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Biomedical subjects

K Amano

Publications and source records attributed to K Amano.

At least 109 records · Page 6Linked to original sources
PubMed1998

Filter leukapheresis for patients with ulcerative colitis: clinical results and the possible mechanism.

To certify the feasibility of leukapheresis, 37 ulcerative colitis (UC) patients, who had failed to recover by conventional treatment were enrolled in this treatment. Imugard (Terumo Co., Ltd., Tokyo Japan) or Cellsorba (Asahi Medical) filters were used. The schedule was one session weekly for 3 weeks and then twice monthly for 2 months. The laboratory tests performed were complete blood count, complements, immunoglobulins, and lymphocyte subsets. Endoscopic examination was done before and 3 months after initiation. Thirty-four of thirty-seven patients had some beneficial effects, and no patient's condition deteriorated. Corticosteroids were tapered or stopped in 18 patients out of 21. Seventeen of twenty patients experienced endoscopical remission. In laboratory data, leukocytes decreased with time. The C-reactive protein (CRP) levels and erythrocyte sedimentation rates (ESRs) improved. The percentage of CD3+HLA-DR+ cells, CD8+HLA-DR+ cells decreased. Six patients discontinued the treatment. Three of them showed no favorable effects. No severe side effects were observed. This treatment is cost effective and will be a feasible treatment.

Adult↗
PubMed1998

[Respiratory failure in polymyositis and dermatomyositis: differential diagnosis between pulmonary infection and interstitial pneumonitis].

Pulmonary diseases are important cause of morbidity and mortality in patients with PM/DM. Thirteen (27%) out of 49 PM/DM patients in the study had developed respiratory failure. Respiratory failure resulted form interstitial pneumonitis (i.p.) in 6, pulmonary infection in 2 and both in 5 patients with PM/DM. Respiratory failure was fatal in PM/DM patients with pulmonary diseases and eleven of the 13 patients expired. More importantly, 2 PM/DM patients with respiratory failure had responded to chemotherapy, if it was due to pulmonary infection. Accordingly, it is almost important to distinguish i.p. and infection for the cause of respiratory failure. However, plain chest X-ray as well as standard laboratory tests failed to differentiate i.p. and pulmonary infection. On the other hand, high resolution CT of the lungs, serum endotoxin and serum beta-D-glucan were found to be useful for the differentiation of these conditions associated with respiratory failure in PM/DM patients. And additionally low serum level of IgG and lymphopenia at the onset of respiratory failure may suggest that the patients may have pulmonary infection rather than i.p.

Adult↗
PubMed1998

Effect of rebamipide, a novel antiulcer agent, on Helicobacter pylori adhesion to gastric epithelial cells.

Helicobacter pylori is a major etiological agent in gastroduodenal disorders. The adhesion of H. pylori to human gastric epithelial cells is the initial step of H. pylori infection. Inhibition of H. pylori adhesion is thus a therapeutic target in the prevention of H. pylori infection. Experiments were performed to evaluate the effect of rebamipide, a novel antiulcer agent, on H. pylori adhesion to gastric epithelial cells. MKN-28 and MKN-45 cells, derived from human gastric carcinomas, were used as target cells. Ten H. pylori strains isolated from patients with chronic gastritis and gastric ulcer were used in the study. We evaluated the effect of rebamipide on H. pylori adhesion to MKN-28 and MKN-45 cells quantitatively using our previously established enzyme-linked immunosorbent assay. The adhesion of H. pylori to MKN-28 and MKN-45 cells was significantly inhibited by pretreatment of these cells with 100 microg of rebamipide per ml. However, the adhesion was not affected by the pretreatment of H. pylori with rebamipide. On the other hand, the viabilities of H. pylori, MKN-28 cells, and MKN-45 cells were not affected by rebamipide. Our studies suggest that rebamipide inhibits the adhesion of H. pylori to gastric epithelial cells.

Alanine↗
PubMed1998

Qualitative and quantitative detection of cytomegalovirus DNA in sera by PCR as a clinical marker.

The amount of human cytomegalovirus (CMV) DNA in sera is considered to be a direct marker for CMV infection. We established conditions for nested PCR that detected one copy of CMV DNA, and for competitive PCR, which detected five or more copies of CMV DNA quantitatively. We tested 50 microl each of 16 freeze-stored and 5 fresh sera from patients, for CMV DNA. In sera obtained from the same patient at different time points, small amounts of CMV DNA were detected before the onset of CMV pneumonia. In sera from certain CMV-infected patients who were treated with the anti-CMV agent, ganciclovir, CMV DNA was not detected. Quantitative PCR detection of CMV DNA seems to be suitable for predicting early recurrent CMV infection and monitoring the efficacy of antiviral therapy. The qualitative nested PCR examination of CMV DNA in 40 cord blood plasma samples was carried out for the purpose of preventing CMV infection by cord blood stem cell transplantation, and they were all negative for CMV DNA.

