 1 antitrypsin in complex (F.XIa-alpha 1 AT) in plasma with the use of a newly produced anti-F.XI monoclonal antibody (KMXI-1). This assay was completed within about 5 hours, and the minimum assay range extended sensitivity about 5-fold over the former assay (Thromb. Res. 44, 489-501, 1986). In 20-fold diluted plasma samples, this assay was not affected by co-existing F.XI or nonspecific color development of the plasma. Normal levels of F.XIa-alpha 1 AT (11 +/- 4.1 ng/ml plasma [n = 96]) increased with the aging of healthy adults. The F.XIa-alpha 1 AT levels of patients with disseminated intravascular coagulation (DIC) rose along with the progression of the disease, and the appearance of high levels and the peak of F.XIa-alpha 1 AT developed faster than FDP-E or alpha 2 plasmin inhibitor-plasmin-complex in most patients. These results indicate that, in addition to FDP, F.XIa-alpha 1 AT is a useful molecular marker for DIC.

Adult↗
PubMed1989

Change of membrane fluidity of rat neutrophils accompanying Escherichia coli inoculation.

Membrane fluidity of rat neutrophils was studied following Escherichia coli inoculation, and characteristic changes were observed. Membrane fluidity was assessed by the excimer-forming lipid technique using pyrenedecanoic acid and flow cytometry and expressed as the fluorescence intensity ratios of excimer and monomer pyrenedecanoic acid (IE/IM ratio). High IE/IM ratios indicated high membrane fluidity. The IE/IM ratio of rat neutrophils (0.50 +/- 0.048) increased after E. coli inoculation, reaching a maximum of almost 1.00 after 10-20 min and then returning to its starting value. Intravenous injection of heat-killed E. coli or E. coli-conditioned culture supernatants into rats induced a rapid increase of IE/IM ratios, which returned to initial levels after 20 min. The effect on membrane fluidity of in vitro neutrophil incubation with E. coli, heat-killed E. coli, or E. coli-conditioned culture supernatants was similar to that observed in vivo. Addition of 5 mM ethylenediaminetetraacetic acid (EDTA) did not affect neutrophil membrane fluidity. Addition of either 5 micrograms/ml cytochalasin B or 10(-5) M colchicine did not directly affect neutrophil membrane fluidity but did block the change observed following incubation with bacteria.

Actin Cytoskeleton↗
PubMed1989

Spontaneous injuries in the aortic endothelium of the inherited cataract rats and their prevention by tocopherol. A study by scanning electron microscopy.

The aortic endothelium of inherited cataract rats (ICR), which spontaneously develop cataracts and neutrophilia, was examined by scanning electron microscopy using silver nitrate staining and pressure fixation. In ICR aged 4 weeks, the luminal surface of the aorta was similar to that in Wistar rats from which they had been derived. However, 8 weeks after birth, endothelial cells were upraised and partially detached from an underlying tissue. At 16 weeks, morphological changes exhibited by such detaching cells were more evident than at 8 weeks and fibrin was seen to be adhering to the surface of these cells; no platelet involvement was noted, however. Oral administration of DL-alpha-tocopheryl acetate for 2 weeks resulted in a reduction in the extent of endothelial injury and the luminal surface of the aorta became similar to that seen in 4- or 8-week-old animals. We found that the number of age-associated spontaneous injuries occurring in the aortic endothelium of ICR could be reduced by tocopherol administration.

Aging↗
PubMed1986

Factor XIa-alpha 1 antitrypsin complex--elevation in the patients with DIC.

We developed an assay for the factor XIa-alpha 1 antitrypsin complex (F.XIa-alpha 1AT complex) in plasma. The purified factor XI (F.XI) activated with beta-XIIa and treated with alpha 1 antitrypsin (alpha 1 AT) served as the standard complex. The assay is an enzyme-linked differential antibody immunosorbent assay. The complex level of tested plasma was measured with peroxidase-labeled anti-alpha 1AT Fab' after the addition of 10-fold diluted test plasma (200 microliter) to the anti-F.XI monoclonal antibody beads. To eliminate the effects of plasma, the standard F.XIa-alpha 1AT complex was diluted with F.XI-deficient plasma (10-fold diluted) which did not contain the complex. Purified F.XI (0.08 micrograms/assay, i.e. 100%) was added to the standard F.XIa-alpha 1AT complex, because the absorbance of the standard complex containing F.XI (0.016-0.12 micrograms/assay, i.e. 20-150%) was a little lower than that of the complex alone. The recovery of the F.XIa-alpha 1AT complex added was over 90%. Neither F.XI nor alpha 1AT alone had the color development. The complex level of 25 normal individuals was below the detectable limit (less than 0.18 ng/assay), whereas the 30 patients with disseminated intravascular coagulation (DIC) had a high level complex (0.18-4.2 ng/assay). This assay may be helpful for the diagnosis of DIC.

Disseminated Intravascular Coagulation↗
PubMed1986

Murine monoclonal antibodies to human factor XI.

Murine monoclonal antibodies to human factor XI (F.XI) are described. The monoclonal antibodies (2-1, 4-1, 7-1 and 10-1) consisted of IgG1. 4-1 inhibited the activation of F.XI completely in the presence of high molecular weight kininogen and kaolin and the others did so partially, whereas these antibodies had no effect on the activation of F.XI with activated factor XII (beta-XIIa). Four antibodies had no effect directly on the amidolytic activity of activated F.XI (F.XIa). 10-1 inhibited the activation of factor IX in coagulant assay for F.XIa by Mannhalter. And 4-1 and 7-1 did so partially, whereas 2-1 did not. In immunoblotting analysis, all antibodies bound to F.XI, its reduced form and F.XIa. All were directed against the heavy chain of F.XI. All antibodies recognized F.XIa-alpha 1 antitrypsin complex.

Antibodies, Monoclonal↗