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Biomedical subjects

H Kawaguchi

Publications and source records attributed to H Kawaguchi.

At least 217 records · Page 12Linked to original sources
PubMed1995

Reduction in risk of mortality from colorectal cancer by fecal occult blood screening with immunochemical hemagglutination test. A case-control study.

Fecal occult blood testing by immunochemical hemagglutination has been shown to be superior to the Hemoccult test, both in sensitivity and in specificity. The test has been widely used as a tool for population screening in Japan, but there has been no study to evaluate the efficacy of screening using this test. A case-control study to evaluate the screening was conducted in study areas where no previous and no other concomitant colorectal cancer screening had been performed. Case series in the study were 193 cases who died of colorectal cancer. Three controls were selected randomly from the list of individuals who were alive at the time of diagnosis of the corresponding case and had been living in the same area as the case, matched by gender and by age. Odds ratios (OR) of dying of colorectal cancer for those screened within 1, 2 and 3 years of case diagnosis vs. those not screened were 0.40 [95% confidence interval (CI) 0.17-0.92], 0.41 (95% CI 0.20-0.82), and 0.48 (95% CI 0.25-0.92), respectively. OR increased towards 1.0 as the duration during which screening histories were compared was extended, and showed similar tendencies when analyzed by number of years since the most recent screening history. These results suggest that colorectal cancer screening by the immunochemical fecal occult blood test would reduce mortality from colorectal cancer.

Adult↗
PubMed1995

Effects of surface modification of materials on human neutrophil activation.

The properties of a polymer surface affect the cellular functions and morphology of cells in contact with the polymer. In this paper, we will demonstrate the effects of surface modification of materials on various neutrophil markers of activation. The sulfonation of a polystyrene surface caused increases in its negative charge and hydrophilicity. The sulfonation did not affect the number of adhered neutrophils, but the shape of the neutrophils adhered on the material was different; a round shape on highly sulfonated polystyrene and a spread shape on weakly sulfonated or non-sulfonated polystyrene. Expression of the adhesion molecule, CD11b, on neutrophils was also affected by the properties of the polymer surface. CD11b was expressed in neutrophils adhered on polystyrene and the expression decreased with increasing sulfonation of the surface. The expression of CD11b on the neutrophils on highly sulfonated polystyrene was the same as that on non-adhered neutrophils. In contrast, the expression of CD11a was not affected by the properties of the material surface. The F-actin content of activated neutrophils and the production of active oxygen groups detected by means of luminol-dependent chemiluminescence were also dependent on the sulfo-group content of the material surface. Finally, the translocation of protein kinase C (PKC) was determined in neutrophils adhered to these materials. Compared to non-adhered cells, the ratio of membrane bound to cytosolic PKC increased in adhered cells, but the increase was suppressed by sulfonation of the material surface. These data suggest that activation of neutrophils on polystyrene is suppressed by surface modification with increasing negative charge and/or hydrophilicity.

Actins↗
PubMed1995

Conversion of xanthine dehydrogenase to xanthine oxidase in bovine carotid artery endothelial cells induced by activated neutrophils: involvement of adhesion molecules.

