Biomedical subjects

H Iishi

Publications and source records attributed to H Iishi.

At least 19 recordsLinked to original sources

PubMed1995

Suppression by amiloride of bombesin-enhanced peritoneal metastasis of intestinal adenocarcinomas induced by azoxymethane.

The effects of concomitant administration of bombesin and of the diuretic drug amiloride on the development of large and small intestinal tumors induced by azoxymethane (AOM), the incidence of their metastasis to the peritoneum and the labeling index of intestinal adenocarcinomas were investigated in inbred Wistar rats. From the start of the experiment, rats were given weekly s.c. injections of AOM for 10 weeks and s.c. injections of bombesin and/or a higher or lower dose of amiloride hydrochloride (amiloride) every other day until the end of the experiment in week 45. Administration of bombesin significantly increased the incidence of intestinal tumors and cancer metastasis to the peritoneum in week 45. It also significantly increased the labeling index of intestinal adenocarcinomas. Although administration of both doses of amiloride with bombesin had little or no influence on the enhancement of intestinal tumorigenesis by bombesin, the location, histological type, depth of involvement or labeling index of intestinal adenocarcinomas, a higher dose of amiloride significantly reduced the incidence of cancer metastasis to the peritoneum. Our findings indicate that amiloride possesses an anti-metastatic activity.

Adenocarcinoma↗

PubMed1995

Promotion by substance P of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of prolonged administration of neuropeptide substance P (SP) on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and on the labeling index of gastric mucosa were investigated in Wistar rats. Rats received subcutaneous injections of 12 micrograms/kg body weight of SP every other day after 25 weeks of oral treatment with MNNG. Long-term administration of SP significantly increased the incidence of gastric cancers in week 52. However, it did not affect the histological type and depth of involvement of gastric cancers. SP also caused a significant increase in the labeling index of the antral and fundic epithelial cells in week 52. These findings indicate that SP promotes gastric carcinogenesis and suggest that this effect may be related to its stimulation of antral epithelial cell proliferation.

Animals↗

PubMed1995

Enhancement by peptide histidine isoleucine of experimental carcinogenesis in the colon of rats induced by azoxymethane.

The effects of peptide histidine isoleucine (PHI) on the incidence and histology of colon tumors induced by azoxymethane (AOM), and on the labeling index of colon mucosa were investigated in Wistar rats. Rats received weekly s.c. injections of 7.4 mg/kg body weight of AOM for 10 weeks, and of 1.0 or 4.0 nmol/kg body weight of PHI until the end of the experiment in week 35. Administration of PHI at the higher, but not the lower dosage, significantly increased the incidence of colon tumors. PHI had no influence on the histology of colon tumors or adenocarcinomas. It also caused significant increase in the labeling index of colon epithelial cells. These findings indicate that PHI enhances colon carcinogenesis, and that its effect may be related to increasing proliferation of colon epithelial cells.

Adenocarcinoma↗

PubMed1995

Attenuation of vasoactive intestinal peptide enhancement of colon carcinogenesis by ornithine decarboxylase inhibitor.

The effects of combined administration of vasoactive intestinal peptide (VIP) and the ornithine decarboxylase (ODC) inhibitor, 1,3-diaminopropane (DAP), on development of colon tumors induced by azoxymethane (AOM), on ODC activity of the colon wall, and on the labelling index of colon epithelial cells were investigated in inbred Wistar rats. Rats received weekly subcutaneous injections of AOM for 10 weeks and subcutaneous injections of VIP every other day and drinking water containing DAP (2.5 milligrams) ad libitum until the end of the experiment at week 45. Administration of VIP significantly increased the incidence of colon tumors at week 45. It also resulted in significant increases in colon ODC activity and in the labelling index during administration of AOM, but not after its cessation. Administration of both DAP and VIP significantly reduced the enhanced colon carcinogenesis by VIP. The DAP significantly attenuated the VIP enhancement of colon ODC activity and of the labelling index during AOM administration. These findings indicate that ODC inhibition attenuated enhancement of colon carcinogenesis, and suggest that enhancement of colon carcinogenesis by VIP may be mediated through its polyamine biosynthesis.

Adenocarcinoma↗

PubMed1995

Chemoprevention by galanin against colon carcinogenesis induced by azoxymethane in Wistar rats.

The effects of the neuropeptide galanin on the development of colon tumors induced by azoxymethane (AOM) and on the labeling index of colon epithelial cells were investigated in Wistar rats. Treatment with galanin significantly decreased the incidence of colon tumors at week 45. Galanin did not influence the histological appearance of the colon tumors, but it slightly increased the frequency of sub-mucosal adenocarcinomas. Furthermore, it significantly decreased the labeling index of colon mucosa during and after AOM treatment. These findings indicate that galanin inhibited the development of colon tumors and that this effect may be related to its suppression of colon-epithelial-cell proliferation.

