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Biomedical subjects

H Asakura

Publications and source records attributed to H Asakura.

At least 163 records · Page 9Linked to original sources

Topographic distribution of Helicobacter pylori in the resected stomach.

OBJECTIVES: The aim of this study was to elucidate the prevalence of Helicobacter pylori and its distribution in order to clarify the frequency of H. pylori infection and the most appropriate site of endoscopic biopsy for studies of H. pylori infection associated with different gastric diseases. DESIGNS AND METHODS: Swiss role mucosal strips from 275 resected stomachs, which included the greater curvature, anterior wall and lesser curvature of the antrum, incisura and corpus, were stained with haematoxylin-eosin and H. pylori antibody. RESULTS: The prevalence of H. pylori infection was 97% in duodenal ulcers, 98% in gastric ulcers, 98% in intestinal-type carcinomas and 99% in diffuse-type carcinomas. H. pylori was present at a rate of 100% in any site in cases of duodenal ulcer, but was diffusely distributed in the antrum and patchily distributed in the corpus. The detection rate of H. pylori was 50-100% in gastric ulcers, 30-100% in intestinal-type adenocarcinomas and 63-100% in diffuse-type adenocarcinomas depending on the site of the stomach examined. CONCLUSIONS: The prevalence of H. pylori infection was very high in peptic ulcers of the duodenum and stomach and gastric carcinomas of Japanese patients. Biopsy specimens for evaluation of H. pylori infection should be taken routinely from both the greater curvature of the antrum and corpus. Immunohistochemical staining should be used to assay for H. pylori when few organisms are present or eradication therapy has been used.

Adenocarcinoma↗

Detection and long-term existence of Shiga toxin (Stx)-producing Escherichia coli in sheep.

The isolation and characterization of Shiga-like toxin (Stx)-producing Escherichia coli (STEC) from sheep are described. The distribution of stx genes in E. coli isolates was detected by PCR. When brain heart infusion (BHI) broth and novobiocin supplemented m-EC broth (N-mEC) were used as enrichment culture for the isolation of STEC, N-mEC, compared to BHI, showed clearly lower efficiency. Finally, 5 STEC isolates from 4 sheep were isolated and characterized by biochemical and genetical analysis. All of them were confirmed by ELISA and Vero cell cytotoxicity assay for the production of Stx. Moreover, some strains carried hemolysin and eaeA genes and harbored large plasmids. Based on their plasmid profiles, antibiotic patterns and PCR-based DNA fingerprinting analysis using random amplified polymorphic DNA (RAPD), all isolates were different from each other. Three of the isolates were identified to belong to serogroups O2, O153 and O165, respectively, and the STEC strains belonging to these serogroups had been isolated from STEC outbreaks in humans. Four months after the first isolation in July 1997, STEC from sheep #1 was isolated again. A new isolate, HI-11, was identified as STEC O2:Hnt. Simultaneously, 2 STEC, which were genetically and phenotypically different from each other, were isolated from the same sheep at intervals of 4 months. These results demonstrate that sheep may be an important animal for studying human STEC infections, and that further epidemiological surveys on STEC are necessary.

Animals↗

Detection and genetical characterization of Shiga toxin-producing Escherichia coli from wild deer.

Shiga toxin (Stx)-producing Escherichia coli (STEC) strains isolated from wild deer in Japan were examined. A total of 43 fecal samples were collected 4 times from 4 different sites around Obihiro City, Hokkaido, Japan, in June and July 1997. Seven STEC strains were isolated by PCR screening, all of them were confirmed by ELISA and Vero cell cytotoxicity assay to be producing only active Stx type 2 (Stx2). Moreover, they seemed to carry the hemolysin and eaeA genes of STEC O157:H7, and some isolates harbored large plasmids which were similar to the 90-kilobase virulence plasmid of STEC O157:H7. Based on their plasmid profiles, antibiotic resistance patterns, PCR-based DNA fingerprinting data obtained by using random amplified polymorphic DNA (RAPD) and the stx2 gene sequences, all isolates were divergent from each other except for 3 isolates from the first and second samplings. A DNA sequence analysis of representative isolates revealed that deer originating STEC strains were closely related to each other, but not to the Stx2-producing STEC strains isolated from a mass outbreak in Obihiro at the same time. A phylogenic analysis of the deduced Stx2 amino acid sequences demonstrated that three distinct clusters existed in the deer originating STEC strains and that the Stx of deer originating STEC was closely associated with that originating from humans, but not those of STEC originating from other animals. These results suggest that STEC contamination of deer carcasses should be considered as a potential source of human infection and adequate sanitary inspection of meat for human consumption is also essential for wild animals.

