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S Tsuda

Publications and source records attributed to S Tsuda.

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

Comparison of the S RNA segments among Japanese isolates and Taiwanese isolates of Watermelon silver mottle virus.

The complete nucleotide sequences of the S RNA of two Japanese isolates of Watermelon silver mottle virus were determined. One was isolated from naturally infected watermelon and causes malformation on upper leaves of Tetragonia expansa. The other was isolated from melon and causes characteristic yellow necrotic lesions on upper leaves of T. expansa. The total nucleotide sequences of the S RNA of WS-O and WS-Y were 3553 nt and 3558 nt long, respectively. Both the nucleotide sequences and the deduced amino acid sequences of WS-O and WS-Y were quite similar even though the symptoms on T. expansa are quite different. They were also significantly similar to those of the Taiwanese isolates, Topso-W and Tospo-To. These results suggested that the Japanese isolates and the Taiwanese isolates of WSMoV were classified as one group not only serologically but also genetically. Within the S RNA sequences, the most variable region was the intergenic region between the N gene and the NSs gene. This was due to a 20 nt insertion between the Japanese isolates and the Taiwanese isolates.

Amino Acid Sequence↗
PubMed2001

External doses in the environment from the Tokai-mura criticality accident.

On 30 September 1999, a criticality accident occurred at a uranium processing plant operated by JCO in Tokai-mura, Japan and the criticality remained for about 20 h. Almost all doses to the neighbouring residents were brought by neutrons and gamma rays emitted from the facility rather than fission products released to the environment. External doses in the environment were evaluated using radiation monitoring data and radiation transport calculation. A pattern of the dose rate evolution was modelled based on the records of gamma ray monitors in the JCO facilities. Relations between the ambient dose equivalent rates of neutrons/gamma rays and the distance from the facility were determined from the monitoring data obtained around the accident site. Conversion from the ambient dose equivalent to the effective dose equivalent was made assuming the energy spectra calculated by the radiation transport code, ANISN. It was estimated that the people who stayed outside the 350 m zone would receive doses of less than 1 mSv.

Gamma Rays↗
PubMed2001

Fluence to effective dose conversion coefficients for electrons with energy from 1 MeV to 100 GeV.

Fluence to organ dose and effective dose conversion coefficients have been calculated for electrons from 1 MeV to 100 GeV using an anthropomorphic phantom and the EGS4 code. The conversion coefficients were calculated for six typical irradiation geometries taking electromagnetic cascade shower and photonuclear reactions into account. The contribution to the absorbed dose due to the photonuclear reactions in energies up to 140 MeV was evaluated to be less than 0.2%. Even at energies above 140 MeV the dose contributions of the photonuclear reactions were insignificant.

Electrons↗
PubMed2001

DNA damage induced by red food dyes orally administered to pregnant and male mice.

We determined the genotoxicity of synthetic red tar dyes currently used as food color additives in many countries, including JAPAN: For the preliminary assessment, we treated groups of 4 pregnant mice (gestational day 11) once orally at the limit dose (2000 mg/kg) of amaranth (food red No. 2), allura red (food red No. 40), or acid red (food red No. 106), and we sampled brain, lung, liver, kidney, glandular stomach, colon, urinary bladder, and embryo 3, 6, and 24 h after treatment. We used the comet (alkaline single cell gel electrophoresis) assay to measure DNA damage. The assay was positive in the colon 3 h after the administration of amaranth and allura red and weakly positive in the lung 6 h after the administration of amaranth. Acid red did not induce DNA damage in any sample at any sampling time. None of the dyes damaged DNA in other organs or the embryo. We then tested male mice with amaranth, allura red, and a related color additive, new coccine (food red No. 18). The 3 dyes induced DNA damage in the colon starting at 10 mg/kg. Twenty ml/kg of soaking liquid from commercial red ginger pickles, which contained 6.5 mg/10 ml of new coccine, induced DNA damage in colon, glandular stomach, and bladder. The potencies were compared to those of other rodent carcinogens. The rodent hepatocarcinogen p-dimethylaminoazobenzene induced colon DNA damage at 1 mg/kg, whereas it damaged liver DNA only at 500 mg/kg. Although 1 mg/kg of N-nitrosodimethylamine induced DNA damage in liver and bladder, it did not induce colon DNA damage. N-nitrosodiethylamine at 14 mg/kg did not induce DNA damage in any organs examined. Because the 3 azo additives we examined induced colon DNA damage at a very low dose, more extensive assessment of azo additives is warranted.