Animals↗

PubMed1995

Liver with hypoechoic nodular pattern as a risk factor for hepatocellular carcinoma.

BACKGROUND/AIMS: Ultrasonography should be used for screening of hepatocellular carcinoma, but there are few reports on the relationship between liver ultrasonographic findings and the development of hepatocellular carcinoma (HCC). Using prospective follow-up studies, we examined the role of liver with a hypoechoic nodular pattern as a high-risk factor in HCC. METHODS: The study was performed by follow-up on 593 patients with chronic liver disease recorded at our hospital. The ultrasonographic pattern of the liver parenchyma was classified either as a small or large hypoechoic nodular pattern or as a nonnodular pattern. Patients were followed up from the time of initial ultrasonographic examination (1985-1987) until January 1, 1991. RESULTS: During the follow-up period (average, 4.2 years, range, 0.3-6.0 years), 62 patients were found to have HCC (12%). Patients whose livers showed small or large hypoechoic nodular pattern had a significantly higher risk of HCC than did patients whose livers showed a nonnodular pattern (rate ratios were 14.0 and 20.0, respectively, adjusted for age, sex, hepatitis virus markers, ICG R15, alpha-fetoprotein concentration, and ultrasonographic pattern of the liver). CONCLUSIONS: Liver showing a hypoechoic nodular pattern is a major risk factor in HCC.

Adult↗

PubMed1995

No effect of RU 486 (mifepristone) on hepatocellular tumorigenesis in orchiectomized male mice induced by 3'-methyl-4-dimethylaminoazobenzene.

Effects of RU 486 (mifepristone) on hepatocellular tumorigenesis in orchiectomized male mice induced by 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) were investigated. Male mice that had been treated with 3'-Me-DAB neonatally were orchiectomized at one month of age, and injected daily with vehicle only or RU 486 at 0.2 or 0.4 mg/day thereafter. In the liver of orchiectomized males injected with vehicle only, adenomatous nodules developed at incidences of 16.2 and 38.5% at 9 and 12 months of age, respectively, but no carcinomas developed at these ages. Injections of RU 486 at 0.2 or 0.4 mg/day neither affect incidences of adenomatous nodules in the liver, their numbers per mouse, and their areas, nor promote the development of carcinomas. The present results suggest that the long term administration of RU 486 has no effects on hepatocellular tumorigenesis.

Animals↗

PubMed1995

Correlation between serum prolactin levels and hepatocellular tumorigenesis induced by 3'-methyl-4-dimethylaminoazobenzene in mice.

Ovariectomy at 1 month of age promotes development of hepatocellular adenomatous nodules in female C57BL/6 x DS-F1 mice treated neonatally with 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB). Implantation of oestradiol-17 beta (E2) pellets at 1 month of age suppresses nodule development. Since E2 increases serum levels of prolactin, high serum levels of prolactin in mice that have received implants of E2 pellets may play a role in the suppression of hepatocellular tumorigenesis. Therefore, to investigate the role of prolactin in hepatocellular tumorigenesis, we examined development of adenomatous nodules in female mice that had been treated neonatally with 3'-Me-DAB and had undergone ovariectomy at 1 month of age, under various serum levels of prolactin. Treatment of these mice with perphenazine (dopamine antagonist) from 6 months of age or transplantation of pituitary glands under the renal capsule at 6 months of age markedly increased serum levels of prolactin and significantly suppressed the incidence of adenomatous nodules at 12 months of age. Implantation of E2 pellets at 1 month of age increased serum levels of prolactin to a greater extent and further decreased the incidence of adenomatous nodules. Treatment of mice that had received implants of E2 pellets at 1 month of age with bromocriptine (dopamine agonist) from 6 months of age decreased serum levels of prolactin, and was accompanied by an increase in the incidence of nodules. The present results showed that an increase in serum levels of prolactin was accompanied by a decrease in incidence of liver tumours induced by 3'-Me-DAB in mice, suggesting a suppressive effect of prolactin on liver tumorigenesis in mice. Thus, it is possible that the suppressive effect of oestrogen on liver tumorigenesis in mice is mediated, at least in part, by prolactin.

Adenoma↗

PubMed1995

Chemoprevention by amiloride of experimental carcinogenesis in rat colon induced by azoxymethane.

