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Currently, many diabetic cardiomyopathy (DC) studies focus on either in vitro molecular pathways or in vivo whole-heart properties such as ejection fraction. However, as DC is primarily a disease caused by changes in structural and functional properties, such studies may not precisely identify the influence of hyperglycemia or hyperlipidemia in producing specific cellular changes, such as increased myocardial stiffness or diastolic dysfunction. To address this need, we developed an in vitro approach to examine how structural and functional properties may change as a result of a diabetic environment. Particle-tracking microrheology was used to characterize the biomechanical properties of cardiac myocytes and fibroblasts under hyperglycemia or hyperlipidemic conditions. We showed that myocytes, but not fibroblasts, exhibited increased stiffness under diabetic conditions. Hyperlipidemia, but not hyperglycemia, led to increased cFos expression. Although direct application of reactive oxygen species had only limited effects that altered myocyte properties, the antioxidant N-acetylcysteine had broader effects in limiting glucose or fatty-acid alterations. Changes consistent with clinical DC alterations occur in cells cultured in elevated glucose or fatty acids. However, the individual roles of glucose, reactive oxygen species, and fatty acids are varied, suggesting multiple pathway involvement. 相似文献
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Xinzhu Deng David Michaelson Jason Tchieu Jin Cheng Diana Rothenstein Regina Feldman Sang-gyu Lee John Fuller Adriana Haimovitz-Friedman Lorenz Studer Simon Powell Zvi Fuks E. Jane Albert Hubbard Richard Kolesnick 《PloS one》2015,10(6)
Mammalian NOTCH1-4 receptors are all associated with human malignancy, although exact roles remain enigmatic. Here we employ glp-1(ar202), a temperature-sensitive gain-of-function C. elegans NOTCH mutant, to delineate NOTCH-driven tumor responses to radiotherapy. At ≤20°C, glp-1(ar202) is wild-type, whereas at 25°C it forms a germline stem cell⁄progenitor cell tumor reminiscent of human cancer. We identify a NOTCH tumor phenotype in which all tumor cells traffic rapidly to G2⁄M post-irradiation, attempt to repair DNA strand breaks exclusively via homology-driven repair, and when this fails die by mitotic death. Homology-driven repair inactivation is dramatically radiosensitizing. We show that these concepts translate directly to human cancer models. 相似文献
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Lead poisoning was produced in suckling rats by lead fed to lactating mother rats being transmitted to newborns maternal milk. The brain of 25 day old lead poisoned rats contained 6.0 to 12.5 ppm lead. Zinc was depressed 56% (cerebral cortex), 45% in cerebellum and 43% (caudate nucleus) whereas copper was depressed 52% in the cerebellum. Inhibition of monoamine oxidase (pargyline) or partial depletion of serotonin and norepinephrine did not alter the concentration of Fe, Cu, Zn, or Mn in brain. 相似文献
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The influence of neonatal growth retardation on subsequent spontaneous activity and activity following d-amphetamine (10 mg/kg, i.p.) was studied in CD-1 mice. Different growth rates were obtained by raising mice in litters of either 8 or 16 sucklings per lactating dam. The testing protocol was specifically designed to duplicate a procedure used to assess the influence of neonatal lead exposure on locomotor activity. At 35 to 37 days of age mice were individually tested for general locomotor activity and drug response. Developmental growth retardation influenced their pattern of habituation to the test apparatus and their locomotor response to emphetamine. It was concluded that growth retardation may partially account for behavioral effects previously attributed to the neurotoxic effects of viruses, 6-hydroxydopamine or inorganic lead. 相似文献
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