Mediated mutagenesis of dimethylnitrosamine in Neurospora crassa by various metabolic activation systems.

Four metabolic activation systems (growth mediated mycelium extract mediated, host mediated, and organ homogenate mediated) were used to study the mutagenic activity of dimethylnitrosamine (DMN) in both forward and reverse mutation systems in the ad-3 (adenine-3) region of Neurospora crassa. DMN was not mutagenic in Neurospora if conidia alone were treated. It was highly mutagenic, however, if conidia were treated with this compound under any of the four activation systems. Quantitative differences in DMN-induced mutation frequencies were observed between in vivo (growth and host mediated) and in vitro (mycelium extract and organ homogenate mediated) activations. The efficiency of the conversion of DMN to a mutagenic metabolite by the organs of rats and mice appeared to be in a reversed order between the host-mediated (liver greater than kidney greater than lung) and the in vitro organ homogenate-mediated (lung greater than kidney greater than liver) assays. Inductions of reverse mutations in strain N23 indicated that DMN induces base-pair substitution in N. crassa.     

Detection of genomic instability in lung cancer tissues by random amplified polymorphic DNA analysis

Genomic instability resulting in multiple mutations is believed to be a driving force in the carcinogenic process. In this study, the random amplified polymorphic DNA (RAPD) technique, a simple PCR-based DNA polymorphism assay system, was used for detecting genomic instability in lung cancer tissues. DNAs from 20 lung cancer (18 non-small cell lung cancers and two small cell lung cancers) and their corresponding normal tissues were amplified individually by RAPD with seven different 10-base arbitrary primers. PCR products from RAPD were electrophoretically separated in agarose gels and banding profiles were visualized by ethidium bromide staining. The ability to detect genomic instability in 20 cancer tissues by each single primer ranged from 15 to 75%. DNA changes were detected by at least one primer in 19 (95%) cancer tissues. These results seem to indicate that genomic rearrangement is associated with lung carcinogenesis and that RAPD analysis is useful for the detection of genomic instability in lung cancer tissues.      

Preneoplastic potential of morphologically distinct transformed foci induced by 3-methylcholanthrene

Individual variability of scoring foci positive for transformation presents a difficult problem in assessing the transformation assay. In this study, an attempt was made to identify five morphologically distinct types of transformed foci based on size (2–3, 3–4, and ≥4 mm in diameter), invasiveness (smooth vs. invading margins), and other properties (piling vs. spread) induced by 3-methylcholanthrene in Balb/c-3T3 cells. The transformed focal cells were used in in vitro studies including anchorage-independent analysis, focal reconstruction, gene transfection using NIH-3T3 host cells, and Southern blotting to assess amplification of five proto-oncogenes (K-ras, H-ras, c-fos, c-jun, c-myc) and a tumor suppressor (p53) gene. Results showed that 1) there was a significant increase in anchorage-independent growth of all five types of foci ranging from 7–12%; 2) all five morphological types of transformed foci showed 8–15% focal reconstruction; 3) DNA from all five types of transformed foci induced transformation in NIH-3T3 cells at a level significantly above the control DNA; 4) gene amplification studies indicated amplification in both K-ras and H-ras proto-oncogenes; however, c-fos, c-jun, and c-myc did not show DNA amplification. The tumor suppressor gene (p53) was activated and the increase was up to 3-fold over the normal Balb/c-3T3 DNA. These findings are consistent with our hypothesis that all five morphologically different foci have preneoplastic potential and that any foci of size ≥ 2 mm regardless of invasiveness and piling should be scored as positive during the transformation assay. Environ. Mol. Mutagen. 32:369–376, 1998 © 1998 Wiley-Liss, Inc.     

闭角型青光眼行复合式小梁切除术后早期高眼压的原因分析

目的：分析闭角型青光眼患者行复合式小梁切除术后1mo内发生高眼压(>21mmHg)的原因及处理方法。

方法：回顾性研究我院2010-03/2013-03应用复合式小梁切除术治疗闭角型青光眼术后1mo内高眼压的病例34例38眼,分析其原因,总结处理方法。

结果：导致术后早期高眼压的因素有：恶性青光眼8例9眼,巩膜瓣下血凝块及结缔组织阻塞13例15眼,术后前房积血5例5眼,巩膜瓣内切口被虹膜组织嵌顿3例3眼,术前高眼压持续时间长4例5眼,原因不明1例1眼。经对症治疗后,患者眼压均控制在21mmHg以下。

