Blockchain-based product traceability systems are receiving increasing attention from both industry and academia. Existing systems make full use of the traceability and non-modification characteristics of blockchain technology and realize the openness and transparency of product traceability information in the entire supply chain. However, existing systems do not consider government regulation, cannot protect enterprise sensitive private data effectively, and have performance bottlenecks. To address these problems, this paper proposes a product traceability scheme based on the permissioned blockchain within a doublelayer framework. We introduce the double-layer framework and describe its advantages in detail. We also describe the smart contracts (chain code) in the double-layer framework. Finally, we test the performance of the proposed scheme through simulation experiments. The simulation results demonstrate the performance of nodes in the main layer, which is very important for consumers to obtain product traceability information, is optimized.
CpG island promoters often lack canonical core promoter elements such as the TATA box, and have dispersed transcription initiation sites. Despite the prevalence of CpG islands associated with mammalian genes, the mechanism of transcription initiation from CpG island promoters remains to be clarified. Here we investigate the mechanism of transcription initiation of the CpG island-associated gene, insulin-degrading enzyme (IDE). IDE is ubiquitously expressed, and has dispersed transcription initiation sites. The IDE core promoter locates within a 32-bp region, which contains three CGGCG repeats and a nuclear respiratory factor 1 (NRF-1) binding motif. Sequential mutation analysis indicates that the NRF-1 binding motif is critical for IDE transcription initiation. The NRF-1 binding motif is functional, because NRF-1 binds to this motif in vivo and this motif is required for the regulation of IDE promoter activity by NRF-1. Furthermore, the NRF-1 binding site in the IDE promoter is conserved among different species, and dominant negative NRF-1 represses endogenous IDE expression. Finally, TATA-box binding protein (TBP) is not associated with the IDE promoter, and inactivation of TBP does not abolish IDE transcription, suggesting that TBP is not essential for IDE transcription initiation. Our studies indicate that NRF-1 mediates IDE transcription initiation in a TBP-independent manner, and provide insights into the potential mechanism of transcription initiation for other CpG island-associated genes.
Several observational studies have investigated the relation between cadmium exposure and risk of any fracture. However, the results from epidemiological studies for the association are inconsistent.We conducted a meta-analysis to evaluate the relationship between cadmium exposure and risk of any fracture. The pertinent studies were identified by a search of PubMed and Embase databases from 1966 to June 2015.Seven articles involving 21,941 fracture cases and 504,346 participants were included. The meta-analysis showed that the pooled relative risk of any fracture for the highest versus lowest category of cadmium concentration was 1.30 (95% confidence interval = 1.13–1.49). In subgroup analyses, the significant association remained consistent when stratified by study type, geographical region, method of cadmium exposure assessment, and gender.Our meta-analysis showed that a high cadmium exposure may be a risk factor for any fracture. However, this result should be interpreted cautiously because of the heterogeneity among studies and existence of publication bias. Additional large, high-quality prospective studies are needed to evaluate the association between cadmium exposure and the risk of development of fracture.
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