A Strategy for the Commons: Business-driven Networks for Collective Action and Policy Dialogue. The Example of Global Compact Local Networks

The current challenges involved with ensuring global sustainability are daunting. Climate change is increasing the incidence of severe weather events, natural resources are undergoing rapid depletion, labor conditions in global supply chains are often inhumane and degrading, and corruption around the globe is undermining competition and destroying wealth. These and other global challenges pose serious problems not only to mankind in general, but also to the sustainability of companies. Indeed, companies rely on enabling environments, local and global alike, for long-term success. Companies depend on a reliable legal framework conducive to investment and competition, a healthy and viable natural environment, and a secure social environment that facilitates the wellbeing of its inhabitants. However, given the overexploitation of shared resources, also known as the “tragedy of the commons,” companies often find it difficult to address global sustainability challenges and invest in enabling environments. All sustainability challenges face this tragedy: Although each societal actor ought to have an interest in creating or ensuring the viability of these common goods, the incentive to “free ride” on the efforts of others and let them bear the costs is exceedingly high. As a result, short-term profit maximization often damages the longterm growth prospects of companies. Since governments lack the capacity to address the complexity and global scope of sustainability challenges alone, a “strategy for the commons” is needed that allows companies, governments and other actors to overcome the free rider dilemma and invest in sustainable development

Голодомор 1932 –– 1933 рр. в Україні як геноцид

Given its fundamental role in development and cancer, the Wnt-beta-catenin signaling pathway is tightly controlled at multiple levels. RING finger protein 43 (RNF43) is an E3 ubiquitin ligase originally found in stem cells and proposed to inhibit Wnt signaling by interacting with the Wnt receptors of the Frizzled family. We detected endogenous RNF43 in the nucleus of human intestinal crypt and colon cancer cells. We found that RNF43 physically interacted with T cell factor 4 (TCF4) in cells and tethered TCF4 to the nuclear membrane, thus silencing TCF4 transcriptional activity even in the presence of constitutively active mutants of beta-catenin. This inhibitory mechanism was disrupted by the expression of RNF43 bearing mutations found in human gastrointestinal tumors, and transactivation of the Wnt pathway was observed in various cells and in Xenopus embryos when the RING domain of RNF43 was mutated. Our findings indicate that RNF43 inhibits the Wnt pathway downstream of oncogenic mutations that activate the pathway. Mimicking or enhancing this inhibitory activity of RNF43 may be useful to treat cancers arising from aberrant activation of the Wnt pathwa

Interaction of hyperalgesia and sensory loss in complex regional pain syndrome type I (CRPS I)

Sensory abnormalities are a key feature of Complex Regional Pain Syndrome (CRPS). In order to characterise these changes in patients suffering from acute or chronic CRPS I, we used Quantitative Sensory Testing (QST) in comparison to an age and gender matched control group