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Biomedical subjects

H Iishi

Publications and source records attributed to H Iishi.

At least 145 records · Page 8Linked to original sources
PubMed1991

Protective effect by potassium chloride against gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in spontaneously hypertensive rats.

The effects of oral potassium supplementation on the enhanced induction of gastric carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in spontaneously hypertensive rats (SHR), and the norepinephrine concentration in their gastric wall were investigated. The SHR and normotensive Wistar Kyoto rats (WKY) as controls were given a solution of the carcinogen for 25 weeks and then 1% KCl solution or tap water to drink. In Week 52, the incidence of gastric cancers and their number per rat and the norepinephrine concentration in the gastric wall were significantly greater in SHR than in WKY. Prolonged oral treatment of SHR with potassium significantly reduced the incidence of gastric cancers and their number per rat, as well as the blood pressure and the norepinephrine concentration in the antral portion of the gastric wall. These findings indicate that prolonged treatment with KCl attenuated the enhancement of gastric carcinogenesis by MNNG in SHR.

Animals↗
PubMed1991

Inhibition by xiao-chai-hu-tang (TJ-9) of development of hepatic foci induced by N-nitrosomorpholine in Sprague-Dawley rats.

The effect of Xiao-chai-hu-tang (TJ-9) on hepatocarcinogenesis induced by N-nitrosomorpholine (NNM) was investigated in male Sprague-Dawley rats. Rats were given normal chow pellets containing 0.5% or 1.0% TJ-9 until the end of the experiment, and drinking water containing NNM for 8 weeks. Pre-neoplastic and neoplastic lesions staining for gamma-glutamyl transpeptidase (GGT) or the placental type of glutathione-S-transferase (GST-P) were examined histochemically. In Week 15, quantitative histological analysis showed that prolonged treatment with 0.5% TJ-9 significantly reduced the number and volume of GGT-positive and GST-P-positive hepatic lesions. Treatment with 1.0% TJ-9 inhibited the development of GGT-positive and GST-P-positive lesions, but was less effective than 0.5% TJ-9. Administration of 0.5% TJ-9 also caused a significant increase in the proportion of helper T lymphocytes and a significant decrease in the labeling index of pre-neoplastic lesions. These findings indicate that TJ-9 inhibits the development of hepatic foci.

Animals↗
PubMed1990

Effect of tetragastrin on azaserine-induced carcinogenesis in rat pancreas.

The effect of tetragastrin on pancreatic tumors induced by azaserine was investigated in Wistar rats. Rats were given 25 weekly injections of 10 mg/kg body weight of azaserine and 1 mg/kg body weight of tetragastrin as a suspension in olive oil every other day. Carcinogen-induced pancreatic lesions were examined by histochemical techniques, and were classified as ATPase-positive or ATPase-negative. In week 62, quantitative histological analysis showed that prolonged administration of tetragastrin had little or no influence on the number and size of the carcinogen-induced pancreatic lesions, although it caused significantly increased cell proliferation, indicated by a greater labelling index of the pancreatic acinar cells.

Adenosine Triphosphatases↗
PubMed1990

Attenuating effect of bromocriptine on cysteamine anticarcinogenesis of stomach cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine.

The effect of bromocriptine on inhibition by cysteamine of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine was investigated in inbred Wistar rats. After 25 weeks of p.o. treatment with N-methyl-N'-nitro-N-nitrosoguanidine, rats were given injections every other day: cysteamine (50 mg/kg body weight); cysteamine (50 mg/kg body weight) plus bromocriptine (0.5 or 0.25 mg/kg body weight); or bromocriptine (0.5 or 0.25 mg/kg body weight). In week 52, the group treated with cysteamine showed a significantly decreased incidence of gastric cancers. Concomitant treatment with bromocriptine at 0.5 but not at 0.25 mg/kg body weight significantly attenuated the inhibitory effect of cysteamine on gastric carcinogenesis. Administration of bromocriptine alone at either dosage had no influence on gastric carcinogenesis. The labeling index of the antral mucosa was significantly reduced in rats treated with cysteamine and significantly higher in those treated concomitantly with bromocriptine at 0.5 mg/kg body weight than in those treated with cysteamine alone. These findings indicate that cysteamine suppressed gastric carcinogenesis and that bromocriptine at high dosage attenuated this inhibition. These findings also suggest that dopamine is involved in the mechanism of inhibition of gastric carcinogenesis by cysteamine.

