To examine the role of apoptosis in neuromuscular disease progression, we have determined whether pathogenesis in dystrophin-deficient (mdx) and laminin alpha2-deficient (Lama2-null) mice is ameliorated by overexpression of the anti-apoptosis protein BCL2 in diseased muscles. The mdx mice are a model for the human disease, Duchenne muscular dystrophy (DMD), and the Lama2-null mice are a model for human congenital muscular dystrophy type 1A (MDC1A). For these studies, we generated transgenic mice that overexpressed human BCL2 under control of muscle-specific MyoD or MRF4 promoter fragments. We then used cross-breeding to introduce the transgenes into diseased mdx or Lama2-null mice. In mdx mice, we found that overexpression of BCL2 failed to produce any significant differences in muscle pathology. In contrast, in the Lama2-null mice, we found that muscle-specific expression of BCL2 led to a several-fold increase in lifespan and an increased growth rate. Thus, BCL2-mediated apoptosis appears to play a significant role in pathogenesis of laminin alpha2 deficiency, but not of dystrophin deficiency, suggesting that therapies designed to ameliorate disease by inhibition of apoptosis are more likely to succeed in MDC1A than in DMD.

The incidence of anastomotic stricture tends to be lower with a handsewn technique with lower operative time. No difference was appreciated in the anastomotic leak or reexploration rate with either technique.

Traumatic celiac artery injuries are rare and highly lethal with reported mortality rates of 38–62%. The vast majority are caused by penetrating trauma with only 11 reported cases due to blunt trauma (Graham et al., 1978; Asensio et al., 2000, 2002). Only 3 of these cases were complete celiac artery avulsions. Management options described depend upon the type of injury and have included medical therapy with anti-platelet agents or anti-coagulants, endovascular stenting, and open ligation. We report a case of a survivor of complete celiac artery avulsion from blunt trauma managed by open bypass.

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Background: Upon serial passaging of mouse skeletal muscle cells, a small number of cells will spontaneously develop the ability to proliferate indefinitely while retaining the ability to differentiate into multinucleate myotubes. Possible gene changes that could underlie myogenic cell immortalization and their possible effects on myogenesis had not been examined.

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direct comparison of information derived from these databases, it is critical that these differences be taken into account in making policy decisions and guidelines based on these data repositories.

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