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Biomedical subjects

M Imamura

Publications and source records attributed to M Imamura.

At least 181 records · Page 10Linked to original sources
PubMed2000

Early detection of haemobilia associated with percutaneous ethanol injection for hepatocellular carcinoma.

OBJECTIVE: Haemobilia often results from iatrogenic injury caused by therapeutic procedures. The objective of this study was to evaluate the efficacy of early diagnosis of haemobilia based on ultrasonography in patients with hepatocellular carcinoma undergoing percutaneous ethanol injection. PATIENTS AND METHODS: A combination retrospective and prospective study on the early detection of haemobilia caused by percutaneous ethanol injection was conducted on 365 patients in 1995-1996. The retrospective study reviewed the clinical, laboratory and imaging data of 172 patients who had undergone ethanol injection therapy in 1995. The results showed that ultrasonographic changes in the gallbladder, namely the rapid appearance of echogenic material in the gallbladder lumen, are a useful early sign of haemobilia. Based on the results of the retrospective study, a prospective study on the early detection of haemobilia was carried out in 1996. In the prospective study, percutaneous ethanol injection was halted as soon as haemobilia was detected. RESULTS: The incidence of haemobilia in the prospective group (3.6%) was not different from that in the retrospective group (4.7%). However, the mean duration between percutaneous ethanol injection and diagnosis of haemobilia was only 0.3 +/- 0.2 days in the prospective group, compared with 2.8 +/- 2.1 days in the retrospective group (P < 0.001), and the mean duration of jaundice in the prospective group (4.3 days) was significantly shorter than in the retrospective group (40.0 days) (P< 0.05). CONCLUSION: Early diagnosis of haemobilia based on ultrasonographic findings of the gallbladder lumen effectively reduces the severity of haemobilia-related complications due to immediate interruption of the interventional procedure.

Administration, Cutaneous↗
PubMed2000

Nonrandom chromosomal imbalances in esophageal squamous cell carcinoma cell lines: possible involvement of the ATF3 and CENPF genes in the 1q32 amplicon.

Using comparative genomic hybridization (CGH), we investigated copy number aberrations in 29 esophageal squamous cell carcinoma (ESC) cell lines. All lines displayed numerous chromosome imbalances. The most frequent losses were observed on chromosome 18q (65.5%), Xp (48. 3%), 3p (44.8%), 4q (44.8%), 8p (41.4%), 11q23 - 25 (34.5%) and 4p (27.6%), whereas the most common copy number gains were noted at 8q (86.2%), 3q (82.8%), 5p (69%), 7p (69%), 20q (65.5%), 9q (55.2%), 11q (55.2%), 1q (48.3%), Xq (44.8%) and 18p (37.9%). High-level gains (HLGs) were detected at 3q26 (9 cases), 8q23 (6 cases), 5p14 - 15 (6 cases), 18p11.2 - 11.3 (6 cases), 3q27 - 28 (5 cases), 5p13 (3 cases), 7p14 - 15 (3 cases), 20q12 - 13 (3 cases), 11q13 (3 cases), 14q21 (2 cases), 20p11.2 (2 cases), 13q32 (2 case), and 1q32 (1 case). Among them, HLGs of 1q32 have been reported in other types of cancer, including glioblastoma and breast cancers. We successfully narrowed down the smallest common amplicon involving 1q-gain to the genomic segment between D1S414 and D1S2860 by fluorescence in situ hybridization (FISH). Southern and northern blot analysis clearly demonstrated that ATF3, human activating transcription factor-3 and CENPF, centromere protein F, mapped within this region, were significantly amplified and over-expressed in 1q32 amplicon.

Activating Transcription Factor 3↗
PubMed2000

Evolution to acute myeloblastic leukemia from chronic neutrophilic leukemia with dysplastic features in granulocytic lineage.