We have demonstrated that the endothelial cell-derived superoxide anion is deeply involved in the endothelial cell injury induced by activated neutrophils (Fujita, H., Morita, I. and Murota, S. (1994) Arch. Biochem. Biophys. 309, 62-69). To clarify the mechanism underlying the increase in the endothelial cell-derived superoxide anion induced by activated neutrophils, the conversion of xanthine dehydrogenase (XD) to xanthine oxidase (XO) in cultured endothelial cells isolated from bovine carotid arteries was investigated. Although the endothelial cells expressed both XD and XO activity, the XO activity of unstimulated cells comprised about 12% of the total (XD + XO) activity. When endothelial cells were exposed to neutrophils activated with phorbol 12-myristate 13-acetate (PMA), XO activity rapidly increased about 3-fold over the control. Whereas treatment of endothelial cells with PMA alone or unstimulated neutrophils alone did not increase the XO activity at all. The increase in XO activity in endothelial cells was also observed on the treatment of the cells with neutrophils activated with leukotriene B4 or thrombin. To determine whether or not proteases released from activated neutrophils are involved in the increased conversion of XD to XO in endothelial cells, the effects of the elastase specific inhibitor, ONO-5046, and protease inhibitors, such as aprotinin, gabexate mesylate and urinastatin, were examined. However, these protease inhibitors did not suppress the conversion of XD to XO induced by PMA-activated neutrophils. Moreover, the treatment of endothelial cells with purified human neutrophil elastase and H2O2 also did not affect the conversion at all. In contrast, monoclonal antibodies against CD11a and CD18 significantly inhibited the increased conversion of XD to XO induced by PMA-activated neutrophils. Moreover, tyrosine kinase inhibitors such as staurosporin and herbimysine also inhibited the increased conversion of XD to XO induced by PMA-activated neutrophils. These results indicate that the adhesion of activated neutrophils to endothelial cells via CD11a/CD18-ICAM-1 is involved in the conversion of XD to XO in endothelial cells induced by activated neutrophils.

Animals↗
PubMed1995

Cytosolic localization of beta 3-subunit of heterotrimeric GTP binding protein in rat hearts.

The expression of three different subtypes of GTP binding protein beta-subunits (beta 1, beta 2 and beta 3) was examined in rat hearts at both mRNA and protein levels. Among three subtypes, beta 3 mRNA was more abundant in ventricles while beta 1 and beta 2 mRNAs were expressed ubiquitously among ventricles, atria and aortas. The immunodetectable beta 1- and beta 3-proteins were predominantly found in the cytosolic fraction of rat ventricles. In this study, we demonstrate ventricle-specific expression of beta 3-subunit and localization of G protein beta 3-subunit in the cytosol of rat hearts. This unusual cytosolic localization of G protein beta 3-subunit might indicate subtype-specific function of G protein beta (gamma)-subunits in rat hearts.

Animals↗
PubMed1995

Autoregulation of inducible prostaglandin G/H synthase in osteoblastic cells by prostaglandins.

Prostaglandins (PGs) have been postulated to amplify their own production by stimulating cyclic adenosine monophosphate activity, which in turn stimulates PG production. We examined regulation of messenger RNA levels for the inducible and constitutive prostaglandin G/H synthases, PGHS-2 and PGHS-1, in murine osteoblastic MC3T3-E1 cells, which express both PGHS-1 and PGHS-2, and in rat osteoblastic Py1a cells, which express only PGHS-2. Prostaglandins E2, F2 alpha, and D2 induced PGHS-2 mRNA in both cell lines under serum-free conditions and stimulated small increases in PGHS-1 mRNA levels in MC3T3-E1 cells. PGE2 (1 microM) increased the transcription rate of PGHS-2 mRNA 9-fold at 2 h in serum-free cells and also induced PGHS-2 protein. In the presence of arachidonic acid or serum, PGs also increased medium PGE2. Both forskolin, a protein kinase A activator, and phorbol 12-myristate 13-acetate (PMA), a protein kinase C (PKC) activator, have previously been shown to induce PGHS-2 mRNA in MC3T3-E1 cells, but in the present study only PMA induced PGHS-2 expression in Py1a cells. The induction of PGHS-2 mRNA in Py1a cells by PGs was inhibited by chelerythrine, a PKC inhibitor, and blocked by 24 h of pretreatment with PMA. The 2 h serum stimulation of PGHS-2 mRNA in MC3T3-E1 cells was inhibited 40-50% by three structurally unrelated nonsteroidal anti-inflammatory drugs (NSAIDs), suggesting that endogenous PGs also amplify PG production through induction of PGHS-2.(ABSTRACT TRUNCATED AT 250 WORDS)

3T3 Cells↗
PubMed1995

Significance of rapid urease test for identification of Helicobacter pylori in comparison with histological and culture studies.

