Incipient plasticity and fully plastic contact behavior of copper coated with a graphene layer

Cu coated with a graphene layer increases the elastic modulus from 163.4 GPa to 176.7 GPa, as analyzed for the initial elastic loading during nanoindentation by the Hertzian contact theory. This is attributed to stiffening, due to the ultra-high elastic modulus of the graphene layer, and the compressive in-plane residual stresses in the Cu surface volume introduced by the lattice mismatch between graphene and Cu. The graphene layer induces incipient plasticity, manifested by pop-in events during nanoindentation loading, at shallower indentation depths. This could be due to the compressive in-plane residual stress in the Cu surface volume; however, this compressive stress does not significantly change the critical resolved shear stress for the incipient plasticity. Even in the fully plastic contact region, at an indentation depth of 100 nm, the graphene layer affects the stress distribution underneath the indenter, resulting in a lower pile-up height. When considering this reduced pile-up height, the graphene layer is found to enhance elastic modulus by 5%, whereas it has no effect on hardness

Vav1 inhibits RANKL-induced osteoclast differentiation and bone resorption

Vav1 is a Rho/Rac guanine nucleotide exchange factor primarily expressed in hematopoietic cells. In this study, we investigated the potential role of Vav1 in osteoclast (OC) differentiation by comparing the ability of bone marrow mononuclear cells (BMMCs) obtained from Vav1-deficient (Vav1−/−) and wild-type (WT) mice to differentiate into mature OCs upon stimulation with macrophage colony stimulating factor and receptor activator of nuclear kappa B ligand in vitro. Our results suggested that Vav1 deficiency promoted the differentiation of BMMCs into OCs, as indicated by the increased expression of tartrate-resistant acid phosphatase, cathepsin K, and calcitonin receptor. Therefore, Vav1 may play a negative role in OC differentiation. This hypothesis was supported by the observation of more OCs in the femurs of Vav1−/− mice than in WT mice. Furthermore, the bone status of Vav1−/− mice was analyzed in situ and the femurs of Vav1−/− mice appeared abnormal, with poor bone density and fewer number of trabeculae. In addition, Vav1-deficient OCs showed stronger adhesion to vitronectin, an αvβ3 integrin ligand important in bone resorption. Thus, Vav1 may inhibit OC differentiation and protect against bone resorption

The Three Strikes Policy in Korean Copyright Act 2009: Safe or Out?

Korea has grown to be one of the Internet powers in a short period. Because of insufficient copyright protection, Korea recently revised the Korean Copyright Act to reinforce protection of copyright and promote sound distribution of copyrighted works. The new law allows the Minister of Culture, Sports and Tourism to issue orders and the Korea Copyright Commission to issue recommendations. Orders and recommendations are distinguished by the subject of the issuance and the legal force. Orders and recommendations enable online service providers to delete or stop transmission of illegal reproductions, give warning notices to infringers, or suspend the account of repetitive infringers. The “three strikes” policy is controversial and has raised several constitutional concerns. First, the suspension of the repeat infringer’s account may be an unconstitutional violation of the infringer’s freedom of speech. Second, an executive agency’s decision to issue a correction order could be an unconstitutional violation of the separation of powers. The final concern is that the policy violates the principles of due process. This Article examines the “three strikes” policy, the constitutional concerns regarding the policy, and possible policy revisions for more effective copyright protection

Substrate Competition as a Source of Ultrasensitivity in the Inactivation of Wee1

SummaryThe mitotic regulators Wee1 and Cdk1 can inactivate each other through inhibitory phosphorylations. This double-negative feedback loop is part of a bistable trigger that makes the transition into mitosis abrupt and decisive. To generate a bistable response, some component of a double-negative feedback loop must exhibit an ultrasensitive response to its upstream regulator. Here, we experimentally demonstrate that Wee1 exhibits a highly ultrasensitive response to Cdk1. Several mechanisms can, in principle, give rise to ultrasensitivity, including zero-order effects, multisite phosphorylation, and competition mechanisms. We found that the ultrasensitivity in the inactivation of Wee1 arises mainly through two competition mechanisms: competition between two sets of phosphorylation sites in Wee1 and between Wee1 and other high-affinity Cdk1 targets. Based on these findings, we were able to reconstitute a highly ultrasensitive Wee1 response with purified components. Competition provides a simple way of generating the equivalent of a highly cooperative allosteric response