We experienced the case of an 82-year-old man with chronic neutrophilic leukemia (CNL) with dysplastic features in the granulocytic lineage which subsequently progressed to acute myeloblastic leukemia (AML) with myelofibrosis. The patient had hepatosplenomegaly, but there was no evident cause of neutrophilic leukocytosis. The cytogenetic study showed that he had a normal karyotype. Concentrations of the serum granulocyte colony-stimulating factor (G-CSF) were not detectable. Two years after the diagnosis of CNL, blastic transformation to AML occurred with myelofibrosis and significant morphological abnormalities in neutrophils. The blasts were positive for myeloperoxidase, CD33, CD34, and HLA-DR, and the presence of dysplasia within the granulocytic lineage suggested that he had an abnormality at the level of the granulocyte-committed progenitors. Heterogeneous origins of CNL might lead to various clinicopathological features in each case.

Aged↗
PubMed2000

Squamous cell carcinoma of the prostate without evidence of recurrence 5 years after operation.

A 54-year-old man underwent radical cystoprostatectomy after prostatic needle biopsy which revealed squamous cell carcinoma of the prostate. However, the positive surgical margin of the pubis suggested residual disease. He received chemotherapy with methotrexate, peplomycin and cisplatin (MPD regimen). He is at present still alive without evidence of recurrence 5 years after the operation. This suggests that MPD chemotherapy is effective for squamous cell carcinoma of the prostate.

Carcinoma, Squamous Cell↗
PubMed2000

Immunohistochemical analysis of apoptosis-related proteins in human embryonic and fetal pancreatic tissues.

BACKGROUND: The growth of both cancer cells and fetal tissue is rapid; however, cancer cells de-differentiate and proliferate in a disorderly manner, whereas fetal tissues differentiate and proliferate in an orderly manner. Thus, there may be both common and different factors that are involved in the process of the uncontrolled cell growth of pancreatic cancers and the development of the fetal pancreas. The common part of the mechanisms should be in the regulation of the cell cycle, resulting in rapid proliferation via such mechanisms as growth stimulation and avoidance of apoptosis. Therefore, in the current study we investigated the expression of apoptosis-related proteins in fetal pancreatic tissues. METHODS: Sixteen human embryonic and fetal pancreatic tissues obtained between 6 and 32 wk of gestation were used. We immunohistochemically examined the protein expression of Bcl-2, Bcl-XL, Mcl-1, and Bax. Further, the expression of insulin, glucagon, and proliferting cell nuclear antigen (PCNA), and TdT-mediated dUTP-biotin nick-end labeling (TUNEL) staining were examined. RESULTS: In embryonic and fetal pancreatic tissues, Bcl-2 was not detected in any type of pancreatic cell (acinar, ductal, or islet). Bcl-XL was expressed in all types of pancreatic cells throughout the gestation. Mcl-1 was expressed in all types of pancreatic components, and strongly expressed in the margin of the islets. Bax, a pro-apoptotic protein, was expressed in all components. PCNA was strongly expressed in the embryonic and fetal pancreas, especially in early stages of gestation; however, TUNEL staining was negative in all samples. At least one antiapoptotic protein was expressed in all types of pancreatic cells. CONCLUSION: The results of the current study indicate that active proliferation and avoidance of apoptosis take place in embryonic and fetal pancreatic tissues, which may be controlled by particular combinations of apoptosis-related proteins. Among these proteins, Bcl-XL and Mcl-1 may play an important role in the proliferation and differentiation of the embryonic and fetal pancreas.

Apoptosis↗
PubMed2000

Chronic sulfonylurea treatment and hyperglycemia aggravate disproportionately elevated plasma proinsulin levels in patients with type 2 diabetes.

