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Biomedical subjects

A Terano

Publications and source records attributed to A Terano.

At least 37 records · Page 2Linked to original sources
PubMed2001

[The perspectives of upper GI tract diseases].

Recently, most of the upper GI tract diseases, peptic ulcer, chronic gastritis, gastric cancer as well as MALT lymphoma, have been explained by the infection of Helicobacter pylori (H. pylori). However, it is not evident whether or not gastric cancer is induced solely by the bacterial infection at this stage. On the other hand, it is reported that the eradication of H. pylori might evoke the reflux esophagitis as well as esophageal and fundic cancer. These important issues remain to be elucidated for the investigation of upper GI tract in the 21st century. The development of new endoscopic technology may be another promising field of upper GI tract.

Endoscopy, Gastrointestinal↗
PubMed2000

Hepatocyte growth factor protects gastric epithelial cells against ceramide-induced apoptosis through induction of cyclooxygenase-2.

Forced overexpression of cyclooxygenase-2 (COX-2) in intestinal cells has been shown to be associated with resistance to apoptosis. However, the role of physiologically-induced COX-2 in the regulation of apoptosis remains unclear. In the present study, we examined whether hepatocyte growth factor (HGF)-induced COX-2 affects ceramide-induced apoptosis in RGM-1 gastric epithelial cells. An externally applied cell permeable ceramide analogue, C2-ceramide, caused RGM-1 cell death in a dose-dependent manner, whereas an inactive ceramide analogue, C2-dihydroceramide, did not. TdT-mediated dUTP nick end labeling (TUNEL) assay showed that the C2-ceramide-induced cell death was apoptosis. Application of HGF rapidly induced the expression of COX-2, and HGF prevented the apoptotic cell death induced by C2-ceramide. However, the anti-apoptotic action of HGF was antagonized by coapplication of NS-398, a selective inhibitor of COX-2. Thus, these results indicate that COX-2 is involved in the survival signaling from HGF in gastric epithelial cells, and suggest a role for physiologically-induced COX-2 in the protection of the cells from apoptosis.

Animals↗
PubMed2000

The effects of aspirin on antioxidant defences of cultured rat gastric mucosal cells.

BACKGROUND: Helicobacter pylori-associated inflammation leads to exposure of the gastric epithelium to reactive oxygen species (ROS) generated in the gastric mucosa. In some pathological conditions, such as those induced by nonsteroidal anti-inflammatory drugs, the gastric mucosa may become more susceptible to ROS. AIM: To examine the effects of aspirin on antioxidant defenses as well as on oxidant injury in cultured rat gastric mucosal cells. METHODS: Primary monolayer cultures of rat gastric fundic mucosa were exposed to an ROS-generating system, hypoxanthine/xanthine oxidase (XOD). Cytotoxicity was quantified by measuring 51Cr release from prelabelled cells. The effects of aspirin on antioxidants and on cellular injury brought about by the ROS-generating system were determined. RESULTS: XOD, in the presence of hypoxanthine, caused a dose-dependent increase in specific 51Cr release, which corresponded to the ability of XOD to produce ROS (as assessed by the production of uric acid from hypoxanthine). Incubation of cells with aspirin (1-100 microM) produced a dose-dependent increase in XOD-induced 51Cr release. Aspirin did not affect cellular glutathione content or activity of glutathione peroxidase, glutathione reductase or endogenous catalase. By contrast, aspirin caused a dose-dependent reduction in mucus synthesis. as assessed by incorporation of [3H]-glucosamine hydrochloride into the cells. CONCLUSIONS: Aspirin at therapeutically relevant concentrations rendered cultured gastric cells more susceptible to subsequent exposure to ROS. Aspirin affected neither the glutathione redox cycle nor catalase activity. Thus, the enhancement of ROS-induced injury by aspirin may be accomplished through diminished gastric mucus synthesis, since mucus is a potent scavenger of ROS. These findings provide insight into how gastric inflammation and injury (such as that induced by H. pylori infection) in human gastric mucosa is modulated by the administration of nonsteroidal anti-inflammatory drugs.

Animals↗
PubMed2000

The effect of NSAIDs and a COX-2 specific inhibitor on Helicobacter pylori-induced PGE2 and HGF in human gastric fibroblasts.

