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Biomedical subjects

Y Fujiyama

Publications and source records attributed to Y Fujiyama.

At least 19 recordsLinked to original sources
PubMed1999

Increased growth of Bifidobacterium and Eubacterium by germinated barley foodstuff, accompanied by enhanced butyrate production in healthy volunteers.

Germinated barley foodstuff (GBF) derived from the aleurone and scutellum fractions of germinated barley mainly consists of low-lignified hemicellulose and glutamine-rich protein. GBF improves the proliferation of intestinal epithelial cells and defecation, through the bacterial production of short chain fatty acids (SCFA), especially butyrate. In this study we investigated the mechanism of production of butyrate by microflora in humans and in vitro. Daily administration of 9 g GBF for 14 successive days significantly increased fecal butyrate content. Fecal Bifidobacterium and Eubacterium were also significantly increased by GBF administration in healthy volunteers. Ten anaerobic micro-organisms selected from intestinal microflora were cultured in vitro in the medium containing GBF as a sole carbon source (GBF medium). After a 3-day incubation, 7 strains (Bifidobacterium breve, Bifidobacterium longum, Lactobacillus acidophilus, Lactobacillus casei subsp. casei, Bacteroides ovatus, Clostridium butyricum, and Eubacterium limosum) lowered the medium pH producing SCFA. Eubacterium grown together with Bifidobacterium in GBF medium efficiently produced butyrate. On the other hand, GBF changed the intestinal microflora and increased probiotics such as Bifidobacterium in the intestinal tract. As a result, butyrate was produced by the mutual action of Eubacterium and Bifidobacterium. This butyrate is considered to enhance the proliferation of colonic epithelial cells.

Adult↗
PubMed1998

Contribution of two missense mutations (G71R and Y486D) of the bilirubin UDP glycosyltransferase (UGT1A1) gene to phenotypes of Gilbert's syndrome and Crigler-Najjar syndrome type II.

In our mutation analyses of bilirubin UDP glycosyltransferase (UGT1A1) gene, we encountered six patients with Crigler-Najjar syndrome type II who were double homozygotes for G71R and Y486D, a patient with Gilbert's syndrome who was a single homozygote for G71R and six patients with Gilbert's syndrome who were single heterozygote for G71R. To clarify the role of each mutation in the occurrence of the two syndromes, we made four mutant expression models. Relative UGT1A1 activity of a single homozygous model of G71R was 32.2+/-1.6% of normal, that of a single homozygous model of Y486D was 7.6+/-0.5%, that of a double homozygous model of G71R and Y486D was 6.2+/-1.6% and that of a heterozygous model of G71R was 60.2+/-3.5%. The decreased activities of the single homozygous model of G71R and the double homozygous model were at an appropriate level to be diagnosed as Gilbert's syndrome and CN-II, respectively. The activity of a single heterozygous model of G71R was somewhat high to develop to the phenotype of Gilbert's syndrome, suggesting the presence of additional factors for the etiology of Gilbert's syndrome.

Animals↗
PubMed1998

Aggressive jejunal gamma deltaT-cell lymphoma derived from intraepithelial lymphocytes: an autopsy case report.

A 69-year-old man with massive ascites was referred to our hospital. Paracentesis revealed exudative ascites with many abnormal lymphocytes, which expressed T-natural killer (T-NK) cell surface markers and gamma deltaT-cell receptor (TCR). Although the ascites resolved for a short time with chemotherapy, gastrointestinal bleeding occurred and acute retention of ascites was observed. The patient died of panperitonitis. At autopsy, part of the jejunum revealed ulceration and marked mucosal thickening, and was perforated at the site of the severe ulceration. Histological examination showed massive infiltration of abnormal lymphocytes that were positive for CD45RO. Therefore, the cells responsible for the jejunal lymphoma and ascites were thought to be derived from gamma deltaIEL.

Aged↗
PubMed1998

Primary gastric Burkitt's lymphoma presenting with c-myc gene rearrangement.