Animals↗
PubMed1990

Inhibition by gamma-amino-n-butyric acid and baclofen of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effect of gamma-amino-n-butyric acid (GABA), the GABA(A) receptor agonist muscimol (5-aminomethyl-3-hydroxyisoxazole), and the GABA(B) receptor agonist baclofen [4-amino-3-(4-chlorophenyl)butanoic acid] on the incidence and number of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine was investigated in Wistar rats. Rats received alternate-day i.p. injections of 500 or 1000 mg/kg of body weight GABA, 0.25 or 0.5 mg/kg of body weight muscimol, or 4 or 8 mg/kg of body weight baclofen after 25 wk of p.o. treatment with the carcinogen. Prolonged administration of GABA at 1000 mg/kg of body weight, but not at 500 mg/kg of body weight, and of baclofen at 4 and 8 mg/kg of body weight significantly decreased the incidence and number of gastric cancers of the glandular stomach in Wk 52, but long-term muscimol administration had no influence. Histologically, GABA at the high dosage and baclofen at both dosages significantly decreased the labeling index of the antral mucosa and significantly increased the serum gastrin level. Furthermore, baclofen at both dosages significantly decreased antral pH and significantly increased gastric acid secretion. These findings indicate that GABA inhibits gastric carcinogenesis via the GABAB receptor and that this effect may be related to its effect in decreasing the proliferation of antral mucosa.

Animals↗
PubMed1990

Enhancement of azoxymethane-induced colon carcinogenesis in spontaneously hypertensive rats.

The incidence, number, location, and histological types of colon tumors induced by azoxymethane (AOM) and the tissue norepinephrine concentration of the colon wall were investigated in spontaneously hypertensive (SH) rats and in control normotensive Wistar Kyoto (WKY) rats. All rats received 10 weekly s.c. injections of AOM. At week 30, the incidence of colon tumors were significantly higher in SH than in WKY rats. Colon tumors were chiefly located in the proximal colon in WKY but were found with significant frequency in the distal colon in SH rats. The colon tumors induced were mainly adenocarcinomas, but no significant difference in histological type of adenocarcinoma was found between the 2 strains of rat. At weeks 8 and 30, the norepinephrine concentration and labelling index of the distal colon, but not of the proximal colon, were significantly higher in SH than in WKY rats. These findings indicate that increased sympathetic nervous system activity enhances the development of colon tumors.

Adenocarcinoma↗
PubMed1990

Effect of calcium channel blockers on gastric carcinogenesis and caerulein enhancement of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of the organic calcium channel blocker verapamil and the inorganic calcium channel blocker MgCl2 on gastric carcinogenesis, on caerulein enhancement of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine, and on the labeling index of gastric mucosa were investigated in inbred Wistar rats. After 25 weeks of treatment with N-methyl-N'-nitro-N-nitrosoguanidine (50 micrograms/ml p.o.), rats received one of the following alternate-day injections: caerulein (2 micrograms/kg body weight, s.c.), MgCl2 (150 mg/kg, s.c.), verapamil (20 mg/kg body weight, i.p.), caerulein (2 micrograms/kg body weight, s.c.) plus MgCl2 (150 mg/kg body weight, s.c.), or caerulein (2 micrograms/kg body weight, s.c.) plus verapamil (20 mg/kg body weight, i.p.). At Week 52, prolonged administration of caerulein had significantly increased the incidence and number of adenocarcinomas in the glandular stomach and the incidence of gastric cancers that penetrated through or beyond the muscle layer. Concomitant administration of MgCl2 significantly attenuated the enhancing effect of caerulein on gastric carcinogenesis. Combined administration of caerulein and verapamil did not affect the incidence and number of gastric cancers but significantly reduced the incidence of cancers penetrating through or beyond the muscle layer. Administration of MgCl2 or verapamil alone had no influence on gastric carcinogenesis. Rats treated with caerulein had a significantly elevated labeling index of the antral mucosa which was significantly decreased by concomitant administration of MgCl2 and/or of verapamil, as compared with the labeling index observed after treatment with caerulein alone. Either MgCl2 or verapamil alone had no influence on the labeling index of the antral mucosa. These findings indicate that caerulein enhances gastric carcinogenesis and that MgCl2 and verapamil attenuate this enhancement. These findings also indicate that calcium may play an important role in caerulein enhancement of gastric carcinogenesis.

Adenocarcinoma↗
PubMed1990

Effect of ornithine decarboxylase inhibitor on tetragastrin treatment of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of combined administration of tetragastrin and the ornithine decarboxylase inhibitor 1,3-diaminopropane (DAP) on the incidence and number of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and the BUdR labelling indices of the fundic and antral mucosae, were investigated in inbred Wistar rats. Rats were given drinking water containing 2.5 g/l of DAP ad libitum and received alternate-day injections of 1 mg/kg body weight of tetragastrin in depot form after 25 weeks of oral treatment with MNNG. At week 52, prolonged administration of tetragastrin alone resulted in a significant reduction in the incidence and number of gastric cancers and a significant increase or decrease in the labelling indices of the fundic and antral mucosae, respectively. Concomitant administration of tetragastrin and DAP had no effect on the inhibition by tetragastrin of gastric carcinogenesis. With this treatment, the labelling index was significantly reduced in the fundic mucosa but not in the antral mucosa. These results suggest that ODC inhibitor does not attenuate tetragastrin inhibition of gastric carcinogenesis, and that anti-trophic action of tetragastrin on antral mucosa may be related to tetragastrin inhibition of gastric carcinogenesis.

