Search PubMed⌕ Search

Biomedical subjects

H Yoshida

Publications and source records attributed to H Yoshida.

At least 991 records · Page 55Linked to original sources
PubMed1996

Affinity-purified Dermatophagoides farinae antigen induces CD23 on T and B lymphocytes and monocytes specifically in patients with atopic dermatitis.

The purpose of this work is to analyze CD23 expression on subpopulations of peripheral blood mononuclear cells (PBMC) from the patients with atopic dermatitis (AD) after stimulation with affinity-purified Dermatophagoides farinae antigen (Af-DF). PBMC from mite-allergic AD patients stimulated with Af-DF induced striking expression of CD23 after the culture. The frequencies of CD23-positive (CD23+) PBMC in the culture were significantly higher than those without stimulation. Most of the CD23+ cells belonged to B lymphocytes and monocytes subsets. CD23 was induced in less than 1% of CD3+, CD4+ and CD8+ lymphocytes by Af-DF. However, significant differences were observed compared to the spontaneous expression, and dose-dependencies were confirmed. No significant increase in the frequencies of CD23+ PBMC was found in non-mite-allergic AD patients and non-atopic donors after stimulation with Af-DF. The kinetics of CD23 expression by Af-DF showed similar patterns to that by IL-4 stimulation. Our results demonstrate that Af-DF can induce CD23 expression on PBMC in mite-allergic AD patients. Based on the high titer of mite-specific IgE antibody in blood of AD, mite antigen may, at least in part, contribute to high CD23 expression in AD.

Adolescent↗
PubMed1996

Hexamethylene bisacetamide as a chemopreventive agent in hamster cheek pouch tumorigenesis.

The chemopreventive effect of oral and intraperitoneal (i.p.) administration of hexamethylene bisacetamide (HMBA) on 9,10-dimethyl-1,2-benzanthracene (DMBA)-induced tumour formation in hamster cheek pouches was investigated. Male Syrian hamsters were treated by painting both cheek pouches with a 0.5% solution of DMBA twice weekly for 11 weeks. In addition to DMBA application, Group 1 hamsters were given 1% HMBA continuously in the drinking water and Group 2 hamsters received i.p. injection of HMBA at a dose of 500 mg/kg three times per week during the experiment. Group 3 animals received DMBA application alone. Thirteen weeks after the start of the experiment, the numbers of cheek pouch tumours and tumour volume were significantly decreased by oral but not i.p. administration of HMBA. Low levels of HMBA were detected in the plasma of the hamsters which were given 1% HMBA in drinking water. These results indicate that oral administration of HMBA can act as a chemopreventive agent against hamster cheek pouch tumorigenesis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1996

Early effects of electrical stimulation on osteogenesis.

The mechanism by which electrical stimulation causes osteogenesis is unknown. Bone marrow of the rabbit was stimulated by direct electrical current or electromagnetic fields to clarify the mechanism of osteogenesis by electrical stimulation. A total of 105 rabbits were separated into five groups: a direct current stimulation by Kirshner wire insertion group; a pulsed electromagnetic fields stimulation (PEMF) group; a PEMF with Kirshner wire insertion group; a Kirshner wire insertion group; and an intramedullary drilling control group. Measurement of intramedullary new bone formation and determination of alkaline phosphatase activity within the bone marrow were performed. Argylophilic nuclear organizer region (AgNOR) staining was done to evaluate the change in proliferative activity of the osteoblasts during electrical stimulation. In the direct current stimulation group and the PEMF accompanied by the insertion of the Kirshner wire group, alkaline phosphatase activity in the bone marrow and AgNOR staining increased at 7 days after surgery. At 14 days after surgery, alkaline phosphatase activity and proliferative activity of osteoblast were significantly higher in these two groups than in the other groups (PEMF group, Kirshner wire insertion alone group, intramedullary drilling group). Intramedullary new bone formation was most active in the direct current stimulation group. Electromagnetic stimulation of the inserted Kirshner wire also promoted bone formation significantly. The Kirshner wire insertion alone group and the intramedullary drilling group showed bone formation, but it was significantly less. Electromagnetic stimulation without the insertion of the Kirshner wire showed little bone formation. These findings revealed that the degree of osteogenesis induced by electrical stimulation is influenced by the tissue environment, and that osteogenesis is promoted markedly when electrical stimulation is provided in the environment of inflammation and reactive cells.

