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Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice
- Nature
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Evaluation of the mechanism of nucleoplasmic bridge formation due to premature telomere shortening in agricultural workers exposed to mixed pesticides: Indication for further studies
"... h i g h l i g h t s Effects of pesticide exposure on relative telomere length was evaluated by Q-FISH. Theory of nucleoplasmic bridge formation due to telomere shortening was considered. No significant correlation between exposure and telomere shortening was found. Exposure significantly increased ..."
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h i g h l i g h t s Effects of pesticide exposure on relative telomere length was evaluated by Q-FISH. Theory of nucleoplasmic bridge formation due to telomere shortening was considered. No significant correlation between exposure and telomere shortening was found. Exposure significantly increased formation of nucleoplasmic bridges (NPB). Telomere-end fusion is not a way of NPB formation in studied pesticide exposure. a r t i c l e i n f o Handling Editor: Tamara S. Galloway Keywords: Relative telomere length Nucleoplasmic bridges Occupational exposure Pesticides a b s t r a c t Agricultural workers are often exposed to high levels of pesticides over prolonged periods of time. We attempted to determine whether exposure to multiple pesticides shortens relative telomere length (RTL) and causes nucleoplasmic bridge (NPB) formation via the mechanism of telomere-end fusion in the lymphocytes of agricultural workers. For measuring RTL, we used quantitative fluorescent in situ hybridization, while NPB frequency was measured as part of the cytome assay. Multivariate analysis of variances taking into account confounding factors (age, gender, years of exposure, smoking, and alcohol intake) did not show a decrease, but rather an increase of RTL in agricultural workers compared to control individuals. In the exposed population, NPB frequency was significantly higher compared to controls (6 times, p < 0.05). Multiple regression between NPB, RTL, and confounding factors was not significant. Using Spearman correlation, we did not find proof for our initial hypothesis. Our hypothesis that telomere shortening is a mechanism of NPB origin was not proven, indicating that telomere-end fusion is not a mechanism of NPB formation under our experimental conditions for agricultural workers.
Amancio Carnero*, Carmen Blanco-Aparicio1, Hiroshi Kondoh2, Matilde E.Lleonart3,
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doi:10.4061/2011/620601 Review Article Molecular Characteristics of Pancreatic Ductal Adenocarcinoma
, 2010
"... Copyright © 2011 Niki A. Ottenhof et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Pancreatic cancer is an almost universally l ..."
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Copyright © 2011 Niki A. Ottenhof et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Pancreatic cancer is an almost universally lethal disease and despite extensive research over the last decades, this has not changed significantly. Nevertheless, much progress has been made in understanding the pathogenesis of pancreatic ductal adenocarcinoma (PDAC) suggesting that different therapeutic strategies based on these new insights are forthcoming. Increasing focus exists on designing the so-called targeted treatment strategies in which the genetic characteristics of a tumor guide therapy. In the past, the focus of research was on identifying the most frequently affected genes in PDAC, but with the complete sequencing of the pancreatic cancer genome the focus has shifted to defining the biological function that the altered genes play. In this paper we aimed to put the genetic alterations present in pancreatic cancer in the context of their role in signaling pathways. In addition, this paper provides an update of the recent advances made in the development of the targeted treatment approach in PDAC. 1. Pancreatic Ductal Adenocarcinoma Annually, approximately 43,140 people are diagnosed (incidence 10–12: 100,000) with pancreatic ductal adenocarcinoma (PDAC) in the Unites States and the mortality rate of
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, 2011
"... telomere ends and telomerase and reduces telomerase activity within cells ..."
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telomere ends and telomerase and reduces telomerase activity within cells
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, 2012
"... Developmental dyslexia: dysfunction of a left hemisphere reading network ..."
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