It is established that disproportionately elevated plasma proinsulin levels occur in patients with Type 2 diabetes. In the present study, multivariate analysis was performed to determine what factors contributed to the disproportionately elevated plasma proinsulin levels in Japanese patients with Type 2 diabetes (n=276). Results from univariate analysis showed that both fasting proinsulin/C-peptide ratio and proinsulin/IRI ratio were approximately 2-fold higher in patients with Type 2 diabetes than those in healthy nondiabetic subjects (n=45). In patients with Type 2 diabetes, both proinsulin/C-peptide ratio and proinsulin/IRI ratio were significantly positively correlated with fasting plasma glucose level (FPG) and HbA1c. Neither proinsulin/C-peptide ratio nor proinsulin/IRI ratio was significantly correlated with BMI. Sulfonylurea-treated subjects had a significant elevation in both proinsulin/C-peptide ratio and proinsulin/IRI ratio compared with diet-treated subjects, whereas nonsulfonylurea hypoglycemic agent-treated subjects did not. Multivariate analysis confirmed that sulfonylurea treatment and FPG were significant determinants of both fasting proinsulin/C-peptide ratio (P=0.006 and P=0.030, respectively) and proinsulin/IRI ratio (P=0.003 and P=0.016, respectively) in patients with Type 2 diabetes. These results imply that disproportionate hyperproinsulinemia may reflect an excessive overwork of beta cells under chronic sulfonylurea treatment as well as hyperglycemia.

Body Mass Index↗
PubMed2000

Bile acid metabolism, bacterial bowel flora and intestinal function following ileal pouch-anal anastomosis in dogs, with reference to the influence of administration of ursodeoxycholic acid.

The pathophysiology following a total colectomy with ileal pouch-anal anastomosis (IPAA) has not been sufficiently clarified yet. We investigated bile acid metabolism, bacterial bowel flora and transit of the alimentary tract after IPAA, with reference to administration of ursodeoxycholic acid (UDCA) in dogs undergoing IPAA. Ten adult beagle dogs underwent IPAA at one stage, and were observed for 12 months. UDCA (100 mg/day) was administered orally to five dogs, and the other five did not. In the UDCA(+) group, UDCA replaced other bile acids, especially cholic acid, accounting for 16.5% of gallbladder bile at 12 months after surgery. Both plasma levels and postprandial increase of total bile acids remained unchanged in the UDCA(+) group, but decreased in the UDCA(-) group at 12 months. Fecal excretion of bile acids tended to be smaller in the UDCA(+) group, and the ratio of secondary to primary bile acids was larger in the UDCA(-) group. Almost all the bile acids were in free form in stool, and UDCA constituted 19% in the UDCA(+) group. The transit time of the whole alimentary tract was elongated by administering UDCA, especially at an early period after IPAA. Although both anaerobic and aerobic bacteria decreased after IPAA, the latter decreased more in stool, resulting in an increase in the ratio of total anaerobes/total aerobes, especially in the UDCA(-) group. The decrease in Bacteroidaceae and Lactobacillus after IPAA was slightly smaller in the UDCA(+) group. Administration of UDCA following IPAA was efficient to induce rapid intestinal adaptation and also to keep the bile acid fraction in the ileal pouch less harmful.

Administration, Oral↗
PubMed2000

High glucose level and free fatty acid stimulate reactive oxygen species production through protein kinase C--dependent activation of NAD(P)H oxidase in cultured vascular cells.

Recent studies have revealed that vascular cells can produce reactive oxygen species (ROS) through NAD(P)H oxidase, which may be involved in vascular injury. However, the pathological role of vascular NAD(P)H oxidase in diabetes or in the insulin-resistant state remains unknown. In this study, we examined the effect of high glucose level and free fatty acid (FFA) (palmitate) on ROS production in cultured aortic smooth muscle cells (SMCs) and endothelial cells (ECs) using electron spin resonance spectroscopy. Exposure of cultured SMCs or ECs to a high glucose level (400 mg/dl) for 72 h significantly increased the free radical production compared with low glucose level exposure (100 mg/dl). Treatment of the cells for 3 h with phorbol myristic acid (PMA), a protein kinase C (PKC) activator, also increased free radical production. This increase was restored to the control value by diphenylene iodonium, a NAD(P)H oxidase inhibitor, suggesting ROS production through PKC-dependent activation of NAD(P)H oxidase. The increase in free radical production by high glucose level exposure was completely restored by both diphenylene iodonium and GF109203X, a PKC-specific inhibitor. Exposure to palmitate (200 micromol/l) also increased free radical production, which was concomitant with increases in diacylglycerol level and PKC activity. Again, this increase was restored to the control value by both diphenylene iodonium and GF109203X. The present results suggest that both high glucose level and palmitate may stimulate ROS production through PKC-dependent activation of NAD(P)H oxidase in both vascular SMCs and ECs. This finding may be involved in the excessive acceleration of atherosclerosis in patients with diabetes and insulin resistance syndrome.