Helicobacter pylori in the stomach is an etiological factor of gastritis and peptic ulcer. It is now considered that gastric cancer can be, at least in some cases, a late complication of H. pylori infection. In 123 consecutive endoscopic antral biopsies obtained from patients with the Okamoto Hospital, the specimens were subjected to the rapid urease test (RUT), histology (H&E stain), and culture, for the identification of H. pylori. The results of these methods were compared semi-quantitatively in order to evaluate these detection methods for identifying H. pylori. The results of these methods were found to agree well, with the Spearman's rank correlation coefficient between RUT and culture being 0.90 (P < 0.01) and that between histology and culture being 0.80 (P < 0.01). RUT is considered to be a very simple, sensitive, and highly specific test which enables the endoscopist to diagnose H. pylori infection.

Adult↗
PubMed1995

Expression of renin and angiotensin-converting enzyme in human hearts.

To understand the significance of the tissue renin-angiotensin system in the heart, we examined the expression of renin and angiotensin-converting enzyme (ACE) in autopsied human hearts. Samples were taken from organs obtained at autopsy from 15 patients without heart disease and 3 patients with heart disease (old myocardial infarctions, acute myocardial infarctions, and hypertrophic cardiomyopathy). We examined the expression of renin and ACE mRNA by using the reverse transcription-polymerase chain reaction (RT-PCR). RT-PCR showed the expression of renin in the right atria in all patients. However, expression of renin mRNA in the left ventricles was not found in any of the 15 hearts without heart disease. In contrast, renin mRNA was detected in the left ventricles in hearts with heart disease. ACE mRNA was detected in both the atria and the ventricles in normal hearts, and its expression did not alter in diseased hearts. These findings suggest that renin mRNA is expressed mainly in the right atria in normal hearts, but that its expression in the left ventricle can be activated in some pathological conditions.

Adult↗
PubMed1995

Serum glycoproteins and severity of coronary atherosclerosis.

The relation of serum glycoproteins and C-reactive protein (CRP) to severity of coronary atherosclerosis was examined in 133 men and 92 women undergoing coronary angiography. The following serum glycoproteins were determined: alpha 1-antitrypsin, alpha 1-acid glycoprotein, alpha 2-macroglobulin, ceruloplasmin, haptoglobin, fibrinogen, C4b binding protein, and lipoprotein (a) [Lp(a)]. Sex- and age-adjusted levels of alpha 1-antitrypsin, alpha 1-acid glycoproteins, alpha 2-macroglobulin, ceruloplasmin, Lp(a) and CRP were significantly associated with the severity of coronary atherosclerosis as determined by the Gensini score; these associations remained significant even after adjustment for body-mass index, smoking history, hypertension, and total cholesterol, except for Lp(a) (p = 0.075). These findings suggest that certain serum glycoproteins and CRP can serve as independent indicators for the progression of coronary atherosclerosis.

Aged↗
PubMed1995

Angiotensin-converting enzyme gene polymorphism in Japanese patients with hypertrophic cardiomyopathy.

To examine the contribution of the angiotensin-converting enzyme (ACE) gene to hypertrophic cardiomyopathy (HCM), we determined the ACE insertion/deletion (I/D) polymorphism in 80 patients with HCM and 88 of their unaffected siblings and children. Patients were divided into familial or solitary HCM (FHCM or SHCM) groups with or without affected family members. Genotypes were identified by the polymerase chain reaction (PCR) with oligonucleotide primers flanking the polymorphic region in intron 16 of the ACE gene to amplify template DNA prepared from peripheral leukocytes. D-allele frequencies were 0.38 in all subjects, 0.42 in patients with HCM, and 0.35 in relatives (p < 0.05). The probability ratios were 1.98, 1.46, and 2.97 in patients with HCM, FHCM, and SHCM, respectively. The D allele frequency was higher in SHCM than in FHCM (p < 0.05). The findings suggest that HCM, especially in solitary cases, is partially determined by genetic disposition. Findings imply that the ACE D allele is one of the genetic contributing factors associated with cardiac hypertrophy in HCM.

