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November: My Life in Blue is a collection of abstract poetry, consisting of 105 individual poems. November is new beginnings; it is the end of old things; it is paper; magic; dark days; dark blue.

A moving holiday story from New York Times bestselling author Andrew Clements. For Hart Evans, being the most popular kid in sixth grade has its advantages. Kids look up to him, and all the teachers let him get away with anything -- all the teachers except the chorus director, Mr. Meinert. When Hart's errant rubber band hits Mr. Meinert on the neck during chorus practice, it's the last straw for the chorus director, who's just learned he's about to lose his job due to budget cuts. So he tells the class they can produce the big holiday concert on their own. Or not. It's all up to them. And who gets elected to run the show? The popular Mr. Hart Evans. Hart soon discovers there's a big difference between popularity and leadership, and to his surprise, discovers something else as well -- it's really important to him that this be the best holiday concert ever, and even more important, that it not be the last.

Mechanism-based therapies that mitigate phenotypic modulation of vascular smooth muscle cells (SMC) represent appealing targets to improve outcomes of vascular intervention by limiting restenosis. Canonical transient receptor potential channel subtype-6 (TRPC6) is upregulated in arterial segments following balloon angioplasty, though its role in the pathogenesis of neointimal hyperplasia (IH) is unclear. We hypothesized that TRPC6 is required for maintenance of myocardin expression and stabilizes the contractile phenotype in SMC to reduce stenosis in a model of arterial intervention. In this study, histologic evaluation of TRPC6-/- common carotid arteries (CCA) demonstrated subtle structural deficits, including luminal dilation, medial thinning and decreased elastin lamella compared to WT CCA. These structural deficits were associated with reduced myocardin expression in TRPC6-/- CCA homogenates. To assess the effects of TRPC6 on arterial healing after vascular intervention, WT and TRPC6-/- mice were subjected to carotid wire injury. Evaluation at 28 days post injury demonstrated that luminal stenosis, negative arterial remodeling and neointimal hyperplasia were accentuated in TRPC6-/- mice compared to WT mice. TRPC6-/- carotid arteries showed increased medial and neointimal cell proliferation after injury. Immunohistochemistry suggested persistent attenuation of contractile biomarker expression in the media of TRPC6-/- CCA but complete restoration of contractile biomarker expression in in the media of WT CCA 28 days after wire injury. In vitro, cultured primary aortic TRPC6-/- SMC showed decreased expression of SM22, MYH11 and myocardin. Loss of contractile biomarker expression in TRPC6-/- SMC was accompanied by the emergence of IH-related behaviors including enhanced proliferation and migration. Acute siRNA-mediated knockdown of TRPC6 in immortalized arterial SMC was sufficient to induce myocardin downregulation and phenotypic modulation. In total, these results suggest that TRPC6 plays a protective and deterministic role in maintenance of the SMC contractile phenotype, and that absence of TRPC6 promotes IH and luminal stenosis following vascular intervention.