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Biomedical subjects

E K Onuma

Publications and source records attributed to E K Onuma.

10 recordsLinked to original sources
PubMed2001

A phenotypic change of small intestinal epithelium to colonocytes in small intestinal adenomas and adenocarcinomas.

OBJECTIVE: Using a novel monoclonal antibody (mAb Das-1) that specifically reacts with colon epithelium, we examined if there is a phenotypic change of small intestinal enterocytes toward colonocytes in small intestinal neoplastic tissue. METHODS: Tissue sections of the small intestine consisting of adenomas (n = 20, five with histories of familial polyposis), adenocarcinomas (eight primary and one metastatic from colon). carcinoids (n = 2), and hyperplastic polyps (n = 3) were examined by a sensitive immunoperoxidase assay using mAb Das-1 (IgM isotype). Normal jejunal (n = 10) and colonic (n = 10) biopsy specimens were also included as additional controls. RESULTS: mAb Das-1 reacted with normal colonic epithelium but not with jejunal mucosa. However, mAb Das-1 reacted strongly with each of the five adenomas (100%) from patients with histories of familial polyposis, but only five of 15 (33%) of the adenomas from nonfamilial polyposis patients, and each of the eight (100%) adenocarcinomas of the small intestine (p < 0.001). The reactivity with the adenomas from nonfamilial polyposis patients was very focal, whereas in the adenomas with familial polyposis the reactivity was more extensive. Each of the eight carcinomas reacted strongly with mAb Das-1. Adjacent normal small intestinal mucosa did not react. Hyperplastic polyps and the carcinoids did not react with mAb Das-1. CONCLUSION: These data demonstrate a phenotypic change in small intestinal epithelium toward the colonic phenotype, particularly in familial polyposis and in adenocarcinomas. mAb Das-1 may be clinically useful in identifying small intestinal adenomas with "high risk" for malignancy, such as in familial polyposis.

Adenocarcinoma↗
PubMed2000

Autoimmunity in ulcerative colitis (UC): a predominant colonic mucosal B cell response against human tropomyosin isoform 5.

We set out to examine if the IgG-producing cells in the colonic mucosa in UC are committed to tropomyosin isoform 5 (hTM5), a putative autoantigen in UC. Lamina propria mononuclear cells (LPMC) were isolated from colonoscopic biopsy specimens from recto-sigmoid and proximal colon. Twenty-three patients with UC, eight with Crohn's colitis (CC), and 10 non-inflammatory bowel disease (non-IBD) controls were included. The ELISPOT assays were used to quantify lamina propria B cells producing total immunoglobulin (IgA, IgG, IgM), IgG, IgA, as well as IgG against hTM5 isoform. The median value of percentage of total IgG-producing lymphocytes was similar in UC (12%) and CC (11%), but was significantly (P < 0.0002) higher than non-IBD controls (6%). However, in UC, but not in CC and non-IBD, a large number of lamina propria B cells produced IgG against hTM5 (median values: UC 42%, CC 2.5%, non-IBD 0%). This difference in UC when compared with CC and non-IBD was highly significant (P < 0.00001). Twenty-one of 23 (91%) patients with UC had percentage of anti-hTM5 IgG-producing immunocytes more than 2 s. d. above the mean for non-UC patients. In UC but not in CC and non-IBD controls, the increased number of IgG-producing cells are largely committed to produce IgG against hTM5-related epitope(s).

Adult↗
PubMed2000

Long-term follow-up after treatment of Mirizzi syndrome by peroral cholangioscopy.

BACKGROUND: The standard treatment for Mirizzi syndrome is surgical, although endoscopic and percutaneous management have also been described. The aim of this study was to evaluate the usefulness of shock wave lithotripsy combined with peroral cholangioscopy and its long-term outcome in patients with Mirizzi syndrome. METHODS: The records of 25 patients with Mirizzi syndrome who underwent endoscopic treatment between April 1990 and November 1998 were retrospectively reviewed. Shock wave lithotripsy was performed under direct vision with a "mother-baby" endoscope system in 2 patients with type I and 23 with type II Mirizzi syndrome (12 men and 13 women, mean age 60 years). Follow-up data were obtained from clinical records or through telephone interviews. RESULTS: In the two patients with type I, the cholangioscopic approach failed and both patients underwent open cholecystectomy. The 23 patients with type II were all successfully treated with shock wave lithotripsy alone. The cholangioscopic approach was unsuccessful in the treatment of residual gallbladder stones. Follow-up data were obtained in all but one patient (mean 43.6 months, range 4 to 103 months). Of the 23 patients with type II, 12 with no gallbladder stones had remained asymptomatic during the follow-up period. Of the 6 patients with type II with large residual gallbladder stones, 4 had acute cholangitis due to stone migration 6, 9, 28, and 34 months after endoscopic treatment. Two patients died during the follow-up period, one of non-biliary causes and the other of coexistent gallbladder carcinoma. CONCLUSIONS: Endoscopic treatment of Mirizzi syndrome using peroral cholangioscopy is a safe and effective alternative to surgery, especially in patients with the type II syndrome. A favorable long-term outcome depends on the absence of large residual gallbladder stones.

Adult↗
PubMed1998

[Barrett's esophagus].

