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Biomedical subjects

A Terano

Publications and source records attributed to A Terano.

At least 163 records · Page 9Linked to original sources
PubMed1990

Percutaneous ethanol injection therapy for neoplasms located on the surface of the liver.

There has been a reluctance to perform percutaneous ethanol injection therapy on lesions located on the surface of the liver because of the possibility of complications. We treated 16 lesions located on the surface of the liver in 14 patients by percutaneous ethanol injection and evaluated the complications and efficacy. Bleeding and seeding of malignant cells did not occur in any case. However, transient pain after injection of ethanol was more intense in these patients than in those whose lesions were not on the surface of the liver. Histopathologic examinations, imaging findings, and decrease in the serum alpha-fetoprotein levels showed that percutaneous ethanol injection was effective for tumors located on the surface of the liver. Our experience suggests that percutaneous ethanol injection can be performed safely even when lesions are located on the surface of the liver.

Adult↗
PubMed1990

Percutaneous ethanol injection therapy of hepatocellular carcinoma: analysis of 77 patients.

Although sonographically guided percutaneous ethanol injection therapy has been attracting a great deal of attention in the treatment of liver neoplasms, few reports regarding long-term results of this therapy have been published. We report here our 4-year experience, in which ethanol injection was performed 419 times on 108 lesions in 77 patients with hepatocellular carcinoma. Histopathologic examination performed in 14 cases after the therapy revealed that the lesion was completely necrotic in 10 cases, 90% necrotic in three cases, and 70% necrotic in the remaining case. Angiography performed after the therapy showed complete disappearance of tumor stain in 37 of 42 cases treated with ethanol injection. CT after the therapy showed no enhancement of the treated lesion in 55 of 56 cases. Elevated serum levels of alpha-fetoprotein decreased in 21 of 24 cases. Ethanol injection improved the long-term prognosis of the patients. Among the 50 patients in whom there were three or fewer lesions and all lesions were treated by ethanol injection, the 1-, 2-, 3-, and 4-year survival rates were 89%, 74%, 68%, and 60%, respectively. Factors that significantly affected the prognosis were the goal of the treatment, liver function, and size of the largest lesion. Serious complications rarely occurred even in patients with severe liver dysfunction. Percutaneous ethanol injection therapy appears to be valuable for treatment of hepatocellular carcinoma.

Adult↗
PubMed1990

Ultrasound-guided percutaneous injection of ethanolamine oleate for hypersplenism. An experimental study in dogs.

In order to evaluate a possible therapy for hypersplenism, an experiment with animals was done. In nine dogs, 0.6 ml/kg body weight of 5% ethanolamine oleate was injected percutaneously into the spleen under ultrasound guidance. The injection was repeated three times at intervals of 1 week. Three dogs each were killed at 1, 4, and 8 weeks after the final injection. All dogs tolerated the procedure well and lived until they were killed. The platelet count and leukocyte count increased after the injections, and remained higher than the pretreatment level until death. This effect probably is due to depressed splenic function. The autopsy showed 40% of the spleen to be infarcted with complete destruction of the normal structure. No serious complications occurred. In addition, injection of ethanolamine oleate in six fully heparinized dogs showed that there was little risk of hemorrhage. Ultrasound-guided percutaneous injection of ethanolamine oleate might be a simple and effective therapy for hypersplenism.

Administration, Cutaneous↗
PubMed1989

Effect of adenosine and adenosine analogs on [14C]aminopyrine accumulation by rabbit parietal cells.

