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Biomedical subjects

M Hirose

Publications and source records attributed to M Hirose.

At least 415 records · Page 23Linked to original sources
PubMed1993

Carcinogenicity of catechol in F344 rats and B6C3F1 mice.

Carcinogenicity of catechol, a naturally occurring and industrial chemical which has been shown to have strong cell proliferating potential on rat glandular stomach epithelium, was investigated in male and female F344 rats and B6C3F1 mice. Groups of 30 male and female F344 rats and B6C3F1 mice were treated with 0.8% catechol in powdered diet continuously for 104 weeks (rats) or 96 weeks (mice). At necropsy, neoplastic lesions were observed mainly in the glandular stomach of both species. Adenomas were found in all rats and in the majority of mice: 29 out of 30 (97%) in males and 21 out of 29 (72%) females. In addition 15 out of 28 (54%) and 12 out of 28 (43%) of the male and female rats respectively, had well differentiated adenocarcinomas. No adenocarcinomas were found in mice of either sex. In the forestomach epithelium, although significant increase in papilloma development was not evident, incidences of squamous cell hyperplasia were significantly increased in rats and mice of both sexes. In other organs examined, incidence and numbers of liver hyperplastic foci per cm2 liver section were significantly lower in male rats. Although the incidence was not different, the numbers of hyperplastic foci were also significantly reduced in female rats. Thus the present experiment clearly demonstrated that catechol exerts carcinogenic activity in rodent glandular stomach epithelium.

Adenocarcinoma↗
PubMed1993

Modification of BHA forestomach carcinogenesis in rats: inhibition by diethylmaleate or indomethacin and enhancement by a retinoid.

The long-term effects of butylated hydroxyanisole (BHA), in combination with various other chemicals on the development of forestomach lesions in rats were investigated. BHA is a synthetic antioxidant, and the other agents included the glutathione-depleting agent diethylmaleate (DEM), the anti-inflammatory drugs indomethacin (IM), dexamethazone (DEX), 6-aminocaproic acetate (6-ACA) and FOY (gabexate mesilate), and the vitamin all-trans-retinol acetate (RA). Concurrent treatment with BHA (1% in diet) and DEM, IM, DEX or FOY for 52 weeks inhibited development of forestomach epithelial hyperplasia as compared to BHA alone, while simultaneous treatment with RA enhanced hyperplastic development. However, the inhibition by DEX or FOY was only partial and in the DEX case, in particular, might have been due to weight loss. Since the most effective inhibitory influence on BHA-induced forestomach lesions exerted in this 1-year experiment was by DEM, a further 2-year experiment was conducted to confirm whether DEM actually can exert inhibitory effects on BHA (2% in diet)-induced forestomach carcinogenesis. The results demonstrated that induction of forestomach hyperplasias and papillomas by BHA was significantly reduced by combination treatment with DEM. Both multiplicity and incidence of forestomach papillomas were significantly decreased, while squamous cell carcinoma development showed a tendency for decrease only.

Animals↗
PubMed1993

DNA methylation of the pepsinogen 1 gene during rat glandular stomach carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine or catechol.

The methylation patterns of the rat pepsinogen 1 (Pg1) gene in preneoplastic and neoplastic stomach lesions induced by genotoxic N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) or the non-genotoxic carcinogen catechol were investigated. Male WKY/Ncrj rats were given MNNG in their drinking water (50 mg/l) for 30 weeks or 0.8% catechol throughout the experiment (60 weeks). MNNG induced Pg1 altered pyloric glands (PAPG), adenomatous hyperplasias and well-differentiated adenocarcinomas. Catechol also induced PAPG and adenomatous hyperplasias although cancers did not develop. Adenomatous hyperplasias and adenocarcinomas all consisted of gastric type cells resembling surface mucous cells or pyloric gland cells with little or no Pg1 expression. In MNNG-induced stomach cancers generally lacking Pg1, altered Pg1 gene methylation was observed with both CCGG and GCGC sites being methylated more than normal pyloric mucosa. MNNG or catechol-induced adenomatous hyperplasias also demonstrated essentially the same methylation changes in the CCGG, but not in the GCGC sites. In the mucosa containing PAPG in groups treated with MNNG or catechol the methylation patterns of the Pg1 gene were quite similar to those of normal pyloric mucosa, although the CCGG sites tended to demonstrate slightly increased methylation. The results suggest that the altered methylation of the Pg1 gene observed in stomach cancers is acquired early in the carcinogenic process and progressive methylation changes occur with tumor development.