Animals↗
PubMed1990

Diagnosis of hepatic cavernous hemangioma by fine needle aspiration biopsy under ultrasonic guidance.

Percutaneous aspiration biopsy of the liver using a heparinized 22-gauge needle was performed under ultrasonic guidance in 11 patients with hepatic cavernous hemangioma. Ten (91%) of 11 biopsy specimens obtained were cytologically diagnostic for hemangioma. No indications of malignancy were found. There was no relation between the cytological diagnosis and the location, size, or ultrasonographic findings. No complications were encountered. These findings indicate that cytological examination of the liver by fine needle aspiration biopsy is useful in diagnosing hepatic cavernous hemangioma of any size and in any location, provided optimal route to the lesions is chosen.

Aged↗
PubMed1990

Enhancement of mucus accumulation in a human gastric scirrhous carcinoma cell line (KATO-III) by fibroblast-tumor cell interaction.

Human fibroblasts (WI-38 cells) were found to enhance mucus accumulation by human scirrhous carcinoma cells (KATO-III cells). Coculture of KATO-III with WI-38 cells resulted in enlargement of the KATO-III cells and increases in the proportions of PAS- and colloidal iron-positive KATO-III cells. These morphological alterations were reversed when the KATO-III cells were again cultured without WI-38 cells. Conditioned media from cultures of WI-38 cells or cocultures of KATO-III and WI-38 cells induced the same morphological alterations in KATO-III cells, suggesting that WI-38 cells produce a factor or factors that enhance mucus accumulation in KATO-III cells. This factor seemed to be a protein with a molecular weight of more than 10,000 daltons.

Adenocarcinoma, Scirrhous↗
PubMed1990

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

The effect of oral administration of L-phenylalanine on the incidence and histology of gastric adenocarcinomas induced by N-methyl-N'-nitro-N-nitrosoguanidine was investigated in inbred Wistar rats. Oral administration of 6% phenylalanine after 25 weeks of treatment with the carcinogen significantly reduced the incidence and number of adenocarcinomas of the glandular stomach at experimental week 52. Oral administration of high dose phenylalanine significantly increased the basal serum gastrin level and significantly decreased the norepinephrine concentration in the antral portion of the gastric wall, as well as the labelling indices of antral mucosa. These findings indicate that orally administered phenylalanine inhibits the development of gastric cancers.

Adenocarcinoma↗
PubMed1990

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

The effects of neurotensin on the incidence, number, size, and histology of colon tumours induced by azoxymethane (AOM) were investigated in Wistar rats. Rats were given 10 weekly injections of AOM (7.4 mg kg-1 body weight) and were also given 200 micrograms kg-1 of neurotensin in depot form every other day until the end of the experiment. In week 40, prolonged alternate-day administration of neurotensin resulted in significant increases in the number and size of colon tumours and the incidence of adenocarcinomas penetrating muscle layer and deeper. However, neurotensin did not influence the incidence of tumour-bearing rats and the histological appearance of colon tumours. Administration of neurotensin caused a significant increase in the labelling index of the colon cancers but not that of colon mucosa. These findings indicate that neurotensin enhanced the growth of colon tumours, possibly related to its effect in increasing proliferation of colon cancer cells.

Adenocarcinoma↗
PubMed1990

Gastric emptying in patients with fundal gastritis and gastric cancer.

Gastric emptying was compared in patients with gastric cancers and fundal gastritis to determine its value in identifying patients at high risk of gastric cancer. Gastric emptying was measured by the acetaminophen absorption method, and the extent of fundal gastritis was determined by the endoscopic Congo red test. The results showed that gastric emptying was significantly slower in patients with severe fundal gastritis than in those without. Gastric emptying in patients with differentiated adenocarcinomas was significantly slower than in those with undifferentiated adenocarcinoma, its value being similar to that in patients with severe fundal gastritis. The Congo red test showed that the incidence of severe fundal gastritis was significantly greater in patients with differentiated adenocarcinomas than in those with undifferentiated cancers. These findings suggest that delayed gastric emptying may allow prolonged contact between dietary carcinogens and the stomach.

Adenocarcinoma↗
PubMed1990

Reduction of gastric ulcer recurrence after suppression of Helicobacter pylori by cefixime.

