China and the crisis : global power, domestic caution and local initiative

Even though the global crisis had a quick and dramatic impact on Chinese exports, the Chinese government responded with a range of policy responses that have helped maintain high rates of growth. This success has helped propel China to the centre of global politics, accelerating what many perceive to be a power shift from the West to China. But these gains were achieved by reversing policy in previous years designed to make a fundamental shift in China‟s mode of development, and have highlighted the problems associated with making such a transition. At the moment that many are looking at the Chinese "model" as a potential alternative to the Washington Consensus, one of the consequences of the crisis is to further question the long term efficacy of this "model" in China itself

Effects of Transcriptional Pausing on Gene Expression Dynamics

Stochasticity in gene expression affects many cellular processes and is a source of phenotypic diversity between genetically identical individuals. Events in elongation, particularly RNA polymerase pausing, are a source of this noise. Since the rate and duration of pausing are sequence-dependent, this regulatory mechanism of transcriptional dynamics is evolvable. The dependency of pause propensity on regulatory molecules makes pausing a response mechanism to external stress. Using a delayed stochastic model of bacterial transcription at the single nucleotide level that includes the promoter open complex formation, pausing, arrest, misincorporation and editing, pyrophosphorolysis, and premature termination, we investigate how RNA polymerase pausing affects a gene's transcriptional dynamics and gene networks. We show that pauses' duration and rate of occurrence affect the bursting in RNA production, transcriptional and translational noise, and the transient to reach mean RNA and protein levels. In a genetic repressilator, increasing the pausing rate and the duration of pausing events increases the period length but does not affect the robustness of the periodicity. We conclude that RNA polymerase pausing might be an important evolvable feature of genetic networks

The Chromatin Remodelling Complex B-WICH Changes the Chromatin Structure and Recruits Histone Acetyl-Transferases to Active rRNA Genes

The chromatin remodelling complex B-WICH, which comprises the William syndrome transcription factor (WSTF), SNF2h, and nuclear myosin 1 (NM1), is involved in regulating rDNA transcription, and SiRNA silencing of WSTF leads to a reduced level of 45S pre-rRNA. The mechanism behind the action of B-WICH is unclear. Here, we show that the B-WICH complex affects the chromatin structure and that silencing of the WSTF protein results in a compaction of the chromatin structure over a 200 basepair region at the rRNA promoter. WSTF knock down does not show an effect on the binding of the rRNA-specific enhancer and chromatin protein UBF, which contributes to the chromatin structure at active genes. Instead, WSTF knock down results in a reduced level of acetylated H3-Ac, in particular H3K9-Ac, at the promoter and along the gene. The association of the histone acetyl-transferases PCAF, p300 and GCN5 with the promoter is reduced in WSTF knock down cells, whereas the association of the histone acetyl-transferase MOF is retained. A low level of H3-Ac was also found in growing cells, but here histone acetyl-transferases were present at the rDNA promoter. We propose that the B-WICH complex remodels the chromatin structure at actively transcribed rRNA genes, and this allows for the association of specific histone acetyl-transferases

Cars, corporations, and commodities: Consequences for the social determinants of health

Social epidemiologists have drawn attention to health inequalities as avoidable and inequitable, encouraging thinking beyond proximal risk factors to the causes of the causes. However, key debates remain unresolved including the contribution of material and psychosocial pathways to health inequalities. Tools to operationalise social factors have not developed in tandem with conceptual frameworks, and research has often remained focused on the disadvantaged rather than on forces shaping population health across the distribution. Using the example of transport, we argue that closer attention to social processes (capital accumulation and motorisation) and social forms (commodity, corporation, and car) offers a way forward. Corporations tied to the car, primarily oil and vehicle manufacturers, are central to the world economy. Key drivers in establishing this hegemony are the threat of violence from motor vehicles and the creation of distance through the restructuring of place. Transport matters for epidemiology because the growth of mass car ownership is environmentally unsustainable and affects population health through a myriad of pathways. Starting from social forms and processes, rather than their embodiment as individual health outcomes and inequalities, makes visible connections between road traffic injuries, obesity, climate change, underdevelopment of oil producing countries, and the huge opportunity cost of the car economy. Methodological implications include a movement-based understanding of how place affects health and a process-orientated integration of material and psychosocial explanations that, while materially based, contests assumptions of automatic benefits from economic growth. Finally, we identify car and oil corporations as anti-health forces and suggest collaboration with them creates conflicts of interest