Adenocarcinoma↗
PubMed1993

Effects of green tea catechins in a rat multi-organ carcinogenesis model.

The effects of dietary administration of green tea catechins (GTC) were examined using a multi-organ carcinogenesis model. Groups of 15 F344 male rats were initially treated with a single i.p. administration of 100 mg/kg body wt N-diethyl-nitrosamine, 4 i.p. administrations of 20 mg/kg body wt N-methylnitrosourea, 4 s.c. doses of 40 mg/kg body wt 1,2-dimethylhydrazine, together with 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine for 2 weeks and then 0.1% 2,2'-dihydroxy-di-n-propylnitrosamine for 2 weeks, both in the drinking water, for a total initiation period of 4 weeks. GTC in the diet, at doses of 1.0 or 0.1%, was administered from 1 day before and during carcinogen exposure, after carcinogen exposure or both during and after carcinogen exposure. Further groups of animals were treated with carcinogen, 1% GTC or basal diet alone as controls. All animals were killed at the end of week 36, and all major organs examined histopathologically. The numbers of small intestinal tumors (adenomas and carcinomas) per rat were significantly reduced in the groups treated with 1% GTC during (0.13 +/- 0.35) and after carcinogen exposure (0.31 +/- 0.48) and in those receiving 1% and 0.1% GTC both during and after carcinogen exposure (0.14 +/- 0.36, 0.46 +/- 0.97 respectively) as compared with the carcinogen alone group (1.07 +/- 1.21). On the other hand, numbers of glutathione S-transferase placental form positive liver foci per cm2 were slightly but significantly increased in the groups treated with 1 and 0.1% GTC during carcinogen exposure, 1% GTC after carcinogen exposure and 1% GTC both during and after carcinogen exposure. The results indicated that while GTC inhibits small intestinal carcinogenesis it slightly enhances hepatocarcinogenesis in a dose dependent manner when applied both during and after carcinogen exposure.

1,2-Dimethylhydrazine↗
PubMed1993

Exanthema subitum and human herpesvirus 6 infection: clinical observations in fifty-seven cases.

Exanthema subitum had been speculated to be a viral disease although its pathogen is unknown. Human herpesvirus 6 (HHV-6), first isolated in 1986, was proved by Yamanishi et al. to be the causal agent of exanthema subitum. To evaluate the role of HHV-6 as the causal agent in clinically diagnosed exanthema subitum, we tested for HHV-6 antibody in 57 infants with clinical exanthema subitum and exanthema subitum-like rash without fever. Of the 53 patients with clinical exanthema subitum 43 showed seroconversion or a significant rise in antibody titer to HHV-6, 7 were seropositive without significant rise and 3 remained seronegative. The clinical manifestations of these 43 infants with serologically confirmed HHV-6 infection were consistent with the classical characteristics of exanthema subitum. The 4 patients with atypical exanthema subitum showed significant rises in antibody titer. Our results therefore show that the majority of cases with typical clinical manifestations of exanthema subitum had HHV-6 infection. Most cases with HHV-6 infection had the typical clinical course of exanthema subitum, and a few cases might show an afebrile exanthema subitum-like rash.

Antibodies, Viral↗
PubMed1993

Strong inhibition of 2-amino-6-methyldipyrido[1,2-a:3',2'-d] imidazole-induced mutagenesis and hepatocarcinogenesis by 1-O-hexyl-2,3,5-trimethylhydroquinone.