Adenosine receptors that modulate adenylate cyclase activity have been identified recently in a number of tissues. Adenosine A2 receptor is stimulatory to adenylate cyclase, whereas adenosine A1 receptor is inhibitory to adenylate cyclase. We investigated the effect of adenosine and its analogs on [14C]aminopyrine accumulation by rabbit parietal cells. Rabbit gastric mucosal cells were isolated by enzyme digestion. Parietal cells were enriched by nonlinear percoll gradients. [14C]Aminopyrine accumulation was used as an indicator of acid secretion. The effect of 2-chloroadenosine on histamine-stimulated [14C]aminopyrine accumulation was studied. The effects of N-ethylcarboxamideadenosine, 2-chloroadenosine, stable analogs of adenosine, and adenosine on [14C]aminopyrine accumulation were assessed. Cyclic AMP content of parietal cells was determined by radioimmunoassay. Histamine and carbachol, known secretagogues, stimulated [14C]aminopyrine accumulation. 2-Chloroadenosine did not suppress histamine-stimulated [14C]aminopyrine accumulation. 2-Chloroadenosine, N-ethylcarboxamideadenosine, and adenosine dose dependently increased [14C]aminopyrine accumulation. The order of potency was N-ethylcarboxamideadenosine greater than 2-chloroadenosine greater than adenosine. 8-Phenyltheophylline and theophylline, adenosine-receptor antagonists, or cimetidine did not have significant effects on the increase of AP uptake induced by 2-chloroadenosine. Coadministration of dipyridamole, and adenosine uptake inhibitor, augmented the effect of adenosine on [14C]aminopyrine accumulation. 2-Chloroadenosine, N-ethylcarboxamideadenosine, and adenosine each induced a significant increase in cellular cyclic AMP. We conclude that there may be adenosine A2 receptors on rabbit parietal cells which modulate gastric acid secretion.

2-Chloroadenosine↗
PubMed1989

Role of superoxide and hydroxyl radicals in rat gastric mucosal injury induced by ethanol.

It has been reported that oxygen-derived free radicals play an important role in the pathogenesis of mucosal injury in the small intestine as well as in the stomach. The aims of this study were to test whether ethanol-induced damage in the rat stomach was prevented by the administration of (1) superoxide dismutase (SOD; a scavenger of superoxide radicals), (2) allopurionol (ALP; an inhibitor of xanthine oxidase), (3) dimethyl sulfoxide (DMSO; a scavenger of hydroxyl radicals). SOD significantly decreased the ulcer index from 100 +/- 8.5% (control) to 39.6 +/- 8.2% (P less than 0.001). Ethanol-induced damage was reduced by the administration of ALP by 37.4% (P less than 0.01). DMSO also diminished the ulcer index from 100 +/- 8.5% (control) to 31.6 +/- 5.8% (P less than 0.01). Histochemical studies supported these results. A scanning EM study, however, revealed that surface epithelial cells were not protected by SOD against ethanol-induced damage. These results demonstrated that SOD, ALP and DMSO had the ability to protect gastric mucosa against ethanol-induced injury. Accordingly, oxygen-derived free radicals may be involved in the pathogenesis of ethanol-induced gastric mucosal damage. Surface epithelial cells, however, were not protected even by SOD against ethanol-induced injury.

Allopurinol↗
PubMed1989

Regulation of prostaglandin production in cultured gastric mucosal cells.

The aims of this study were to investigate whether exogenous prostaglandin modulates prostaglandin biosynthesis by cultured gastric mucosal cells, and to clarify the role of cyclic nucleotides in the possible modulation of prostaglandin production. After pretreatment for 30 min with buffer alone (control) or 1 to 100ng/ml PGE2, cells were incubated with 4 uM arachidonic acid for 30 min. Pretreatments with greater than 5ng/ml PGE2 inhibited arachidonate-induced PGE2 and PGI2 production in a dose-dependent fashion, as compared with control, with inhibition by 64 +/- 8% and 75 +/- 4% respectively, at 100ng/ml PGE2. PGE2, at 100ng/ml, significantly increased intracellular cAMP accumulation, but pretreatment with dibutyryl cAMP (0.01-mM) did not alter the amounts of arachidonate-induced PGE2 production. Furthermore, while greater than 10ng/ml PGE2 increased cGMP production dose-dependently, preincubation with dibutyryl cGMP (0.001-0.1mM) also failed to affect PGE2 synthesis significantly. In addition, pretreatment with isobutyl-methyl-xanthine, while increasing accumulation of cellular cyclic nucleotides, did not significantly change PGE2 production. Calcium ionophore A23187-induced PGE2 production was also inhibited by pretreatment with PGE2. These results indicate that exogenous PG inhibits subsequent arachidonate or A23187-induced PG biosynthesis in rat gastric mucosal cells, and suggest the possibility that PG regulates its own biosynthesis via feedback inhibition independent of cyclic nucleotides in these cells.

Animals↗
PubMed1989

[Establishment and characterization of a tumor marker producing cell line (JR-1) derived from a gastric scirrhous cancer].