Amino Acid Sequence↗

Autoantibodies against a 210 kDa glycoprotein of the nuclear pore complex as a prognostic marker in patients with primary biliary cirrhosis.

It has been reported that the presence of anti-nuclear antibody against a 210 kDa glycoprotein of nuclear pore complex (anti-gp210) is highly specific for primary biliary cirrhosis (PBC). The aim of the present study was to investigate the significance of anti-gp210, especially as a prognostic marker. The presence of anti-gp210 was ascertained in 113 patients with PBC and 162 controls by indirect immunofluorescence assay using HepG2 cells and immunoblotting analysis using nuclear extracts from HeLa cells. Anti-gp210 was detected in 25 of the 113 (22.1%) patients. None of the 162 controls was positive for anti-gp210. The appearance and titre of anti-gp210 in the patients with PBC did not vary from the time of diagnosis and through their clinical course. Anti-mitochondrial antibodies (AMA), including antibodies against pyruvate dehydrogenase complex, branched chain alpha-ketoacid dehydrogenase complex and alpha-ketoglutarate dehydrogenase complex, were not detected by enzyme-linked immunosorbent assay in five of the 113 (4.4%) patients with PBC. However, anti-gp210 alone was positive in one of these five patients. The difference in prognosis was statistically significant; patients with PBC positive for anti-gp210 died from hepatic failure more frequently than those who were negative (P < 0.01), although there were no statistically significant differences in the frequency of jaundice and the histological stage at the time of diagnosis between the two groups. We suggest that the presence of anti-gp210 is one of the independent prognostic markers able to predict, at the time of diagnosis, a poor outcome in patients with PBC.

Adult↗

Fibrosing cholestatic hepatitis after living related-donor renal transplantation.

A 43-year-old man underwent living related-donor renal transplantation because of chronic renal failure in 1991. During the transplant period, both donor and recipient were seronegative for hepatitis B surface antigen (HBsAg). The donor was seropositive for antibody to hepatitis B surface antigen (anti-HBs) due to hepatitis B virus (HBV) vaccination. After transplantation, FK506 and methylprednisolone had been administered to the patient as immunosuppressants. In 1993, HBsAg appeared in his serum. His alanine aminotransferase level elevated gradually during 1995 and then in 1996, general fatigue, ascites and jaundice developed. At this time his serum was positive for hepatitis B e antibody, contained more than 100000 Meq/mL HBV-DNA and 100% precore mutant. Despite subsequent intensive therapy, liver dysfunction progressed and this patient died of hepatic failure 2 months following admission. At autopsy, the liver exhibited cholestasis, fibrosis extending from the portal tracts, mild inflammation and hepatocytes with a ground-glass appearance. In addition, HBsAg and hepatitis B core antigens had accumulated in the hepatocytes. Consequently, the final diagnosis was fibrosing cholestatic hepatitis (FCH) due to precore mutant HBV infection contracted after renal transplantation. It is unclear when and where the recipient liver became HBV infected. Nevertheless, after renal transplantation, while receiving immunosuppressive drugs, HBV appeared to have the potential to cause hepatic failure and FCH may have been a fatal complication for the recipient.

Adult↗

Serum N-acetylglucosaminyltransferase III activities in hepatocellular carcinoma.