Amaranth Dye↗
PubMed2001

Role of dihydropyridine-sensitive calcium channels in the regulation of norepinephrine release in hypertension.

In the present study, in order to elucidate the role of dihydropyridine (DHP)-sensitive calcium (Ca) channels in the regulation of neurotransmitter release in hypertension, we examined the effects of the DHP-sensitive Ca channel blocker nicardipine on norepinephrine (NE) release in blood vessels of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. The stimulation-evoked pressor responses and NE release were significantly greater in the mesenteric arteries of SHR than in the mesenteric arteries of WKY rats. Nicardipine significantly inhibited the stimulation-evoked NE release as well as vasoconstrictor responses in the mesenteric arteries to a greater extent in SHR than in WKY rats. These results demonstrated that nicardipine markedly reduced the stimulation-evoked NE release in blood vessels of SHR, which might suggest that the DHP-sensitive Ca channels could be involved, at least in part, in the regulation of NE release in hypertension.

Animals↗
PubMed2001

[Evaluation of bone metastases from renal cell carcinoma].

Forty-two cases of bone metastasis from renal cell carcinoma were examined. Thirty of the cases had bone metastases at the time of renal cell carcinoma. Bone metastasis appeared after treatment of the primary site in 12 cases. Fifteen cases had only bone metastasis and another 27 had metastasis in multiple organs. The total cause-specific survival curve of these patients was 10% at 5 years. All patients with bone metastases died of cancer within 5 years after the bone metastases had developed. There was no significant difference in the survival rate between patients with bone metastases and patients with lung metastases. We investigated the prognostic value of laboratory studies in bone metastases of renal cell carcinoma. However, no significant markers were detected for bone metastases. The 6 patients were treated with decompressed laminectomy (2), wide resection (3) and excision of the metastatic lesions (3). The quality of life was improved in all the patients although they died of cancer.

Adult↗
PubMed2001

[Long-term experience with renal transplantation in systemic amyloidosis: a case report].

Renal transplantation was performed on a 39-year old woman with secondary amyloidosis due to rheumatoid arthritis. She remains alive and renal function has been maintained satistfactorily with the exception of proteinuria ten years after transplantation. Recent renal biopsy showed no amyloid recurrence, but the presence of chronic rejection reaction and mild cyclosporin arteriolopathy. Symptoms related to systemic amyloidosis and rheumatoid arthritis improved after transplantation. Renal transplantation is the recommended therapy for the type AA systemic amyloidosis. This is the second report of long-term experience with renal transplantation in systemic amyloidosis in Japan.

Aged↗
PubMed2001

The diagnostic value of bone scan in patients with renal cell carcinoma.

PURPOSE: Bone scan is performed as part of the evaluation of bone metastasis. We assessed the diagnostic value of bone scan in patients with renal cell carcinoma. MATERIALS AND METHODS: Bone scan was performed at presentation in 205 patients with confirmed renal cell carcinoma. Abnormal hot areas were further evaluated by x-ray, computerized tomography or surgery. RESULTS: Of the 56 patients (27%) with an abnormal bone scan 32 (57%) had osseous metastatic lesions. Overall bone metastasis was present in 34 of the 205 patients (17%). Bone scan had 94% sensitivity and 86% specificity. Of the 124 patients with clinically localized, stages T1-2N0M0 disease exclusive of bone metastasis 6 (5%) had bone metastasis only, whereas 28 of 81 (35%) with locally advanced or metastatic disease had bone metastasis, including 12 (35%) who complained of bone pain and 19 (56%) who presented with other symptoms due to local tumor growth or metastasis at other sites. Three patients (9%) were asymptomatic. There was osseous metastasis without other metastasis, enlarged regional lymph nodes or bone pain in 7 patients, including 1 with stage T1b (2% of all with that stage), 2 with stage T2 (5%), 1 with stage T3a (4%), 1 with stage T3b (6%), 1 with stage T3c (14%) and 1 with stage T4 (6%) disease. CONCLUSIONS: Bone scan may be omitted in patients with stages T1-3aN0M0 tumors and no bone pain because of the low proportion of missed cases with bone metastasis.