AIDS-Related Opportunistic Infections↗
PubMed1998

Validity of a self-administered diet history questionnaire for assessment of sodium and potassium: comparison with single 24-hour urinary excretion.

We developed a self-administered diet history questionnaire (DHQ) for use in prevention and control of cardiovascular diseases and cancer, and validated it by comparison with single 24-h urinary excretion of sodium (Na) and potassium (K). The subjects were 154 male and 69 female freshmen university students. Mean intakes (mmol/day) assessed by DHQ and the urinary excretion of Na were 196 and 165 respectively for men and 179 and 136 respectively for women. Those of K were 61.5 and 43.9 respectively for men and 56.8 and 41.6 respectively for women. The ratios of urinary excretion to dietary intake of Na were 0.97 in men and 0.84 in women. Those of K were 0.78 in men and 0.80 in women. The results for both Na and K were reasonable, except for Na in men. When Pearson correlation was examined between dietary and urinary Na and K, no significant correlations for Na in men (r=0.14) or women (r=0.23, p=0.06), or significant correlations for K in men (r=0.34, p<0.001) or women (r=0.40, p<0.001) were observed. The results suggest a reasonable ability to estimate a subject mean for Na in women, K in both sexes, and individual level for K for both sexes. The validity for individual level for Na intake is not conclusive because the duration of urine collection was too short.

Adult↗
PubMed1998

Self-administered diet history questionnaire developed for health education: a relative validation of the test-version by comparison with 3-day diet record in women.

A self-administered diet history questionnaire has been developed for the use in health education in Japan. The relative validity of the test-version was examined using 3-day diet record (DR) as a reference method. Subjects were mildly hypercholesterolemic 47 women aged 38-69 years living in Hikone, Japan. The questionnaire provided close estimation of nutrients compared to the DR (mean of the 3-days), 1-25% differences between the two methods were observed for total energy and 17 nutrients examined. The differences were in general smaller for macronutrients, 1-3%, than for micronutrients, 1-25%. Pearson correlation coefficients between the questionnaire and the DR (mean of the 3-days) ranged from 0.16 for niacin to 0.60 for saturated fatty acid (mean = 0.41). The energy-adjustment using regression analysis and the correction of attenuation due to error from a limited number of days of DR slightly improved the results. The correlations ranged from 0.19 for niacin to 0.75 for saturated fatty acid (mean = 0.48). Average 37 and 6% subjects were classified into same quartile and opposite quartile respectively between the two methods. This questionnaire may be useful to assess individual nutrient intake level at least for the subjects examined.

Adult↗
PubMed1998

Mutation at either Arg336 or Arg562 in factor VIII is insufficient for complete resistance to activated protein C (APC)-mediated inactivation: implications for the APC resistance test.

Activated protein C (APC)-mediated inactivation of factor VIII (FVIII) correlates with cleavage at either Arg336 and/or Arg562. To elucidate the APC cleavage requirements for inactivation of FVIII, APC cleavage site mutants in FVIII (R336I, R562K and R336I/R562K) were made by site-directed mutagenesis. Analysis of these FVIII mutants expressed in COS-1 monkey cells demonstrated the thrombin-cleaved mutant R562K was resistant to APC cleavage at residue 562 but not at Arg336 and the thrombin cleaved mutant R3361 was mostly resistant to APC cleavage at residue 336, but was sensitive to APC cleavage at Arg562. The double mutant R336I/R562K was mostly resistant to cleavage at residue 336 and completely resistant to cleavage at residue 562. Thus, APC cleavage of FVIII does not require a specific order of cleavage at either residue. The functional inactivation by APC was studied using partially purified preparations of FVIII expressed in Chinese hamster ovary cells. Both single mutants were inactivated at similar rates but slower than wild-type FVIII, whereas the double mutant R336I/R562K was resistant to inactivation. The ability of a commercially available APC-resistance assay kit to detect APC resistant FVIII was tested by reconstituting FVIII deficient plasma with the APC resistant mutants. Only the R336I/R562K demonstrated a reduced APC-resistance ratio, indicating that this assay can not detect the single APC cleavage site mutant of FVIII. These results suggest that APC-mediated cleavage at either Arg336 or Arg562 partially inactivate FVIII.

Animals↗
PubMed1998

Serum IgG antibodies in children and adults reacting with Helicobacter pylori lipopolysaccharides.

The presence of IgG antibodies reacting with Helicobacter pylori lipopolysaccharides (LPSs) in sera from children and adults diagnosed as H. pylori-infected, as well as healthy persons, was tested. There was no correlation between the production of antibodies reacting with H. pylori surface proteins and LPSs. Also no correlation between reactivity of tested sera with H. pylori antigens and deep rough mutant (Re types) enterobacterial LPSs was revealed. The prevalence of anti-LPS IgG in randomly selected children was relatively high.