BACKGROUND: There is compelling evidence for the pivotal role of Helicobacter pylori in the pathogenesis of gastrointestinal ulcer disease. However, despite the bacterium's toxicity, the majority of H. pylori infections are not accompanied by gastric ulcers. This implies the existence of a host mechanism offsetting H. pylori toxicity. AIMS: To evaluate gastric fibroblasts' expression of hepatocyte growth factor (HGF), which is known to facilitate gastric ulcer healing, in the presence of H. pylori; to compare the effect on H. pylori-induced HGF expression of a COX-2 selective inhibitor with that of nonselective nonsteroidal anti-inflammatory drugs METHODS: Human gastric fibroblasts were cultured from human gastric mucosa obtained at surgery. Prostaglandin E2 (PGE2) and HGF were measured by EIA. The expression of COX-2 mRNA was assessed by the TaqMan quantitative RT-PCR system. RESULTS: H. pylori increased PGE2 release in gastric fibroblasts. H. pylori induced expression of COX-2 mRNA, which indicates that PG induction by H. pylori is through COX-2. Sulindac sulphide, etodolac and NS 398 all inhibited H. pylori-induced PGE2 release to the same extent. These agents also inhibited H. pylori-induced HGF release. CONCLUSION: Gastric fibroblasts produce PG and HGF in response to the presence of H. pylori, which may be considered part of the human body's defensive reaction to H. pylori toxicity. This defensive mechanism is inhibited not only by COX-2 nonselective NSAIDs but also by a COX-2 selective inhibitor. These findings indicate the importance of COX-2 in chronic H. pylori infection.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2000

Suspected intestinal myiasis due to Dryomyza formosa in a Japanese schizophrenic patient with symptoms of delusional parasitosis.

A third-stage larva of Dryomyza formosa (Wiedemann) (Diptera: Dryomyzidae) was found in the fresh stool of a 27-year-old Japanese woman resident of Shiobara, 150 km north of Tokyo, on 16 November 1998. This is the first record of myiasis due to Dryomyza. Detection of this maggot (2cm long) by the patient herself was associated with her longstanding delusion of abdominal parasitosis as a symptom of chronic schizophrenia. Circumstantial evidence agreed with this being a genuine case of intestinal myiasis, apparently due to accidental ingestion of the insect, with no signs that the patient had contrived the report, nor that the maggot had invaded the stool post-defaecation. This case draws attention to the likelihood that some personality states are predisposed to noticing and reporting myiasis, when it occurs. We review other conditions (mental and physical) that are more prone to myiasis.

Adult↗
PubMed2000

Incidence of P53 and K-ras alterations in ovarian mucinous and serous tumors.

Clarification of the pathogenic relationships existing among ovarian cystadenomas, tumors of low malignant potential (LMP) and various adenocarcinoma types, a series of 29 mucinous and 19 serous ovarian tumors including adenomas, LMP tumors and adenocarcinomas were examined. P53 protein was detected by the streptavidin-biotin method and point mutation of K-ras codon 12 was detected by polymerase chain reaction-restriction fragment length polymorphism analysis. P53 overexpression was observed more frequently in serous adenocarcinomas (5/8, 63%) than in mucinous adenocarcinomas (2/9, 22%) and was correlated with the malignant potential of serous tumors. Furthermore, the proportion of P53-positive cells was significantly higher in serous adenocarcinomas than in mucinous adenocarcinomas. P53 overexpression may therefore be closely related to the early events of carcinogenesis in serous tumors. Although mutation of the K-ras oncogene appears to be an important event in the early tumorigenesis of mucinous tumors, mutation of the K-ras oncogene in serous tumors may be dependent on morphology. Different complex pathways of oncogene and/or tumor suppressor gene abnormalities may be involved in the development of mucinous and serous adenocarcinomas.

Cell Transformation, Neoplastic↗
PubMed2000

[Clinical update of GERD].

In our country, it is reported that reflux esophagitis(GERD) has been increasing like in European countries. One of the reasons for this tendency may be the arrival of the aging society. Another explanation is the lowering of Helicobacter pylori infection rate in the younger generation. Though the Los Angeles classification is mainly used at present, the Savary-Miller classification is also clinically important. For the initial treatment of GERD, proton pump inhibitor(PPI) has been mainly used, while there is large problems in the ideal way of maintenance therapy. The guideline on the GERD treatment is also being considered, based on EBM.

Gastroesophageal Reflux↗
PubMed2000

[Prognostic factors of hepatocellular carcinoma: analysis by the proportional hazard model].

Five hundred fifty patients hospitalized to our hospital during 1990 to 1999 were studied. Subjects consisted of 413 males and 102 females and mean age was 62.1 years. Association with HBV infection, HCV infection and both infection was 11.1%, 78.4% and 2.5% respectively. According to the criteria based in Liver Cancer Study of Japan, 5 year survival rate in clinical stage I, II, III was 42.3%, 38.8% and 17.5%. Tumor morphology was nodular type in 78.9%, massive type in 9.1% and diffuse type in 10.5% of cases. Portal tumor thrombus and distal metastasis were observed in 19.9% and 6.3% of all cases. The 1-, 3- and 5-year survival rate in patients received any therapy was 80.8%, 44.6% and 28.7%, respectively. Analysis by the proportional hazard model showed that HBV infection, advanced clinical stage, multiple tumors, a tumor diameter in excess of 5 cm and AFP positivity were shown as significant factors on poor prognosis.

