Mutation Research/Genetic Toxicology最新文献

{"title":"The Ames test: The two-fold rule revisited","authors":"Neal F. Cariello ,&nbsp;Walter W. Piegorsch","doi":"10.1016/S0165-1218(96)90044-0","DOIUrl":"10.1016/S0165-1218(96)90044-0","url":null,"abstract":"<div><p>Mutagenicity in the Ames assay is evaluated by comparing the number of revertants observed in treated cultures to those in untreated cultures. Often, some form of the ‘2-fold rule’ is employed, whereby a compound is judged mutagenic if a 2-fold or greater increase is seen in a treated culture. In order to understand the underpinnings of this approach, we study some of its statistical properties. We assume that the number of revertants on any plate from a given two-group experiment follows a Poisson distribution and we address the following questions: (1) what is the false-positive error probability of observing at least a doubling of the number of colonies from the control to the treatment group?; (2) if a given mean number of colonies is postulated for a control group, what number of colonies above the observed control mean provides a false-positive rate of 5%? We also present results for question 1 in the case where the number of revertants follows a negative binomial distribution.</p></div>","PeriodicalId":100938,"journal":{"name":"Mutation Research/Genetic Toxicology","volume":"369 1","pages":"Pages 23-31"},"PeriodicalIF":0.0,"publicationDate":"1996-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1218(96)90044-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19675228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sister chromatid exchange analysis in workers exposed to noise and vibration","authors":"M.J. Silva ,&nbsp;A. Carothers ,&nbsp;N. Castelo Branco ,&nbsp;A. Dias ,&nbsp;M.G. Boavida","doi":"10.1016/S0165-1218(96)90055-5","DOIUrl":"10.1016/S0165-1218(96)90055-5","url":null,"abstract":"<div><p>Workers chronically exposed to whole-body vibration and noise are known to develop pathophysiological and psychological disturbances. The frequencies of sister chromatid exchanges (SCEs) and of cells with high frequencies of SCEs (HFCs) were analyzed in lymphocytes of 50 workers occupationally exposed to vibration and noise and of 34 controls. The exposed group included: individuals operating hand-vibrating tools (group 1), ‘test-cell operators’ (group 2) and ‘run-up’ operators (group 3) from an air base and helicopter pilots (group 4). The statistical analysis of the mean SCE count per cell was carried out by multiple regression analysis, comparing various predictor variables: exposure group, duration of exposure, age and cigarette consumption. Only cigarette consumption and exposure group were found to be significantly correlated with the mean SCE frequency. After allowing for the effects of smoking, the analysis indicates that: (1) there was no significant difference between group 1 and controls (<em>p</em> &gt; 0.05); (2) the differences between group 2 and group 0, group 3 and group 0 and group 4 and group 0 were all highly significant (<em>p</em> &lt; 0.001); (3) there was no significant difference between groups 2 and 3 (<em>p</em> &gt; 0.05), nor between groups 2 and 3 combined and group 4 (<em>p</em> &gt; 0.05); (4) exposure groups 2, 3 and 4 combined, had a significantly elevated mean SCE frequency compared to the control group (<em>p</em> &lt; 0.0001). Statistical analysis of the proportion of HFCs was consistent with these results. Our data suggest that chronic exposure to whole-body vibration and noise may lead to an increase in the level of SCEs in man. The observed effects may not reflect a direct action of these physical agents on DNA. Alternative explanations may include some of the whole-body vibration and noise-induced or stress-induced pathophysiological alterations which may indirectly induce SCE formation.