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S Honda

Publications and source records attributed to S Honda.

At least 181 records · Page 10Linked to original sources
PubMed1998

The prevalence and pattern of insomnia in Japanese industrial workers: relationship between psychosocial stress and type of insomnia.

We examined the prevalence of insomnia among Japanese male industrial workers and analyzed the effect of psychosocial stress on the prevalence of three types of insomnia: 'difficulty in falling asleep', 'frequent sleep interruption' and 'early morning arousal'. The study population consisted of male day workers (n = 319) in a manufacturing heavy industry company located in Nagasaki City, Japan. The subjects answered a questionnaire consisting of six sleep-related items and 24 questions related to occupational and private life conditions. A total of 271 men (average age 40.9 years) completed the questionnaire; a response rate of 85%. Insomnia within the month preceding the survey was present in 27.7% of the workers (75/271). Multiple logistic regression analysis demonstrated that different psychosocial stressors were associated with different types of insomnia. Visual display terminal (VDT) work overload was significantly associated with all types of insomnia, while 'over-involvement in the job' was associated with difficulty in falling asleep and early morning arousal. Our results demonstrated that the prevalence of insomnia in Japanese workers is similar to that reported among European and American general adult population. Our results also indicate that the use of VDT in the workfield is associated with insomnia.

Adolescent↗
PubMed1998

Renal involvement in Henoch-Schönlein purpura: a multivariate analysis of prognostic factors.

This study is the first report in which the relationship between the progression of renal involvement in Henoch-Schönlein purpura (HSP) and various factors was evaluated using a multivariate analysis. Sixty-five (33.5%) of 194 patients with HSP developed renal involvement from three days to 17 months after the onset of the disease. The plasma coagulation factor XIII (F XIII) activity of 97 patients was examined, and 51 (54.3%) of them showed a decreased activity. A univariate analysis showed that an age at the onset of more than seven years, persistent purpura and a decreased F XIII activity all increased the risk of developing renal involvement. A Cox regression model analysis indicated severe abdominal symptoms, persistent purpura and decreased F XIII activity to be significant risk factors and their hazard ratios were 3.26, 11.53 and 2.27, respectively. Corticosteroid treatment had a hazard ratio of 0.36 and was considered to decrease the risk of developing renal involvement. Based on these findings, patients who have the risk factors for renal involvement should be treated with corticosteroids at the onset of the disease to prevent developing renal involvement.

Adolescent↗
PubMed1998

Gastric ulcer, atrophic gastritis, and intestinal metaplasia caused by Helicobacter pylori infection in Mongolian gerbils.

BACKGROUND: Helicobacter pylori infection is associated with gastroduodenal disease in humans. In this study we aimed to show this relationship directly in Mongolian gerbils. METHODS: The animals were challenged orally with H. pylori and killed 1, 2, 3, and 6 months after inoculation for histologic and anti-H. pylori antibody titer examination. RESULTS: The spiral bacteria were observed in the mucus and gastric pits of all infected animals. A severe infiltration of the lamina propria by polymorphonuclear and mononuclear cells was seen 1 month after H. pylori inoculation. The submucosa was infiltrated by mainly mononuclear cells with formation of lymphoid follicles. Erosion of the gastric mucosa appeared soon after inoculation, whereas gastric ulcers, gastritis cystica profunda, and atrophy with goblet cell metaplasia occurred between 3 and 6 months after inoculation. In the duodenal mucosa a mild inflammatory cell infiltration with ballooning and diminished number of duodenal glands was seen. The IgG anti-H. pylori antibody titer increased gradually after 2 months of inoculation. CONCLUSIONS: Since the gastritis, gastric ulcers, atrophic gastritis, and intestinal metaplasia that developed in Mongolian gerbils were similar to those observed in humans, this model may be useful to study the therapy of gastric ulcer and, with a longer observation period, to confirm a possible relationship between H. pylori and malignancy.

Animals↗
PubMed1998

Possible involvement of autoreactive CD4 T cells in generation of cytotoxic T lymphocytes on in vitro stimulation with H-2 class I-binding tumor antigen peptide.