Animals↗
PubMed2000

Gastric stromal tumor with CD34 immunoreactivity--a case report.

Gastric stromal tumors are the most common mesenchymal tumors, and such submucosal mass lesions of the upper gastrointestinal tract occur frequently. A 54-year-old woman with no major complaint was admitted to our hospital for evaluation of a mass located between the stomach and the pancreas. Abdominal ultrasonography, computed tomography and endoscopic ultrasonography demonstrated a mass lesion which was located near the lesser curvature of the stomach. Selective left gastric arterial angiography revealed a hypervascular mass, and we diagnosed it as a leiomyosarcoma of the stomach. At laparotomy, there was a large solid mass 5 cm in diameter along the minor curvature of the stomach. Tumor resection with partial gastrectomy was performed, and the histological diagnosis was a gastric stromal tumor with CD34 immunoreactivity. We report a case of stromal tumor of the stomach with extramural growth and review the literature.

Antigens, CD34↗
PubMed2000

The Epstein-Barr virus is rarely associated with esophageal cancer.

The Epstein-Barr virus is an agent that causes African Burkitt's lymphoma, infectious mononucleosis, and Hodgkin's disease. It is also related to nasopharyngeal carcinoma and gastric carcinoma. The aim of this study was to evaluate the prevalence of the Epstein-Barr virus in esophageal cancer. Polymerase chain reaction and in situ hybridization were used to detect the Epstein-Barr virus. We detected 103 Epstein-Barr virus positive cells out of 107 of KYSE 273 cells using first standard-PCR. Epstein-Barr virus DNA could not be detected in 30 of the esophageal squamous cell carcinoma cell lines and 2 of the Barrett's esophageal adenocarcinoma cell lines. Out of 77 esophageal cancer patients, 3 cases were found positive for Epstein-Barr virus DNA using polymerase chain reaction. However, by in situ hybridization we found signals in only 1 of the 3 cases, the signal was located in the infiltrating lymphocytes. The Epstein-Barr virus is rarely associated with esophageal cancer.

Adenocarcinoma↗
PubMed2000

TGF-alpha as well as VEGF, PD-ECGF and bFGF contribute to angiogenesis of esophageal squamous cell carcinoma.

It has been demonstrated that vascular endothelial growth factor (VEGF) is associated with tumor progression as an angiogenic factor in esophageal squamous cell carcinoma (SCC)s. However, the role of other angiogenic factors such as transforming growth factor-alpha (TGF-alpha), platelet-derived endothelial cell growth factor (PD-ECGF), and basic fibroblast growth factor (bFGF) are still unknown in esophageal SCCs. In this study, we detected the expression of VEGF, TGF-alpha, PD-ECGF and bFGF in tissue specimens from 96 patients with SCC of the esophagus by immunohistochemical staining. To evaluate angiogenesis, endothelial cells were stained immunohistochemically and microvessel density (MVD) was counted in 24 cases. The positive rates for VEGF, TGF-alpha, PD-ECGF and bFGF were 65% (62/96), 67% (64/96), 66% (63/96), and 49% (47/96), respectively. Only TGF-alpha expression had a strong correlation with the average MVD (p=0.0059). However, the MVD increased as the number of positive factors for these 4 factors increased (p=0.0023). The expression of all of these factors significantly correlated to the depth of tumor invasion, and lymph node metastasis. Finally, survival analysis of the patients revealed that VEGF, TGF-alpha, and PD-ECGF were significant prognostic factors. However, multivariate analysis revealed that these factors were not prognostic. Thus, we suggest that TGF-alpha as well as VEGF, PD-ECGF and bFGF may be associated with angiogenesis, and the progression and metastasis of esophageal squamous cell carcinoma.