结论：闭角型青光眼行复合式小梁切除术后早期高眼压是由多因素造成的,早期预防、及时处理是手术成功的关键。     

The chest tube inserted into the stomach after a transthoracic operation for esophageal cancer: case report

Surgical complications after the transthoracic operation for esophageal cancer mainly include anastomatic fistula, gastric wound thoraco-stomach fistula, stenosis of anastomosis, perforation, gastric volvulus, diaphragmatic hernia, infection, and some other pulmonary complications. Unfortunately, there are few reports about the complications caused by position change of the chest tube until now. We presented an unusual case of a patient who underwent a transthoracic operation for esophageal cancer in our department on August 17, 2006, and a lot of intragastric material was found in his chest tube 17 days later, endoscopic examination suggested that the chest tube had inserted into the stomach. We tried to discuss the etiology and clinical management for this case as well.[第一段]     

Induction of 6-thioguanine resistance in Chinese hamster lung cells treated with dimethylnitrosamine' 2-amino-anthracene or 7,12-dimethylbenz(A)anthracene in the presence of rat liver microsomes

Chemically non-reactive carcinogens require metabolization in order to exert such biological effects as mutagenicity. The mutagenic activities of dimethylnitrosamine (DMN), 2-aminoanthracene (2-AA) and 7,12-dimethylbenz(a)anthracene (7,12-DMBA) have been studied at the hypoxanthine guanine phosphoribosyl transferase (HGPRT) locus in Chinese hamster lung cells. These compounds induce 6-thioguanine (6TG) resistance in the presence of rat liver microsomes, but they do not induce 6TG resistance in the absence of rat microsomes. The frequencies of mutations induced by these compounds are dose-dependent.     

Transplacental genotoxicity of triethylenemelamine, benzene, and vinblastine in mice.

Transplacental cytogenetic effects of triethylenemelamine (TEM), benzene, and vinblastine on maternal mice and their fetuses have been investigated using micronucleus and sister chromatid exchange (SCE) as genetic endpoints. CD-1 mice were treated on day 14 and 15 of gestation with TEM (0.125, 0.25, and 0.5 mg/kg), benzene (439,878, and 1,318 mg/kg), and vinblastine (0.5, 1, and 2 mg/kg) by intraperitoneal injection at 24 hr intervals, and sacrificed 40 hr after the first injection. Erythrocytic precursor cells in maternal bone marrow and fetal livers (2-4) from each pregnant mouse were used for the micronucleus and/or the SCE analyses. Significant dose-related increases in both micronuclei and SCE were found in maternal bone marrow and fetal liver following TEM treatment. Benzene at the highest dose (1,318 mg/kg) also caused a significant increase in micronuclei and SCE in both maternal bone marrow and fetal liver cells. The embryonic genotoxic effect of TEM was much higher than that of benzene for both genetic endpoints, and the frequency of micronuclei induced by benzene was higher in fetal liver than in maternal bone marrow cells. Vinblastine, a spindle poison, induced micronuclei but not SCE. Micronuclei induction by vinblastine was 7 fold greater in maternal bone marrow than in fetal liver cells. All three chemicals were cytotoxic in maternal bone marrow cells, but not in fetal liver cells except for TEM, which showed a weak cytotoxicity in fetal liver cells in the micronucleus assay. These results indicate that TEM, benzene, and vinblastine are transplacental genotoxicants in mice.     

Studies of the mutagenic response of salmonella typhimurium TA98 to size-fractionated air particles: Comparison of the fluctuation and plate incorporation tests

The high-volume Andersen sampler was used to study the mutagenic activity of size-fractionated airborne particles from ambient air in Morgantown, West Virginia. Mutagenicity was studied by the Ames Salmonella assay and the bacterial fluctuation test and was dependent on particle size in both systems, ie, the greatest activity was associated with the smallest particles. Comparison of the two systems was based on identical aliquots of each extract, cells prepared under identical conditions at the same time, and on mutagenic response at a predetermined level of statistical significance (P < 0.05). The results suggest a slight advantage in sensitivity for the Ames test for the air samples under study.     

Mutagenicity detection of in vivo nitrosation of dimethylamine by nitrite

In vivo nitrosation of dimethylamine by nitrite was measured with an intrahepatic host-mediated mutagenicity assay using Salmonella typhimurium as the detecting organism. It was possible to detect the product, N-nitrosodimethylamine, at much lower doses with this system than with previously reported in vivo systems. This and other improvements made it possible to detect the formation of nitrosodimethylamine from relatively low levels of gavaged precursors.