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This digital document is an article from Issues in Science and Technology, published by National Academy of Sciences on March 22, 1993. The length of the article is 4463 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.

From the supplier: The increase over the years in noise pollution demands a renewed effort by the EPA to reduce excessive noise across the US. The Office of Noise Abatement and Control must be refunded, or Congress can repeal the Noise Control Act so that state and local governments can adopt standards more appropriate to their vicinity. Moreover, the EPA should capitalize on market forces and public education, and reevaluate its scientific, technical, training and infrastructure activities. Another difficult but necessary task for the EPA is to coordinate with the private sector and other federal agencies. Finally, the bad effects of noise pollution are described.

Citation Details
Title: Rejoining the battle against noise pollution.
Author: Sidney A. Shapiro
Publication:Issues in Science and Technology (Refereed)
Date: March 22, 1993
Publisher: National Academy of Sciences
Volume: v9 Issue: n3 Page: p73(7)

Distributed by Thomson Gale.
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This digital document is a journal article from DNA Repair, published by Elsevier in . The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.

Description:
A PFGE method was adapted to measure DNA double-strand breaks (DSBs) in mammalian cells after low (0-25Gy) doses of ionising radiation. Instead of radionuclide incorporation, DNA staining in the gel by SYBR-Gold was used, which lowered the background of DNA damage and could be applied to non-cycling cells. DSB level was defined as a product of a fraction of DNA released to the gel (FR) and a number of DNA fragments in the gel (DNA"f"r"a"g"m) and expressed as a percentage above control value. The slope of the dose-response curve was two-fold higher compared to that with FR alone as DSB level indicator (31.4 versus 15.6% per Gy). Two alternative ways were proposed to determine the total amount of DNA, used for FR calculation: measurement of DNA content in a plug not subjected to electrophoresis, with the use of Pico-Green, or estimation of DNA released to the gel from a plug irradiated with 600Gy of @c-rays. The limit of DSB detection was 0.25Gy for human G1-lymphocytes and 0.5-1Gy for asynchronous cultures of human glioma M059 K and J or mouse lymphoma L5178Y-R and -S cells. Specificity of our PFGE assay to DSB was confirmed by the fact that no damage was detected after treatment of the cells with H"2O"2, an inducer of single-strand DNA breaks (SSBs). On the contrary, the H"2O"2 inflicted damage was detected by neutral comet assay, attaining 160% above control (equivalent to 2.5Gy of X-radiation). DSB rejoining, measured in cells after X-irradiation with a dose of 10Gy, generally proceeded faster than that measured previously after higher (30-50Gy) doses of ionising radiation. Clearly seen were defects in DSB rejoining in radiosensitive M059 J and L5178Y-S cells compared to their radioresistant counterparts, M059 K and L5178Y-R. In some cell lines, a secondary post-irradiation increase in DSB levels was observed. The possibility is considered that these additional DSBs may accumulate during processing of non-DSB clustered DNA damage or/and represent early apoptotic events. .
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This digital document is a journal article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, published by Elsevier in . The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.

Description:
In our previous study, we found that colcemid, an inhibitor of mitotic spindle, promotes UVC-induced apoptosis in Chinese hamster ovary cells (CHO.K1). In this study, a brief treatment of colcemid on cells after but not before UV irradiation could synergistically reduce the cell viability. Although colcemid did not affect the excision of UV-induced DNA damages such as [6-4] photoproducts or cyclobutane pyrimidine dimers, colcemid accumulated the DNA breaks when it was added to cells following UV-irradiation. This colcemid effect required nucleotide excision repair (NER) since the same accumulation of DNA breaks was barely or not detected in two NER defective strains of CHO cells, UV5 or UV24. Furthermore, the colcemid effect was not due to semi-conservative DNA replication or mitosis since the colcemid-caused accumulation of DNA breaks was also seen in non-replicating cells. Moreover, colcemid inhibited rejoining of DNA breaks accumulated by hydroxyurea/cytosine arabinoside following UV irradiation. Nevertheless, colcemid did not affect the unscheduled DNA synthesis as assayed by the incorporation of bromodeoxyuridine. Taken together, our results suggest that colcemid might inhibit the step of ligation of NER pathways. ication or mitosis since the colcemid-caused accumulation of DNA breaks was also seen in non-replicating cells. Moreover, colcemid inhibited rejoining of DNA breaks accumulated by hydroxyurea/cytosine arabinoside following UV irradiation. Nevertheless, colcemid did not affect the unscheduled DNA synthesis as assayed by the incorporation of bromodeoxyuridine. Taken together, our results suggest that colcemid might inhibit the step of ligation of NER pathways. .
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