We demonstrated that RL male 1-specific cytotoxic T lymphocytes (CTL) were generated in spleen cells from the tumor-rejected CB6F1 mice on in vitro stimulation with Ld-binding pRL1a peptide. We showed that CD4 T cells and antigen-presenting cells were necessary for CTL generation. Furthermore, CTL generation was inhibited by the addition of anti-I-Ad mAb, but not anti-I-Ek/d mAb, to the culture. However, no binding of the pRL1a peptide to the I-Ad molecule could be demonstrated. No inhibition by the pRL1a peptide of I-Ad-restricted IL-2 production by ovalbumin (OVA)-specific CD4 T cell hybridoma DO-11.10 was observed on stimulation with the specific OVA peptide. Moreover, no specific proliferative response or IL-2 production was observed with CD4 T cells in spleen cells from the tumor-rejected mice on stimulation with a range of mitomycin C-treated RL male 1 cells, or with RL male 1 lysate or the pRL1a peptide. Rather, the activation of autoreactive CD4 T cells and the IL-2 production from them were observed. CD4 T cells from CB6F1 mice that had rejected other tumors such as EL4 or MOPC-70A also helped the generation of pRL1a-specific CTL. These findings suggested the involvement of autoreactive CD4 T cells in CTL generation against the pRL1a peptide.

Animals↗
PubMed1998

Abnormal neurohumoral responses to exercise in patients with heart disease: inhibition of an increase in endothelin-1 production during exercise.

We have reported that the plasma endothelin-1 (ET-1) level is significantly increased by exercise in healthy athletes and that it is elevated in the circulation of the non-working leg but not the working leg, suggesting that ET-1 plays an important role in redistribution of blood during exercise. This study was designed to compare alterations of neurohumoral substances by exercise in normal subjects and patients with heart disease. Study patients comprised three groups: eight patients with congestive heart failure (CHF) due to Ebstein's anomaly or single-ventricle heart after Fontan operation; six patients with complete transposition of the great arteries (TGA) after an anatomic surgical correction who may be candidates for ischemic heart disease; and five age-matched normal subjects. All patients were in New York Heart Association functional class I. All subjects performed symptom-limited treadmill exercise. It is suggested that patients with CHF or TGA have a manifest or latent exercise intolerance, respectively. In failed to increase plasma ET-1 level, although it caused a greater increase in norepinephrine, angiotensin II, and arginine vasopressin than in the controls. Exercise also caused a delay in the increased response of plasma ET-1 levels in patients with TGA after an anatomic surgical repair. On the other hand, plasma brain natriuretic peptide (BNP) level was augmented by exercise in patients with CHF and patients with TGA but not in the controls. The present results suggest that an increase in ET-1 production during exercise is absent in patients with heart disease. The mechanisms of inhibition of ET-1 production during exercise in patients with heart disease remain to be elucidated. However, the present study suggests that ET-1 plays an important role in redistribution of blood during exercise, and proposes the possibility that failure of an increase in ET-1 production results in exercise intolerance in patients with heart disease.

Child↗
PubMed1998

Long-term prospective study of body composition and lipid profiles during and after growth hormone (GH) treatment in children with GH deficiency: gender-specific metabolic effects.

GH has many effects on metabolism in addition to promoting growth. We studied changes in body composition and lipid profiles during and after GH treatment in 94 children with GH deficiency. Sixty-two subjects (46 boys and 16 girls) were evaluated at the beginning and during 36 months of GH treatment. The other 32 (21 boys and 11 girls) who had already been treated with GH were examined after the discontinuation of GH for a 6-month period. The height SD scores at the beginning and the discontinuation of GH treatment were -2.81 and -1.34 in boys and -3.14 and -1.38 in girls, respectively. The percent body fat (BF) significantly decreased from 16.5% to 11.7% in boys and from 16.7% to 11.6% in girls during the first 6 months of GH treatment (P < 0.01). BF subsequently remained constant in boys, but started to increase in girls from the 18th month of treatment. Lean body mass (kilograms) increased linearly throughout the treatment in both sexes (P < 0.01). Mean total cholesterol (TC) values decreased as a result of marked declines in low density lipoprotein cholesterol in both sexes, although statistical significance was detected only in boys (P < 0.01). High density lipoprotein cholesterol (HDLC) and apolipoprotein AI (Apo-AI) rapidly increased only in boys (P < 0.01). Triglyceride, Apo-AII, Apo-B, Apo-CII, Apo-CIII, Apo-E, and lipoprotein(a) showed no significant changes compared with baseline levels. Mean TC/HDLC and Apo-B/Apo-AI ratios decreased during treatment in both sexes, but the difference from baseline was significant only in boys (P < 0.01). After discontinuation of GH treatment, BF increased, and lean body mass decreased in boys (P < 0.01), whereas these variables did not change in girls. TC and low density lipoprotein cholesterol increased in boys within 6 months of discontinuing GH (P < 0.05). Other lipoproteins did not change in either sex, except for lipoprotein(a), which decreased significantly 6 months after the cessation of GH treatment in boys (P < 0.01). The mean TC/HDLC and Apo-B/Apo-AI ratios increased in boys slightly, but insignificantly. We concluded that GH treatment has beneficial effects on body composition and lipid profiles in both boys and girls with GH deficiency, although there are considerable gender differences. These beneficial effects of GH were reversed after the discontinuation of GH treatment, suggesting an important role of GH for GH-deficient children in the maintenance of normal metabolism even after the completion of linear growth.