A 54-year-old man with primary gastric Burkitt's lymphoma is described. He was evaluated for appetite loss and intermittent midepigastric pain. Upper gastroduodenal endoscopy detected an ulcer in the lesser curvature of the body, and biopsy specimens revealed infiltration of medium-sized lymphoblasts with "starry sky" macrophages. The infiltrated cells were positive for a B-cell marker. Abdominal computed tomography scan demonstrated marked enlargement of the gastric wall, but no enlargement of lymph nodes. These findings led us to diagnose primary gastric Burkitt's lymphoma. The patient responded dramatically to CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy, but 6 months after his initial admission, the disease recurred in the stomach and bone marrow. Lymphoblastic cells were positive for B-cell markers (CD 10, 19, 20, and human leukocyte antigen [HLA]-DR) and showed an abnormal karyotype, 47, XY, t(8;14)(q24;q32), +12. In these cells, the Epstein-Barr virus genome was detected by polymerase chain reaction. Southern blot analysis revealed rearrangement of Ig heavy and light chain genes. In addition, c-myc gene rearrangement was detected. Eight months after the beginning of chemotherapy, the patient died of central nervous system involvement. To our knowledge, this is the first description of a genetic analysis of primary gastric Burkitt's lymphoma.

Blotting, Southern↗
PubMed1998

Analysis of bilirubin uridine 5'-diphosphate (UDP)-glucuronosyltransferase gene mutations in seven patients with Crigler-Najjar syndrome type II.

Crigler-Najjar syndrome (CN) type II is caused by a reduction in hepatic bilirubin uridine 5'-diphosphate (UDP)-glucuronosyltransferase activity. Recently, there has been progress in mutation analysis of patients with CN type II. Here, we analyzed both the coding and the promoter regions of the gene in seven Japanese patients with CN type II from five unrelated families. The mutations found in this study were classified into three types. The first type was composed of double homozygous missense mutations (Gly71Arg and Tyr486Asp) in exons 1 and 5. These mutations, which were detected in five patients from three unrelated families, were the commonest. The second type, which was detected in one patient, consisted of a single homozygous missense mutation (Arg209Trp) in exon 1. The third type, which was detected in one patient and was a new type of mutation combination, was composed of a homozygous insertion mutation of the TATAA element and a heterozygous missense mutation (Pro229Gln) in exon 1. Although the first and the second type of mutations are recessive, the third type appears to be dominant with incomplete penetrance, since the allele frequency of the insertion mutation of the TATAA element is very high (40%).

Adult↗
PubMed1998

Detection of complement C3 and factor B gene expression in normal colorectal mucosa, adenomas and carcinomas.

Local secretion of complement components in the human intestine has been previously reported. However, the cellular source has not been identified. In this study, we demonstrate complement C3 and factor B mRNA expression in the normal colonic mucosa by in situ hybridization analysis. C3 and factor B genes were found to be expressed at high levels in the epithelial cells of the lower parts of the crypts in colonic mucosa, and this expression decreased gradually from the crypt base to the luminal surface. At the upper crypt and the luminal surface, these genes almost disappeared. C3 and factor B genes were expressed in all crypts at the same level. Furthermore, C3 and factor B gene expression was also identified in adenomas and carcinomas. In these neoplastic tissues, C3 and factor B genes were expressed uniformly, and the polarized distribution observed in the normal crypts was not detected. It is likely that complement components are locally synthesized in the intestine, and that these complement components may actively participate in normal immune and inflammatory responses over the enormous surface area of the intestinal mucosa.

Adenoma↗
PubMed1998

A blockade of complement activation prevents rapid intestinal ischaemia-reperfusion injury by modulating mucosal mast cell degranulation in rats.