N-Acetylglucosaminyltransferase III (GnT III) catalyses the addition of N-acetylglucosamine through a beta 1-4 linkage to the mannose of the trimannosyl core, resulting in conversion of the concanavalin A (Con A)-reactive glycan into a non-reactive state. In this study, we measured GnT III activity to evaluate its diagnostic efficacy and its therapeutic effect on hepatocellular carcinoma (HCC). Concanavalin A-non-reactive fraction of serum transferrin (Tf) was also determined since the sugar chains of Tf are one of the possible candidates for the product of GnT III. Serum samples (159) were used from patients with HCC (89), liver cirrhosis (30), chronic hepatitis (19), alpha-fetoprotein (AFP) producing gastric carcinoma metastatic to the liver (five) and healthy controls (16). N-Acetylglucosaminyltransferase III activity was determined by high performance liquid chromatography. The reactivity of serum Tf to Con A was also analysed in 21 paired HCC samples before and after treatment by crossed immuno-affinoelectrophoresis. N-Acetylglucosaminyltransferase III activity from the HCC group (153 +/- 72pmol/mL/h) was significantly higher than that from liver cirrhosis (99 +/- 67 pmol/mL per h), chronic hepatitis (84 +/- 39 pmol/mL per h) and the normal controls (62 +/- 16 pmol/mL per h). N-Acetylglucosaminyltransferase III activity of 21 patients with HCC was significantly reduced after treatment such as transcatheter arterial chemoembolization and/or percutaneous ethanol infection therapy, (123 +/- 77 to 100 +/- 60 pmol/mL per h). Commensurate decreases of AFP and des-gamma-carboxy prothrombin with GnT III activity were also observed after treatment. The Con A-non-reactive fraction (n = 21; 6.4 +/- 2.3%) in patients with HCC after treatment was significantly lower than before (8.2 +/- 2.4%). The present study suggests that GnT III activity is a possible aid in the diagnosis and evaluation of HCC, especially when other tumour markers are negative.

Adult↗

Reduced expression of thrombopoietin is involved in thrombocytopenia in human and rat liver cirrhosis.

It is widely accepted that thrombocytopenia associated with liver cirrhosis is caused by increased platelet destruction in the enlarged spleen, but this issue has not yet been analysed sufficiently in terms of platelet production. Thrombopoietin is produced mainly in the liver and strongly promotes platelet production. We studied serum thrombopoietin and the levels of its mRNA in liver tissue of cirrhotic patients and also in a rat model of liver cirrhosis. Furthermore, to clarify the influence of the spleen, we investigated thrombopoietin mRNA in splenectomized rats. The serum thrombopoietin level in humans with liver cirrhosis was not significantly reduced instead of thrombocytopenia. The expression of thrombopoietin mRNA in liver tissue decreased with the progression of liver cirrhosis in both patients and the rat model and no compensatory expression was observed in other organs or non-parenchymal cells. The level of thrombopoietin mRNA did not differ significantly in splenectomized cirrhotic rats before or after administration of dimethylnitrosamine, but was lower than that in splenectomized rats without cirrhosis. We conclude that thrombocytopenia in liver cirrhosis is caused not only by platelet destruction but also by decreased platelet production, perhaps due to reduction of thrombopoietin mRNA in the liver.

Adult↗

Areas of sinusoidal surface hepatocyte nuclear predominance in type C chronic hepatitis.

AIMS/BACKGROUND: Thick hepatic plates have been considered one of the morphological characteristics of hepatocyte regeneration in cirrhotic nodules. They can be recognized by the sinusoidal surface predominance of their nuclei. We have investigated the prevalence of this in HBV and HCV infections. METHODS AND RESULTS: This feature was more frequently present in type C chronic hepatitis with low activity of inflammation and low grade of fibrosis, than with type B chronic hepatitis. Additionally, this area of sinusoidal surface hepatocyte nuclear predominance (ASSHNP) was seen in zone II, rather than in periportal zones, in type C chronic hepatitis. Clinical data were analyzed statistically. Immunohistochemical reactivity of type IV collagen, laminin, Ulex europaeus agglutinin 1 lectin (UEA-1), and factor VIII-related antigen were increased in ASSHNP. Immunohistochemical staining of Ki-67 antigen was performed in order to assess the regenerative capacity of this area and showed a low level of regeneration. Ultrastructure of this area in type C chronic hepatitis showed a decrease in the number of mitochondria and an increase of nuclear pleomorphism together with basement membrane formation in the space of Disse. CONCLUSION: Although the cause of these abnormalities was not clarified in this study, it is suggested that they are related to chronic hepatitis C virus (HCV) infection per se, rather than regeneration or inflammatory activity. These changes may be significant in HCV-associated hepatocarcinogenesis.

