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Nobuhide Hayashi

Publications and source records attributed to Nobuhide Hayashi.

8 recordsLinked to original sources
PubMed2006

Serum cystatin C levels to predict serum concentration of digoxin in Japanese patients.

Cystatin C (Cys-C) has been recently paid great attention as a better endogenous marker of the glomerular filtration rate than creatinine (Cr). In this study, the usefulness of Cys-C was compared with Cr in terms of the estimation of the steady-state serum trough concentrations of digoxin in Japanese patients. Forty patients treated with digoxin and 56 healthy elderly subjects were participated in this study. The serum levels of Cys-C and Cr in the patients were higher than those in the healthy elderly subjects, but the increase of Cys-C was more predominant in the patients. Their levels were well-correlated for both of the healthy elderly subjects (r=0.691) and patients (r=0.774), but the serum concentrations of digoxin were better correlated with those of the reciprocal values of Cr (r=0.667) than those of Cys-C (r=0.383), presumably due to the fact that digoxin and Cr were excreted via both glomerular filtration and tubular secretion. Cys-C is useful for the substratification of the patients diagnosed to have normal renal function with Cr of < 1.3 mg/dL into those with normal and pseudo-normal renal function, resulting in the corresponding serum concentrations of digoxin.

Journal Article↗
PubMed2006

Performance evaluation and cross-reactivity from insulin analogs with the ARCHITECT insulin assay.

BACKGROUND: Insulin measurement is used for the diagnosis of hypoglycemia and for insulin pharmacokinetic evaluations. We assessed the analytical and clinical performance of the ARCHITECT insulin assay, a chemiluminescent immunoassay recently introduced for the ARCHITECT i2000 fully automated immunoassay analyzer (Abbott Laboratories). We also tested whether major insulin analogs cross-reacted with the immunoassay reagents. METHODS: We used Clinical and Laboratory Standards Institute protocols to assess the analytical performance of the ARCHITECT insulin assay and compared its accuracy with that of the E-test TOSOH II (IRI) from TOSOH Corporation. We used 3 recombinant insulin analogs (lispro, aspart, and glargine) to evaluate the cross-reactivity of insulin analogs with the ARCHITECT immunoassay reagent. RESULTS: The total CV for the ARCHITECT assay was < 5%. Correlation between the ARCHITECT insulin assay and the E-test TOSOH II (IRI) was satisfactory in the measured range, but we detected a slope deviation between the assays. The ARCHITECT insulin assay showed low cross-reactivity to the insulin analog aspart, whereas it detected the other insulin analogs, lispro and glargine, in concentrations as high as the theoretical concentrations. CONCLUSIONS: The ARCHITECT insulin assay showed favorable basic performance, including reproducibility, dilution linearity, detection limit, and effects of interfering substances. When interpreting results, clinicians and laboratory pathologists should be aware of the cross-reactivity of the ARCHITECT and other immunoassays to specific insulin analogs prescribed to diabetes patients.

Autoanalysis↗
PubMed2004

[Topics on immunological tests for rheumatoid arthritis].

To prevent joint destruction, it is important to diagnose RA early and to speculate the prognosis. Several new laboratory tests have been developed for this purpose. In addition to rheumatoid factor (RF), IgG-RF, anti-agalactosyl IgG antibodies (CARF), and matrix metalloproteinase 3 (MMP-3) have become available as diagnostic tests for RA. Among them, anti-cyclic citrullinated peptide antibodies (anti-CCP antibodies) have the sensitivity and specificity of 81.0% and 92.4%, respectively, which are superior to other laboratory tests by ROC analysis. Moreover, the specificity of anti-CCP antibodies to diagnose early RA was much higher than that of RF, although the sensitivity of CARF was slightly high compared with that of RF. In contrast, MMP-3 is thought to be an evaluative test for the activity of RA because a significant correlation was found between MMP-3 and CRP, but MMP-3 has a possibility as a prognostic test to know the joint damage of RA. We have shown that the progression of joint damage (Sharp score) was faster in MMP-3-positive patients than negative patients. Anti-CCP antibodies was also reported to associate with the progression of joint damage and may be used also as a prognostic test. We next examined how efficiently was the diagnosis of RA made by combining these laboratory tests. Although anti-CCP antibodies are highly specific to RA, the specificity of RF was not so high but became up to 92% when combined with MMP-3. In order to diagnose RA efficiently, we may firstly examine RF, next MMP-3 if RF is positive, and anti-CCP antibodies if RF is negative.

Arthritis, Rheumatoid↗
PubMed2004

[Usefulness of anti-cyclic citrullinated peptide antibodies (anti-CCP) for the diagnosis of rheumatoid arthritis].

Rheumatoid factor (RF) has been commonly used as a marker of rheumatoid arthritis (RA). RF can be detected in 60-80% of RA patients, but the specificity is low against other rheumatic diseases patients. We evaluated the diagnostic accuracy of anti-cyclic citrullinated peptide antibody (anti-CCP), a new diagnostic test for RA. Anti-CCP demonstrated higher sensitivity (81.0%) and specificity (92.4%). By the receiver operating characteristic (ROC) curve analysis, anti-CCP was superior to other markers (ie. RF, CARF, IgG-RF, and MMP-3). In early RA patients (RA patients who had had disease symptoms for < 2 years), sensitivity was 68.8%. Positivities of anti-CCP in RA patients became higher as the advance of stage defined by the Steinbrocker classification. We concluded that anti-CCP is a very valuable tool for the diagnosis of RA. Moreover, anti-CCP is a useful for finding RA of recent onset.