We attempted to define the putative role of complement activation in association with mucosal mast cell (MMC) degranulation in the pathogenesis of rapid intestinal ischaemia-reperfusion (I/R) injury. We prepared complement activity-depleted rats by the administration of the anti-complement agent K-76COOH and the serine-protease inhibitor FUT-175. Autoperfused segments of the jejunum were exposed to 60 min of ischaemia, followed by reperfusion for various time periods, and the epithelial permeability was assessed by the 51Cr-EDTA clearance rate. The number of MMC was immunohistochemically assessed. In control rats, the maximal increase in mucosal permeability was achieved by 30-45 min of reperfusion. This increase was significantly attenuated by the administration of either K-76COONa alone or in combination with FUT-175. In contrast, the administration of carboxypeptidase inhibitor (CPI), which prevents the inactivation of complement-derived anaphylatoxins such as C5a, significantly enhanced the increase in I/R-induced mucosal permeability. These findings were confirmed morphologically by light microscopy and scanning electron microscopy. In addition, the I/R-induced mucosal injury was accompanied by a marked decrease in the number of MMC, and administration of K-76COOH significantly inhibited this change. These results indicate that complement activation and the generation of complement-derived anaphylatoxins are key events in I/R-induced mucosal injury. It is likely that intestinal I/R-induced mucosal injury may be partially mediated by MMC activation associated with the complement activation.

Anaphylatoxins↗
PubMed1998

Macrolipasemia in Crohn's disease.

A 38-year-old male patient who had been treated for Crohn's disease was found to have serum lipase activity that was persistently increased approximately 10-fold above the normal upper limit. He was diagnosed with chronic pancreatitis based on slightly elevated elastase-1 level and retrograde pancreatography showing slight dilatation of the main pancreatic duct. Therefore, the hyperlipasemia was thought to be due to pancreatitis. However, the serum amylase and trypsin was not increased at any time, and no serious findings suggestive of pancreatitis were detected on morphologic examination. Thus, there were discrepancies between the serum lipase activity and other laboratory and clinical findings. Exclusion chromatography of the patient's serum suggested macromolecular lipase, and further immunologic testing including affinity chromatography, enzyme-linked immunosorbent assay, and immunoprecipitation assay showed that serum lipase was bound to immunoglobulin Gkappa. Therefore, the hyperlipasemia was caused by immunoglobulin-linked lipase, termed "macrolipasemia." Macrolipasemia has rarely been reported, and this is the first reported case of macrolipasemia accompanied by Crohn's disease.

Adult↗
PubMed1998

Proliferative effect of phospholipase A2 on rat periacinar fibroblastoid cells of the pancreas.

We have shown previously that rat pancreatic periacinar fibroblastoid cells (PFCs) can be cultured from isolated pancreatic acini. In the present study, immunocytochemical examination of the PFC extracellular matrix was performed using antibodies against prolyl hydroxylase alpha and beta subunits, types I, III, and IV collagen, fibronectin, and laminin. The PFC content of alpha-smooth muscle actin and platelet-derived growth factor (PDGF) receptor were studied by immunoblotting. We demonstrated that PFCs synthesized extracellular matrix and expressed alpha-smooth muscle actin and PDGF receptors. These results suggested that PFCs resemble myofibroblasts and may play a critical role in pancreatic fibrosis. Conversely, pancreatic-type phospholipase A2 (P-PLA2), one of the pancreatic digestive enzymes, has been shown to induce DNA synthesis of Swiss 3T3 fibroblasts. To determine whether this enzyme is involved in pancreatic fibrosis, we studied P-PLA2's proliferative and chemotactic effects on PFCs as well as its digestive activity. The proliferative and chemotactic effects were investigated using 3H-thymidine incorporation and a chemotactic assay, respectively. P-PLA2 had both proliferative and chemotactic effects. P-PLA2 is considered a growth factor for PFCs and is implicated in pancreatic fibrosis.

Actins↗
PubMed1998

Case report: Haemangioma of the small intestine complicated by protein-losing gastroenteropathy.

