12 research outputs found

    Stable isotope analysis of local avian diets

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    Stable Isotope Analysis (SIA) quantifies the proportion of 13C and 15N within an organism’s tissue and may be used in trophic and nutrient assimilation analysis (Hobson and Sealy 1991). Birds were mist-netted at the North Maple River MAPS site between July 17 and August 1, 2008. Birds were identified and banded according to MAPS protocol and blood samples of 100 μl were taken. Food items were also collected at site and sorted into three groups: berries, aquatic insects, and terrestrial insects. Blood and diet samples were dried and analyzed for δ 13C and δ 15N. Bird isotope signatures were adjusted with discrimination factors and plotted within a mixing model. Proportions for species within model were calculated using IsoSource (interval=1.0, tolerance=0.05). All species, excluding Yellow Warblers, Black-capped Chickadees, and Gray Catbirds, assimilated at least 50% of nutrients from the terrestrial food group. SIA is a new tool for diet analysis and more research is necessary to determine more accurate discrimination factors for North American avifauna.http://deepblue.lib.umich.edu/bitstream/2027.42/61426/1/Bakhurin_Burtch_Latta_2008.pd

    Haploinsufficiency of myostatin protects against aging‐related declines in muscle function and enhances the longevity of mice

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/112228/1/acel12339-sup-0003-TableS1.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/112228/2/acel12339.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/112228/3/acel12339-sup-0004-TableS2.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/112228/4/acel12339-sup-0002-FigureS1.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/112228/5/acel12339-sup-0001-DataS1.pd

    Physiological loading of tendons induces scleraxis expression in epitenon fibroblasts

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    Scleraxis is a basic helix–loop–helix transcription factor that plays a central role in promoting fibroblast proliferation and matrix synthesis during the embryonic development of tendons. Mice with a targeted inactivation of scleraxis ( Scx −/− ) fail to properly form limb tendons, but the role that scleraxis has in regulating the growth and adaptation of tendons of adult organisms is unknown. To determine if scleraxis expression changes in response to a physiological growth stimulus to tendons, we subjected adult mice that express green fluorescent protein (GFP) under the control of the scleraxis promoter ( ScxGFP ) to a 6‐week‐treadmill training program designed to induce adaptive growth in Achilles tendons. Age matched sedentary ScxGFP mice were used as controls. Scleraxis expression was sparsely observed in the epitenon region of sedentary mice, but in response to treadmill training, scleraxis was robustly expressed in fibroblasts that appeared to be emerging from the epitenon and migrating into the superficial regions of tendon fascicles. Treadmill training also led to an increase in scleraxis, tenomodulin, and type I collagen gene expression as measured by qPCR. These results suggest that in addition to regulating the embryonic formation of limb tendons, scleraxis also appears to play an important role in the adaptation of adult tendons to physiological loading. © 2011 Orthopaedic Research Society. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 30:606–612, 2012Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90076/1/21550_ftp.pd

    Haploinsufficiency of myostatin protects against aging-related declines in muscle function and enhances the longevity of mice

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    Summary The molecular mechanisms behind aging-related declines in muscle function are not well understood, but the growth factor myostatin (MSTN) appears to play an important role in this process. Additionally, epidemiological studies have identified a positive correlation between skeletal muscle mass and longevity. Given the role of myostatin in regulating muscle size, and the correlation between muscle mass and longevity, we tested the hypotheses that the deficiency of myostatin would protect oldest-old mice (28-30 months old) from an aging-related loss in muscle size and contractility, and would extend the maximum lifespan of mice. We found that MSTN +/À and MSTN À/À mice were protected from aging-related declines in muscle mass and contractility. While no differences were detected between MSTN +/+ and MSTN À/À mice, MSTN +/À mice had an approximately 15% increase in maximal lifespan. These results suggest that targeting myostatin may protect against aging-related changes in skeletal muscle and contribute to enhanced longevity
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