Adult↗
PubMed2000

Chitin-binding proteins in invertebrates and plants comprise a common chitin-binding structural motif.

Tachycitin, a 73-residue polypeptide having antimicrobial activity is present in the hemocyte of horseshoe crab (Tachypleus tridentatus). The first three-dimensional structure of invertebrate chitin-binding protein was determined for tachycitin using two-dimensional nuclear magnetic resonance spectroscopy. The measurements indicate that the structure of tachycitin is largely divided into N- and C-terminal domains; the former comprises a three-stranded beta-sheet and the latter a two-stranded beta-sheet following a short helical turn. The latter structural motif shares a significant tertiary structural similarity with the chitin-binding domain of plant chitin-binding protein. This result is thought to provide faithful experimental evidence to the recent hypothesis that chitin-binding proteins of invertebrates and plants are correlated by a convergent evolution process.

Amino Acid Sequence↗
PubMed2000

The alkaline single cell electrophoresis assay with eight mouse organs: results with 22 mono-functional alkylating agents (including 9 dialkyl N-nitrosoamines) and 10 DNA crosslinkers.

The genotoxicity of 22 mono-functional alkylating agents (including 9 dialkyl N-nitrosoamines) and 10 DNA crosslinkers selected from IARC (International Agency for Research on Cancer) groups 1, 2A, and 2B was evaluated in eight mouse organs with the alkaline single cell gel electrophoresis (SCGE) (comet) assay. Groups of four mice were treated once intraperitoneally at the dose at which micronucleus tests had been conducted, and the stomach, colon, liver, kidney, bladder, lung, brain, and bone marrow were sampled 3, 8, and/or 24 h later. All chemicals were positive in the SCGE assay in at least one organ. Of the 22 mono-functional alkylating agents, over 50% were positive in all organs except the brain and bone marrow. The two subsets of mono-functional alkylating agents differed in their bone marrow genotoxicity: only 1 of the 9 dialkyl N-nitrosoamines was positive in bone marrow as opposed to 8 of the 13 other alkylating agents, reflecting the fact that dialkyl N-nitrosoamines are poor micronucleus inducers in hematopoietic cells. The two groups of mono-functional alkylating agents also differ in hepatic carcinogenicity in spite of the fact that they are similar in hepatic genotoxicity. While dialkyl N-nitrosoamines produce tumors primarily in mouse liver, only one (styrene-7,8-oxide) out of 10 of the other type of mono-functional alkylating agents is a mouse hepatic carcinogen. Taking into consideration our previous results showing high concordance between hepatic genotoxicity and carcinogenicity for aromatic amines and azo compounds, a possible explanation for the discrepancy might be that chemicals that require metabolic activation show high concordance between genotoxicity and carcinogenicity in the liver. A high percent of the 10 DNA crosslinkers were positive in the SCGE assay in the gastrointestinal mucosa, but less than 50% were positive in the liver and lung. In this study, we allowed 10 min alkali-unwinding to obtain low and stable control values. Considering that DNA crosslinking lesions can be detected as lowering of not only positive but also negative control values, low control values by short alkali-treatment might make it difficult to detect DNA crosslinking lesions. In conclusion, although both mono-functional alkylating agents and DNA crosslinkers are genotoxic in mouse multiple organs, the genotoxicity of DNA crosslinkers can be detected in the gastrointestinal organs even though they were given intraperitoneally followed by the short alkali-treatment.