Adult↗
PubMed2000

PTEN/MMAC1 expression in esophageal squamous cell carcinomas.

The PTEN/MMAC1 gene at 10q23.3 is a novel tumor suppressor gene candidate. Various kinds of tumors have mutations in this gene. However, in some cancers PTEN/MMAC1 gene may be inactivated by mechanisms other than gene deletion and mutation, including promoter methylation or translational modification. The aim of this study was to determine whether there are abnormalities in the expression of PTEN/MMAC1 gene in esophageal cancer. Reverse transcription polymerase chain reaction and western blot were used to examine PTEN/MMAC1 expression in human esophageal squamous cell lines and normal cultured esophageal epithelial cells. Immunohistochemical staining was carried out to detect PTEN/MMAC1 expression in surgically resected esophageal squamous cell carcinomas and normal esophageal epithelium. All 30 esophageal cancer cell lines (KYSE series) and normal cultured esophageal epithelial cells expressed PTEN/MMAC1 mRNA. Western blot analysis confirmed that all the cell lines expressed PTEN/MMAC1 protein and there was no difference in expression level. Immunohistochemical study showed that the PTEN/MMAC1 protein was localized dominantly in the cytoplasm and strongly stained in all 42 surgically resected esophageal squamous cell carcinomas and normal esophageal epithelium. PTEN/MMAC1 is rarely associated with esophageal squamous cell carcinoma carcinogenesis.

Carcinoma, Squamous Cell↗
PubMed2000

Auto-induction and growth stimulatory effect of betacellulin in human pancreatic cancer cells.

Betacellulin (BTC) was identified in mouse pancreatic beta cell tumors as a member of the epidermal growth factor (EGF) family, and was found to bind and activate the EGF receptor. BTC is also expressed in some human malignancies and may have an important role in tumor growth progression. We examined whether BTC and EGF have a growth stimulatory effect on human pancreatic cancer cell lines both in vitro and in vivo. We also investigated the BTC expression and autonomous induction of BTC in pancreatic cancer cells. in vitro, both BTC and EGF had almost the same proliferative effect on Panc-1, MIA PaCa-2 and AsPC-1. in vivo, in a Panc-1 inoculated athymic mice model, BTC-treated tumors grew approximately five times larger than in control. Immunocytochemistry showed that BTC expression occurred in three pancreatic cancer cell lines, with MIA PaCa-2 showing the strongest intensity. Semi-quantitative RT-PCR of MIA Paca-2 showed that mRNA levels of BTC gradually increased after treatment with 1 nM BTC. Immunocytochemistry also demonstrated that the intensity of BTC-like immunoreactivity was increased when treated with 1 nM BTC but was reduced after treatment with 100 nM of AG1478, an EGF receptor tyrosine kinase inhibitor. BTC has thus a significant growth stimulatory effect on pancreatic cancer cells and might function as an autocrine and paracrine growth factor. BTC expression in pancreatic cancer cells is, at least in part, controlled by an auto-induction mechanism.

Animals↗
PubMed2000

Enhancement of angiogenesis, tumor growth, and metastasis by transfection of vascular endothelial growth factor into LoVo human colon cancer cell line.