Alkaline Phosphatase↗
PubMed1996

Impaired fibrinolysis early after percutaneous transluminal coronary angioplasty is associated with restenosis.

This study examined the role of fibrinolytic components in the process of restenosis after percutaneous transluminal coronary angioplasty (PTCA). Seventy-two patients with single-vessel disease who underwent successful PTCA were prospectively selected. Tissue plasminogen activator (TPA), free plasminogen activator inhibitor-1 (free PAI-1), TPA/PAI-1 complex, and total PAI-1 antigen levels were measured before, at 1 week after, and at 3 months after PTCA. Six months after PTCA, the study patients were divided into two groups: 41 patients without restenosis and 31 patients with restenosis. There were no significant differences with regard to sex, age, coronary risk factors, or morphologic changes in the target lesions between the two groups. There were no significant differences in plasma TPA, TPA/PAI-1 complex, or total PAI-1 levels at each sampling period, or in the time courses between the two groups, except for total PAI-1 levels at 1 week after PTCA. Although no significant differences in free PAI-1 levels before PTCA were observed, free PAI-1 levels after PTCA in the patients with restenosis were significantly higher than those in the patients without restenosis. In addition, each group had a significant change in the time course of free PAI-1 levels. The results suggest that impaired fibrinolysis early after PTCA might affect the repair process of vascular injury, which leads to restenosis, and also that serial determination of free PAI-1 levels could help predict restenosis.

Angioplasty, Balloon, Coronary↗
PubMed1996

An immunohistochemical and in situ hybridization study of the expression of tenascin in synovial membranes from human temporomandibular joints with internal derangement.

In samples of 27 human temporomandibular joints (internal derangement, ankylosis and control specimens) the distribution of immunoreactive tenascin was restricted to the walls of blood vessels, at the perineurium, and at the surface of the disc. Tenascin staining was intense in the stroma of hypertrophic synovial membranes, particularly on the surface of severely hypertrophic synovial membranes with inflammation, proliferation, irregular lining structures and new capillary growth. In situ hybridization of fresh discs and synovial membranes demonstrated that synovial cells as well as fibroblasts and endothelial cells expressed tenascin mRNA. The expression of tenascin mRNA was most evident in synovial cells. It is concluded that synovial cells in the synovial membrane produce tenascin in the diseased human temporomandibular joint.

Adult↗
PubMed1996

Renal impairment after surgical resection of neuroblastoma.

Postoperative renal impairment was observed in 6 of 58 patients with neuroblastoma treated between November 1982 and March 1994. To clarify the clinical characteristics of these patients (renal-impairment group), they were compared with 26 patients treated during the same period who did not have renal impairment (no-impairment group). The incidence of primary retroperitoneal tumor and invasion of the hilum renalis was clearly higher in the renal-impairment group than in the group with no impairment. However, no significant difference was observed with respect to age, tumor laterality, or stage of disease. The results of postoperative biochemical examinations showed that the serum concentrations of lactic dehydrogenase were significantly higher in the renal-impairment group. In the group with renal impairment, the mean maximal body temperatures on the first, second, and third postoperative days were 38.7 degrees C, 38.6 degrees C, and 38.1 degrees C, respectively. These were higher than those of the no-impairment group. For patients with these risk factors, intraoperative prophylactic measures and early postoperative renal blood flow evaluation (in anticipation of postoperative renal impairment) are considered necessary.

Adrenal Gland Neoplasms↗
PubMed1996

An improved computer-assisted diagnostic scheme using wavelet transform for detecting clustered microcalcifications in digital mammograms.