Barrett's esophagus (BE) has recently gained the interest of Japanese physicians. In BE, the squamous epithelium of the distal esophagus is replaced by metaplastic columnar epithelium. This intestinal metaplasia usually occurs as a complication of severe reflux esophagitis and its association with adenocarcinoma of the esophagus is well established. In 1950 Norman Barrett described a tubular, intrathoracic structure that appeared to be the esophagus, except that the distal portion was lined with columnar epithelium. Although he believed that the distal portion was not the esophagus, the condition in which the distal esophagus is lined with columnar epithelium became known as BE. From animal and clinical studies, the intestinal metaplasia is generally believed to arise from multipotential stem cells located in the basal layer of the squamous epithelium and at the base of the glandular epithelium. Evidence for a genetic basis underlying the dysplasia-adenocarcinoma sequence is now being accumulated. It is known that gastric acid reflux as well as bile reflux can cause distal esophagitis. Therefore, treatment with a proton pump inhibitor alone may not be sufficient therapy for all patients. Antireflux surgery can cause regression of BE in up to 50% of patients. Overall 1-, 2-, and 5-year survival rates for patients with adenocarcinoma arising from BE after surgical resection is reported to be 63%, 41%, and 32%, respectively. Therefore, endoscopic surveillance of patients with BE is suggested.

Animals↗
PubMed1988

Electric field-directed cell shape changes, displacement, and cytoskeletal reorganization are calcium dependent.

C3H/10T1/2 mouse embryo fibroblasts were stimulated by a steady electric field ranging up to 10 V/cm. Some cells elongated and aligned perpendicular to the field direction. A preferential positional shift toward the cathode was observed which was inhibited by the calcium channel blocker D-600 and the calmodulin antagonist trifluoperazine. Rhodaminephalloidin labeling of actin filaments revealed a field-induced disorganization of the stress fiber pattern, which was reduced when stimulation was conducted in calcium-depleted buffer or in buffer containing calcium antagonist CoCl2, calcium channel blocker D-600, or calmodulin antagonist trifluoperazine. Treatment with calcium ionophore A23187 had similar effects, except that the presence of D-600 did not reduce the stress fiber disruption. The calcium-sensitive photoprotein aequorin was used to monitor changes in intracellular-free calcium. Electric stimulation caused an increase of calcium to the micromolar range. This increase was inhibited by calcium-depleted buffer or by CoCl2, and was reduced by D-600. A calcium-dependent mechanism is proposed to explain the observed field-directed cell shape changes, preferential orientation, and displacement.

Actin Cytoskeleton↗
PubMed1985

A calcium requirement for electric field-induced cell shape changes and preferential orientation.

C3H/10T1/2 mouse embryo fibroblasts stimulated by a steady electric field (10 V/cm) for 30 min exhibited lamellar retraction on the sides facing the electrodes. Some cells elongated and preferentially oriented with their long axis perpendicular to the field direction. Depletion of external calcium or blockage of calcium influx with lanthanum or the calcium channel blocker D-600 resulted in a reduction of the field-induced response. When external calcium was elevated stepwise from 0 to 10 mM, the field-induced response increased correspondingly. Electric stimulation in the presence of the calcium ionophore A23187 resulted in an increase of spindle-shaped cells with no preferential orientation. This response was blocked by calcium depletion and lanthanum, but not by D-600. The anticalmodulin drug W-13 inhibited the field-induced responses observed in normal buffer as well as in the presence of A23187. Some cell death resulted from prolonged electric field exposure, and the mortality was reduced by calcium depletion, lanthanum or D-600, but was not affected by W-13. We postulate that local calcium influx through channels opened by the electric field produces areas of high intracellular calcium which stimulate the cytoskeletal network to induce lamellar retraction. Prolonged field-induced calcium influx may eventually overcome the cell's mitochondrial calcium-buffer system, leading to necrotic calcification.

Animals↗
PubMed1984

Response of C3H/10T1/2 fibroblasts to an external steady electric field stimulation. Reorientation, shape change, ConA receptor and intramembranous particle distribution and cytoskeleton reorganization.

C3H/10T1/2 mouse embryo fibroblasts were stimulated by a steady electric field ranging up to 15 V/cm. The percentage of spindle-shaped cells increased with the field strength and duration of the stimulation. These cells oriented preferentially with their long axis perpendicular to the field direction. A small percentage of the cells were found to move slightly toward the cathode during the course of electric stimulation. Although no apparent field-induced redistribution of fluorescent-labelled concanavalin A (conA) receptor along the cell periphery was observed, the bright perinuclear area appeared preferentially on the anode side. Correlative fluorescence and scanning electron microscopy (SEM) revealed no difference in the density of conA-gold microsphere labels on either side of the cell. The density of intramembranous particles on the E-face of the plasma membrane was 54% higher on the anode side than on the cathode side of the cell. The microfilament bundles were observed to be disrupted after 30 min of 10 V/cm stimulation by rhodamine phalloidin labelling of F-actin. The cell sensitivity to electric field-induced reorientation and cell shape changes was reduced by pretreatment with conA, and to a lesser extent, with succinyl conA or wheat germ agglutinin (WGA). ConA pretreatment alone also reduced the prominence of microfilament bundles. However, post-field lectin binding to the cell has no effect on cell recovery. It is possible that the generally flat 10T1/2 cells retract and realign in order to minimize the disruption of their membrane potential. The conA binding-mediated receptor-cytoskeletal linkage temporarily immobilizes the cell and inhibits subsequent field-induced shape changes.

Actins↗