Adult↗
PubMed1998

[A case with rheumatoid arthritis complicated with ANCA-associated vasculitis].

A 50-year-old woman with rheumatoid arthritis (RA) developed constitutive symptoms such as fever and weight loss, mononeuritis multiplex and rapidly progressive glomerulonephritis (RPGN). The renal biopsy revealed crescentic glomerulonephritis (CrGN) with few immune deposits such as IgG and C 3 and necrotizing vasculitis, which led to the pathological diagnosis of microscopic polyangiitis (MPA). Moreover the high serum level of anti-myeloperoxidase (MPO) antibody, one of the anti-neutrophil cytoplasmic antibody (ANCA), suggested that she had ANCA-associated vasculitis. The renal prognosis of the ANCA-associated vasculitis is said to be poor unless patients were treated in the early phase of the disease. As we started to treat the patient when her serum creatinine level (sCr) was 1.7 mg/dl and creatinine clearance (CCr) was 27 ml/min, her renal function returned to the almost normal level (sCr = 0.6, CCr = 91). It is well known that patients with RA may develop various kinds of extraarticular manifestations which are usually related to immune-complex mediated vasculitis, what we call malignant RA. We emphasize that ANCA-associated vasculitis is another important complication of RA. When we see a RA patient with constitutional symptom, abnormal urinary sediments and other clinical signs of vasculitis such as mononeuritis multiplex, ANCA-associated vasculitis should be considered. Since the early diagnosis and treatment of ANCA-associated vasculitis is a key to prevent renal failure, it is encouraged to measure the serum ANCA titer for not only the diagnosis of such patients but the evaluation of their clinical course.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1997

Functional domain mapping of HIV-1 Gag proteins.

A series of human immunodeficiency virus type 1 (HIV-1) proviral gag gene mutants carrying bacterial CAT gene were constructed and monitored for the expression of reverse transcriptase and CAT in a highly sensitive single-round replication assay system to determine the defective replication phase in lymphocytic cells. All the mutants displayed no abnormality in the process of transcription and translation at late replication stage. In contrast, some matrix, capsid, and p6 mutants were defective at final phase, that is, assembly and virion release. Most of the mutants including nucleocapsid mutants, which showed normal phenotype at late stage, were defective at early replication phase. From the functional domain map thus obtained, it is evident that HIV-1 Gag proteins are required for both early and late replication phases.

CD4-Positive T-Lymphocytes↗
PubMed1997

Cleavage of Gag precursor is required for early replication phase of HIV-1.

A mutant of human immunodeficiency virus type 1 (HIV-1), which is deficient for Gag precursor cleavage and noninfectious, was characterized with respect to its defective step in the viral replication phase. Upon transfection, the mutant produced a normal level of progeny virions as monitored by electron microscopy and RNA hybridization. Single-round replication assay demonstrated, in contrast, that the mutant was defective at the early phase of the replication cycle. Furthermore, no viral DNA was detected in the cells infected with the mutant. Taken together, it is concluded that maturation of Gag precursor protein of HIV-1 is required for an early event(s) before or during a coupled process of uncoating/reverse transcription.

Blotting, Southern↗
PubMed1997

HIV-1 capsid mutants inhibit the replication of wild-type virus at both early and late infection phases.

In-frame mutations were introduced into various portions of the human immunodeficiency virus type 1 (HIV-1) gag gene, and potentials of the mutants to suppress the replication of wild-type HIV-1 were monitored. In contrast to results obtained with matrix and nucleocapsid mutants, almost all capsid mutants blocked HIV-1 replication completely in single-round replication assays. A capsid mutant designated C6b was demonstrated to be one of the most efficient inhibitors for HIV-1 reported to date, and to be effective at both early and late viral replication phases. T-cells, which are engineered to express the C6b Gag in response to HIV-1 infection, were perfectly resistant to HIV-1.

Blotting, Western↗
PubMed1997

Mouse and human SHPS-1: molecular cloning of cDNAs and chromosomal localization of genes.