</p></div>","PeriodicalId":100938,"journal":{"name":"Mutation Research/Genetic Toxicology","volume":"369 1","pages":"Pages 113-121"},"PeriodicalIF":0.0,"publicationDate":"1996-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1218(96)90055-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19675225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genotixicity in vivo of phenazine and aminophenazines assayed in the wing spot test and the DNA-repair test with Drosophila melanogaster","authors":"Tetsushi Watanabe,&nbsp;Terue Kasai,&nbsp;Mikito Arima,&nbsp;Kazuko Okumura,&nbsp;Naoyoshi Kawabe,&nbsp;Teruhisa Hirayama","doi":"10.1016/S0165-1218(96)90050-6","DOIUrl":"10.1016/S0165-1218(96)90050-6","url":null,"abstract":"<div><p>The genotoxicity and DNA-damaging activity of 6 phenazine and aminophenazine derivatives were assayed in the wing spot and DNA-repair tests in <em>Drosophila melanogaster</em>. Phenazine (Pz), and all aminophenazines tested, namely, 1-aminophenazine (APz), 2-APz, 2,3-diaminophenazine (DAPz), 2,7-DAPz and 2,7-diamino-3,8-dimethylphenazine (DADMPz), exhibited mutagenicity significantly in the wing spot test. The activities in the wing spot test were ranked in a sequence DADMPz &gt; (2,7-DAPz, 2,3-DAPz) &gt; (2-APz 1-APz, Pz). In the DNA-repair test, 2,3-DAPz, 2,7-DAPz, and DADMPz clearly showed DNA-damaging activity, but Pz, 1-APz and 2-APz were inactive. Based on these results, we predict that DADMPz, 2,3-DAPz and 2,7-DAPz are likely to be more carcinogenic than 2-APz, 1-APz or Pz.</p></div>","PeriodicalId":100938,"journal":{"name":"Mutation Research/Genetic Toxicology","volume":"369 1","pages":"Pages 75-80"},"PeriodicalIF":0.0,"publicationDate":"1996-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1218(96)90050-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19673582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of eugenol on the mutagenicity of benzo[a]pyrene and the formation of benzo[a]pyrene-DNA adducts in the λ-lacZ-transgenic mouse","authors":"C.J.M. Rompelberg,&nbsp;M-J.S.T. Steenwinkel,&nbsp;J.G. van Asten,&nbsp;J.H.M. van Delft,&nbsp;R.A. Baan,&nbsp;H. Verhagen","doi":"10.1016/S0165-1218(96)90052-X","DOIUrl":"10.1016/S0165-1218(96)90052-X","url":null,"abstract":"<div><p>To study the possible reduction by eugenol of the mutagenicity and genotoxicity of benzo[<em>a</em>]pyrene (B[<em>a</em>]P) in vivo, the λ-<em>lac</em>Z-transgenic mouse strain 40.6 (Muta^TMMouse) was used. Male mice were fed a diet containing 0.4% (w/w) eugenol or a control diet for 58 days. On day 10, half of the mice received an i.p. dose of 100 mg/kg b.w. B[<em>a</em>]P. The <em>lac</em>Z mutants were recovered by packaging of DNA isolated from liver into lambda phage, and expressed in <em>E. coli</em> <em>C</em> lacZ⁻<em>rec</em>A⁻<em>gal</em>E⁻ bacteria. In both control mice and mice fed the eugenol diet, B[<em>a</em>]P treatment resulted in a similar, significant increase in <em>lac</em>Z mutant frequency. Eugenol was not mutagenic by itself. By ³²P-postlabelling analysis of the liver DNA using an analysis method with chromatographic conditions for B[<em>a</em>]P-DNA adducts, no effect of eugenol on the formation of B[<em>a</em>]P-DNA adducts in the λ-<em>lac</em>Z-transgenic mouse was found. By ³²P-postlabelling analysis using an alkenybenzene solvent system the amount of B[<em>a</em>]P-DNA adducts was lower in mice fed the eugenol diet than in mice fed the control diet but the decrease was not statistically significant. However, one spot indicative of an eugenol-associated DNA adduct was detected. The present data provide no evidence for antimutagenic or antigenotoxic potential of eugenol in vivo. Furthermore, they suggest genotoxicity in vivo of eugenol per se.