16 research outputs found

    Industrial Relations Experiments in China: Balancing Equity and Efficiency the Chinese Way

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    China should build socialism by "crossing the river by feeling for stones" (Deng Xiaoping). Chinese industrial relations are changing accordingly. Local union experiments have implemented local-level changes experimenting with institutional reforms that address efficiency and equity imbalances. Local union leaders have exercised autonomy to develop multi-employer “community unions” in Changchun’s Chaoyang District to represent peasant migrant workers employed by small firms by targeting small geographic zones and hiring union presidents as organizers, aggregating union members into amalgamated units. While the union’s role still includes social harmonization, unions have undertaken an additional representative role. Similar efforts elsewhere have given the union representation experience. Unions have organized multi-employer federations across industries. Unions also have collaborated with local governments on innovative structures to ensure that companies in some industries, such as construction, post a “bond” to guarantee end-of-year compensation. Finally, this paper discusses the role of the new Labor Contract Law in institutionalizing these changes. The LCL defines more precisely employment relationships and workers’ legal rights and seems to increase unions’ legal authority to ensure that employers respect individual workers’ rights, supports the extension of collective contracts to more enterprises, and appears to give unions greater authority to represent workers within the employment relationship and before legal authorities. These changes may provide a material basis for balancing efficiency with equity. We think these experiments have political foundations, whether it is “harmonious society” or simply to extend the union’s organizing maintain political status. Further research will determine whether these experiments are successful

    Major Vault Protein Prevents Atherosclerotic Plaque Destabilization by Suppressing Macrophage ASK1-JNK Signaling

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    Background: Macrophages are implicated in atherosclerotic plaque instability by inflammation and degradation of extracellular matrix. However, the regulatory mechanisms driving these macrophage-associated processes are not well understood. Here, we aimed to identify the plaque destabilization-associated cytokines and signaling pathways in macrophages. Methods: The atherosclerotic models of myeloid-specific MVP (major vault protein) knockout mice and control mice were generated. Atherosclerotic instability, macrophage inflammatory signaling, and active cytokines released by macrophages were examined in vivo and in vitro by using cellular and molecular biological approaches. Results: MVP deficiency in myeloid cells exacerbated murine plaque instability by increasing production of both MMP (matrix metallopeptidase)-9 and proinflammatory cytokines in artery wall. Mechanistically, expression of MMP-9 was mediated via ASK1 (apoptosis signal-regulating kinase 1)-MKK-4 (mitogen-activated protein kinase kinase 4)-JNK (c-Jun N-terminal kinase) signaling in macrophages. MVP and its α-helical domain could bind with ASK1 and inhibit its dimerization and phosphorylation. A 62 amino acid peptide (MVP-[686-747]) in the α-helical domain of MVP showed a crucial role in preventing macrophage MMP-9 production and plaque instability. Conclusions: MVP may act as an inhibitor for ASK1-JNK signaling-mediated MMP-9 production in macrophages and, thereby, attenuate unstable plaque formation. Our findings suggest that suppression of macrophage ASK1-JNK signaling may be a useful strategy antagonizing atherosclerotic diseases
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