N NANOTECHNOLOGY CHANGES HOW METALS CAN INFLUENCE CELL GROWTH
cientists have expanded on recent advances in nanotechnology to change how metals can influence cell growth and development in the body, according to an article published online Jan. 21 in advance of print publication in the journal Nano Letters. Researchers in Canada and Brazil applied etching compounds to the surfaces of common biomedical metals such as titanium, which caused a sponge-like pattern of nanopits to appear on the metal surfaces. Researchers then tested the effects of the chemically produced nanoporous titanium surfaces on cell growth and development. Compared with the untreated smooth surfaces, bone cell growth increased, unwanted cell growth decreased and stem cells were stimulated on the treated surfaces. Additionally, the expression of genes required for cell adhesion and growth increased when they were in contact with the nanoporous surfaces. A critical aspect of the study is that the surfaces can directly stimulate cells, which can eliminate the need for pharmaceuticals and the resulting side effects. “Our study is groundbreaking,” said Dr. Antonio Nanci, senior author and a professor at the Université de Montréal’s Faculty of Dentistry. “We use simple yet very efficient chemical treatments to alter metals commonly used in the operating room. This innovative approach may ultimately hold the key to developing intelligent materials that are not only easily accepted
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by the human body but that can actively respond to the surrounding biological environment.” The study was funded by the Canadian Institutes of Health Research, the Natural Science and Engineering Research Council of Canada, the Canada Foundation for Innovation, the Fonds de la recherche sur la nature et les technologies, the São Paulo State Research Foundation and the Canadian Bureau for International Education. RESEARCHERS DISCOVER HOW CHEMOTHERAPEUTIC AGENTS BLOCK BLOOD VESSEL GROWTH
he means by which a class of commonly used chemotherapeutic agents can block cancer growth has been discovered, report researchers in a study published online in January in the Proceedings of the National Academy of Sciences Early Edition. Researchers at Johns Hopkins University, Baltimore, screened more than 3,000 drugs in the Johns Hopkins Drug Library. They treated modified liver cancer cells growing in low oxygen with each of the drugs in the library and examined whether the drug could stop hypoxia-inducible factor 1 (HIF1) from turning on genes. HIF-1 proteins help cells survive under low-oxygen conditions by turning on genes that grow new blood vessels to help oxygenstarved cells—like those found in fast-growing solid tumors— survive. One of the drugs in the anthracycline class of chemotherapeutic agents—daunorubicin— reduced HIF-1’s gene-activating ability by more than 99 percent. Other drugs in the same class—
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doxorubicin, epirubicin and idarubicin—also blocked HIF-1 activity. Further examination, however, showed that both treated and untreated cells contained similar amounts of HIF-1 protein. Researchers concluded that the drugs did not affect whether HIF-1 was made. To turn on genes, HIF-1 must bind to DNA. So researchers evaluated treated and untreated cells and compared regions of DNA known to be bound by HIF-1. The sites bound by HIF-1 in untreated cells were unbound in anthracyclinetreated cells. “This is the first direct evidence that anthracycline agents prevent HIF-1 from binding to and turning on target genes,” said study coauthor Gregg L. Semenza, MD, PhD, director of the vascular program at the Johns Hopkins Institute for Cell Engineering and a member of the McKusick-Nathans Institute of Genetic Medicine, Baltimore. Researchers grew tumors in mice from human prostate cancer cells to see if interfering
JADAPreview COMING IN APRIL
dSealing, repairing and refurbishing defective Class I and Class II restorations dManaging severe dental discoloration in porcelain veneers dAssessing the importance of oral health dRespecting patient autonomy Look for this and more in the April issue of JADA.
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Copyright © 2009 American Dental Association. All rights reserved. Reprinted by permission.
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