Adolescent↗
PubMed1998

[A case of systemic lupus erythematosus overlapping with progressive systemic sclerosis accompanied by deposition of AA amyloid in the stomach].

A 52-year-old woman was admitted to our department because of fever and dysphasia in November 1994. She had noticed Raynaud's phenomenon, arthralgia, and stiffness in the skin for the past 20 years without receiving specific treatment. A diagnosis of progressive systemic sclerosis (PSS) was made based on the presence of sclerosis of the skin, sclerodactyly, pulmonary fibrosis, and the dilatation of the lower esophagus. It was also confirmed that systemic lupus erythematosus (SLE) overlapped based on the presence of an oral ulcer, polyarthralgia, leukocytopenia, renal dysfunction, positive tests for antinuclear antibodies and anti-DNA antibodies. A gastric biopsy specimen revealed amyloid deposits which showed green birefrigence by Congo red staining under polarized light microscopy. The disappearance of the green birefrigence after potassium permanganate treatment indicated that the deposits consisted of AA amyloid. No amyloid deposits were detected in the rectum or the kidney. The average of the SAA level in active SLE patients is 174 micrograms/ml in our department and the SAA level in the present case was 280 micrograms/ml. Although AA amyloidosis is rarely associated with SLE and PSS, a long-term elevation of SAA level could cause the development of amyloidosis even in the cases of SLE and PSS.

Amyloidosis↗
PubMed1998

Establishment and characterization of Epstein-Barr virus-specific human CD4+ T lymphocyte clones.

We developed a simple method for establishing Epstein-Barr virus (EBV)-specific, human CD4+ T cell clones. The method originates from our experience that the regression of cell growth in in vitro EBV transformation of B cells occurs when round lymphoid cells appear in the culture. Peripheral blood mononuclear cells (PBMCs) were cultured with EBV, and IL-2 (20 U/ml) was added to the culture on day 17 after the virus addition. The phenotype of the growing cells was CD3+, CD4+, and CD8-. The cells were cytotoxic for autologous lymphoblastoid B cell line (LCL) and EBV-superinfected autologous LCL. The cytotoxic T lymphocytes (CTLs) were confirmed to be CD4+ T cells but not CD8+ T cells in the culture. CTL clones were established by a limiting dilution method. All the CTL clones had the phenotype of CD3+, CD4+ and CD8-, and proliferated in response to autologous LCL. They produced interferon (IFN)-gamma, interleukin 2 (IL-2) and tumour necrosis factor (TNF)-beta but not IL-4. All but one clone responded to both autologous, EBV-superinfected and non-superinfected LCLs. Proliferative and cytotoxic responses to allogenic LCLs were heterogeneous. These results suggest that this method induces heterogeneous, EBV-specific CD4+ CTL clones and is useful for analysis of CD4+ T cells in EBV infections.

Adult↗
PubMed1998

Changes in morphology of neuroblastoma cells treated with all-trans retinoic acid combined with transfer of the C-terminal region of the amyloid precursor protein.

Alzheimer disease is a progressive neurodegenerative disorder that is characterized by a loss of cognitive and memory functions. Amyloid fibrils deposited in neuritic plaque is mainly beta-amyloid protein (Abeta) that is derived from amyloid precursor protein (APP). The secreted form of APP, which is corresponded to N-terminal portion of APP, shows neurotrophic activities. On the other hand, Abeta and cytoplasmic domains of APP are thought to be neurotoxic. In order to investigate the effect of C-terminal fragment of APP covering Abeta and the cytoplasmic domain upon cell growth and differentiation, we established a stably transfected cell line producing the C-terminal 100 amino acid peptide of APR The transfected clones stained positively with anti-Abeta monoclonal antibody, TB-1. The growth rate of the transfected cells was not significantly different from that of mock-transfected cells or native NB39 cells. After treatment with all-trans retinoic acid (ATRA), mock-transfected cells extended neurite processes and showed neuronal-like differentiation, while a transfected clone overexpressing C-terminal fragment did not present neuronal-like morphology. These results suggest that ATRA-induced neurite extension may be suppressed by overexpression of the C-terminal fragment of APP.