Aged↗
PubMed1995

The secretory granule matrix-electrolyte interface: a homologue of the p-n rectifying junction.

When placed at the tip of a glass micropipette electrode the polymeric matrix of the secretory granule behaves like a diode. The measured current was 100-fold greater at negative potentials compared to positive potentials, and up to sixfold greater than that measured with the pipette alone. By manipulating the geometry of the electric field we show that these electrical properties result from focusing an electric field at the gel-electrolyte interface. We also show, by using pulsed-laser imaging with fluorescein as the ionic probe, that there is a rapid accumulation and depletion of ions at the gel-electrolyte interface. A voltage pulse of -9 V applied to the gel caused a severalfold increase in the fluorescence intensity within 5 ms. This correlated with an increase in the measured current (approximately 1 microA). In contrast, within 5 ms of applying +9 V we recorded a decrease in the fluorescence intensity, which paralleled the twofold decrease in the measured current. This is similar to a p-n junction where an applied voltage causes the accumulation and depletion of charge carriers. Using synthetic gels (diameter 3-6 microns) with different charge characteristics we observed no rectification of the current with neutral gels and confirmed that rectification and amplification of the current were dependent on the fixed charge within a gel. In addition, we modeled the conduction at the gel-electrolyte interface using the Nernst-Planck electrodiffusion equation and accurately fitted the experimental current-voltage relationships. This study provides some insight into how biological interfaces may function. For example, we suggest that neurotransmitter release during exocytosis could be regulated by voltage-induced accumulation and depletion of ions at the interface between the secretory granule and the fusion pore.

Animals↗
PubMed1995

Renin-angiotensin system in failing heart.

Extrahepatic synthesis and localization of angiotensinogen have been described in animals, thus establishing the tissue renin-angiotensin system. We examined angiotensinogen messenger RNA synthesis by northern blotting. It was detected not only in the liver, but also in both the atrial and ventricular heart tissues, suggesting that angiotensinogen is synthesized in the human heart. Immunohistochemical studies using a specific antibody to angiotensinogen revealed a stronger reaction in the endocardial layer of the human left ventricle, than in the epicardial layer, and intense immunoreactivity in the conduction system and right atrium. Furthermore, our experiments revealed a widespread immunopositive reaction for angiotensinogen in the left ventricle of diseased hearts. We examined the participation of the collagen in the occurrence and progression of cardiomyopathy. The acetic acid solubility of collagen and reducible crosslink decreased in cardiomyopathic hamsters as the fibrosis progressed, but was unchanged in controls. These findings indicate that in the early phase of cardiomyopathy the extracellular matrix of the myocardium is similar to immature tissues. In the later phase, the matrix resembles that of hard tissues, and is insoluble. Furthermore, we examined the relationship between angiotensin II and collagen synthesis. Basal collagen synthesis in cardiac fibroblasts from spontaneously hypertensive rats was 1.6-fold greater than that in Wistar-Kyoto rats. The responsiveness of collagen production to Ang II was significantly enhanced in SHR. This effect was angiotensin receptor-specific, because it was blocked by the competitive inhibitor. These results indicate angiotensin II may play an important role in collagen accumulation in hypertensive cardiac hypertrophy.

Angiotensin II↗
PubMed1995

Macrophages in childhood IgA nephropathy.

