Skeletal muscle contractility is defined as the capability of the contractile proteins in a muscle to interact and generate force. All body movement are dependent on contractions of skeletal muscles. Consequently, any decline in skeletal muscle contractility results in some degree of immobility. Contractility is impaired by many muscle disease, random and engineered genetic mutations, and even healthy aging. Quantitative knowledge of the contractility of skeletal muscles of skeletal muscles is necessary to test hypotheses regarding the interactions between deficits in basic cellular and molecular processes and musculoskeletal frailty and immobility. Briefly, the specific aims of the Contractility Core are to provide for NSC investigators: (1) facilities, expertise, and technical support for measuring contractility of whole skeletal muscles and small strips of intact fibers from the diaphragm muscle (2) instruction and training in the knowledge and skills necessary to measure contractility; and (3) development of techniques and/or construction of specialized apparatus for the study of the contractility. Contractility is measured initially at the level of the whole skeletal muscle to provide the broadest spectrum of functional changes arising from cellular and molecular changes in skeletal muscle fibers due to aging or experimental interventions. At later stages in a project, more sophisticated evaluations may be required at the cellular or molecular levels. The Contractility Core was developed to ensure that all NSC investigators are able to include valid and reliable measurements of skeletal muscle contractility in their experiments. Consequently, the Contractility Core provides reliable measurements of skeletal muscle contractility in their experiments. Consequently, the Contractility Core provides free to a NSC investigators: (1) one study of six pairs of control and experimental rodents; (2) assistance in education and training NSC investigators, their staff, or their trainees to set-up the apparatus and measure contractility independently; and (3) assistance in the development of one innovative technique, or the construction of one specialized instrument for the measurement of contractility per year. Subsequent use of the Core is generally on a fee-for-service basis, but if results are promising and particularly if the NSC investigator proposes to seek outside funding, additional experiments may be supported by the Core budget from unallocated charge-back-fees. Through the provision of state-of-the-art facilities, techniques and expertise, the Core enhances and encourages multi-disciplinary research in the basic biology of aging at UM and Worldwide. The significance of the Contractility Core to NSC investigators is evidenced by the increase in the number of users from the seven UM scientists in 1995 to nineteen UM and fourteen external scientists in 1999.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Center Core Grants (P30)
Project #
3P30AG013283-08S1
Application #
6615149
Study Section
Special Emphasis Panel (ZAG1)
Project Start
2002-08-01
Project End
2003-06-30
Budget Start
Budget End
Support Year
8
Fiscal Year
2002
Total Cost
Indirect Cost
Name
University of Michigan Ann Arbor
Department
Type
DUNS #
791277940
City
Ann Arbor
State
MI
Country
United States
Zip Code
48109
Xiong, Yi; Torsoni, Adriana Souza; Wu, Feihua et al. (2018) Hepatic NF-kB-inducing kinase (NIK) suppresses mouse liver regeneration in acute and chronic liver diseases. Elife 7:
Liu, Yan; Jiang, Lin; Sun, Chengxin et al. (2018) Insulin/Snail1 axis ameliorates fatty liver disease by epigenetically suppressing lipogenesis. Nat Commun 9:2751
Ghosh, Amiya Kumar; Mau, Theresa; O'Brien, Martin et al. (2018) Novel role of autophagy-associated Pik3c3 gene in gonadal white adipose tissue browning in aged C57/Bl6 male mice. Aging (Albany NY) 10:764-774
Shen, Hong; Sheng, Liang; Xiong, Yi et al. (2017) Thymic NF-?B-inducing kinase regulates CD4+ T cell-elicited liver injury and fibrosis in mice. J Hepatol 67:100-109
Julius, Annabelle; Desai, Anjali; Yung, Raymond L (2017) Recombinant human erythropoietin stimulates melanoma tumor growth through activation of initiation factor eIF4E. Oncotarget 8:30317-30327
Kim, Evelyn H; Galchev, Vladimir I; Kim, Jin Young et al. (2016) Differential protein expression and basal lamina remodeling in human heart failure. Proteomics Clin Appl 10:585-96
Ghosh, Amiya Kumar; Mau, Theresa; O'Brien, Martin et al. (2016) Impaired autophagy activity is linked to elevated ER-stress and inflammation in aging adipose tissue. Aging (Albany NY) 8:2525-2537
Feinstein, Lydia; Ferrando-Martínez, Sara; Leal, Manuel et al. (2016) Population Distributions of Thymic Function in Adults: Variation by Sociodemographic Characteristics and Health Status. Biodemography Soc Biol 62:208-21
Figueroa-Romero, Claudia; Hur, Junguk; Lunn, J Simon et al. (2016) Expression of microRNAs in human post-mortem amyotrophic lateral sclerosis spinal cords provides insight into disease mechanisms. Mol Cell Neurosci 71:34-45
Sharma, Naveen; Arias, Edward B; Cartee, Gregory D (2016) Inhibition of Akt2 phosphorylation abolishes the calorie restriction-induced improvement in insulin-stimulated glucose uptake by rat soleus muscle. Appl Physiol Nutr Metab 41:1208-1211

Showing the most recent 10 out of 219 publications