Amyloid beta-Peptides↗
PubMed1998

Difference of (Ca2+)i movements in platelets stimulated by thrombin and TRAP: the involvement of alpha(IIb)beta3-mediated TXA2 synthesis.

This study investigated the difference of [Ca2+]i movement in platelets in response to thrombin and TRAP. The involvement of alpha(IIb)beta3 in this signaling was also studied. Stimulation of platelets with thrombin at 0.03 U/ml caused platelet aggregation and a two-peak increase in [Ca2+]i. The second peak of [Ca2+]i, but not the first peak was abolished by the inhibition of platelet aggregation with alpha(IIb)beta3 antagonists or by scavenging endogenous ADP with apyrase. A cyclooxygenase inhibitor, aspirin, and a TXA2 receptor antagonist, BM 13505, also abolished the second peak of [Ca2+]i but not the first peak, although these regents did not inhibit aggregation. Under the same assay conditions, measurement of TXB2 demonstrated that alpha(IIb)beta3 antagonists and aspirin almost completely inhibited the production of TXB2. In contrast to thrombin-stimulation, TRAP caused only a single peak of [Ca2+]i even in the presence of platelet aggregation, and a high level of [Ca2+]i increase was needed for the induction of platelet aggregation. The inhibition of aggregation with alpha(IIb)beta3 antagonists had no effect on [Ca2+]i change and TXB2 production induced by TRAP. Inhibition studies using anti-GPIb antibodies suggested that GPIb may be involved in the thrombin response, but not in the TRAP. Our findings suggest that low dose thrombin causes a different [Ca2+]i response and TXA2 producing signal from TRAP. Endogenous ADP release and fibrinogen binding to alpha(IIb)beta3 are responsible for the synthesis of TXA2 which results in the induction of the second peak of [Ca2+]i in low thrombin- but not TRAP-stimulated platelets.

Adenosine Diphosphate↗
PubMed1998

Differential expression of nitric oxide synthase isoforms in form-deprived chick eyes.

PURPOSE: To clarify whether nitric oxide synthase (NOS) is involved in development of myopia, we examined the influence of form deprivation on the expressions of NOS isoform mRNA. METHODS: NOS isoform cDNAs were amplified from total RNA extracted from control and 7-day-form-deprived chick retina-RPE (retinal pigment epithelium)-choroid, using competitive RT-PCR (reverse-transcription polymerase chain reaction). Each NOS isoform protein was also analyzed by Western blotting and immunohistochemistry. RESULT: Expression of inducible NOS (iNOS) mRNA was highest in the control chick retina-RPE-choroid, followed by the expression of brain NOS (bNOS) mRNA. Expression of endothelial NOS (eNOS) mRNA was faint. The iNOS protein level, however, was only slightly higher than the levels of the bNOS and eNOS proteins and was found mainly in the outer part of the photoreceptor layer and inner and outer parts of RPE and choroid. bNOS alone was found in the outer nuclear layer. Although form deprivation reduced the iNOS and bNOS mRNA expressions, only the iNOS protein showed significant reduction. CONCLUSION: All three NOS isoforms were expressed in chick retina-RPE-choroid. Predominant expression of iNOS, instead of bNOS and eNOS, suggested the existence of ocular tissue-specific regulation of the iNOS gene. In addition to differences in expression level, bNOS displayed regional differential expression. Moreover, only iNOS was reduced in response to form deprivation. It is suggested that NOS isoforms may be differentially involved in the mechanisms regulating the posterior eye tissues, including myopic eye growth.

Animals↗
PubMed1997

Amidophosphoribosyltransferase limits the rate of cell growth-linked de novo purine biosynthesis in the presence of constant capacity of salvage purine biosynthesis.