The role of glomerular macrophages in IgA nephropathy in children was investigated using a new monoclonal antibody (KP1) as a probe. The average number of glomerular macrophages per patient (ANM/P) was closely correlated with the degree of hematuria (P < 0.01) as well as with the degree of leukocyturia (P < 0.01) in the absence of any correlation with proteinuria, serum IgA levels or the interval between the detection of urine abnormalities and renal biopsy. ANM/P was significantly higher in patients diagnosed pathologically as having focal and diffuse proliferative glomerulonephritis than in patients with minor glomerular abnormalities or advanced sclerosis (P < 0.05). Among various types of glomerular morphology in individual patients, macrophages predominantly infiltrated glomeruli with cell-proliferative lesions despite an absence of any increase in glomeruli with minor abnormalities or with sclerosis. Macrophages were mainly localized within the capillary lumen in association with endocapillary proliferative lesions (tuft necrosis), they accumulated in areas of mesangial proliferation, and they were attached to Bowman's capsule in segmental lesions. Macrophages were less evident in sclerosis. Furthermore, ultrastructural analysis revealed macrophages in the paramesangial areas in close proximity to lytic changes in the glomerular basement membrane and effacement of epithelial foot processes. In addition, some cases in repeat biopsy shows prolonged or increased values of ANM/P after several years of interval in association with progression of proliferative lesions. These results suggest that macrophages infiltrate glomeruli during acute glomerular inflammation, and that they are involved in mesangial proliferation or the development of extracapillary lesions in the absence of apparent clinical symptoms. Furthermore, recurrence or prolonged infiltration may promote progression of IgA nephropathy.

Antibodies, Monoclonal↗
PubMed1995

ABO incompatible kidney transplantation in children.

We have performed 7 pediatric kidney transplantations from living related donors of ABO incompatibility. All patients preoperatively underwent plasmapheresis with or without immunoadsorption to reduce anti-A and/or anti-B antibodies. Immunosuppression initially consisted of methylprednisolone, cyclosporine, azathioprine, antilymphocyte globulin and deoxyspergualin. At transplantation splenectomy was simultaneously performed in all patients. Median followup is 44 months (range 31 to 58). Patient and graft survival rates are 100% to date. There were no uncontrollable vascular rejection episodes, and post-transplant anti-A and/or anti-B antibody titers were always less than 1:32. Transplantation across the ABO blood barrier remains challenging today. However, our small series clearly shows that the preoperative reduction of ABO antibody, simultaneous splenectomy and strict immunosuppressive therapy cause successful long-term results in children.

ABO Blood-Group System↗
PubMed1995

Low expression of adhesion molecules in a case of cutaneous T-cell lymphoma.

A case of cutaneous T-cell lymphoma (CTCL) with low expression of the adhesion molecules lymphocyte function-associated antigen-1 (LFA-1), intercellular adhesion molecule-1 (ICAM-1), and very late antigen-4 (VLA-4) is described. The patient was a 90-year-old man with red round homogeneous tumors on his scalp, trunk, and extremities. He had no history of definite erythema or plaque stage. A biopsy sample taken from a tumor revealed massive infiltration of atypical lymphocytes in the reticular dermis and subcutis with a definite clear zone. The atypical lymphocytes were medium-sized with slightly convoluted nuclei. Immunohistochemically, the infiltrates showed the phenotype of so-called memory T cells. On the basis of these features, the case was diagnosed as CTCL. Expression of LFA-1, ICAM-1 and VLA-4 on the infiltrates was 9%, 13% and 11%, respectively, which is much lower than that in classic mycosis fungoides. This finding suggests that loss of these adhesion molecules may contribute to loss of epidermotropism in the advanced stage of CTCL.

Aged↗
PubMed1995

Hypercalciuria and nephrocalcinosis in patients with idiopathic low-molecular-weight proteinuria in Japan: is the disease identical to Dent's disease in United Kingdom?

Idiopathic low-molecular-weight (LMW) proteinuria is a newly described renal disease in Japan and Italy. We report on 7 patients who manifested bilateral or unilateral nephrocalcinosis, as demonstrated by abdominal computed tomography scans. Renal histology revealed calcinosis of renal tubules in 2 patients. Computed tomography is a reliable method for the detection of nephrocalcinosis in this disorder. Hypercalciuria was also seen in 6 patients. A calcium-loading test performed in 2 patients suggested that hypercalciuria was of renal origin. Although the true pathogenesis is still not known, hypercalciuria and nephrocalcinosis appear to be a common complication in patients with idiopathic LMW proteinuria. These complications and clinical features suggest that idiopathic LMW proteinuria in Japan is likely to be identical to Dent's disease in the United Kingdom.