We report a case of haemangioma of the small intestine complicated by protein-losing gastroenteropathy. A 32-year-old female had suffered from hypoproteinaemia for 6 years, but the cause of this condition had not been determined. On diagnosis and therapy for hypoproteinaemia, intra-operative endoscopy and histological examination were performed and she was subsequently diagnosed with capillary haemangioma of the small intestine. Angiography was not useful for the detection of capillary haemangioma of the small intestine in this case. Although intestinal haemangioma is an important cause of gastrointestinal bleeding, protein loss is an extremely rare complication and this case is the first to be reported in Japan.

Adult↗
PubMed1998

Germinated barley foodstuff increases fecal volume and butyrate production at relatively low doses and relieves constipation in humans.

Germinated barley foodstuff (GBF), derived from the aleurone layer, scutellum and germ of germinated barley, contains a large quantity of fermentable dietary fibers, especially hemicellulose. GBF was given to 9 healthy volunteers in a dose of 9 g of GBF per day for 10 consecutive days, and subsequently 18 g of GBF for another 10 days. As a control, no GBF was given for 3 days before administration of GBF (control period). Fecal weight, water content and short chain fatty acid content were measured before and during the last 3 days of each experimental period. Feeding of GBF significantly increased the fecal butyrate content as well as fecal weight at both dose-levels (9 and 18 g/day), compared with those during the control period. Daily administration of 9 g GBF induced the maximum level of defecation in humans. Relatively mild but chronic constipated volunteers (n = 16) were administered 9 g of GBF daily for 14 days. In this experiment, the condition of defecation (frequency, volume) was estimated by a questionnaire survey. GBF significantly improved defecation within a short period without severe adverse effects. No major abnormalities in laboratory findings were found in hematologic and urinary analyses. In conclusion, daily administration of 9 g GBF was effective for improving defecation in healthy but constipated humans. GBF is a highly safe and effective foodstuff for improving defecation.

Adult↗
PubMed1998

[A case of hepatocellular carcinoma with reduction of primary tumor and disappearance of multiple lung metastasis].

A 56-year-old male had suffered from hepatocellular carcinoma treated by operation, PHoT and TAE since 1994. In December 1995, he had multiple metastases of lung in addition to recurrence of primary hepatic lesions. We discontinued treatment of TAE and decided to administer UFT (400 mg/day) orally as an outpatient. After seven months, the primary hepatic lesions were decreased in size, and metastatic lesions of lung were completely eliminated with reduction of AFP level. Generally, hepatocellular carcinoma with metastasis is refractory to treatment. However, this result suggests that UFT is one of the effective treatments for such advanced cases as having lung metastasis.

Administration, Oral↗
PubMed1998

The role of mucosal mast cell degranulation and free-radical generation in intestinal ischaemia-reperfusion injury in rats.

OBJECTIVES: In this study, we determined the role of mucosal mast cell (MMC) activation in the pathogenesis of intestinal ischaemia-reperfusion (I/R) injury by immunohistochemical analysis using anti-RMCP II antibody. In addition, we investigated the role of free-radical generation in the activation of MMCs in this model. METHODS: In the first experiment, rats were divided into four groups: (1) sham operated; (2) I/R + saline; (3) I/R + the mast cell stabilizer, MAR-99 (30 mg/kg); and (4) I/R + MAR-99 (100 mg/kg). Treatment with MAR-99 was started 1 h before the occlusion of the superior mesenteric artery (SMA). In the second experiment, rats were divided into five groups: (1) sham operated; (2) I/R + saline; (3) I/R + superoxide dismutase (SOD; 50,000 U/ml); (4) I/R + catalase (90,000 U/ml); and (5) I/R + allopurinol (50 mg/kg/day). Intravenous administration of SOD and catalase was performed 1 h before SMA occlusion. Oral administration of allopurinol was started 2 days before I/R surgery. We measured several parameters of intestinal mucosal injury and evaluated the degranulation of MMCs by using an immunohistochemical technique. RESULTS: The number of resting MMCs, detected by anti-RMCP II antibody, was significantly decreased in the I/R-treated rats. The I/R treatment induced a decrease in the mucosal histamine content and an increase in plasma histamine levels. Mucosal permeability in the small intestine was significantly enhanced by I/R treatment. However, these changes were significantly prevented by pretreatment with the MMC stabilizer, MAR-99. Furthermore, administration of several free-radicals scavengers (SOD, catalase, and allopurinol) also blocked the I/R-induced degranulation of MMCs. CONCLUSION: These data indicate that activation of MMCs was involved in the pathogenesis of I/R-induced intestinal mucosal injury. In addition, some parts of the I/R-induced MMC activation pathway were mediated by free-radical generation.