</p></div>","PeriodicalId":100938,"journal":{"name":"Mutation Research/Genetic Toxicology","volume":"369 1","pages":"Pages 87-96"},"PeriodicalIF":0.0,"publicationDate":"1996-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1218(96)90052-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19673584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mutagenic activity of some coal-derived humic compounds evaluated by the Ames test","authors":"Francesca Bernacchi,&nbsp;Isabella Ponzanelli,&nbsp;Roberto Barale,&nbsp;Nicola Loprieno","doi":"10.1016/S0165-1218(96)90054-3","DOIUrl":"10.1016/S0165-1218(96)90054-3","url":null,"abstract":"<div><p>Two coal-derived humic substances (Sulcis and South Africa, Eniricerche, Italy) have been evaluated for their mutagenic activity on TA98 and TA100 <em>Salmonella typhimurium</em> strains, either in presence or in absence of metabolic activation (S9). Both compounds showed no effect on the two strains, as observed with natural humic acid (Fluka). After chlorination, coal-derived humic acids induced a strong dose-related increase in the number of revertants on TA100 without S9, whose extent was directly proportional to the chlorination ratios. Such effect was completely suppressed when a sodium thiosulfate solution (10%) was added at the end of the chlorination period (about 90 h). The analogies with natural humic acid mutagenicity are discussed.</p></div>","PeriodicalId":100938,"journal":{"name":"Mutation Research/Genetic Toxicology","volume":"369 1","pages":"Pages 107-112"},"PeriodicalIF":0.0,"publicationDate":"1996-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1218(96)90054-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19675224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cytogenetic effects of piperonyl butoxide and safrole in CHO-K1 cells","authors":"Sumiko Tayama","doi":"10.1016/S0165-1218(96)90066-X","DOIUrl":"10.1016/S0165-1218(96)90066-X","url":null,"abstract":"<div><p>Recently, hepatocarcinogenicity in rats and mice was reported with regard to the methylenedioxyphenyl compound, piperonyl butoxide (PB), which is used as a synergist for pyrethrins and related insecticides. Induction of sister-chromatid exchanges (SCEs) and chromosomal aberrations (CAs) due to PB were investigated using CHO-K1 cells with or without rat liver S9 fraction (S9); at the same time, the effects of safrole (SF), a methylenedioxyphenyl compound and a weak hepatocarcinogen, were also examined. PB (0.25 and 0.3 mM) and SF (0.8 mM) caused a slight but significant increase in SCEs followed by a cell-cycle delay in the 3-h treatment without S9. In the presence of S9 (4.5%), the cytotoxicity of PB or SF was weakened greatly or slightly, the top dose capable of cell division was raised to 0.6 mM (2-fold) or 1 mM, respectively. PB with S9 induced SCE at doses of 0.4 and 0.5 mM, and caused endoreduplications (ERDs, 7%) at a dose of 0.6 mM, while SF caused a dose-related significant increase in SCE at all doses used (0.4–1 mM) with S9. Genotoxicity of the metabolites of PB or SF was cleared by changing the dose of S9 (1.5–9%) while holding the dose of each chemical constant. In the case of SF (0.6 mM), induction of SCE, ERD and cell-cycle delay intensified almost in a dose-effect relationship, and CAs and a high level of ERD (14%) were caused by a 9% dose of S9. The concentration of unchanged SF in the incubated medium was certainly in inverse proportion to the dose of S9. This strongly suggests that the metabolites of SF are genotoxic. In the case of PB (0.3 mM), no positive responses were produced in the cultures, even with a high level of S9, though the amount of unchanged PB left in the incubated medium was very slight. This indicates that the metabolites of PB may not be genotoxic. In conclusion, PB and SF are possible to somewhat induce SCE at high dose(s) in the absence of S9, and the genotoxic effects of SF are more intensified in the presence of S9 than in its absence, while PB is probably no genotoxic in the presence of sufficient metabolic activation.