The effects of amiloride on the incidence and histology of colon tumors induced by azoxymethane, on the labeling index of the colon mucosa and on the activity of ornithine decarboxylase in the colon wall were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body wt azoxymethane and s.c. injections of 5 or 7.5 mg/kg body wt amiloride in depot form every other day for 35 weeks. Prolonged administration of amiloride at a dose of 7.5 mg/kg, but not 5 mg/kg, significantly reduced the incidence of colon tumors at week 35. However, administration of amiloride had little or no significant influence on the histological types of colon tumors and cancers. Administration of amiloride at 7.5 mg/kg significantly decreased the labeling index of the colon mucosa and ornithine decarboxylase activity in the colon wall during and after administration of azoxymethane. These findings suggest that amiloride inhibits development of colon tumors. A possible mechanism of inhibition of colon carcinogenesis by amiloride is its suppression of proliferation of colon tumor cells.

Amiloride↗

PubMed1995

Ornithine decarboxylase inhibitor attenuates NaCl enhancement of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine.

The effects of combined administration of NaCl and the ornithine decarboxylase (ODC) inhibitor 1,3-diaminopropane (DAP) on the incidence and number of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and on the ODC activity of the gastric wall and the labeling index of the gastric mucosa were investigated in inbred Wistar rats. Rats were given drinking water with or without 2.5 g/l DAP and chow pellets with and without 10% NaCl ad libitum after 25 weeks of oral administration of MNNG. At week 52 feeding 10% NaCl resulted in significant increases in the incidence of gastric cancers, in the ODC activity of the antral portion of the gastric wall and in the labeling index of antral epithelial cells. Administration of both NaCl and DAP significantly reduced the enhancements by NaCl of gastric carcinogenesis, ODC activity of the antral wall and the labeling index of antral epithelial cells. These results suggest that inhibition of ODC attenuates NaCl enhancement of gastric carcinogenesis and that enhancement by NaCl of gastric carcinogenesis is mediated by polyamine biosynthesis.

Animals↗

PubMed1995

Scanning electron microscopic observations on gastric mucus secretion in rats, and the effects of tetraprenylacetone.

Mucus secretion in the gastric mucosa of rats was studied with a scanning electron microscope. After stimulation, two types of mucus secretion were observed: exocytosis and apical expulsion. Prolonged administration of tetraprenylacetone (TPA) significantly increased the number of mucus-secreting cells in both the gastric corpus and antrum 12 h after the last administration of TPA. In the secreting cells, apical expulsion was significantly more frequent among TPA-treated than in untreated rats. TPA also significantly increased the hexosamine concentration in both gastric corpus and antrum. These findings indicate that TPA stimulates both the content and the secretion of gastric mucus, and that its secretion is chiefly through apical expulsion.

Animals↗

PubMed1994

Protection by galanin against gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of prolonged administration of the neuropeptide galanin on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine, the norepinephrine concentration in the gastric wall, and the labeling index of the gastric mucosa were investigated in Wistar rats. The rats received 2 or 4 micrograms/kg body weight of galanin s.c. every other day after 25 weeks oral treatment with the carcinogen. Prolonged administration of galanin at 4 micrograms/kg body weight, but not at 2 micrograms/kg body weight, significantly decreased the incidence of gastric cancers in experimental week 52. However, it did not influence the histological types of cancers. Galanin at 4 micrograms/kg body weight also significantly decreased the labeling index of the antral epithelial cells but not the norepinephrine concentration in the gastric wall. These findings indicate that galanin inhibits gastric carcinogenesis and suggest that its effect may be related to the suppression of proliferation of the antral epithelial cells.

Animals↗

PubMed1994

Diagnosis of colorectal tumors by the endoscopic Congo red-methylene blue test.

The endoscopic Congo red-methylene blue test was performed on 51 tumors of the large intestine. Results revealed that colorectal adenocarcinomas and adenomas bleached the Congo red and methylene blue sprayed over their surface and so appeared in sharp contrast to the bluish red mucosa of unaffected areas. No bleaching of the dyes was observed on the surface of non-neoplastic polyps. Moderately differentiated adenocarcinomas, submucosal or advanced cancers, and adenomas with severe atypia bleached the dyes most frequently. Thus this test facilitates early detection of colorectal tumors.

Adenocarcinoma↗

PubMed1992

Protection by muscimol against gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in spontaneously hypertensive rats.

The effects of prolonged administration of the gamma-aminobutyric acid receptor agonist muscimol on enhanced induction of gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in spontaneously hypertensive rats (SHR), and on the norepinephrine concentration in the gastric wall and the labeling index of gastric mucosa were investigated. SHR and normotensive Wistar Kyoto (WKY) rats as controls were given a solution of MNNG (25 micrograms/ml) for 25 weeks and then i.p. injections of 0.5 mg/kg body weight of muscimol every other day. In control WKY rats, gastric cancers were found in 1 (7%) of 14 rats examined at week 52. In SHR treated with NaCl solution only, the incidence of gastric cancers was significantly increased to 50% compared with that in control WKY rats. However, treatment of SHR with muscimol significantly increased its incidence to 12% compared with the value in SHR treated with NaCl solution only. The norepinephrine concentration in the gastric wall and the labeling index of the gastric mucosa were significantly greater in SHR than in WKY rats. Prolonged administration of muscimol to SHR significantly reduced the norepinephrine concentration in the antral portion of the gastric wall or the labeling index of the antral epithelial cells. These findings indicate that long-term treatment of SHR with muscimol attenuated the enhancement of gastric carcinogenesis in SHR.

