In some cavernous sinus dAVFs with palliative transarterial embolization or observational management, there was a change in the venous drainage patterns, consisting of a decrease in the number of venous drainage routes. There was a trend for the posterior route to close before the anterior drainage or cortical drainage route. This suggests the occurrence of a staged progression in a regular direction in cavernous sinus dAVFs. Without treatment aiming at a complete cure, most cavernous sinus dAVFs can behave benignly, with a low possibility of development of cortical venous reflux during follow-up.
Skeletal myogenesis is a multistep process by which multinucleated mature muscle fibers are formed from undifferentiated, mononucleated myoblasts. However, the molecular mechanisms of skeletal myogenesis have not been fully elucidated. Here, we identified muscle-restricted coiled-coil (MURC) protein as a positive regulator of myogenesis. In skeletal muscle, MURC was localized to the cytoplasm with accumulation in the Z-disc of the sarcomere. In C2C12 myoblasts, MURC expression occurred coincidentally with myogenin expression and preceded sarcomeric myosin expression during differentiation into myotubes. RNA interference (RNAi)-mediated knockdown of MURC impaired differentiation in C2C12 myoblasts, which was accompanied by impaired myogenin expression and ERK activation. Overexpression of MURC in C2C12 myoblasts resulted in the promotion of differentiation with enhanced myogenin expression and ERK activation during differentiation. During injury-induced muscle regeneration, MURC expression increased, and a higher abundance of MURC was observed in immature myofibers compared with mature myofibers. In addition, ERK was activated in regenerating tissue, and ERK activation was detected in MURC-expressing immature myofibers. These findings suggest that MURC is involved in the skeletal myogenesis that results from modulation of myogenin expression and ERK activation. MURC may play pivotal roles in the molecular mechanisms of skeletal myogenic differentiation.
Background-Carbon dioxide-rich water bathing has the effect of vasodilatation, whereas it remains undetermined whether this therapy exerts an angiogenic action associated with new vessel formation. Methods and Results-Unilateral hindlimb ischemia was induced by resecting the femoral arteries of C57BL/J mice.Lower limbs were immersed in CO 2 -enriched water (CO 2 concentration, 1000 to 1200 mg/L) or freshwater (control) at 37°C for 10 minutes once a day. Laser Doppler imaging revealed increased blood perfusion in ischemic limbs of CO 2 bathing (38% increase at day 28, PϽ0.001), whereas N G -nitro-L-arginine methyl ester treatment abolished this effect. Angiography or immunohistochemistry revealed that collateral vessel formation and capillary densities were increased (4.1-fold and 3.7-fold, PϽ0.001, respectively). Plasma vascular endothelial growth factor (VEGF) levels were elevated at day 14 (18%, PϽ0.05). VEGF mRNA levels, phosphorylation of NO synthase, and cGMP accumulation in the CO 2 -bathed hindlimb muscles were increased (2.7-fold, 2.4-fold, and 3.4-fold, respectively) but not in forelimb muscles. The number of circulating LinϪ/Flk-1ϩ/CD34Ϫ endothelial-lineage progenitor cells was markedly increased by CO 2 bathing (24-fold at day 14, PϽ0.001). The LinϪ/Flk-1ϩ/CD34Ϫ cells express other endothelial antigens (endoglin and VE-cadherin) and incorporated acetylated LDL. Conclusions-Our present study demonstrates that CO 2 bathing of ischemic hindlimb causes the induction of local VEGF synthesis, resulting in an NO-dependent neocapillary formation associated with mobilization of endothelial progenitor cells.
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