The effects of 3-O-dodecylcarbomethylascorbic acid (3-O-DAsA), 3-O-ethylascorbic acid (3-O-EAsA) and 1-O-hexyl-2,3,5-trimethylhydroquinone (HTHQ) on 2-amino-6-methyldipyrido[1,2-a:3',2'-d]-imidazole (Glu-P-1)-induced mutagenesis and hepatocarcinogenesis were examined. In a Salmonella assay, addition of 2.5 to 20.0 mg of HTHQ to Salmonella TA 98 in the presence of S-9 mixture dose-dependently inhibited Glu-P-1-induced mutagenesis. The highest dose showed a 99% reduction in revertants. 3-O-DAsA and 3-O-EAsA were without effect. In an animal study using the medium-term bioassay system for the detection of hepatocarcinogens or hepatopromoters in F344 male rats, treatment with Glu-P-1 alone was associated with a significant increase in the number and area of GST-P-positive foci (47.5 +/- 8.9 and 11.1 +/- 4.7, respectively). Combined treatment with 1.0% HTHQ significantly reduced the number and area of GST-P-positive foci (to 8.1 +/- 2.1 and 0.6 +/- 0.2) while 3-O-DAsA exerted marginal inhibition and 3-O-EAsA had no effect. On the other hand, all three of these compounds slightly enhanced the numbers and areas of foci when given alone. The results indicate that HTHQ is a potent chemopreventer of Glu-P-1-induced hepatocarcinogenesis.

Animals↗
PubMed1993

Comparison of reversibility of rat forestomach lesions induced by genotoxic and non-genotoxic carcinogens.

Reversibility of forestomach lesions induced by genotoxic and non-genotoxic carcinogens was compared histopathologically. Groups of 30 to 33 male F344 rats were given dietary 0.1% 8-nitroquinoline, dietary 0.4-0.2% 2-(2-furyl)-3-(5-nitro-2-furyl)acrylamide, an intragastric dose of 20 mg/kg body weight N-methyl-N'-nitro-N-nitrosoguanidine once a week, or 20 ppm N-methylnitrosourethane in the drinking water as a genotoxic carcinogen, or 2% butylated hydroxyanisole, 2% caffeic acid, 2% sesamol or 2% 4-methoxyphenol in the diet as a non-genotoxic carcinogen for 24 weeks. Ten or 11 rats in each group were killed at week 24. Half of the remainder were maintained on basal diet alone for an additional 24 weeks and the other half were given the same chemical for 48 weeks, and then killed. Forestomach lesions induced by genotoxic carcinogens did not regress after removal of carcinogens. In contrast, simple or papillary hyperplasia (SPH), but not basal cell hyperplasia (BCH), induced by non-genotoxic carcinogens clearly regressed after cessation of insult. SPH labeling indices in the non-genotoxic carcinogen-treated cases decreased after removal of the carcinogenic stimulus whereas BCH values were low irrespective of treatment. Atypical hyperplasia (AH), observed at high incidences in rats treated with genotoxic carcinogens, was also evident in animals receiving non-genotoxic agents, even after their withdrawal, albeit at low incidences. AH labeling indices remained high even without continued insult. These results indicate that even with non-genotoxic carcinogens, heritable alterations at the DNA level could occur during strong cell proliferation and result in AH development. This putative preneoplastic lesion might then progress to produce carcinomas.

Animals↗
PubMed1993

[Epidemiology of sporadic pediatric enteritis patients due to verotoxin-producing Escherichia coli].

We tried to isolate verotoxin-producing Escherichia coli (VTEC) from 323 sporadic pediatric enteritis patients who came to three clinics in the Fukuoka area. We used the sorbitol-MacConkey medium for the isolation of VTEC O157:H7. For non-O157 VTEC strains we used the V1/PECS method. VT/PECS method was applied. VTEC strains were isolated from three patients (0.9%). None of the patients were seriously, ill or developed the hemolytic uremic syndrome. The three patients were all seen in the summer season, July and August. O157:H7 strains were isolated from two patients, and O145:NM from one. This study showed that sporadic enteritis cases due to VTEC exist in the Fukuoka area. In the future a rapid and easy method for the detection of VT or VTEC should be developed and commercialized to proceed with epidemiological studies of VTEC infections throughout Japan.

Bacterial Toxins↗
PubMed1993

Effect of the head-down tilt position during lower abdominal surgery on endocrine and renal function response.

