Cal Poly and the Wayward Field of Home Economics

Since its establishment in 1901 California Polytechnic State University at San Luis Obispo has gone through a number of identity crises. What began as a progressive institution that aimed to educate the state’s future blue-collar workers has matured into a recognized academic institution. As the school grew, its faculty and administrators had to decide which features of Cal Poly fit into their vision of its future, and which should be left behind as the university progressed. Many aspects of Cal Poly’s curriculum were scrapped somewhere between rural-secondary school, and comprehensive polytechnic university. The now defunct Department of Home Economics falls into this unfortunate second category

Age-Dependent Effect of Myostatin Blockade on Disease Severity in a Murine Model of Limb-Girdle Muscular Dystrophy

Myostatin (MSTN) is a muscle-specific secreted peptide that functions to limit muscle growth through an autocrine regulatory feedback loop. Loss of MSTN activity in cattle, mice, and humans leads to a profound phenotype of muscle overgrowth, associated with more and larger fibers and enhanced regenerative capacity. Deletion of MSTN in the mdx mouse model of Duchenne muscular dystrophy enhances muscle mass and reduces disease severity. In contrast, loss of MSTN activity in the dy(W)/dy(W) mouse model of laminin-deficient congenital muscular dystrophy, a much more severe and lethal disease model, does not improve all aspects of muscle pathology. Here we examined disease severity associated with myostatin (mstn(−/−)) deletion in mice nullizygous for δ-sarcoglycan (scgd(−/−)), a model of limb-girdle muscular dystrophy. Early loss of MSTN activity achieved either by monoclonal antibody administration or by gene deletion each improved muscle mass, regeneration, and reduced fibrosis in scgd(−/−) mice. However, antibody-mediated inhibition of MSTN in late-stage dystrophic scgd(−/−) mice did not improve disease. These findings suggest that MSTN inhibition may benefit muscular dystrophy when instituted early or if disease is relatively mild but that MSTN inhibition in severely affected or late-stage disease may be ineffective