Adult↗

[Enterohemorrhagic Escherichia coli O157 outbreak in Obihiro-City--study on antibiotic susceptivity and plasmid profiles].

The drug-resistance patterns and plasmid profiles of 147 isolates (patient origin 142 and food origin 5 isolates) from the outbreak of enterohemorrhagic Escherichia coli (EHEC) O157:H7 infection in Obihiro-city Hokkaido in late October, 1996, were examined. Thirty-six isolates were resistant to tetracycline (TC) (24.5%), 15 of which were resistant to both streptomycin and TC. The minimal growth inhibitory concentration (MIC) of fosfomycine (FOM) was examined, confirming that MIC changed by the cultivation conditions, that is 12.5 micrograms/ml at the aerobic condition, 1.6 micrograms/ml at the anaerobic condition and 3.2 micrograms/ml on blood agar plates. Furthermore, though E. coli O157 could not be detected once by the FOM medication, FOM sensitivity of the patient origin O157 isolates who became O157-positive again was examined. Any changes in FOM sensitivity were not observed. Plasmid profiles of all isolates were divided by 4 patterns from A to D. The most dominant pattern was type A, and plasmid profiles of food origin O157 belonged to pattern A. In 9 examples of the person-to-person infection in the family, plasmid patterns of O157 isolates were the same to each other, even though drug-resistant patterns were different. In 13 patients developing the duration of excretion of EHEC, the changes of the drug-resistance patterns were correlated with the changes of plasmid profiles. By comparing plasmid profiles and TC resistance, it was suggested that TC resistance was controlled on a plasmid. Since food origin O157 isolates were sensitive to all drugs and presenting the same plasmid profiles, demonstrating that TC resistance and plasmid are newly added to the bacterial cells while food origin O157 isolates passe inside the human body.

Adolescent↗

Spectrum of cytokine gene expression in intestinal mucosal lesions of Crohn's disease and ulcerative colitis.

BACKGROUND/AIMS: We investigated the mRNA expression of spectrum of cytokines in the colonic mucosa in inflammatory bowel disease (IBD). METHODS: The expression of cytokine gene was evaluated by using the reverse transcription-polymerase chain reaction and the radioactivity of amplified cDNA standardized by coamplified beta-actin cDNA. RESULTS: Crohn's disease and ulcerative colitis showed significantly increased expression of IL-1beta, IL-6, IL-8 and TNF-alpha mRNA as compared with controls (p < 0.05). CONCLUSION: Proinflammatory cytokines such as IL-1beta, IL-6, IL-8 and TNF-alpha are closely involved in the immune abnormalities of inflammatory mucosal lesions in IBD.

Adolescent↗

Corticotropin-releasing factor inhibits luteinizing hormone-stimulated P450c17 gene expression and androgen production by isolated thecal cells of human ovarian follicles.