</p></div>","PeriodicalId":100938,"journal":{"name":"Mutation Research/Genetic Toxicology","volume":"368 3","pages":"Pages 249-260"},"PeriodicalIF":0.0,"publicationDate":"1996-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1218(96)90066-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19666038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Squalene inhibits sodium arsenite-induced sister chromatid exchanges and micronuclei in Chinese hamster ovary-K1 cells","authors":"Shyh-Rong Fan,&nbsp;I-Ching Ho,&nbsp;Fenny Lai-Fun Yeoh,&nbsp;Chi-Jen Lin,&nbsp;Te-Chang Lee","doi":"10.1016/S0165-1218(96)90058-0","DOIUrl":"10.1016/S0165-1218(96)90058-0","url":null,"abstract":"<div><p>Arsenic, widely distributed throughout our environment, is a well-established human carcinogen. We report here that squalene, a natural fish oil, is a potential agent in the reduction of sodium arsenite-induced sister chromatid exchange (SCE) and micronuclei in Chinese hamster ovary (CHO-K1) cells. Squalene dose-dependently inhibited sodium arsenite-induced SCE. At the highest concentration (160 μM), squalene reduced the SCE frequency from 8.85 to 6.47 SCEs per cell which is very close to the background level (5.82 SCEs per cell). Sodium arsenite dose-dependently induces micronuclei in CHO-K1 cells, and squalene at 80 μM significantly inhibits arsenite-induced micronuclei. However, squalene did not eliminate the killing effects of arsenite on the cells and only slightly decreased intracellular accumulation of arsenic.</p></div>","PeriodicalId":100938,"journal":{"name":"Mutation Research/Genetic Toxicology","volume":"368 3","pages":"Pages 165-169"},"PeriodicalIF":0.0,"publicationDate":"1996-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1218(96)90058-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19667402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urinary mutagenicity and thioethers in nonsmokers: Role of environmental tobacco smoke (ETS) and diet","authors":"Gerhard Scherer ,&nbsp;David J. Doolittle ,&nbsp;Thomas Ruppert ,&nbsp;Irmtrud Meger-Kossien ,&nbsp;Kirsten Riedel ,&nbsp;Anthony R. Tricker ,&nbsp;Franz Adlkofer","doi":"10.1016/S0165-1218(96)90061-0","DOIUrl":"10.1016/S0165-1218(96)90061-0","url":null,"abstract":"<div><p>The urinary excretion of mutagens and thiothers was investigated in a controlled diet study and in two field studies. A diet containing charcoal-broiled meat and other items rich in mutagenic compounds increased the urinary mutagenicity as assessed in <em>Salmonella typhimurium</em> strain TA98 with metabolic activation ∼ 46-fold compared to a diet low in mutagens. The excretion of thiothers after ingestion of the diet rich in mutagens also increased significantly when compared to the diet low in mutagens. The increase was associated with the content of preformed thiothers in the diet. In the first field study with 21 nonsmokers, urinary mutagenicity as assessed in <em>Salmonella typhimurium</em> strain TA98 and excretion of thiothers showed no relation to either the self-reported exposure to environmental tobacco smoke (ETS) or to serum cotinine concentrations used as an objective marker for ETS exposure. In the second field study, urinary mutagenicity was determined with a tobacco-smoke sensitive <em>Salmonella typhimurium</em> strain YG1024 with metabolic activation. No correlation was found between the mutagenic activity in urine and ETS exposure duration, nicotine on the personal sampler, cotinine in saliva and cotinine in urine. Our results suggest that real-life ETS exposure does not measurably increase either urinary mutagen or urinary thioether excretion. Furthermore, diet seems to be the most important source for both urinary mutagen and thioether excretion in nonsmokers.</p></div>","PeriodicalId":100938,"journal":{"name":"Mutation Research/Genetic Toxicology","volume":"368 3","pages":"Pages 195-204"},"PeriodicalIF":0.0,"publicationDate":"1996-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1218(96)90061-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19667405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of the ability of paracetamol to produce chromosome aberrations in man","authors":"Ph. Hantson ,&nbsp;L. de Saint-Georges ,&nbsp;P. Mahieu ,&nbsp;E.D. Léonard ,&nbsp;M.C. Crutzen-Fayt ,&nbsp;A. Léonard","doi":"10.1016/S0165-1218(96)90071-3","DOIUrl":"10.1016/S0165-1218(96)90071-3","url":null,"abstract":"<div><p>The ability of paracetamol to induced structural