Carcinoma, Hepatocellular↗
PubMed1999

Role of calcitonin gene-related peptide and capsaicin-sensitive afferents in central thyrotropin-releasing hormone-induced hepatic hyperemia.

The involvement of capsaicin-sensitive afferent neurons and calcitonin gene-related peptide (CGRP) in the central thyrotropin-releasing hormone (TRH)-induced hepatic hyperemia was investigated in urethane anesthetized rats. Both systemic capsaicin pretreatment and intravenous administration of CGRP receptor antagonist, human CGRP-(8-37), completely abolished the stimulatory effect of hepatic blood flow induced by intracisternal injection of TRH analog (RX-77368; p-Glu-His-(3,3'-dimethyl)-Pro-NH2, 100 ng), assessed by the hydrogen gas clearance method. These data demonstrate the involvement of capsaicin-sensitive afferent neurons and CGRP in the central TRH-induced stimulation of hepatic blood flow.

Animals↗
PubMed1999

Cyclooxygenase (COX)-2 immunoreactivity and relationship to p53 and Ki-67 expression in colorectal cancer.

The tumor-suppressive effects of nonsteroidal antiinflammatory drugs (NSAIDs) have been suggested to be due to a reduction in cyclooxygenase (COX)-2 activity, although the effects of COX-2 in the colonic mucosa and in colorectal cancer have not been determined. Ki-67 immunoreactivity in cancers is also attracting attention, as Ki-67 reflects cell proliferation, while p53 immunoreactivity is also of interest, as it reflects the malignancy of colorectal lesions. Accordingly, to determine these correlation, we investigated the distribution and intensity of COX-2, p53 and Ki-67 expression in both cancerous and non-cancerous tissues from patients with sporadic and ulcerative colitis (UC)-associated colorectal cancer. We selected 21 colorectal cancer specimens, obtained by surgical resection or colonoscopic biopsy, from 21 patients, including 3 with UC (13 men and 8 women; aged 42-78 years). Histological examination of hematoxylin and eosin-stained specimens revealed that 9 were well differentiated; 11. moderately differentiated: and 1 was a poorly differentiated adenocarcinoma. We used anti-COX-2, p53, and Ki-67 antisera to perform immunohistochemical staining by the labelled streptavidin biotin method and then assessed and graded the staining intensity and distribution. COX-2 staining was more intense in cancer tissue than in non-cancerous areas. Colorectal cancers associated with UC were not stained intensely. COX-2, p53, and Ki-67 positivity rates in were 38.1%, 38.1%, and 47.6%, respectively. There were no relationships among the distributions or intensities of COX-2, p53, and Ki-67 expression. Our results indicate that colorectal cancer tissues overexpress COX-2, but that there are no relationships between COX-2, p53, and Ki-67 expression, suggesting that COX-2 expression may not be related to cell proliferation or to the grade of malignancy. However, it is necessary to determine whether COX-2 in cancer tissue is involved in carcinogenesis or whether it is simply a product of cancer.

Adult↗
PubMed1999

Treatment of gastric tumors by endoscopic mucosal resection with a ligating device.

BACKGROUND: This study attempted to determine the indication for endoscopic mucosal resection with a ligating device (EMRL) and to assess the efficacy of radical (complete) resection of early gastric carcinoma and adenoma. METHODS: Sixteen patients with early gastric carcinoma (17 lesions) and 21 patients with gastric adenoma (23 lesions) underwent EMRL with an endoscope with a ligating device. After epinephrine solution was injected into the submucosa, the lesions were aspirated, ligated, and resected. RESULTS: Twelve of 17 early carcinomas (70.6%) and 18 of 23 adenomas (78.3%) were radically resected by EMRL. The average size of the resected specimens was 12.8 x 11.0 mm. The rate of successful radical resection by EMRL, including piecemeal resection, was 100% (15/15) for lesions located in the antrum, 80% (4/5) in the angle, 61.1% (11/18) in the body, and 0% (0/2) for lesions at the cardia. Repeat EMRL was performed successfully in cases of partial resection (n = 3). No serious complication was encountered. No recurrence of the tumors was identified in cases of radical resection during a median follow-up period of 22.8 months. CONCLUSION: EMRL is suitable for the treatment of gastric tumorous lesions. For the treatment of early carcinoma, well-differentiated mucosal carcinomas smaller than 10 mm located in the distal stomach represent the best indication for EMRL.

Adenocarcinoma↗