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Biomedical subjects

O Masamune

Publications and source records attributed to O Masamune.

At least 37 records · Page 2Linked to original sources
PubMed1998

Anterior abdominal wall pathologies detected by high-frequency annular array.

AIM AND METHODS: In 1850 patients, high-frequency (HF: 7.5-10 MHz) annular array US examination was performed to evaluate the value of HF annular US in the detection of pathologies of the anterior abdominal wall. RESULTS: HF annular US revealed pathological lesions (metastasis, benign tumor, lymphoma, hematoma, fistula, hernia, abscess) in 37 patients. The lesions were detected by conventional medium-frequency (3.5-3.75 MHz) US in only 8 of 37 cases (21.6%). HF annular US added information that altered clinical management in 19 cases (51.4%), predominantly in cases with tumors and fistulas. CONCLUSION: The addition of HF annular US to a conventional US examination increases the detectability of small, but clinically important pathologies in the anterior abdominal wall.

Abdominal Muscles↗
PubMed1998

Portal vein thrombosis associated with antiphospholipid syndrome: a case report.

We present a case of portal vein thrombosis associated with antiphospholipid syndrome (APS). The patient had an end-stage renal disease and underwent hemodialysis, and a portal thrombus was incidentally found in the main portal vein by color Doppler sonography. The patient is followed up now with long-term anticoagulant therapy. This experience suggests that color Doppler sonography be performed for patients with APS to improve their management.

Antiphospholipid Syndrome↗
PubMed1998

Sonographic findings of malignant fibrous histiocytoma of the mesentery-report of two cases.

We present two cases of malignant fibrous histiocytoma (MFH) of the mesentery. A whorled internal structure observed on sonogram and large feeding and draining vessels demonstrated on color Doppler sonogram in these cases were worth noticing. When sonography reveals an abdominal tumor with such findings, although very rare, the possibility of a MFH of the mesentery must be considered. We also review briefly the literature.

Histiocytoma, Benign Fibrous↗
PubMed1998

Effect of preinduction of heat-shock proteins on acetic acid-induced small intestinal lesions in rats.

Bowel dysfunction such as irritable bowel syndrome caused by stress is well described. Previous reports suggest that stress is known to cause the release of endogenous substances such as catecholamine, beta-endorphine, 5-hydroxytryptamine, corticotropin-releasing factor, and thyrotropin-releasing hormone (TRH). However, the role played by these neurohormonal mediators in bowel dysfunction under stress conditions is not well known. We investigated the influence of water-immersion stress or TRH administration on the expression of 60-kDa, 72-kDa, and 90-kDa heat-shock proteins (HSP60, HSP72, and HSP90, respectively) in rat small intestinal mucosa by Western blot and immunohistochemical analyses. The cytoprotective function of preinduced HSPs on experimentally induced mucosal damage also was studied. In order to investigate the influence of preinduction of HSP60 on small intestinal damage, the small intestinal lumen was perfused with 1.5% acetic acid 1 ml/min for 15 min with or without pretreatment with water-immersion stress or TRH administration. Expression of HSP60 was significantly increased by water-immersion stress or TRH administration in the small intestinal mucosa, whereas HSP72 and HSP90 did not increase. Interestingly, expression of this protein showed the biphasic peak pattern after water-immersion stress or TRH administration. Each peak was observed 3-6 hr and 21-24 hr after the initiation of water-immersion stress or TRH administration. Immunohistochemical study also showed a significant increment of HSP60 in both the cytoplasm and nuclei of the small intestinal mucosal cells. No histopathologic alteration was observed in rat small intestinal mucosa after each treatment. Small intestinal damage caused by 1.5% acetic acid perfusion was not influenced by preinduction of HSP60. We demonstrated that water-immersion stress or TRH administration specifically induced HSP60, although preinduction of this protein did not show a cytoprotective function in the small intestinal mucosa.

Acetic Acid↗
PubMed1998

Listeria monocytogenes in Crohn's disease.