Factors controlling relative flux rates of the de novo and salvage pathways of purine nucleotide biosynthesis during animal cell growth are not fully understood. To examine the relative role of each pathway for cell growth, three cell lines including CHO K1 (a wild-type Chinese hamster ovary fibroblast cell line), CHO ade -A (an auxotrophic cell line deficient of amidophosphoribosyltransferase (ATase), a presumed rate-limiting enzyme of the de novo pathway), and CHO ade -A transfected with human ATase cDNA (-A+hATase) resulting in 30-350% of the ATase activity of CHO K1, were cultured in purine-rich or purine-free media. Based on the enzyme activities of ATase and hypoxanthine phosphoribosyltransferase, the metabolic rate of the de novo and salvage pathways, the rate of cell growth (growth rate) in three cell lines under various culture conditions, and the effect of hypoxanthine infusion on the metabolic rate of the de novo pathway in rat liver, we concluded the following. 1) In -A+hATase transfectants, ATase activity limits the rate of the de novo pathway, which is closely linked with the growth rate. 2) Purine nucleotides are synthesized preferentially by the salvage pathway as long as hypoxanthine, the most essential source of purine salvage, can be utilized, which was confirmed in rat liver in vivo by hypoxanthine infusion. The preferential usage of the salvage pathway results in sparing the energy expenditure required for de novo synthesis. 3) The regulatory capacity of the de novo pathway (about 200%) was larger than that of the salvage pathway (about 20%) with constant hypoxanthine phosphoribosyltransferase activity.

Amidophosphoribosyltransferase↗
PubMed1997

Expansion of an unusual population of Gr-1+CD3int cells in the lymph nodes and other peripheral organs of mice carrying the lpr gene.

Granulocytes and extrathymic T cells are often activated simultaneously, but they are absolutely separate populations in normal mice. However, some abnormal extrathymic T cells (i.e., CD3int cells) seen in mice carrying the lpr gene were found to express a granulocyte marker, Gr-1. Such mice include MRL-lpr/lpr mice and SCG mice. In parallel with an age-associated increase of IL-2Rbeta(low)CD3int cells which contained double-negative CD4-8- and B220+CD2- cells, Gr-1+CD3int cells increased in number in the lymph nodes and other peripheral organs. In addition to a major population of IL-2Rbeta(low)CD3int cells, there is a small population of IL-2Rbeta(high)CD3int cells which produce normal Fas mRNA and Fas molecule from the lpr gene. It was found that both IL-2Rbeta(low)CD3int and IL-2Rbeta(high)CD3int cell populations contained Gr-1+ cells. IL-2Rbeta(high)CD3int cells tended to contain a higher proportion of Gr-1+ cells than did IL-2Rbeta(low)CD3int cells. More interestingly, Gr-1+CD3int cells expressed a considerable level of mRNA of the mG-CSF receptor, similar to granulocytes. The present study thus yielded further information on an unusual property of abnormally expanding CD3int cells in mice carrying the lpr gene.

Aging↗
PubMed1997

Reproducibility of urinary beta 2-microglobulin and cadmium excretion among residents in a cadmium-polluted area during a 3-year period.

To assess the measurement error by using single exposure measurement in epidemiologic studies, reproducibility of urinary beta 2-microglobulin and cadmium excretion was evaluated among persons exposed to environmental cadmium. We measured urinary beta 2-microglobulin concentrations in 47 subjects four times and urinary cadmium concentrations in 48 subjects twice, during a 3-year period. Between-person and within-person variance components of these variables were estimated using a random-effects one-way analysis of variance model. The intraclass correlation coefficient (ICC) for urinary beta 2-microglobulin concentration, when expressed as microg/g creatinine and microg/l, was 0.92 and 0.89, respectively. The ICC for standardized urinary cadmium concentration (expressed as microg/g creatinine) was 0.81, while it decreased to 0.33 without standardization. The findings suggest that single measurement of urinary beta 2-microglobulin and cadmium, when expressed as a function of creatinine, can reliably estimate average levels over at least a 3-year period. Standardization of concentration using urinary creatinine improved reproducibility especially for urinary cadmium excretion.

Adolescent↗
PubMed1997

High-performance capillary electrophoresis of hyaluronic acid: determination of its amount and molecular mass.

The amount and the molecular mass of hyaluronic acid (HA) were determined by high-performance capillary electrophoresis. HA was observed at around 15 min by using an untreated fused-silica capillary (75 microns I.D.) of 58 cm length (effective length, 50 cm) at 20 kV in 50 mM phosphate buffer (pH 4.0). Calibration curves showed good linearity from 0.01 mg/ml to 3.3 mg/ml for all HA samples examined. The lower limit of detection by monitoring the absorbance at 185 nm was 1.0 microgram/ml at the signal-to-noise ratio of 5. HA samples were examined in a buffer containing pullulan (PU) as an additive for the matrix formation material. The HA samples showed marked peak-broadening when analyzed in the buffer solution containing PU with a specified molecular mass. The peak broadening was based on the dispersion of the molecular mass of the HA sample analyzed.

Buffers↗