Adolescent↗
PubMed1995

Cytoplasmic calcium level and membrane fluidity of platelets contacting poly(acrylamide-co-methacrylic acid) particles with different surface properties.

Changes in cytoplasmic free calcium levels and membrane fluidity of platelets in contact with poly(acrylamide-co-methacrylic acid) (PAAmMAc) particles were examined to analyze the mechanistic aspect of regulating platelet function. Our previous studies demonstrated interesting features of PAAmMAc particles during interaction with platelets: (1) PAAmMAc particles induce no calcium increase but enhance membrane fluidity of platelets: (2) thrombin induces no calcium increase in platelets when the platelets were mixed previously with PAAmMAc particles; and (3) PAAmMAc particles induce a calcium increase in platelets when they were treated previously with sodium azide (NaN3). These results suggest the possibility that PAAmMAc surfaces may regulate the calcium level by influencing platelet metabolism. In this study, non-cross-linked PAAmMAc solution with the same chemical composition as the particles showed a suppressive effect on thrombin-induced calcium increase, but, no influence on membrane fluidity. This result indicates that aggregated macromolecular surface assemblies of PAAmMAc may dominate the increase in membrane fluidity of platelets although the calcium change is induced by discrete molecular level interaction between the PAAmMAc and platelet membranes. It was also revealed that the suppression of thrombin-induced calcium increase and the membrane fluidity increase in platelets by PAAmMAc particles were reduced by albumin-treatment of the particles. This result suggests that such phenomena may be due to a decrease in any physicochemical interaction of PAAmMAc surfaces with albumin, rather than platelet metabolic change. PAAmMAc particle surfaces with higher carboxyl groups exhibited a more suppressive effect on thrombin-induced calcium increase, whereas those with lower carboxyl groups derived a higher calcium increase when the platelets were treated previously with NaN3. These results suggest the importance of electrostatic and any other physicochemical interaction of PAAmMAc chains on regulating cytoplasmic calcium levels.

Acrylic Resins↗
PubMed1995

Ovariectomy enhances and estrogen replacement inhibits the activity of bone marrow factors that stimulate prostaglandin production in cultured mouse calvariae.

To examine PG production in estrogen deficiency, we studied effects on cultured neonatal mouse calvariae of bone marrow supernatants (MSup) from sham-operated (SHAM), ovariectomized (OVX), or 17 beta-estradiol (OVX+E)-treated mice. MSups were obtained 3 wk after OVX when bone density had decreased significantly. 10-60% MSup increased medium PGE2 and levels of mRNA for inducible and constitutive prostaglandin G/H synthase (PGHS-2 and PGHS-1) and cytosolic phospholipase A2 in calvarial cultures. OVX MSups had twofold greater effects on PGHS-2 and medium PGE2 than other MSups. IL-1 receptor antagonist and anti-IL-1 alpha neutralizing antibody decreased MSup-stimulated PGHS-2 mRNA and PGE2 levels and diminished differences among OVX, sham-operated, and OVX+E groups. In contrast, antibodies to IL-1 beta, IL-6, IL-11, and TNF alpha had little effect. There were no significant differences in IL-1 alpha concentrations or IL-1 alpha mRNA levels in MSups or marrow cells. PGHS-2 mRNA in freshly isolated tibiae from OVX mice was slightly greater than from sham-operated. We conclude that bone marrow factors can increase PG production through stimulation of PGHS-2; that OVX increases and estrogen decreases activity of these factors; and that IL-1 alpha activity, together with additional unknown factors, mediates the differential MSup effects.

Animals↗