The effect on the recurrence of gastric ulcers after suppression of Helicobacter pylori by combined treatment with cimetidine and the antimicrobial drug cefixime was investigated. Twenty one of 43 patients with endoscopically proved gastric ulcer and H pylori infection were randomly assigned to receive cimetidine 800 mg daily for 12 weeks; the remaining 22 patients received cimetidine 800 mg daily for 12 weeks plus cefixime 100 mg daily for the last two weeks. After treatment, 88% of 17 patients on cimetidine only remained H pylori positive, whereas combined administration of cimetidine and cefixime had suppressed H pylori in 78% of 18 patients (p less than 0.05). Seventeen patients in the former group whose ulcers healed but who remained H pylori positive and 18 patients in the latter group whose ulcers healed and who were no longer infected with H pylori continued to be followed after treatment. These patients underwent endoscopy to detect ulcer recurrence if symptomatic, or at 12 and 24 weeks if asymptomatic. At 12 weeks, recurrence was observed in seven of 15 (47%) patients in whom H pylori persisted, but in only one of 14 (7%) patients in whom H pylori had been suppressed (p less than 0.05). At 24 weeks, however, recurrence rates were similar between the two groups. These findings indicate that H pylori infection may be closely related to early ulcer recurrence.

Cefixime↗
PubMed1989

Tissue norepinephrine depletion as a mechanism for cysteamine inhibition of colon carcinogenesis induced by azoxymethane in Wistar rats.

The effects of cysteamine (2-aminoethanethiol hydrochloride) on the incidence, number and histology of colon tumors induced by azoxymethane (AOM), and on the norepinephrine concentration in the colon wall tissue and the labelling indices of colon mucosa and colon cancers were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body weight of AOM and alternate-day subcutaneous injections of 25 mg/kg of cysteamine in 0.9% NaCl solution until the end of the experiment. At week 40, prolonged administration of cysteamine significantly reduced the incidence and number of colon tumors. Histologically, the adenocarcinomas that did develop in rats treated with cysteamine exhibited high mucin-producing activity. Administration of cysteamine caused significant decreases in the norepinephrine concentration in colon tissue and in the labelling indices of colon mucosa and cancers. Our findings indicate that cysteamine inhibits the development of colon tumors. This action may be related to its effect in decreasing norepinephrine concentration in the colon wall tissues and subsequently in decreasing proliferation of colon cancer cells.

Adenocarcinoma↗
PubMed1989

Enhancement by somatostatin of experimental gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of somatostatin on the incidence, number, and histological type of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine were investigated in Wistar rats. Rats received alternate-day s.c. injections of 100 or 200 micrograms/kg body weight of somatostatin in depot form after 25 weeks of p.o. treatment with the carcinogen. Prolonged administration of somatostatin at both dosages significantly increased the incidence and number of gastric cancers of the glandular stomach in Week 52. Furthermore, somatostatin at 200 micrograms/kg caused a significant increase in the incidence of gastric cancers penetrating the muscle layer or deeper layers. However, somatostatin at both dosages did not influence their histological appearance. Histologically, somatostatin at both dosages significantly elevated the labeling index of gastric cancers but not of the antral mucosa and significantly reduced the gastrin levels. These findings indicate that somatostatin enhances gastric carcinogenesis after N-methyl-N'-nitro-N-nitrosoguanidine treatment and that this effect may be related to its effect in increasing proliferation of gastric cancers and decreasing serum gastrin level.

Animals↗
PubMed1989

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

The effects of bombesin on the incidence, number, histological type, and depth of involvement of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in male Wistar rats. Rats received alternate-day s.c. administration of 20 or 40 micrograms/kg body weight of bombesin in depot form after p.o. treatment with the carcinogen for 25 weeks. Prolonged administration of bombesin at 40 micrograms/kg led to a significant increase in the incidence and number per rat of gastric cancers of the glandular stomach at Week 52. In rats that had received alternate-day injections of 20 micrograms/kg of bombesin, the number of gastric cancers per rat, but not the incidence of cancer, was significantly more than in untreated rats. However, bombesin at both dosages did not affect the histological appearance of the lesions or their depth of involvement. At Weeks 30 and 52, norepinephrine concentrations in the fundic and antral portion of the gastric walls and labeling indices in the antral and fundic mucosae were significantly higher in rats treated with bombesin at both dosages than in untreated rats. These findings indicate that bombesin enhances gastric carcinogenesis after administration of N-methyl-N'-nitro-N-nitrosoguanidine is stopped and that this effect may be related to its effects in increasing tissue norepinephrine concentrations in the stomach wall and increasing cell proliferation in the gastric mucosa.

Animals↗