Analysis of Variance↗

PubMed1992

Inhibition by 6-hydroxydopamine of enhanced gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in spontaneously hypertensive rats.

The effects of chemical sympathectomy induced by 6-hydroxydopamine (6-OHDA) on the enhanced induction of gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in spontaneously hypertensive rats (SHR), and the norepinephrine (NE) concentrations in their gastric wall and the labeling index of gastric epithelial cells were investigated. SHR rats and normotensive Wistar Kyoto rats (WKY) as controls were given MNNG (25 micrograms/ml) in their drinking water for 25 weeks and then i.p. injections of 6-OHDA (42 mg/kg twice within 24 hr, and then 105 mg/kg every 2 weeks from 1 week later). In control group (WKY rat + NaCl), gastric cancers were found in 2 (11%) of 18 rats examined in week 52. In SHR rats treated with NaCl solution only, the incidence of gastric cancers significantly increased, to 53% compared with that in control WKY rats. Treatment of SHR rats with 6-OHDA significantly decreased its incidence to 12% compared with the value in SHR rats treated with NaCl solution only. Prolonged administration of 6-OHDA to SHR rats significantly reduced the NE concentration in the antral portion of the gastric wall and the labeling index of antral epithelial cells. These findings indicate that prolonged i.p. treatment with 6-OHDA attenuated the normally higher incidence of MNNG-induced gastric cancer in SHR rats.

Animals↗

PubMed1992

Inhibitions by 6-hydroxydopamine and neostigmine singly or together of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of chemical sympathectomy induced by 6-hydroxydopamine (6-OHDA) and administration of the acetylcholinesterase inhibitor neostigmine, singly or together, on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and on the tissue catecholamine concentration of the gastric wall and the labeling index of the gastric mucosa, were investigated in inbred Wistar rats. Rats received s.c. injections of neostigmine (0.075 mg/kg), and/or i.p. injections of 6-OHDA (42 mg/kg twice within 24 hr, and then 105 mg/kg every 2 weeks from 1 week later) 25 weeks after oral treatment with MNNG. Prolonged administration of 6-OHDA or neostigmine significantly reduced the incidence of gastric cancers by week 52, and in combination they had a significantly greater inhibitory effect. 6-OHDA and/or neostigmine had no influence on the histology of gastric cancers. Administration of 6-OHDA, but not neostigmine, significantly decreased the norepinephrine concentration in the antral portion of the gastric wall. The labeling index of the antral mucosa was decreased significantly by treatment with 6-OHDA or neostigmine, and decreased even more significantly by 6-OHDA plus neostigmine. Our findings indicate that 6-OHDA and neostigmine have protective effects against gastric carcinogenesis and that in combination their effects are additive. These results imply that the activities of the sympathetic and parasympathetic autonomic systems together influence gastric carcinogenesis.

Animals↗

PubMed1992

Early depressed adenocarcinomas of the large intestine.

From January 1987 to December 1990, five cases of early depressed cancer of the large intestine were seen. Endoscopically, almost all of these tumors were located in the proximal colon and looked like a reddish depression (similar to the sucker of an octopus). Histologically, all of these cancers were well differentiated and tended to reach deeper layers at an early stage. Four (80%) of these cancers were not associated with adenoma and were thought to have arisen de novo.

Adenocarcinoma↗

PubMed1992

Enhancement by thyroxine of experimental carcinogenesis induced in rat colon by azoxymethane.

The effect of thyroxine (T4) on the incidence, number and histology of colon tumors induced by azoxymethane (AOM), and on the labeling index of colon mucosa were investigated in Wistar rats. Rats were given AOM by injection once a week for 10 weeks, together with T4 in depot form until the end of the experiment. Administration of T4 resulted in a significant increase in the incidence of colon tumors in week 35. However, it did not influence the histological appearance of the colon tumors or the histological types and depths of involvement of colon adenocarcinomas. Furthermore, it caused a significant increase in the labeling index of the colon during, but not after, AOM treatment. Our findings indicate that T4 enhances the development of colon tumors, which may be related to its effect in increasing proliferation of epithelial cells in the colon mucosa during administration of the carcinogen.

Adenocarcinoma↗