Arthritis, Rheumatoid↗
PubMed2003

[New diagnostic tests for rheumatoid arthritis].

Rheumatoid factor(RF) is one item in the classification criteria for rheumatoid arthritis(RA), with a tolerable sensitivity of 69.3% for RA but low specificity against other rheumatic diseases(76.4%). Anti-agalactosyl IgG antibody(CARF) showed a slightly higher sensitivity(72.0%) but the specificity was even lower(67.9%). Anti-cyclic citrullinated peptide antibody(anti-CCP), a new diagnostic test for RA, demonstrated higher sensitivity(76.0%) and specificity(91.5%), and the ROC analysis revealed the marked superiority of anti-CCP to other markers(i.e. RF, CARF, and IgG-RF). Matrix metalloproteinase-3 (MMP-3) showed a significantly positive correlation with CRP, suggesting it might be more useful for evaluation of RA activity and prediction of the prognosis of joint destruction. On the contrary, two combination assays, "MMP-3 or CARF" and "MMP-3 or anti-CCP", showed the highest sensitivity(86.7%) for RA. Similarly, in early RA the sensitivities of CARF, MMP-3 and anti-CCP were lower than in RA(66.7%, 66.7% and 58.3%, respectively), but the sensitivities of combination assays "MMP-3 or CARF" and "MMP-3 or anti-CCP" were 91.7% and 83.3%, respectively. Thus, we concluded that these combination assays are useful in the diagnosis of RA and detection of early RA.

Arthritis, Rheumatoid↗
PubMed2002

Oxidative stress mediates cell surface expression of SS-A/Ro antigen on keratinocytes.

Exposure to ultraviolet radiation exacerbates the skin lesions of autoimmune diseases, and is known to induce cell surface expression of SS-A/Ro antigen on keratinocytes in vitro. Following up on recent reports on ultraviolet-B (UVB)-induced oxidative stress, we examined the role of oxidative stress in the surface expression of SS-A/Ro antigen on human keratinocytes. First, the exclusive induction by UVB irradiation of the 52-kDa protein (Ro52) but not of the 60-kDa protein (Ro60) of SS-A/Ro antigen was demonstrated by means of indirect immunofluorescence. The surface expression of Ro52 induced by UVB irradiation was concentration-dependently inhibited by N-acetyl-L-cysteine, an antioxidant. Furthermore, surface expression of Ro52 was similarly induced by diamide, a chemical oxidant. We next used Hoechst 33342 staining and the TUNEL assay to demonstrate that a low dose (20 mJ/cm(2)) of UVB did not induce apoptosis but induced the surface expression of Ro52. Moreover, zVAD-fmk, a pan-caspase inhibitor, did not inhibit UVB-induced surface expression of Ro52 even at a high dose (200 mJ/cm(2)) of UVB, which was sufficient to induce apoptosis in keratinocytes in the absence of zVAD-fmk. Taken together, we concluded that UVB-induced surface expression of Ro52 on keratinocytes is mediated by oxidative stress through a pathway other than apoptosis.

Acetylcysteine↗
PubMed2002

2-Chloroadenosine but not adenosine induces apoptosis in rheumatoid fibroblasts independently of cell surface adenosine receptor signalling.

1. The apoptotic effect of adenosine and its analogues was studied in fibroblast-like synoviocytes derived from rheumatoid arthritis patients (RA-FLSs). Evoked cell death was quantitatively examined by assessing DNA fragmentation using an enzyme-liked immunosorbent assay and by measuring phosphatidylserine exposure through flow cytometric analysis of annexin V binding. 2. Exposing cells for 24 h to 2-chloroadenosine (2-CADO), a nonspecific, adenosine deaminase (ADA)-resistant, adenosine receptor (AdoR) agonist, induced DNA fragmentation, and thus apoptosis, in RA-FLSs at concentrations > or =50 microM. By contrast, incubation with adenosine for up to 72 h did not evoke DNA fragmentation, even in the presence of ADA inhibitor coformycin and nucleoside transporter inhibitor nitrobenzylmercaptopurin (NBMPR). Transcription of all four AdoR isoforms was detected in RA-FLSs; nevertheless selective AdoR agonists similarly failed to induce DNA fragmentation. 3. DNA fragmentation evoked by 2-CADO was inhibited by NBMPR and by 5'-iodotubercidin, an adenosine kinase inhibitor, but not by xanthine amine congener, an A(1) and A(2) receptor antagonist, or by selective AdoR antagonists. 4. The nonspecific caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp fluoromethyl ketone abolished the apoptotic effect of 2-CADO. 5. These results suggest that 2-CADO induces apoptosis in RA-FLSs independently of AdoR-mediated signalling. Instead, 2-CADO, but not adenosine, is taken up into RA-FLSs via human equilibrative nucleoside transporter-1, where it is phosphorylated by adenosine kinase. The resultant phospho-2-CADO induces DNA fragmentation by activating a caspase pathway.

2-Chloroadenosine↗