The Rho family of small GTPases is involved in a diverse array of cellular processes, including regulation of the actin cytoskeleton, cell polarity, microtubule dynamics, membrane transport pathways and transcription factor activity. Recent findings have implicated the Rho proteins as key regulators of the skeletal myogenic program; however, much controversy presently exists as to the precise role of these proteins in this process. This review examines the present controversial findings pertaining to the Rho family's regulation of skeletal myogenesis and extrapolates from both other differentiation systems and recently published data the possible mechanisms by which these proteins function in the myogenic cascade.

Transcription factors with helix-loop-helix (HLH) motif play critical roles in controlling the expression of genes involved in lineage commitment, cell fate determination, proliferation, and tumorigenesis. To examine whether the newly identified HLH protein GCIP/CCNDBP1 modulates cell fate determination and plays a role in hepatocyte growth, proliferation, and hepatocarcinogenesis, we generated transgenic mice with human GCIP gene driven by a liver-specific albumin promoter. We demonstrated that in GCIP transgenic mice, the overall liver growth and regeneration occurred normally after liver injury induced by carbon tetrachloride (CCl 4 ). In the diethylnitrosamine (DEN)-induced mouse hepatocarcinogenesis, we demonstrated that overexpression of GCIP in mouse liver suppressed DEN-induced hepatocarcinogenesis at an early stage of tumor development. The number of hepatic adenomas at 24 weeks was significantly lower or not detected in GCIP transgenic male mice compared to the control mice under the same treatment. Although GCIP has little inhibition on the number of hepatic tumors at later stages (40 weeks), hepatocellular tumors in GCIP transgenic mice are smaller and well-differentiated compared to the poorly differentiated tumors in wildtype mice. Furthermore, we demonstrate that GCIP functions as a transcriptional suppressor, regulates the expression of cyclin D1, and inhibits anchorage-independent cell growth and colony formation in HepG2 cells, suggesting a significant role of GCIP in tumor initiation and development.

The fracture mechanics of a stationary crack in a Poly(vinylalcohol) (PVA) hydrogel with a network consisting of chemical and physical crosslinks is studied here. Prior research by the authors has shown that the time-dependent stress strain behavior of this gel can be captured very accurately with a 3D, large deformation nonlinear viscoelastic model based on breaking kinetics of physical crosslinks. This model is used together with a novel time integration scheme to study the stress and deformation fields near the tip of a stationary crack in single edge cracked specimens. The theoretical and finite element results agree remarkably well with experimentally observed crack opening profiles. For the special case of relaxation tests exact asymptotic crack tip solutions are obtained in specimens loaded under predominantly plane stress conditions.

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