BACKGROUND: In an immunohistochemical study a higher rate of reactivity of intestinal tissues to the antibody against Listeria monocytogenes was reported in Crohn's disease as compared with controls. METHODS: Seventy-six intestinal tissues, either therapeutically resected or biopsied, from 31 patients with Crohn's disease, 20 with ulcerative colitis, and 21 with non-inflammatory bowel disease were studied. DNA extracted from intestinal tissues by proteinase K treatment was used for nested polymerase chain reaction (PCR), using two sets of primers. PCR products were analyzed with agarose gel electrophoresis and subsequent Southern blot analysis. RESULTS: Our amplification system could detect 9 pg of L. monocytogenes DNA. L. monocytogenes was detected in only one sample, that from a patient with ulcerative colitis. CONCLUSIONS: Our study does not support the etiologic significance of L. monocytogenes in Crohn's disease.

Adult↗
PubMed1998

Listeria monocytogenes in the colon in a case of fulminant ulcerative colitis.

A case of ulcerative colitis in which the presence of Listeria monocytogenes was confirmed in the resected colon with polymerase chain reaction and subsequent Southern blot analysis and immunohistochemistry using antibody against Listeria is presented. The patient developed ulcerative colitis at the age of 59 years. Prednisolone, 50 mg/day, was given for severe ulcerative colitis. Later the disease became fulminating, indicating colectomy 4 months after the onset. Multiple sealed colonic perforations were observed. Numerous L. monocytogenes were found at the site of perforation, in fissures, and in cracks in the submucosa. This case indicates the possibility that L. monocytogenes contributes to the exacerbation of colitis to fulminating and colonic perforation.

Colectomy↗
PubMed1998

Portal-systemic encephalopathy from a spontaneous gastrorenal shunt diagnosed by three-dimensional computed tomography and treated effectively by percutaneous vascular embolization.

A 67-year-old man with a portal-systemic shunt confirmed by three-dimensional computed tomography (3D-CT) was successfully treated by percutaneous vascular embolization. The patient had aggravated loss of memory, disorientation, and hyperammonemia. A gastrorenal shunt 16 mm in diameter was found by 3D-CT reconstructed by helical computed tomography (CT). Embolization was performed only in the shunt percutaneously through the inferior vena cava. One year after the embolization, no recurrence of portal-systemic encephalopathy and no portal hypertension have appeared, and the clinical course has been good.

Aged↗
PubMed1998

Induction of major histocompatibility complex class II antigens on human colonic epithelium by interferon-gamma, tumor necrosis factor-alpha, and interleukin-2.

Class II antigens are strongly expressed on the inflamed colonic epithelium in inflammatory bowel disease. However, the mechanism of this epithelial class II antigen induction is not fully understood. Increased activities of interferon (IFN)gamma, tumor necrosis factor (TNF)alpha, and interleukin (IL)2 have been shown in the inflamed mucosa of inflammatory bowel disease. Therefore, we studied whether these cytokines could induce class II antigens on the human colonic epithelium. By an organ culture technique, 284 normal colonic biopsy specimens obtained from 49 individuals were cultured in media containing different concentrations of cytokines with/without anti-IFNgamma R antibody. Colonic epithelial class II antigens were identified by the indirect immunoperoxidase staining method with anti-human leukocyte antigen (HLA)-DR, DP, and DQ monoclonal antibodies. IFNgamma, TNFalpha, and IL2 induced epithelial class II antigens in 16 of 16 cases (100%), 2 of 16 cases (12.5%), and 6 of 17 cases (35%), respectively. Epithelial class II antigen expression in response to TNFalpha was induced via IFNgamma but not via IL2. This is the first demonstration that: (i) the induction of class II antigens on the colonic epithelium in response to TNFalpha is mediated via IFNgamma, and (ii) that IL2 induces class II antigens.

Epithelial Cells↗
PubMed1998

[Muscle atrophy in isolated ACTH deficiency].

