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A novel class of secondary amines with long chains containing ether bonds were synthesized by a three-step protection–etherification–deprotection process from diethanolamine. The optimum reaction conditions were examined. This method has the advantages of simplicity, low cost, and high yield. Furthermore, some new downstream products (diglycolamides) were prepared from the ether-containing long-chain secondary amines as reactants, and their loading capacities in extractions of several metal ions were evaluated. [ABSTRACT FROM AUTHOR]

Purpose This study was aimed to discover the combined effects of single nucleotide polymorphisms (SNPs) within the C-reactive protein (CRP) gene and potential environmental factors on the risk and prognosis for diabetic foot osteomyelitis (DFO). Methods A total of 1734 diabetes mellitus patients, 681 with DFO and 1053 without DFO, were successfully recruited, as well as 1261 healthy control individuals. Participants data were recorded regarding age, gender, smoking and drinking history, body mass index (BMI), hypertension, cacosmia, and ulceration. A total of 11 SNPs within the CRP gene were designated for exploration, by logistic regression analyses, of how they might interact with environmental factors to affect susceptibility to DFO. Results Frequencies of smoking and drinking, and incidence of hypertension, cacosmia, or ulceration displayed marked differences (all P <0.05) between DFO and non-DFO patients. Furthermore, allele G of rs11265260 (A>G), allele G of rs1800947 (C>G), and allele T of rs3093059 (T>C) and rs1130864 (C>T) exhibited a trend to increase risk of DFO (all P <0.05). Allele G of rs11265260 (A>G), allele G of rs1800947 (C>G) and rs3093068 (G>C), and allele T of rs1130864 (C>T) were significant predictors of poor prognosis among DFO patients (P <0.05). In addition, genotypes of rs11265260 (i.e., GG and AG), rs1800947 (i.e., CG and GG), rs3093059 (i.e., TT) and rs113084 (i.e., CT and TT) amplified the influence of smoking, alcohol consumption, cacosmia, and ulceration on progression from non-DFO to DFO (all γ >1). Conclusion Genetic mutations within CRP functioned interactively with external factors to affect DFO risk. [ABSTRACT FROM AUTHOR]