A head-down tilt position in awake subjects induces natriuresis, accompanied by reduced plasma levels of catecholamines, renin, angiotensin II, aldosterone, and antidiuretic hormone. We hypothesized that the head-down tilt position would counteract the surgical stress response which induces sodium and water retention and increases plasma levels of these hormones. We studied endocrine and renal function responses in patients during lower abdominal surgery, performed under sevoflurane anesthesia, at a 6 degree head-down tilt position (n = 10) versus a horizontal position (n = 10). The mean arterial pressure was maintained constant by adjusting the inspired concentration of sevoflurane. Heart rate, and the dose of sevoflurane, decreased significantly in the head-down tilt position. Increases in plasma norepinephrine and epinephrine levels during surgery were significantly less in the head-down tilt position; in contrast, plasma aldosterone and cortisol levels were increased significantly in this position compared to the horizontal position. Both fractional and total urinary excretion of sodium increased significantly in the head-down tilt position compared to the horizontal position. Plasma renin activity, and antidiuretic hormone and atrial natriuretic peptide levels, as well as urine volume, creatinine clearance, and water clearance showed no positional variation. We conclude that the 6 degree head-down tilt position reduces increased sympathetic activity and lessens renal tubular sodium reabsorption during lower abdominal surgery under sevoflurane anesthesia. Other stress hormones, however, increase more in the head-down tilt position than in the horizontal position.

Abdomen↗
PubMed1993

Limited proteolysis of disulfide-reduced ovalbumin by subtilisin.

Our previous study [Takahashi et al., J. Biochem., 109, 846-851 (1991)] has shown that the disulfide-reduced form of ovalbumin was proteolyzed by subtilisin into three major fragments. It was investigated whether or not these three fragments would be folded into one molecule. Gel permeation and ion-exchange chromatography indicated that the three fragments were eluted in a single peak. The proteolyzed protein had a CD spectrum that was almost indistinguishable from the disulfide-reduced, non-proteolyzed form of ovalbumin. Differential scanning calorimetry, however, revealed that the proteolyzed ovalbumin was denatured at a lower temperature than that of the disulfide-reduced, non-proteolyzed protein. Thus, it is concluded that the three fragments were folded into a native-like conformation with decreased stability. Chemical analyses of the fragments purified by reverse-phase HPLC revealed that there was a cleavage site in the disulfide-reduced form of ovalbumin, at least at the amino-terminal side of Cys(73), in addition to the well-known cleavage sites in plakalbumin.

Amino Acid Sequence↗
PubMed1993

Cell proliferation and forestomach carcinogenesis.

To analyze the role of cell proliferation in phenolic compound-induced rat forestomach carcinogenesis, early forestomach histopathological changes as well as oncogene expression and reversibility of early forestomach lesions were examined in F344 male rats. For the analysis of early lesions, five animals each were treated with butylated hydroxyanisole (BHA), caffeic acid, sesamol, or 4-methoxyphenol in the diet, each at a dose of 2%, and killed for histopathological examination after 12 hr, 1, 3, or 7 days. For oncogene analysis, three animals each were treated with BHA for 15, 30 min, 1, 3, 6, or 24 hr and then sacrificed. In the reversibility study, groups of animals were treated with BHA, caffeic acid, sesamol or 4-methoxyphenol for 24 weeks, and basal diet alone was supplied for a further 24-week period. Animals were killed at 24 and 48 weeks and forestomach epithelium was examined histopathologically. DNA synthesis increased within 12 hr to 3 days after commencement of chemical treatment in all cases. Toxicity and cell proliferation became evident subsequent to increase in DNA synthesis in each case. Elevated expression of c-fos and c-myc oncogenes was demonstrated 15 min after beginning treatment with BHA. In the reversibility study, although most of the proliferative lesions induced by these antioxidants regressed after cessation of chemical treatment, some dysplastic lesions were still observed at week 48. The results indicate that these phenolic compounds act primarily as mitogens in rat forestomach epithelium, with regeneration due to toxicity further enhancing cell proliferation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Exposure to heterocyclic amines.