RATIONALE AND OBJECTIVES: We evaluated the potential usefulness of a computer-assisted diagnostic (CAD) scheme incorporating the wavelet transform for detecting clustered microcalcifications in mammograms. METHODS: A wavelet transform technique was applied to the detection of clustered microcalcifications. We examined several wavelets to study their effectiveness in detecting subtle microcalcifications. We used a database consisting of 39 mammograms containing 41 clusters of microcalcifications. The performance of the wavelet-based CAD scheme was evaluated using free-response receiver operating characteristic analysis. RESULTS: The CAD scheme with the wavelet transform was useful in detecting some of the subtle microcalcifications that were not detected by our previous scheme, which was based on the difference-image technique. When the two schemes were combined, the overall performance was improved to a sensitivity of approximately 95%, with a false-positive rate of 1.5 clusters per image. CONCLUSION: The wavelet transform approach can improve the detection of subtle clustered microcalcifications.

Calcinosis↗
PubMed1996

Angiotensin I converting enzyme gene polymorphism in non-insulin dependent diabetes mellitus.

A total of 168 patients with non-insulin dependent diabetes (NIDDM) followed over 10 years were recruited in this study. The patients were divided into two groups: Group 1 patients had a stable renal function (N = 96) and Group 2 had a declining renal function (N = 72). Group 1 included those whose serum creatinine was normal five years ago but had increased to > or = 2 mg/dl or those who has reached end-stage renal failure (requiring dialysis) by the time of study. All patients were genotyped for the insertion/deletion (I/D) polymorphism of the ACE gene, the M235T polymorphism of the angiotensinogen (Atg) gene and the A1166C polymorphism of the angiotensin II type 1 receptor (AT1) gene. The genotype frequency distributions of M235T Atg and the A116C AT1 gene polymorphisms were not different between Group 1 versus Group 2. While the frequency of the ACE DD genotype in Group 1 (7.3%) was comparable to that of the general population, the DD frequency was significantly higher in Group 2 (26.4%) than in Group 1 (odds ratio, 4.56; 95% confidence interval, 1.80 approximately 11.56, P < 0.001). Among all 168 patients studied, the renal survival rate was significantly lower among DD than ID (P < 0.005) or II patients (P < 0.001). In patients with a declining renal function (Group 2), those with the DD genotype had a significantly shorter time interval from onset of diabetes to the initiation of dialysis (13.4 +/- 1.4 years) than those with ID (20.7 +/- 1.2 years, P < 0.01) or II genotypes (17.5 +/- 1.1 year, P < 0.01). Analysis of the clinical course of the three ACE genotypes revealed that the majority (95%) of patients with the DD genotype who had albuminuria progressed to end-stage renal disease within 10 years of diagnosis of diabetes. Our analysis also revealed that initiation and continuation of dialysis are associated with a progressive decrease in the frequency of the DD genotype. These results indicate that, in NIDDM, the ACE DD genotype has a high prognostic value for progressive deterioration of renal function. Moreover, the DD genotype appears to increase the mortality once dialysis is initiated.

Albuminuria↗
PubMed1996

Enhanced production of glomerular extracellular matrix in a new mouse strain of high serum IgA ddY mice.

