A quarter century of creative chaos: Xinhua News Agency 1980-2005

Chinese media in the context of China's rise have puzzled many scholars who used to understand media and communications phenomena by employing the theories generated from a few affluent Western democracies, notably the US. As a result, a complex but more accurate picture has been ignored. Under numerous theoretical polarizations, the contemporary social world seems little changed but polarized. This thesis aims to propose a different approach endeavoring to 'de-Westernize' or 'internationalize' media and communications studies. As a starting point, this study focuses on the globalization debate, Chinese media and news agency studies. The thesis has investigated the Chinese news agency, Xinhua, by employing Fuzzy Logic which captures the complexity of the change in the agency's business structure and journalistic practices over last 25 years. The change is also examined by scrutinizing the role of journalists in the interrelations of Xinhua with its news sources, media and nonmedia clients, and other news agencies. A combination of archive study and 94 semistructured interviews conducted in Beijing, Shanghai, Guangzhou, Hong Kong, Macau and London provides an inclusive account of the Chinese news institution. The key research findings drawn from the empirical research into Xinhua have justified the central argument of this thesis: Crisp Logic or the 'either/or' approach has failed to explain the dynamics of the change to the media system based in a 'non-Western' society. The numerous theoretical polarizations generated by Crisp Logic to a large extent have distorted the understanding of the contemporary social world by polarizing it. Fuzzy Logic serves better(though it is not the only choice)than the traditional approach to reflect on the set of variables existing between the two poles created by Crisp Logic. This thesis is the first doctorate research in the UK and other English-speaking countries to investigate Xinhua by 'going inside' the news institution's headquarters, local branches and overseas bureaus. This is the first comprehensive academic study of the agency, which not only examines the agency's recent change in business structure and journalistic practices, but also provides a historical account of the agency and its relationship with other social institutions. This is the first media study that employs Fuzzy Logic to understand the globalization theory, Chinese media and news agencies.

Molecular mechanisms controlling synaptic recruitment of GluA4 subunit-containing AMPAreceptors

Synaptic recruitment of AMPA receptors (AMPARs) represents a key postsynaptic mechanism driving functional development and maturation of glutamatergic synapses. At immature hippocampal synapses, PKA-driven synaptic insertion of GluA4 is the predominant mechanism for synaptic reinforcement. However, the physiological significance and molecular determinants of this developmentally restricted form of plasticity are not known. Here we show that PKA activation leads to insertion of GluA4 to synaptic sites with initially weak or silent AMPAR-mediated transmission. This effect depends on a novel mechanism involving the extreme C-terminal end of GluA4, which interacts with the membrane proximal region of the C-terminal domain to control GluA4 trafficking. In the absence of GluA4, strengthening of AMPAR-mediated transmission during postnatal development was significantly delayed. These data suggest that the GluA4-mediated activation of silent synapses is a critical mechanism facilitating the functional maturation of glutamatergic circuitry during the critical period of experience-dependent fine-tuning.

Studies of the role of nf-κb in controlling osteoclast differentiation and bone loss

Increased osteoclast (OC) bone resorption and/or decreased osteoblast (OB) bone formation contribute to bone loss in osteoporosis and rheumatoid arthritis (RA). Findings of the basic and translational research presented in this thesis demonstrate a number of mechanisms by which cytokine-induced NF-κB activation controls bone resorption and formation: 1) Tumour necrosis factor-α (TNF) expands pool of OC precursors (OCPs) by promoting their proliferation through stimulation of the expression of macrophage colony stimulating factor (M-CSF) receptor, c-Fms, and switching M-CSF-induced resident (M2) to inflammatory (M1) macrophages with enhanced OC forming potential and increased production of inflammatory factors through induction of NF-κB RelB; 2) Similar to RANKL, TNF sequentially activates transcriptional factors NF-κB p50 and p52 followed by c-Fos and then NFATc1 to induce OC differentiation. However, TNF alone induces very limited OC differentiation. In contrast, it pre-activates OCPs to express cFos which cooperates with interleukin-1 (IL-1) produced by these OCPs in an autocrine mechanism by interacting with bone matrix to mediate the OC terminal differentiation and bone resorption from these pre-activated OCPs. 3) TNF-induced OC formation is independent of RANKL but it also induces NF-κB2 p100 to limit OC formation and bone resorption, and thus p100 deletion accelerates joint destruction and systemic bone loss in TNF-induced RA; 4) TNF receptor associated factor-3 (TRAF3) limits OC differentiation by negatively regulating non-canonical NF-κB activation and RANKL induces TRAF3 ubiquitination and lysosomal degradation to promote OC differentiation. Importantly, a lysosomal inhibitor that inhibits TRAF3 degradation prevents ovariectomy-induced bone loss; 5) RelB and Notch NICD bind RUNX2 to inhibit OB differentiation and RelB:p52 dimer association with NICD inhibit OB differentiation by enhancing the binding of RBPjκ to Hes1. These findings suggest that non-canonical NF- κB signaling could be targets to develop new therapies for RA or osteoporosis. For example 1) Agents that degrade TNF-induced RelB could block M1 macrophage differentiation to inhibit inflammation and joint destruction for the therapy of RA; 2)Agents that prevent p100 processing or TRAF3 degradation could inhibit bone resorption and also stimulate bone formation simultaneously for the therapy of osteoporosis.