Recently, we reported that the thecal compartment of the human ovary contains a CRF system replete with gene expression and protein for corticotropin-releasing factor (CRF), CRF-Receptor 1 (CRF-R1), and the blood-derived high affinity CRF binding protein (CRF-BP). Granulosa cells are devoid of the CRF system. The parallel increases in intensity of CRF, CRF-R1, and 17 alpha-hydroxylase messenger ribonucleic acid (mRNA) and proteins in thecal cells with follicular maturation suggest that the intraovarian CRF system may play an autocrine role regulating androgen biosynthesis, with a downstream effect on estrogen production by granulosa cells. The functionality of the ovarian CRF system may be conditioned by the relative presence of plasma-derived CRF-BP by virtue of its localization of protein, but not transcript in thecal cells and its ability to compete with CRF for the CRF receptor. To further these findings, in the present study we have examined the effect of CRF on LH-stimulated 17 alpha-hydroxylase (P450c17) gene expression and androgen production by isolated thecal cells from human ovarian follicles (11-13 mm). During the 48-h culture, addition of LH (10 ng/mL) to the medium increased by 5- and 6-fold dehydroepiandrosterone and androstenedione production by thecal cells. Remarkably, the LH-stimulated, but not basal, androgen production was inhibited by CRF in a time- and dose-dependent manner. The half-maximal (ID50) effect dose of CRF occurred at 5 x 10(-8) mol/L, and at a maximal concentration of 10(-6) mol/L, CRF completely inhibited LH-stimulated androgen production. This inhibitory effect of CRF became evident at 12 h (45%), and by 24 h the effect was more pronounced, with a 70% reduction from baseline. As determined by Northern analyses, CRF dose dependently decreased LH-stimulated P450c17 mRNA levels, with a maximal inhibition of 85% P450c17 gene expression at a CRF concentration of 10(-6) mol/L. With the addition of 10(-6) mol/L of the antagonist alpha-helical CRF-(9-41), the inhibitory effect of CRF was partially reversed for both P450c17 mRNA (75%) and androgen production (50%), indicating the CRF-R1-mediated event. In conclusion, the present study demonstrated a potent inhibitory effect of CRF on LH-stimulated dehydroepiandrosterone and androstenedione production that appears to be mediated through the reduction of P450c17 gene expression. Thus, the ovarian CRF system may function as autocrine regulators for androgen biosynthesis in the thecal cell compartment to maintain optimal substrate for estrogen biosynthesis by granulosa cells. Further studies to define the role of CRF-BP in the endocrine modulation of the intraovarian CRF system are needed.

Adult↗

Correlations between interleukin-8, and myeloperoxidase or luminol-dependent chemiluminescence in inflamed mucosa of ulcerative colitis.

Interleukin-8 (IL-8) is a peptide which induces not only chemotaxis of neutrophils but also the release of reactive oxygen metabolites from the neutrophils. There are few reports which clarify the relationships between IL-8 and mucosal infiltration of neutrophils or reactive oxygen metabolites produced by neutrophils in the colonic mucosa of ulcerative colitis (UC). Biopsy specimens of colonic mucosa obtained from 26 patients with active UC and 21 patients with inactive UC were studied in order to clarify the relationships among the inflammation factors in UC. Levels of IL-8 and myeloperoxidase in organ culture media of the biopsy specimens from active UC (measured by ELISA and EIA) were significantly higher than those from inactive UC and controls. Reactive oxygen metabolites of biopsy specimens in active UC (measured by luminol-dependent chemiluminescence) were also markedly increased compared to those in inactive UC and controls. The levels of IL-8 were closely correlated to luminol-dependent chemiluminescence or myeloperoxidase levels. However, the levels of IL-8 and myeloperoxidase did not correlate with the grades of activity on colonoendoscopic findings. These findings suggest that IL-8 may play a role in the pathophysiology of UC but it does not define the endoscopic activity grades of UC.

Adolescent↗

The effect of calprotectin on the nucleation and growth of struvite crystals as assayed by light microscopy in real-time.