The expression of vascular endothelial growth factor (VEGF), a highly potent angiogenic molecule, is thought to be correlated with the development of colon cancer; however, direct evidence for a role of VEGF in metastasis is lacking. This study was designed to more directly establish the role of VEGF in the growth and metastasis of human colon cancer using a genetically engineered cancer cell line. A stable VEGF gene-transfected human colon cancer cell line, LoVo, was made by genetic manipulation using eukaryotic expression constructs designed to express the complete VEGF121 cDNA in the sense orientation. Transfected clones were screened for VEGF121 mRNA expression by Northern blot analysis and for VEGF121 protein expression by Western blot analysis. Consequently, we obtained S17 cells that expressed a high level of both VEGF mRNA and VEGF protein. A vector-transfected clone (V7 cell) was used as a control. The experiment with the dorsal air sac method revealed that S17 cells elicited a stronger directional out-growth of capillaries than V7 cells. S17 cells formed faster-growing tumors than did V7 cells when xenografted s.c. into nude mice, although there was no significant difference in their in vitro proliferation. Tumors derived from S17 cells had more vascularity, as assessed by counting capillary vessels after staining with factor VIII, than did tumors derived from V7 cells (P < 0.05). With regard to the metastatic potential, S17 cells exhibited a higher capacity for both hepatic metastasis after the splenic portal inoculation and peritoneal dissemination after i.p. injection than did V7 cells. However, S17 cells showed no apparent metastasis, despite their rapid growth after orthotopic implantation. In conclusion, the present study showed clearly that VEGF plays an important role in cancer growth due to stimulation of angiogenesis by accelerating cell growth after reaching the target organs.

Animals↗
PubMed2000

[beta-thalassemia minor diagnosed in a patient with chronic myelogenous leukemia during hydroxyurea therapy].

A 55-year-old man was admitted to our hospital because of leukocytosis and microcytic anemia with hypochromia, target cells, and increased levels of hemoglobin A2 and hemoglobin F. The results of a gene analysis yielded a diagnosis of chronic myelogenous leukemia and beta-thalassemia minor. A gradual increase in hemoglobin was observed during hydroxyurea therapy, which was performed over a 12-week period. This increment appeared to be due to suppressed production of myeloid cells. It was been reported that hydroxyurea increases total hemoglobin due to increased hemoglobin F synthesis in patients with beta-thalassemia. However, hydroxyurea had no clear influence on hemoglobin concentration in this case.

Antineoplastic Agents↗
PubMed2000

[A case of advanced hepatocellular carcinoma with lung and bone metastases effectively treated by orally administered UFT].

A 52-year-old male underwent hepatic subsegmentectomy for hepatocellular carcinoma (HCC). Five months later, a recurrent tumor was found in the liver and transcatheter arterial embolization (TAE) was performed. However, recurrent tumors were growing rapidly with multiple lung and bone metastases. The titer of serum AFP was elevated to 896,095 ng/ml and the titer of serum PIVKA-II was elevated to 1294.5 AU/ml. The patient was treated by oral administration of UFT (600 mg/day). Two weeks later, his general condition was improved, and several months later, the liver tumor, multiple lung metastases and multiple bone metastases had almost disappeared. The titers of serum AFP and PIVKA-II were reduced to the normal range. He has maintained a good state of health for about four years now. This case suggests the clinical usefulness of UFT for advanced HCC.

Administration, Oral↗
PubMed2000

Expression of thioredoxin and glutaredoxin, redox-regulating proteins, in pancreatic cancer.

Pancreatic cancer (pancreatic ductal carcinoma) is one of the most malignant solid tumors with poor prognosis. There is accumulating evidence that cellular reduction/oxidation (redox) status is deeply involved in the growth promotion and drug resistance of cancer cells. We therefore investigated the expression of redox-regulating proteins, such as thioredoxin (TRX) and glutaredoxin (GRX) in surgically resected pancreatic tissues and cis-diamminedichloroplatinum (CDDP)-resistant cells. Plasma levels of TRX were also measured in subjects with pancreatic diseases. Pancreatic ductal carcinoma tissues were immunohistochemically more positive for TRX (24/32 cases) and GRX (29/32 cases) than pancreatic cystadenocarcinoma or normal pancreas tissues. Plasma levels of TRX (mean +/- SD) measured by ELISA were significantly higher in patients with pancreatic ductal carcinoma (54.8 +/- 37.6 ng/ml, n = 60) than in healthy controls (24.4 +/- 12.9 ng/ml, n = 81). CDDP-resistant subclones of HeLa cells, HeLa-CP5 cells, had higher expression of TRX (1.5 fold) and GRX (1.6 fold) compared with parental HeLa cells by immunoblotting. These results indicate the possible association of TRX and GRX with malignant potential of pancreatic ductal carcinoma.

Adult↗