We analyzed muscle area in CT and muscle pathology in a patient with isolated ACTH deficiency who started with the difficulty of elevation of both arms. Cortisol treatment resulted in full recovery from severe muscle atrophy and contracture of major joints. Change of volume of major muscles in arm, thigh and calf was followed. Major muscles were identified in CT and the area of each muscle was calculated with computer assistance. The increase of total muscle area in sequential 3 times in CT was up to 74% after prednisolone treatment. This indicates that the deficiency of cortisol resulted in 42% reduction of muscle volume. This also suggests that reduction of muscle volume induces the limitation of range of motion of shoulder joint. ATPase of muscle biopsy revealed the influence on fiber type proportion; type 1 : type 2A : type 2B = 29.6 : 6.0 : 64.4% and 35.7 : 17.6 : 46.7% in pre-treatment and post-treatment of cortisol, respectively. Mean diameters of muscle fibers in type 1, type 2A and type 2B was 41.8, 41.8, 39.1 microns and 46.2, 44.0, 37.2 microns in pre-treatment and post-treatment of cortisol, respectively. These suggest that deficiency of glucocorticoid introduces the reduction of the activity of the motor neurons innervating type 1 and type 2A muscle fibers.

Adrenocorticotropic Hormone↗
PubMed1997

Effect of pre-induction of heat shock proteins on indomethacin-induced small-intestinal lesion in rats.

Systemic hyperthermia induces the synthesis of heat shock proteins (HSPs) in several organs. However, the mechanism of induction and the functions of HSPs in the small-intestinal mucosa have not been established. We examined the expression of HSPs in the small-intestinal mucosa after systemic hyperthermia, and evaluated the cytoprotective function of pre-induced HSPs on experimentally induced mucosal damage. HSP expression was investigated by Western blot and densitometric analysis before and after hyperthermia (42.5 degrees C; 20 min). Expression of a 72-kDa heat shock protein (HSP72) and a 73-kDa heat shock protein (HSP73), both of which are endogenous cytoprotectants in vitro significantly increased, peaking 6-9 h after hyperthermia, without any pathologic alterations, whereas the expression of a 60-kDa heat shock protein (HSP60) did not increase. To investigate the influence of pre-induction of HSPs on small-intestinal damage, rats received indomethacin (10 mg/kg; orally) with or without pre-treatment with hyperthermia. Small-intestinal damage caused by indomethacin was not influenced by pre-induction of HSP72 and HSP73. We demonstrated that systemic hyperthermia induced HSP72 and HSP73, although pre-induction of these proteins did not have a cytoprotective function in the small-intestinal damage caused by indomethacin.

Animals↗
PubMed1997

Crohn's disease associated with renal amyloidosis successfully treated with an elemental diet.

We report a case of Crohn's disease associated with nephrotic syndrome due to renal amyloidosis in a 21-year-old man in whom remission of both Crohn's disease and the nephrotic syndrome has been maintained with an elemental diet. The patient developed toxic megacolon and nephrotic syndrome due to renal amyloidosis. Intensive intravenous prednisolone therapy with total parenteral nutrition was dramatically effective in treating the toxic megacolon and inducing remission in Crohn's disease and afterward, remission of the nephrotic syndrome. Remission of both conditions has been maintained for more than 2 years with the elemental diet. To our knowledge, this is the first confirmed case of Crohn's disease complicated with renal amyloidosis in which only slight proteinuria (below 0.3 g/day) was shown with an elemental diet used for a long period.

Adult↗
PubMed1997

Three cases of familial ulcerative colitis--in a mother and two of her sons.

A pedigree of familial ulcerative colitis with their HLA haplotypes is reported. The mother and two children, the eldest and second of three sons were affected. The mother developed proctitis at age 35, and the lesion extended to the entire colon at the time of a relapse. The two sons developed ulcerative colitis in a similar fashion; total colitis, of moderate severity, developing at age 16 in both. The analysis of HLA haplotypes of all five family members suggested that the HLA responsible for ulcerative colitis in this family was not HLA B, C, or DR, but Aw24 and DQw1. The third son had the same HLA haplotype as the second son, and it was presumed that he would develop ulcerative colitis in the future. These cases, together with other cases of familial ulcerative colitis indicate that Aw24 and DQw1 are critical phenotypes for ulcerative colitis in Japan.

Adolescent↗
PubMed1997

Metastatic Crohn's disease involving the penis.

