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Biological Sciences Faculty Research & Creative Works

2009

Animals

Articles 1 - 2 of 2

Full-Text Articles in Life Sciences

Identifying Sleep Regulatory Genes Using A Drosophila Model Of Insomnia, Laurent Seugnet, Yasuko Suzuki, Matthew S. Thimgan, Jeffrey Donlea, Sarah I. Gimbel, Laura Gottschalk, Stephen P. Duntley, Paul J. Shaw Jun 2009

Identifying Sleep Regulatory Genes Using A Drosophila Model Of Insomnia, Laurent Seugnet, Yasuko Suzuki, Matthew S. Thimgan, Jeffrey Donlea, Sarah I. Gimbel, Laura Gottschalk, Stephen P. Duntley, Paul J. Shaw

Biological Sciences Faculty Research & Creative Works

Although it is widely accepted that sleep must serve an essential biological function, little is known about molecules that underlie sleep regulation. Given that insomnia is a common sleep disorder that disrupts the ability to initiate and maintain restorative sleep, a better understanding of its molecular underpinning may provide crucial insights into sleep regulatory processes. Thus, we created a line of flies using laboratory selection that share traits with human insomnia. After 60 generations, insomnia-like (ins-l) flies sleep 60 min a day, exhibit difficulty initiating sleep, difficulty maintaining sleep, and show evidence of daytime cognitive impairment. ins-l flies …


N-Acetylcysteine Amide Decreases Oxidative Stress But Not Cell Death Induced By Doxorubicin In H9c2 Cardiomyocytes, Rong Shi, Chuan-Chin Huang, Robert Aronstam, Nuran Ercal, Adam Martin, Yue-Wern Huang Apr 2009

N-Acetylcysteine Amide Decreases Oxidative Stress But Not Cell Death Induced By Doxorubicin In H9c2 Cardiomyocytes, Rong Shi, Chuan-Chin Huang, Robert Aronstam, Nuran Ercal, Adam Martin, Yue-Wern Huang

Biological Sciences Faculty Research & Creative Works

Background: While doxorubicin (DOX) is widely used in cancer chemotherapy, long-term severe cardiotoxicity limits its use. This is the first report of the chemoprotective efficacy of a relatively new thiol antioxidant, N-acetylcysteine amide (NACA), on DOX-induced cell death in cardiomyocytes. We hypothesized that NACA would protect H9c2 cardiomyocytes from DOX-induced toxicity by reducing oxidative stress. Accordingly, we determined the ability of NACA to mitigate the cytotoxicity of DOX in H9c2 cells and correlated these effects with the production of indicators of oxidative stress.

Results: DOX at 5 μM induced cardiotoxicity while 1) increasing the generation of reactive oxygen species (ROS), …