SHPS-1 (SHP substrate-1) is a glycosylated receptor-like protein with three immunoglobulin-like domains in its extracellular region and four YXX(L/V/I) motifs, potential tyrosine phosphorylation and SRC homology 2 (SH2) domain binding sites, in its cytoplasmic region. Various mitogens and cell adhesion induce tyrosine phosphorylation of SHPS-1 and its subsequent association with SHP-2, and SH2 domain-containing protein tyrosine phosphatase, suggesting that SHPS-1 plays a role in cell signaling in response to both growth factors and cell adhesion. The mouse and human cDNAs encoding SHPS-1 have now been isolated. The deduced amino acid sequences of rat, human, and mouse SHPS-1 show identities of 65 to 81%. In addition to the SH2 domain binding sites, a proline-rich putative SH3 domain binding site was detected in the cytoplasmic region of SHPS-1. Northern blot analysis revealed that human SHPS-1 mRNA is most abundant in brain and that the mouse mRNA is present in embryos as early as day 7. Fluorescence in situ hybridization localized the SHPS-1 gene to human chromosome 20p13 and the F3 band of mouse chromosome 2. Furthermore, interspecific backcross analysis placed the mouse SHPS-1 locus 5.0 centimorgans distal and 1.4 centimorgans proximal to the microsatellite markers D2Mit63 and D2Mit19, respectively, in a region associated with the mutations coloboma (Cm), lethal milk (lm), and well-haarig (we).

Amino Acid Sequence↗
PubMed1997

Palytoxin-induced increase in endothelial Ca2+ concentration in the rabbit aortic valve.

Palytoxin (PTX) is one of the most potent toxins isolated from marine coelenterates of the genus Palythoa. It induces depolarization in various types of cells by increasing the permeability for monovalent cations. It has been reported that PTX induces endothelium-dependent relaxation of vascular smooth muscle. In this study, we examined the effect of PTX on the cytosolic Ca2+ concentration ([Ca2+]i) in the endothelium of rabbit aortic valves loaded with fluorescent Ca2+ indicators, fura-PE3 or fluo-3. PTX (10 pM-300 nM) irreversibly increased endothelial [Ca2+]i in a concentration-dependent manner. ATP and thapsigargin also increased [Ca2+]i. Imaging of [Ca2+]i with a confocal microscope revealed that PTX increased [Ca2+]i in all endothelial cells studied (n = 13). An inorganic Ca2+ entry blocker, La3+ (30 microM), had no effect on the increase in [Ca2+]i induced by PTX whereas it inhibited the sustained phase of the increase in [Ca2+]i induced by ATP or thapsigargin. The PTX-induced increase in [Ca2+]i was partially inhibited by ouabain and was abolished by removal of external Ca2+ although decrease of Na+ concentration in the incubation medium was ineffective. Activation of protein kinase C by 1 microM 12-deoxyphorbol 13-isobutyrate or inhibition of phosphatase by 10 nM calyculin-A had no effect on the increase in [Ca2+]i induced by PTX, whereas both agents inhibited the sustained phase of the increase in [Ca2+]i induced by ATP or thapsigargin. Mn2+ influx, measured by the quenching of fura-PE3 fluorescence, was accelerated by ATP or thapsigargin, but not by PTX. These results suggest that PTX increases [Ca2+]i in the endothelium of the rabbit aortic valve by increasing Ca2+ influx through a pathway which is different from that activated by ATP or thapsigargin.

Acrylamides↗
PubMed1997

CD8 cytotoxic T-cell clone rapidly transfers autoimmune diabetes in very young NOD and MHC class I-compatible scid mice.

A CD8 T-cell clone (YNK1.3) generated from acutely diabetic NOD mouse islets, showed proliferation and cytotoxicity when challenged with NOD and BALB/c islet cells and NOD-derived insulinoma cells. When 1-2 x 10(7) YNK1.3 cells were administered to 7-10-day-old NOD mice, the cells transferred overt diabetes very rapidly in each of the 16 recipients within 4 days of cell transfer. However, of 14 recipients receiving YNK 1.3 cells above 14 days of age none became diabetic. Fluorescent dye-labelled YNK1.3 cells extensively accumulated in the islets by 36 h after transfer in 7-day-old NOD recipients, while no significant insulitis was seen in 21-day-old recipients. Over half of NOD-scid recipients (5/9) rapidly became diabetic within 5 days after transfer of 1-2 x 10(7) YNK1.3 cells at 7 days of age, whereas only one of 12 recipients over 14 days of age became diabetic. Furthermore, YNK1.3 cells also transferred diabetes to H-2Kd-matched very young BALB/c-scid and CB17-scid mice, but not to C57BL/6-scid mice. Thus, optimally activated islet-specific CD8 T-cell clones are able to rapidly transfer diabetes to NOD and MHC class I compatible scid mice when a large enough number is administered at 7 days of age. Administration of monoclonal antibodies against adhesion molecules involved in the trafficking of lymphocytes from the circulation into the inflammatory tissues, could not prevent the cellular infiltration of YNK1.3 cells into the islets in 7-day-old NOD recipients. The results indicate that islet cells in the mouse around 7 days of age are generally susceptible to cytotoxic CD8 T cells, suggesting, therefore, that CD8 T cells may play an important role in the initiation of autoimmune diabetes in NOD mice.

Adoptive Transfer↗