chrosomed aberrations in human peripheral blood lymphocytes in vivo was evaluated in volunteers who had been administered a single oral dose of 3 g paracetamol, in patients who has received 2 g of propacetamol by intravenous infusion every 6 h for at least 7 days, and in self-poisoned patients who, for suicidal reasons, had ingested more than 15 g paracetamol. In addition to the in vivo observations, the effectiveness of paracetamol to interfere with fusorial microtubule polymerisation was assayed in vitro in order to detect a possible effect of paracetamol on the distribution of chromosomes during cell division. The negative results obtained in all those assays strongly suggest that paracetamol has no mutagenic properties in human. There was, indeed, no significant difference in the percentage of abnormal cells before and after application of paracetamol in volunteers (0.2% before ingestion of 3 g paracetamol, 0.12% after 24 h, 0.04% after 72 h and 0.04% after 168 h) and in patients (0.5% of abnormal cells before treatment versus 0.44% after intravenous infusion of a total of 28 g paracetamol). Moreover, the yield of abnormal cells was not modified in self-poisoned persons (0.24%), in spite of an important decrease in the mitotic index of the PHA stimulated lymphocytes. In the in vitro assay, no inhibition of microtubule polymerisation was detected with concentrations of 2.5, 5 and 10 mM paracetamol.</p></div>","PeriodicalId":100938,"journal":{"name":"Mutation Research/Genetic Toxicology","volume":"368 3","pages":"Pages 293-300"},"PeriodicalIF":0.0,"publicationDate":"1996-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1218(96)90071-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19666043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Benzene-induced genotoxicity in mice in vivo detected by the alkaline comet assay: reduction by CYP2E1 inhibition","authors":"Jingsheng Tuo,&nbsp;Steffen Loft,&nbsp;Mikael S. Thomsen,&nbsp;Henrik E. Poulsen","doi":"10.1016/S0165-1218(96)90063-4","DOIUrl":"10.1016/S0165-1218(96)90063-4","url":null,"abstract":"<div><p>The myelotoxic and genotoxic effects of benzene have been related to oxidative DNA damage after metabolism by CYP2E1. Single cell gel electrophoresis (alkaline comet assay) detects DNA damage and may thus be a convenient method for the study of benzene genetoxicity. Benzene exposure to NMRI mice as a single oral gavage at 40, 200 or 450 mg/kg resulted in dose-related DNA damage indicated by an increased comet tail length of peripheral blood lymphocytes and bone marrow nucleated cells sampled 6 h after exposure. After a dose of 40 mg/kg, there was a 1.6-fold increase of ‘tail length’ in bone marrow nucleated cells in comparison with the control (<em>p</em> &lt; 0.01). There was no significant increase in DNA damage in peripheral blood lymphocytes in the same animals. At 200 mg/kg, the tail length was 4.8-fold and 4.0-fold increased in the two cell types, respectively (<em>p</em> &lt; 0.01). At 450 mg/kg, the tail length was further increased to 5.4-fold and 6.6-fold of the control values, respectively (<em>p</em> &lt; 0.01). Pretreatment with propylene glycol (5 μl/g b.wt., twice with a 60-min interval), a selective CYP2E1 inhibitor, reduced the increase in the tail length by about half at all doses in both cell types (<em>p</em> &lt; 0.01). By comparing our data with those from genotoxicity studies on benzene using other methods, we conclude that the ‘alkaline comet assay’ is a sensitive method to detect DNA damage induced by benzene. We also infer that CYP2E1 contributes, at least partly, to the formation of the ‘comet’-inducing metabolites in the chosen cell types.</p></div>","PeriodicalId":100938,"journal":{"name":"Mutation Research/Genetic Toxicology","volume":"368 3","pages":"Pages 213-219"},"PeriodicalIF":0.0,"publicationDate":"1996-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1218(96)90063-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19667407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}