Metastatic Crohn's disease is a rare complication in Crohn's disease and there have been only several cases of metastatic Crohn's disease involving the penis. We report one such case. A 22-year-old male student developed anal pain and alternative constipation and diarrhea in December, 1985, followed by diarrhea and lower abdominal pain in January, 1986. He was diagnosed as having Crohn's disease of ileocolitis type. He was admitted to our hospital in July, 1987 because of exacerbation of Crohn's disease. He had anal tags. Soon after admission, two red swollen lesions with central ulcer and erosions were demonstrated at the eversion of the foreskin adjacent to coronal sulcus. Histology of the lesions revealed granulomas with epithelioid cells and giant cells. The lesion responded to a topical steroid. Eight cases of metastatic Crohn's disease involving the penis are briefly reviewed.

Adult↗
PubMed1997

Conserved structural features of nonstructural glycoprotein NSP4 between group A and group C rotaviruses.

The nonstructural glycoprotein NSP4 of group C human rotavirus strain Ehime 9301 was determined to be 150 amino acids in length and 96% identical with the NSP4 of another group C human rotavirus strain Bristol. Both NSP4 sequences were virtually unrelated to group A rotavirus NSP4s. However, the structural features of group A and group C rotavirus NSP4s were similar with hydrophobic domains being in the amino terminus and a coiled coil domain after the membrane-spanning domain, although group C rotavirus NSP4 lacked one amino-terminal hydrophobic domain.

Algorithms↗
PubMed1997

Effect of preinduction of heat shock proteins on acetic acid-induced colitis in rats.

In order to study the cytoprotective function of heat shock proteins (HSPs) in vivo, the effect of preinduction of HSPs by hyperthermia on acetic acid-induced colitis was investigated. Expression of 60-kDa, 72-kDa, and 90-kDa heat shock proteins (HSP60, HSP72, and HSP90, respectively) in rat colonic mucosa was investigated by Western blot analysis and immunohistochemical study before and after hyperthermia. Following pretreatment with or without hyperthermia, the rats received intrarectal infusion of various doses of acetic acid. The colonic mucosal damage was evaluated by macroscopic and microscopic assessments 24 hr after the intrarectal infusion of acetic acid. Expression of HSPs was significantly increased by hyperthermia in rat colonic mucosa. Immunohistochemical study also showed the increments of HSPs in the colonic mucosal cells after hyperthermia. Acetic acid-induced colitis was dramatically prevented by pretreatment with hyperthermia when HSP72 and HSP90 were preinduced. On the other hand, induction of HSP60 did not correlate with mucosal protection. Our findings suggest that HSP72 and HSP90 may have cytoprotective function against acetic acid-induced mucosal damage. These results may be important for understanding the mechanism of "adaptive cytoprotection" mediated by HSPs.

Acetic Acid↗
PubMed1997

Differential induction of HSP60 and HSP72 by different stress situations in rats. Correlation with cerulein-induced pancreatitis.

We previously reported that water-immersion stress specifically induced the synthesis of a 60-kDa heat-shock protein (HSP60, chaperonin homolog) in pancreatic cells and preinduction of HSP60 completely prevented development of cerulein-induced pancreatitis in the rat in an HSP60 quantitatively dependent manner. In order to study the cytoprotective function of a 72-kDa heat-shock protein (HSP72, stress-inducible hsp70), the effect of specific preinduction of HSP72 by hyperthermia on cerulein-induced pancreatitis was investigated and compared with the effect of preinduction of HSP60 in this study. Expression of HSP60 and HSP72 in the pancreas was investigated by immunoblot before and after water immersion or hyperthermia. Following pretreatment with water-immersion stress or hyperthermia, the rats were injected with cerulein (40 micrograms/kg, intraperitoneally). The pancreas wet weight and serum amylase concentration were measured before and after cerulein injection. Hyperthermia (42.5 degrees C, 20 min) specifically induced HSP72 in the pancreas. The synthesis of HSP60 was specifically induced by water-immersion stress in the pancreas. Cerulein-induced pancreatitis was clearly prevented by specific preinduction of HSP60 by water-immersion stress. However, preinduction of HSP72 by hyperthermia had no preventive effect on cerulein-induced pancreatitis. Our findings suggest that HSP60 and HSP72 have distinct functions in the pancreas, and their induction mechanisms are also different in vivo. These results could be important for understanding the mechanism of "adaptive cytoprotection" in the pancreas mediated by heat-shock proteins.

Amylases↗