Animals↗
PubMed1998

[Effective pentostatin-based treatment of adult T cell leukemia in a patient with severe arthritis].

We report a 48-year-old woman with adult T-cell leukemia who had refractory arthralgia, intense headaches, and fever. Leukemic cell infiltration of the cerebrospinal fluid was detected but no other acute signs were observed. Abnormal lymphocytes with lobulated nuclei were found in the synovial fluid, and a histologic examination revealed proliferation into the synovium. Because combination chemotherapy did not elicit a favorable response, the patient was treated with a pentostatin bolus injection. The articular symptoms disappeared and complete remission was obtained. Six months later, she experienced arthralgia again together with a gradual increase of abnormal lymphocytes in peripheral blood. Sixteen months later, the patient was given pentostatin and achieved a complete remission again. She is still free from relapse without further therapy after 36 months, and her articular symptoms have not returned either. There were no adverse effects due to pentostatin. The patient's serum IL-6 level was elevated, suggesting that IL-6 may play a role in arthropathy.

Antibiotics, Antineoplastic↗
PubMed1997

Acute lupus peritonitis successfully treated with steroid pulse therapy.

A 21-year-old man with systemic lupus erythematosus (SLE) who developed acute lupus peritonitis is described. Acute lupus peritonitis appeared during generalized lupus flare, with nausea, vomiting, frequent diarrhea, and abdominal tenderness with rebound and guarding. The patient was afebrile and had decreased bowel sounds. Abdominal ultrasonography and computed tomography revealed marked thickening of the gastric, duodenal, and jejunal walls, massive intraluminal fluid collection, and increasing ascites. Gastrointestinal endoscopy showed edematous mucosa with multiple erosions of the stomach and duodenum. The ascitic fluid was remarkable for low complement levels and elevated anti-DNA antibody. These manifestations of acute lupus peritonitis resolved after steroid pulse therapy with methylprednisolone. We should consider acute lupus peritonitis in a patient with SLE when abdominal symptoms are severe. Experience with our patient indicates that steroid pulse therapy is effective for this rare but severe manifestation of SLE.

Acute Disease↗
PubMed1997

Trophic effects of glicentin on rat small-intestinal mucosa in vivo and in vitro.

To define the role of glicentin the active site of enteroglucagon, we evaluated the trophic effects of recombinant rat glicentin on rat small intestine and IEC-6 cells. In vivo, a significant increase was observed in jejunal wet weight, protein content, DNA content, and alkaline phosphatase activity after the subcutaneous administration of 100 micrograms/kg per day of glicentin for 2 weeks. In the ileum, however, there were no significant differences between the control versus glicentin groups in any of these parameters. Ornithine decarboxylase (ODC) activity 3.5 h after an intraperitoneal injection of glicentin was increased in the jejunal mucosa, but not in the ileal mucosa. In vitro, glicentin, at a dose of more than 100 ng/ml, significantly increased both tritium-thymidine incorporation and the number of IEC-6 cells. These findings indicate that glicentin exerts direct trophic effects on the rat small-intestinal mucosa and on the rat small-intestinal cell line, IEC-6, and that this peptide appears to be an active site of enteroglucagon.

Alkaline Phosphatase↗