To investigate the relationship between high serum levels of IgA and glomerular lesions, selective mating was performed in high serum IgA ddY mice, a murine model of spontaneously developing mesangioproliferative glomerulonephritis mimicking human IgA nephropathy. The selection and mating of high IgA ddY mice were accomplished when the mice were three to four months old. In the 12th generation of high IgA ddY (HIGA) mice, significantly higher levels of serum IgA from 10 age weeks to 60 weeks (P < 0.0002 to 0.0001) were observed in comparison with BALB/c mice. Relatively high proteinuria was observed at 40 weeks of age, although hematuria was consistently negative. Microscopic observations of renal tissue disclosed a marked glomerular mesangial matrix increase and a reduction of cell proliferation with age by both semiquantitative and morphometric analyses with moderate tubulointerstitial damage. These mesangial matrices were stained markedly by antisera for collagen type IV and by fibronectin, but not by collagen type I. Localization of TGF-beta protein was also detected in the mesangium of the HIGA mice. The positive mesangial IgA deposition was maintained consistently by this mating procedure and became more marked with age. Size analysis of IgA from ten pooled HIGA mice aged 50 to 60 weeks revealed dominant polymeric IgA in sera and dimeric IgA in glomerular eluates. Clonal analysis of serum IgA disclosed heterogeneous spectrotypes in a wide pH range (4.5 to 6.5), in contrast to very limited spectrotypes in the acidic pH range (4.5 to 5.2) of IgA in the glomerular eluates from these mice. The analyses of retroviral gp70 antigen involvement in the HIGA mice disclosed a significant increase of serum levels of gp70 anti-gp70 immune complexes with age, with no relationship to the severity of glomerular gp70 deposition. Northern blot analysis of renal tissue revealed markedly high mRNA expression of collagen type I, IV, fibronectin and TGF-beta even in 10-week-old HIGA mice in comparison with BALB/c mice. The expression became more significant in 60-week-old animals. The genetic background required to induce the expansion of IgA-producing B-cell clones is suggested to be closely related to the increased gene expression of TGF-beta, which induces enhanced glomerular extracellular matrix (especially fibronectin) accumulation in HIGA mice, being possibly mediated by the mesangial deposition of dimeric and highly acidic IgA. This newly established strain may provide a model for investigating the relationship between progressive glomerular sclerotic lesions and the induction of pathogenic IgA in human IgA nephropathy.

Aging↗
PubMed1996

Angiotensin converting enzyme gene polymorphism: potential silencer motif and impact on progression in IgA nephropathy.

Since the renin angiotensin system (RAS) is established as an important factor in renal disease progression, we determined whether RAS alleles that have been linked to variability in outcome in several cardiovascular diseases also affect progression of IgA nephropathy. These genetic variants include: (1) angiotensin I converting enzyme deletion polymorphism in intron 16 (ACE I/D), reported to be associated with increased risk of myocardial infarction as well as left ventricular hypertrophy; (2) a point mutation in the angiotensinogen (Agt) gene resulting in a methionine to threonine substitution at residue 235 (M235T), reported to be associated with hypertension in Caucasians; and (3) an angiotensin receptor type I (ATR) A to C transition at bp 1166 (A1166C) which shows synergy with the deleterious effects of the ACE DD genotype in myocardial infarction. We examined these polymorphisms by PCR amplification of genomic DNA samples from 64 Caucasian patients in the USA (age 6 to 83 years) with biopsy-proven IgA nephropathy whose renal status was followed for an average of almost seven years. Patients who presented with and maintained normal serum creatinine (Cr, < 1.5 mg/dl), had ACE genotype frequencies of II:35%, ID:61%, DD:4%. By contrast, in patients with progression (initially normal Cr increased to a mean of 4.5 +/- 0.86 mg/dl), ACE genotype frequencies were II:22%, ID:44%, DD:33% (P = 0.057 by Fishers's exact test, vs. non-progressors). The association of the DD genotype with progression was even more striking when patients with other risk factors (hypertension and/or heavy proteinuria) were excluded. In this subgroup, the genotype frequencies in patients with stable creatinine versus those with deterioration in renal function was 53%, 47%, and 0% versus 0%, 40%, and 60%, respectively, for II, ID, and DD genotypes (P = 0.009 by Fisher's exact test, progressors vs. non-progressors). Further, sequence analysis of the I gene polymorphism revealed a potential 13 bp silence motif. Neither the Agt 235T nor the ATR A 1166C gene variants, however, was associated with deterioration of renal function. Taken together, these results indicate that, although polymorphism in each of the three genes in the RAS system has been linked to cardiovascular diseases, only the ACE I/D polymorphism is associated with progressive deterioration in renal function in IgA nephropathy. Since previous observations link ACE polymorphism with ACE activity, these findings imply a widespread importance of ACE in modulating destructive processes in different organs.

