Power Dependence and Power Paradoxes in Bargaining

[Excerpt] What this article (and our larger program of work) is designed to demonstrate is that these very simple ideas represent a particularly suitable starting point for understanding the power struggle between parties who regularly engage in negotiation. Specifically, in this article we show that the approach contains certain paradoxes regarding the acquisition and use of power in an ongoing bargaining relationship. The dependence framework treats the ongoing relationship as a power struggle in which each party tries to maneuver itself into a favorable power position

Brand innovation and social media: knowledge acquisition from social media, market orientation, and the moderating role of social media strategic capability

The study examines the relationships between knowledge acquisition from social media, two forms of market orientation (proactive and reactive), social media strategic capability, and brand innovation strategy in the context of China’s online technology industry. Analysis of 357 online technology ventures, created during the past 6 years, suggests that brand innovation is affected by both knowledge acquisition from social media and market orientation. Social media strategic capability positively affects brand innovation and acts as a moderator between knowledge acquisition, market orientation, and brand innovation. It further enhances both types of market orientations in achieving brand innovation, suggesting that on social media, a customer’s needs, both expressed and latent (or unexpressed), can be identified more comprehensively than that of the traditional setting. Hence, the context of social media provides a different set of rules for competition and strategic behavior, which online technology ventures should note. Implications are useful to improve the current understanding of social media brand innovation strategy, here in China’s dynamic social media scene

CSF1R inhibitor JNJ-40346527 attenuates microglial proliferation and neurodegeneration in P301S mice

Neuroinflammation and microglial activation are significant processes in Alzheimer's disease pathology. Recent genome-wide association studies have highlighted multiple immune-related genes in association with Alzheimer's disease, and experimental data have demonstrated microglial proliferation as a significant component of the neuropathology. In this study, we tested the efficacy of the selective CSF1R inhibitor JNJ-40346527 (JNJ-527) in the P301S mouse tauopathy model. We first demonstrated the anti-proliferative effects of JNJ-527 on microglia in the ME7 prion model, and its impact on the inflammatory profile, and provided potential CNS biomarkers for clinical investigation with the compound, including pharmacokinetic/pharmacodynamics and efficacy assessment by TSPO autoradiography and CSF proteomics. Then, we showed for the first time that blockade of microglial proliferation and modification of microglial phenotype leads to an attenuation of tau-induced neurodegeneration and results in functional improvement in P301S mice. Overall, this work strongly supports the potential for inhibition of CSF1R as a target for the treatment of Alzheimer's disease and other tau-mediated neurodegenerative diseases

Inflammatory biomarkers in Alzheimer's disease plasma

Introduction: Plasma biomarkers for Alzheimer's disease (AD) diagnosis/stratification are a \u201cHoly Grail\u201d of AD research and intensively sought; however, there are no well-established plasma markers. Methods: A hypothesis-led plasma biomarker search was conducted in the context of international multicenter studies. The discovery phase measured 53 inflammatory proteins in elderly control (CTL; 259), mild cognitive impairment (MCI; 199), and AD (262) subjects from AddNeuroMed. Results: Ten analytes showed significant intergroup differences. Logistic regression identified five (FB, FH, sCR1, MCP-1, eotaxin-1) that, age/APO\u3b54 adjusted, optimally differentiated AD and CTL (AUC: 0.79), and three (sCR1, MCP-1, eotaxin-1) that optimally differentiated AD and MCI (AUC: 0.74). These models replicated in an independent cohort (EMIF; AUC 0.81 and 0.67). Two analytes (FB, FH) plus age predicted MCI progression to AD (AUC: 0.71). Discussion: Plasma markers of inflammation and complement dysregulation support diagnosis and outcome prediction in AD and MCI. Further replication is needed before clinical translation