Many mutagenic heterocyclic amines (HAs) have been isolated from cooked foods and pyrolysates of amino acids and proteins, and the carcinogenicity of 10 of these HAs in rodents and of 1 in monkeys has been reported. Quantification of these carcinogenic HAs in various kinds of cooked foods indicated that the level of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) was highest (0.56-69.2 ng/g), that of 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) was second highest (0.64-6.44 ng/g), and those of other HAs were 0.03-2.50 ng/g. Heterocyclic amines were found in urine samples of 10 healthy volunteers consuming a normal diet, but HAs were not detectable in urine samples of three patients receiving parenteral alimentation. These results strongly suggest that humans are continuously exposed to HAs derived from food in the normal diet. Based on quantitative data on the levels of HAs in cooked foods and urine samples, the daily exposures to PhIP and MeIQx were estimated to be 0.1-13.8 micrograms and 0.2-2.6 micrograms per person, respectively. These levels of carcinogenic HAs are in the same range as those of other carcinogens such as N-nitrosodimethylamine and benzo[a]pyrene to which humans are exposed.

Adolescent↗
PubMed1993

Magnetic resonance angiography of arteriovenous malformation in the brainstem.

The magnetic resonance (MR) angiography appearance of arteriovenous malformation (AVM) in the tegmentum and pons is described. The interpeduncular perforating branches of the posterior cerebral artery and median pontine branches of the basilar artery were seen more clearly by MR angiography than by conventional angiography. MR angiography was very useful for the follow-up of AVM after stereotactic radiosurgery.

Adolescent↗
PubMed1993

Magnetic resonance angiography of arteriovenous malformation in the thalamus.

A comparative study of magnetic resonance angiography and conventional angiography of arteriovenous malformation in the thalamus showed that both methods clearly visualized the feeding arteries: perforating branches of the posterior cerebral artery, posterior choroidal artery and lenticulostriate artery. Draining veins such as the internal cerebral vein were also demonstrated well.

Adolescent↗
PubMed1993

Overcoming of vincristine resistance in HL-60 human promyelocytic leukemia cell line by dipyridamole.

Dipyridamole enhanced the anti-cancer activity of VCR toward both wild type HL-60 and VCR-resistant subline, HL-60/R, which had a 15 fold greater resistance to VCR as compared with the wild type cell line. The resistance to VCR of HL-60/R cells was associated with a marked decrease in the intracellular VCR accumulation. After incubation with VCR for 24 hrs, 0.61 and 0.24 pmol VCR per one million cells were accumulated in the wild and the resistant cells, respectively. Dipyridamole dose-dependently increased the intracellular VCR accumulation in the wild type cells and also it restored the intracellular VCR accumulation in the VCR-resistant cells. Addition of 10 microM dipyridamole to the culture medium enhanced the intracellular accumulation of VCR during 24 hr incubation by 2.6 fold and 6.0 fold in HL-60 and HL-60/R cells, respectively. The VCR-resistance in HL-60/R cells was able to be overcome by the addition of 2.5 microM dipyridamole to the culture medium. This concentration of dipyridamole could be obtained by the intravenous administration without severe adverse effects. These results indicate that dipyridamole should be effective in the treatment of patients with hematologic malignancy resistant to VCR.

Dipyridamole↗
PubMed1993

[The clinical significance of retroperitoneal lymph node metastasis and lymphadenectomy on 3-year survival in ovarian carcinoma].

Fifty-two patients with primary epithelial ovarian cancer received surgical treatment and chemotherapy at the Hospital of Shiga University of Medical Science and retroperitoneal lymph node metastases were evaluated clinico-pathologically. Forty patients underwent paraaortic and pelvic lymphadenectomy, although 12 patients with stage IIIc underwent no lymphadenectomy. In the patients with lymphadenectomy, stage I and II groups had 100% of 3-year survival, stage III group, 40.0% and stage IV group, 0.0%. A series of 27 patients with stage IIIc diagnosed from findings in the abdominal cavity had cytoreductive surgery and chemotherapy including cisplatinum, and were evaluated for 3-year survival. No significant difference in the survival rate was found between the stage IIIc groups with and without para-aortic and pelvic lymphadenectomy. The most important prognostic factors for 3-year survival were retroperitoneal lymph node metastases, complete remission, and residual tumor at second surgery. A three year survival analysis confirmed that para-aortic and pelvic lymphadenectomy is not an important procedure for the treatment for stage III ovarian cancer. However, retroperitoneal lymph node metastases was one of the most important prognostic factors.

Aged↗