Alkylating Agents↗
PubMed2000

The nonreceptor protein-tyrosine kinase c-Fes is involved in fibroblast growth factor-2-induced chemotaxis of murine brain capillary endothelial cells.

Fibroblast growth factor-2 (FGF-2)-induced migration of endothelial cells is involved in angiogenesis in vivo. However, signal transduction pathways leading to FGF-2-induced chemotaxis of endothelial cells are largely unknown. Previous studies have shown that the cytoplasmic protein-tyrosine kinase c-Fes is expressed in vascular endothelial cells and may influence angiogenesis in vivo. To investigate the contribution of c-Fes to FGF-2 signaling, we expressed wild-type or kinase-inactive human c-Fes in the murine brain capillary endothelial cell line, IBE (Immortomouse brain endothelial cells). Wild-type c-Fes was tyrosine-phosphorylated upon FGF-2-stimulation in transfected cells, whereas kinase-inactive c-Fes was not. Overexpression of wild-type c-Fes promoted FGF-2-independent tube formation of IBE cells. Tube formation was not observed with endothelial cells expressing kinase-inactive c-Fes, indicating a requirement for c-Fes kinase activity in this biological response. Expression of kinase-defective c-Fes suppressed endothelial cell migration following FGF-2 treatment, suggesting that activation of endogenous c-Fes may be required for the chemotactic response. Expression of either wild-type c-Fes or the kinase-inactive mutant did not affect the tyrosine phosphorylation FRS2, Shc, or phospholipase C-gamma, nor did it influence the kinetics of mitogen-activated protein kinase activation. These results implicate c-Fes in FGF-2-induced chemotaxis of endothelial cells through signaling pathways not linked to mitogenesis.

Animals↗
PubMed2000

The comet assay in eight mouse organs: results with 24 azo compounds.

The genotoxicity of 24 azo compounds selected from IARC (International Agency for Research on Cancer) groups 2A, 2B, and 3 were determined by the comet (alkaline single cell gel electrophoresis, SCG) assay in eight mouse organs. We treated groups of four mice once orally at the maximum tolerated dose (MTD) and sampled stomach, colon, liver, kidney, bladder, lung, brain, and bone marrow 3, 8, and 24 h after treatment. For the 17 azo compounds, the assay was positive in at least one organ; (1) 14 and 12 azo compounds induced DNA damage in the colon and liver, respectively, (2) the genotoxic effect of most of them was greatest in the colon, and (3) there were high positive responses in the gastrointestinal organs, but those organs are not targets for carcinogenesis. One possible explanation for this discrepancy is that the assay detects DNA damage induced shortly after administration of a relatively high dose, while carcinogenicity is detected after long treatment with relatively low doses. The metabolic enzymes may become saturated following high doses and the rates and pathways of metabolic activation and detoxification may differ following high single doses vs. low long-term doses. Furthermore, considering that spontaneous colon tumors are very rare in rats and mice, the ability to detect tumorigenic effects in the colon of those animals might be lower than the ability to detect genotoxic events in the comet assay. The in vivo comet assay, which has advantage of reflecting test chemical absorption, distribution, and excretion as well as metabolism, should be effective for estimating the risk posed by azo dyes to humans in spite of the difference in dosage regimen.

Animals↗
PubMed2000

Natural history of early colorectal cancer: evolution of a growth curve.