PURPOSE: To use light microscopy to observe the urease-induced growth of struvite crystals in real-time, and to compare the effects of various proteins on that growth. MATERIALS AND METHODS: Artificial urine, with and without citrate, and a minimal urine solution containing only urea and the components of struvite and apatite were incubated with urease and test proteins in the depressions of culture slides. The number and size of rectangular and X-shaped struvite crystals were recorded using a low-power phase contrast microscope. RESULTS: The formation of crystalline struvite appears to occur after the formation of an amorphous calcium- and magnesium-containing phase. The extent of this amorphous phase is dependent on the presence of calcium and citrate, both of which strongly promote its formation over the crystalline phase. alpha-globulin, gamma-globulin and chymotrypsin inhibitor all result in the same amount of crystalline struvite as bovine serum albumin which is used as a control. Calprotectin, on the other hand, causes consistent and significant reductions in the number and size of struvite crystals under a wide range of conditions. No changes in the morphology of the struvite crystals were observed. CONCLUSIONS: Calprotectin, the dominant protein of infection stone matrix, has distinctive properties which affect the formation and growth of struvite crystals. The presence of citrate in synthetic urine dramatically reduces the number of struvite crystals observed. The present method for observing the effects of putative infection stone inhibitors appears to have merit.

Crystallization↗

Increased plasma levels of free tissue factor pathway inhibitor in patients with Graves' disease.

Tissue factor pathway inhibitor (TFPI) is present in a free-form and in lipoprotein-associated forms in plasma. In this study, the plasma concentrations of total TFPI (tTFPI) and free-form TFPI (fTFPI) were measured in 25 patients with Graves' disease and 25 age-matched healthy subjects, and the relationship between thyroid state and plasma TFPI was examined. Plasma concentrations (median) of tTFPI and fTFPI in Graves' patients who were hyperthyroid were significantly increased compared with Graves' patients who were euthyroid (152 ng/ml versus 124 ng/ml, p < 0.01 and 41.3 ng/ml versus 20.2 ng/ml, p < 0.0001, respectively), and control subjects (152 ng/ml versus 96 ng/ml, p < 0.0001 and 41.3 ng/ml versus 18.7 ng/ml, p < 0.0001, respectively). There was no significant difference in plasma fTFPI concentrations between the euthyroid group and the control group. Plasma fTFPI concentrations correlated closely with thyroid hormone (T3) levels in the patients (r = 0.559, p < 0.005). Serial measurement of individual patients revealed that plasma concentrations of fTFPI and tTFPI were significantly decreased, reaching normal control values upon attainment of euthyroidism. In conclusion, the close correlation between plasma fTFPI and serum thyroid hormone levels suggests that thyroid hormones might influence the synthesis or metabolism of TFPI on the surface of endothelial cells in patients with Graves' disease. This is the first report concerning high concentrations of plasma tTFPI in patients with hyperthyroidism.

Adult↗

CD20-positive T-cell chronic lymphocytic leukaemia.

Although CD20 is considered to be a representative marker for B lymphocytes, the antigen is weakly expressed on a small subset of normal T lymphocytes. A 60-year-old man developed pancytopenia and hepatosplenomegaly due to clonal proliferation of atypical lymphocytes that were weakly positive for CD20. The leukaemic cells were also positive for T-cell antigens such as CD2, CD3, CD5, CD7, CD8 and T-cell receptor (TCR) Vbeta8 and for activation antigens such as CD38 and HLA-DR, but were negative for CD19, CD21, CD22, CD25. Southern blot analysis revealed rearrangement of the TCR-beta gene and a germline configuration of the immunoglobulin heavy chain gene. This is the first report of a case of clonal expansion of CD20dim T lymphocytes.

Antigens, CD20↗

[Ulcerative colitis and intestinal bleeding].

Ulcerative colitis is a nonspecific inflammatory disease of large intestine. Its inflammation is limited to intestinal mucosa. The most essential symptom is hematochezia, bloody stool and intestinal bleeding. Differential diagnosis among diseases having intestinal bleeding is clinically important. These diseases include Crohn disease, ischemic colitis, intestinal Behçet disease, Enterohemorrhagic E. coli including O157, antibiotics associated hemorrhagic colitis and so on. Drugs for the treatment of ulcerative colitis are sulphapyridine, 5-aminosalicylic acid, prednisolone, betamethasone and immunosuppressive drugs. Recently, leukocytapheresis and massive immunoglobulin 7S treatment are available for the treatment of ulcerative colitis.

Anti-Infective Agents↗