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New perspectives on the Cultural Revolution./ Ed. William A Joseph ... + Schwarcz, Vera: Time for telling truth is running out. Conversations with Zhang Shenfu. + Enthält Rezensionen u.a. von: Wang Fan-hsi: Memoirs of a Chinese revolutionary

OBJECTIVE: We aimed to describe the rationalisation beliefs endorsed by Chinese male smokers and to examine the association between rationalisation and the intention to quit. SETTING: Questionnaires were conducted among male smokers in three cities (Shanghai, Nanning and Mudanjiang) which represent different geographical locations, economic development levels and legislative status of tobacco control in China. DESIGN AND PARTICIPANTS: It was a multicentre cross-sectional survey involved a total of 3710 male smokers over 18 years. OUTCOME MEASURES: Primary outcomes were intention to quit, smoking rationalisation scores and sub scores in six dimensions. Smoking rationalisation was assessed using a newly developed Chinese rationalisation scale. Multivariable logistic regression was performed to examine the relationship between rationalisation and intention to quit. RESULTS: On average, smokers scored 3.3 out of 5 on the smoking rationalisation scale. With a one point increase in total rationalisation scale, the odds for intention to quit in the next 6 months decreased by 48% (OR=0.52, 95% CI: 0.44 to 0.61; p<0.001). Separate logistic regressions for six subscales of rationalisation shown consistent inverse associations with intention to quit (all p values <0.001). Believing that smoking was socially acceptable was the strongest predictor (OR=0.62, 95% CI: 0.55 to 0.71; p<0.001). CONCLUSIONS: Rationalisation beliefs could be important barriers to smoking cessation. Some beliefs have stronger association with quit intention than others. Eroding rationalisation beliefs endorsed by smokers is a potential strategy for smoking cessation intervention.

Long-range interactions between regulatory elements and gene promoters play key roles in transcriptional regulation. The vast majority of interactions are uncharted, constituting a major missing link in understanding genome control. Here, we use promoter capture Hi-C to identify interacting regions of 31,253 promoters in 17 human primary hematopoietic cell types. We show that promoter interactions are highly cell type specific and enriched for links between active promoters and epigenetically marked enhancers. Promoter interactomes reflect lineage relationships of the hematopoietic tree, consistent with dynamic remodeling of nuclear architecture during differentiation. Interacting regions are enriched in genetic variants linked with altered expression of genes they contact, highlighting their functional role. We exploit this rich resource to connect non-coding disease variants to putative target promoters, prioritizing thousands of disease-candidate genes and implicating disease pathways. Our results demonstrate the power of primary cell promoter interactomes to reveal insights into genomic regulatory mechanisms underlying common diseases. ; This work was supported by the following grants: UK Medical Research Council (MR/L007150/1, MC_UP_1302/1, MC_UP_1302/3, MC_UP_1302/5), UK Biotechnology and Biological Sciences Research Council (BB/J004480/1), ERC (DEVOCHROMO advanced grant), JDRF (9-2011-253, 5-SRA-2015-130), Wellcome Trust (089989, 091157, 095908, 100140, 107212, 107881), European Union 7th Framework Programme (FP7/2007-2013, grant agreements 241447 [NAIMIT] and 282510 [BLUEPRINT]), NHS Blood and Transplant, NIHR (PG-0310-1002), and BHF (RG/09/12/28096). K.D. is funded by NHS Health Education England. M.F. is supported by the BHF Cambridge Centre of Excellence (RE/13/6/30180). S.P.W., M.K., D.R.Z., and O.S. are funded by the European Molecular Biology Laboratory. ; This is the final version of the article. It first appeared from Elsevier (Cell Press) via https://doi.org/10.1016/j.cell.2016.09.037