PURPOSE: There are very few studies on the development of early colorectal cancers, although we have previously reported growth speeds of early colorectal cancer in a radiographic retrospective study. The aim of this study was to estimate a statistical curve for cancer growth from mucosal cancer. METHODS: Subjects of the study were 31 patients with cancer in which initial lesions were diagnosed as mucosal cancer. These lesions were overlooked in the first or second investigations, but were detected later. Initial radiographic features were as follows; 4 pedunculated lesions, 1 semipedunculated lesion, 6 sessile lesions, 9 superficially elevated lesions, and 11 superficially depressed lesions. The diameters of the initial lesions were 12.1+/-6.1 mm. The final depths of invasion were 6 mucosal cancers, 12 submucosal cancers, 6 muscularis propria cancers, and 7 serosal cancers. The observation period between the initial and final examination was 41.5+/-25.8 months. The growth curve was estimated by an exponential curve with the natural logarithm of d = e (a + b x t), where a is the intercept (initial tumor size) and b is the regression coefficient (growth speed). RESULTS: A growth curve was obtained as follows: diameter = 12.5 x 2(t/77) (r = 0.448, P < 0.0001) and 95 percent confidence interval of time = 53 to 173 months. Subsequently, volume = 1 x 10(3) x 2(t/26), and the 95 percent confidence interval of time = 18 to 58 months. CONCLUSION: Growth speed of early colorectal cancer was estimated through a statistically significant growth curve. Estimated doubling time of the volume of early colorectal cancer was 26 (95 percent confidence interval, 18-58) months. From these results we could obtain a rational cancer surveillance program using appropriate procedures with different sensitivities.

Aged↗
PubMed2000

Invasive colon cancer derived from a small superficial depressed cancer: report of a case.

A 64-year-old male in May 1997 was diagnosed by colonoscopy and a barium enema examination as having an invasive cancer in the transverse colon. Pathologic study of the resected surgical specimen revealed a well-differentiated adenocarcinoma invading the muscularis propria. He had a colonoscopic examination in 1991 and was diagnosed as having multiple adenomas, which were endoscopically removed. After that he had annual colonoscopy or barium enema examination follow-ups. At endoscopy in February 1994, a superficial depressed cancer 6 mm in diameter had been detected. However, the cancer was not seen again in several endoscopic examinations until one in 1997. Because the location of the lesion detected in 1994 and that of the invasive carcinoma detected in 1997 were identical, it was considered that the superficial depressed cancer developed, 40 months later, to an advanced cancer. Doubling time was calculated as 8.4 months.

Adenocarcinoma↗
PubMed2000

The comet assay with multiple mouse organs: comparison of comet assay results and carcinogenicity with 208 chemicals selected from the IARC monographs and U.S. NTP Carcinogenicity Database.