Despite the importance of in vitro study of gastric cancer, the established cell lines derived from human gastric carcinoma are very few. We have recently established a new cell line derived from human gastric cancer which has the ability to produce several tumor markers. This cell line has been designated JR-1. The cancer cells were obtained from the cerebrospinal fluid of a 37 year-old female patient who had metastatic brain tumor of the poorly differentiated gastric adenocarcinoma. The cells were inoculated into the tissue culture flask containing Ham's F-12 medium supplemented with 10% fetal bovine serum, antibiotics. Within 24 hours, the cells attached to the surface of the flask and started to grow. The first subcultures were performed at 1 week, and subsequent subcultures have been done once a week. This cell line has been maintained for more than 15 months through 60 passages with a stable growth. Chromosome analysis of the cells was performed. The doubling time of the 20th passage was 72 hours. Under phase contrast microscopy, monolayered pavement-like cell arrangement was observed. PAS staining showed intracellular mucin granules. Transmission and scanning electron microscopy revealed spindle-shaped cells with numerous microvilli and fine projections as well as intracellular granules, indicating mucin. Tumor markers produced by this cell line were CEA, CA19-9, TPA and Procollagen III.

Adenocarcinoma, Scirrhous↗
PubMed1989

[Collaterals of portal hypertension running through the liver. Part 1. Paraumbilical vein].

Seven cases of portosystemic collateral running through the left lobe of the liver (6 in the medial segment and 1 in the lateral segment) were reported. Six cases were diagnosed by CT and/or ultrasound, and one case was confirmed by autopsy. This collateral originated from the umbilical vein recess of the left portal vein and connected with enlarged vein in front of the left lobe of the liver. All the patients had other portosystemic collaterals of severe and moderate degrees. Paraumbilical veins demonstrated on portography did not differ from ordinary paraumbilical veins in portal hypertension except for prominent tortuosity and dilatation noted in half cases. In markedly dilated cases, intrahepatic portosystemic collateral can be a pitfall in the diagnosis of hepatic tumor on CT. Careful examination of portal hypertension with ultrasound, dynamic CT and/or magnetic resonance imaging will detect such portosystemic collaterals running through the hepatic parenchyma.

Collateral Circulation↗
PubMed1989

Pancreatitis in the annulus of annular pancreas demonstrated by the combined use of computed tomography and endoscopic retrograde cholangiopancreatography.

Annular pancreas, an uncommon condition, is often hard to diagnose before operation. We report a case of annular pancreas with pancreatitis of the annulus that was diagnosed by the use of computed tomography followed by endoscopic retrograde cholangiopancreatography. An upper gastrointestinal series and duodenoscopy revealed stenosis of the second portion of the duodenum. Computed tomography revealed enlargement of the annulus of the pancreas. Two years later, follow-up computed tomography demonstrated calcifications of the annulus, although the remaining pancreas seemed to be normal.

Adult↗
PubMed1988

Cytoprotective effect of acetaminophen against taurocholate-induced damage to rat gastric monolayer cultures.

Acetaminophen has recently been reported to protect against drug damage to gastric mucosa in vivo. The present study tested acetaminophen protection in cultured rat gastric mucous cells against sodium taurocholate-induced damage and assessed the role of endogenous prostaglandins. Cell damage was assessed by phase-contrast microscopy and quantitated by Chromium-51 release assay which positively correlated with the trypan blue dye exclusion test (r = 0.98). The effect of acetaminophen on the production of PGE2 and 6-keto-prostaglandin F1a (6KF) was also studied. Sodium taurocholate caused cell death in a dose-dependent manner as indicated by increased 51Cr release. Preincubation with 5 mM acetaminophen significantly reduced 51Cr release caused by 5 mM sodium taurocholate, producing a 40% increase in cell survival. This cytoprotection was not blocked by indomethacin. PGE2 and 6KF of the media did not change after preincubation with nondamaging concentrations of acetaminophen or taurocholate. These results indicate that: (1) acetaminophen exerts a direct protective effect on gastric mucous cells cultured in vitro independent of indirect factors such as blood flow and (2) this protection is not associated with increased prostaglandin production.

6-Ketoprostaglandin F1 alpha↗