Alleles↗
PubMed1996

Signalling from endoplasmic reticulum to nucleus: transcription factor with a basic-leucine zipper motif is required for the unfolded protein-response pathway.

BACKGROUND: Accumulation of unfolded proteins in the endoplasmic reticulum (ER) triggers the transcriptional induction of molecular chaperones and folding enzymes localized in the ER. Thus, eukaryotic cells possess an intracellular signalling pathway from the ER to the nucleus, called the unfolded protein-response (UPR) pathway. In Saccharomyces cerevisiae, such induction is mediated by the cis-acting unfolded protein-response element (UPRE) which has been thought to be recognized by one or more transcription factor(s). RESULTS: Extensive mutational analysis revealed that UPRE contains a partial palindrome with a spacer of one nucleotide (CAGCGTG) that is essential for its function. We then cloned the ERN4 (presumably identical with HAC1) gene using yeast one-hybrid screening, in which the GAL4-ERN4 fusion gene constitutively activates the UPR pathway. The ERN4 gene encodes a basic-leucine zipper protein (Ern4p) that specifically binds to UPRE in vitro and activates transcription in vivo. Cells lacking Ern4p are unable to induce transcription of any of the five target genes tested and exhibit sensitivity to ER stress and inositol requirement for growth. CONCLUSION: We concluded that Ern4p represents a major component of the putative transcription factor (UPRF) responsible for the UPR leading to the induction of ER-localized stress proteins.

Amino Acid Sequence↗
PubMed1996

Analysis of K-ras gene mutation in hyperplastic duct cells of the pancreas without pancreatic disease.

BACKGROUND & AIMS: We and others have previously shown that the mutation of K-ras codon 12 was found in the majority of pancreatic adenocarcinomas. The mutation has also been identified in the pancreatic duct with mucous cell hyperplasia in association with chronic pancreatitis. Ductal hyperplasia is also frequently found in the pancreas free from pancreatic carcinoma or chronic pancreatitis. The aim of this study was to assess the incidence and types of mutations in hyperplastic foci in these cases. METHODS: The nucleotide sequence of the K-ras gene at codon 12 of the DNA extracted from microdissected hyperplastic epithelium of the pancreatic duct obtained at autopsy in patients without pancreatic adenocarcinoma or chronic pancreatitis was analyzed. RESULTS: Of 38 patients with 79 hyperplastic foci, 12 patients (with 19 hyperplastic foci) had mutations. None of the 16 normal ducts in 12 specimens had this mutation. The nucleotide sequence of the codon in 53% of ductal hyperplastic foci was TGT or AGT, both of which were not found in 30 cases of adenocarcinoma. CONCLUSIONS: These results suggest that the ras gene mutation occurs frequently in multifocal hyperplastic foci of pancreatic duct and that the mutations may not have direct relevance to the carcinogenesis of pancreatic cancer.

Adult↗
PubMed1996

Cytokine-induced neutrophil chemoattractant release from hepatocytes is modulated by Kupffer cells.

To clarify the role of intercellular communication in the liver during accumulation of neutrophils, the release of cytokine-induced neutrophil chemoattractant (CINC) (interleukin-8 [IL-8] related protein in rodents) by hepatocytes was investigated in the presence of Kupffer cell-conditioned medium in vitro. Kupffer cells were prepared by perfusion of rat liver with collagenase followed by centrifugation on a metrizamide gradient and were cultured in the presence or absence of lipopolysacharide (LPS). The conditioned medium was collected after 24 hours, and rat hepatocytes were cultured in the presence or absence of Kupffer cell-conditioned medium. An amount of CINC in the culture supernatant was measured by western blotting analysis and enzyme-linked immunosorbent assay (ELISA), and expression of its messenger RNA (mRNA) was assessed by the polymerase chain reaction. LPS-stimulated Kupffer cell-conditioned medium enhanced an expression of CINC mRNA in hepatocytes and increased the production of CINC by hepatocytes. Enhanced production of CINC was not shown when the Kupffer cell-conditioned medium was pretreated with heat (56 degrees C, 30 minutes). The production of CINC by hepatocytes in the presence of the LPS-stimulated Kupffer cell-conditioned medium was reduced by an antibody against interleukin 1 beta (IL-1 beta), but not by antibodies against tumor necrosis factor alpha (TNF-alpha) or LPS. These results suggest that production of CINC by hepatocytes could be regulated by IL-1 beta released from Kupffer cells, leading to neutrophil accumulation during liver injury, because this protein is a strong chemoattractant for neutrophils.

