The price of re-establishing perfect, almost perfect or public monitoring in games with arbitrary monitoring

This paper establishes a connection between the notion of observation (or monitoring) structure in game theory and the one of communication channels in Shannon theory. One of the objectives is to know under which conditions an arbitrary monitoring structure can be transformed into a more pertinent monitoring structure. To this end, a mediator is added to the game. The objective of the mediator is to choose a signalling scheme that allows the players to have perfect, almost perfect or public monitoring and all of this, at a minimum cost in terms of signalling. Graph coloring, source coding, and channel coding are exploited to deal with these issues. A wireless power control game is used to illustrate these notions but the applicability of the provided results and, more importantly, the framework of transforming monitoring structures go much beyond this example.Comment: Proc. of the 4th ACM International Workshop on Game Theory in Communication Networks, 201

From Volume to Value: Transforming Health Care Payment and Delivery Systems to Improve Quality and Reduce Costs

Summarizes presentations on the changes in payment systems and organizational structures required to provide higher-quality health care, including episode-of-care payments for major acute episodes. Suggests pilot projects and implementation strategies

Similarities and differences between the E5 oncoproteins of bovine papillomaviruses type 1 and type 4: Cytoskeleton, motility and invasiveness in E5-transformed bovine and mouse cells

Bovine papillomaviruses (BPVs) are oncogenic viruses. In cattle, BPV-1/2 is associated with urinary bladder cancer and BPV-4 with upper GI tract cancer. BPV E5 is a small hydrophobic protein localised in the endoplasmic reticulum (ER) and Golgi apparatus (GA). E5 is the major transforming protein of BPVs, capable of inducing cell transformation in cultured mouse fibroblasts and, in cooperation with E7, in primary bovine cells. E5-induced cell transformation is accompanied by activation of several cellular protein kinases, including growth factor receptors, and alkalinisation of endosomes and GA. We have reported that BPV E5 causes swelling and fragmentation of the GA and extensive vacuolisation of the cytoplasm. We now show that E5 from both BPV-1 and BPV-4 disturbs the actin cytoskeleton and focal adhesions in transformed bovine cells, where these morphological and behavioural characteristics are accompanied by hyperphosphorylation of the cellular phosphotyrosine kinase c-src. Both BPV-1 and BPV-4 E5 increase the motility of transformed mouse cells, but only BPV-1 E5 causes transformed mouse cells to penetrate a matrigel matrix. BPV-1 transformed mouse cells, but not BPV-4 transformed mouse cells, have hyperhpsphorylated c-src

Tissue-specific calibration of extracellular matrix material properties by transforming growth factor-beta and Runx2 in bone is required for hearing

Publisher version: http://www.nature.com/embor/journal/v11/n10/full/embor2010135.htmlDA - 20100917 IS - 1469-3178 (Electronic) IS - 1469-221X (Linking) LA - ENG PT - JOURNAL ARTICLEDA - 20100917 IS - 1469-3178 (Electronic) IS - 1469-221X (Linking) LA - ENG PT - JOURNAL ARTICLEDA - 20100917 IS - 1469-3178 (Electronic) IS - 1469-221X (Linking) LA - ENG PT - JOURNAL ARTICLEPhysical cues, such as extracellular matrix stiffness, direct cell differentiation and support tissue-specific function. Perturbation of these cues underlies diverse pathologies, including osteoarthritis, cardiovascular disease and cancer. However, the molecular mechanisms that establish tissue-specific material properties and link them to healthy tissue function are unknown. We show that Runx2, a key lineage-specific transcription factor, regulates the material properties of bone matrix through the same transforming growth factor-beta (TGFbeta)-responsive pathway that controls osteoblast differentiation. Deregulated TGFbeta or Runx2 function compromises the distinctly hard cochlear bone matrix and causes hearing loss, as seen in human cleidocranial dysplasia. In Runx2(+/-) mice, inhibition of TGFbeta signalling rescues both the material properties of the defective matrix, and hearing. This study elucidates the unknown cause of hearing loss in cleidocranial dysplasia, and demonstrates that a molecular pathway controlling cell differentiation also defines material properties of extracellular matrix. Furthermore, our results suggest that the careful regulation of these properties is essential for healthy tissue functio