The comet assay is a microgel electrophoresis technique for detecting DNA damage at the level of the single cell. When this technique is applied to detect genotoxicity in experimental animals, the most important advantage is that DNA lesions can be measured in any organ, regardless of the extent of mitotic activity. The purpose of this article is to summarize the in vivo genotoxicity in eight organs of the mouse of 208 chemicals selected from International Agency for Research on Cancer (IARC) Groups 1, 2A, 2B, 3, and 4, and from the U.S. National Toxicology Program (NTP) Carcinogenicity Database, and to discuss the utility of the comet assay in genetic toxicology. Alkylating agents, amides, aromatic amines, azo compounds, cyclic nitro compounds, hydrazines, halides having reactive halogens, and polycyclic aromatic hydrocarbons were chemicals showing high positive effects in this assay. The responses detected reflected the ability of this assay to detect the fragmentation of DNA molecules produced by DNA single strand breaks induced chemically and those derived from alkali-labile sites developed from alkylated bases and bulky base adducts. The mouse or rat organs exhibiting increased levels of DNA damage were not necessarily the target organs for carcinogenicity. It was rare, in contrast, for the target organs not to show DNA damage. Therefore, organ-specific genotoxicity was necessary but not sufficient for the prediction of organ-specific carcinogenicity. It would be expected that DNA crosslinkers would be difficult to detect by this assay, because of the resulting inhibition of DNA unwinding. The proportion of 10 DNA crosslinkers that was positive, however, was high in the gastrointestinal mucosa, stomach, and colon, but less than 50% in the liver and lung. It was interesting that the genotoxicity of DNA crosslinkers could be detected in the gastrointestinal organs even though the agents were administered intraperitoneally. Chemical carcinogens can be classified as genotoxic (Ames test-positive) and putative nongenotoxic (Ames test-negative) carcinogens. The Ames test is generally used as a first screening method to assess chemical genotoxicity and has provided extensive information on DNA reactivity. Out of 208 chemicals studied, 117 are Ames test-positive rodent carcinogens, 43 are Ames test-negative rodent carcinogens, and 30 are rodent noncarcinogens (which include both Ames test-positive and negative noncarcinogens). High positive response ratio (110/117) for rodent genotoxic carcinogens and a high negative response ratio (6/30) for rodent noncarcinogens were shown in the comet assay. For Ames test-negative rodent carcinogens, less than 50% were positive in the comet assay, suggesting that the assay, which detects DNA lesions, is not suitable for identifying nongenotoxic carcinogens. In the safety evaluation of chemicals, it is important to demonstrate that Ames test-positive agents are not genotoxic in vivo. This assay had a high positive response ratio for rodent genotoxic carcinogens and a high negative response ratio for rodent genotoxic noncarcinogens, suggesting that the comet assay can be used to evaluate the in vivo genotoxicity of in vitro genotoxic chemicals. For chemicals whose in vivo genotoxicity has been tested in multiple organs by the comet assay, published data are summarized with unpublished data and compared with relevant genotoxicity and carcinogenicity data. Because it is clear that no single test is capable of detecting all relevant genotoxic agents, the usual approach should be to carry out a battery of in vitro and in vivo tests for genotoxicity. The conventional micronucleus test in the hematopoietic system is a simple method to assess in vivo clastogenicity of chemicals. Its performance is related to whether a chemical reaches the hematopoietic system. Among 208 chemicals studied (including 165 rodent carcinogens), 54 rodents carcinogens do not induce micronuclei in mouse hematopoietic system despite the positive finding with one or two in vitro tests. Forty-nine of 54 rodent carcinogens that do not induce micronuclei were positive in the comet assay, suggesting that the comet assay can be used as a further in vivo test apart from the cytogenetic assays in hematopoietic cells. In this review, we provide one recommendation for the in vivo comet assay protocol based on our own data.

Animals↗
PubMed2000

The influence of antioxidants on cigarette smoke-induced DNA single-strand breaks in mouse organs: a preliminary study with the alkaline single cell gel electrophoresis assay.

According to published information, the lung is the only clear target organ for tumors when mice are exposed to cigarette smoke. Liver, skin, and upper digestive tract are target organs when orally or dermally exposed to cigarette smoke condensate, but not kidney, brain, or bone marrow. We tested the genotoxicity of cigarette smoke in the known target organ (lung), possible target organs (stomach and liver), and non-target organs (kidney, brain, and bone marrow) of the mouse using the alkaline single-cell gel electrophoresis (SCG, or comet) assay, as modified by us. We also tested the effect of free radical scavengers on the genotoxicity of the smoke. Male ICR mice were exposed to cigarette smoke. DNA single-strand breaks (SSB) were measured by the SCG assay 15, 30, 60, 120, and 240 min after the exposure. Fifteen min after the animals were exposed for 1 min to a 6-fold dilution of smoke, SSB appeared in the lungs, stomach, and liver; the damage in the lungs and liver returned to almost control levels by 60 min, and that of the stomach by 120 min. Kidney, brain, and bone marrow DNA were not damaged. Exposure to more dilute smoke (12- or 24-fold dilution) did not cause DNA damage. Single oral pretreatment (100 mg/kg) of either ascorbic acid (VC) or alpha-tocopherol acetate (VE) 1 h before smoke inhalation prevented SSB in the stomach and liver, while VE but not VC significantly reduced SSB in the lung. Five consecutive days of either VC or VE (100 mg/kg/day) pretreatment completely prevented SSB in the lung, stomach, and liver. Thus, the SCG assay detected DNA SSB, induced by cigarette smoke, in the known target organ, two possible target organs, and none of the non-target organs. Antioxidants could prevent those effects, suggesting that free radicals may have been a source of the damage. Our results suggest the importance of the SCG assay as a tool in the study of genotoxicity and carcinogenicity.

Animals↗