Animals↗
PubMed1996

Serum lipid profile in relation to milk consumption in a Japanese population.

OBJECTIVE: To investigate relationships between serum lipid profiles, milk consumption and lifestyle, in a Japanese population. METHODS: A cross-sectional study in 12,610 Japanese men aged 30 to 69 years. Serum total-cholesterol (TC), HDL-cholesterol (HDLC), LDL-cholesterol (LDLC), TC/HDLC ratio, and triglycerides (TG) were determined. Milk consumption was classified into "Yes" (3553 men) and "No" (9057 men) groups by a self-administered questionnaire "Do you drink a glass of cow's milk (180 to 200 mL) or more everyday?". Five variables (age, body mass index, habitual exercise, and smoking and drinking habits) were considered confounding factors for the serum lipids. RESULTS: Regardless of age, the "Yes" group had higher levels of serum TC, HDLC and LDLC than the "No" group except for one comparison (HDLC in 50 to 54 year old group). The differences in serum TC (p < 0.001), HDLC (p < 0.001) and LDLC (p < 0.001) between the two groups were significant by ANOVA. However, milk consumption had no significant relations to serum TC/HDLC ratio or TG level. Multivariate models including the five confounding factors confirmed these results, and indicated that the "Yes" group had higher adjusted means of serum TC by 0.079 mmol/L (+1.5%, 5.280 vs. 5.201 mmol/L, p < 0.001), HDLC by 0.018 mmol/L (+1.4%, 1.260 vs. 1.242 mmol/L, p < 0.01), and LDLC by 0.066 mmol/L (+2.0%, 3.382 vs. 3.316 mmol/L, p < 0.001) than the "No" group. CONCLUSION: Milk consumption is part of a lifestyle related to hypercholesterolemia in the Japanese.

Adult↗
PubMed1996

Endothelium-dependent vasodilatation is not selectively impaired in patients with chronic heart failure secondary to valvular heart disease and congenital heart disease.

This study examined possible selective impairment of endothelial dysfunction in the peripheral vascular bed in patients with chronic heart failure in the absence of confounding factors influencing endothelial function (i.e. hypertension, hypercholesterolaemia and diabetes mellitus). Several recent studies have suggested that endothelium-dependent peripheral vasodilation is impaired but endothelium-independent vasodilation is preserved in patients with chronic heart failure. However, a classical paper has demonstrated that sodium nitrite-mediated calf blood flow is clearly depressed in patients with valvular heart disease and cardiomyopathy. We examined forearm blood flow changes mediated by acetylcholine and nitroprusside in patients with valvular heart disease (n = 55) or congenital heart disease (n = 13), and a comparison was made with healthy volunteers (n = 21). The blood flow changes mediated by acetylcholine and nitroprusside were significantly impaired in both patient groups (P < 0.01). When blood flow responses were collected from all patients, two types of vasodilatory capacity were found to have decreased significantly with increasing clinical severity of heart failure (New York Heart Association functional class; P < 0.01). This suggests that the peripheral vasodilatory responses mediated by endothelium-dependent and endothelium-independent vasodilators are significantly impaired in patients with symptomatic chronic heart failure due to non-ischaemic heart disease.

Acetylcholine↗