Nanograin-Boundary-Abundant Cu2O-Cu Nanocubes with High C2+ Selectivity and Good Stability during Electrochemical CO2 Reduction at a Current Density of 500 mA/cm2.

Surface and interface engineering, especially the creation of abundant Cu0/Cu+ interfaces and nanograin boundaries, is known to facilitate C2+ production during electrochemical CO2 reductions over copper-based catalysts. However, precisely controlling the favorable nanograin boundaries with surface structures (e.g., Cu(100) facets and Cu[n(100)×(110)] step sites) and simultaneously stabilizing Cu0/Cu+ interfaces is challenging, since Cu+ species are highly susceptible to be reduced into bulk metallic Cu at high current densities. Thus, an in-depth understanding of the structure evolution of the Cu-based catalysts under realistic CO2RR conditions is imperative, including the formation and stabilization of nanograin boundaries and Cu0/Cu+ interfaces. Herein we demonstrate that the well-controlled thermal reduction of Cu2O nanocubes under a CO atmosphere yields a remarkably stable Cu2O-Cu nanocube hybrid catalyst (Cu2O(CO)) possessing a high density of Cu0/Cu+ interfaces, abundant nanograin boundaries with Cu(100) facets, and Cu[n(100)×(110)] step sites. The Cu2O(CO) electrocatalyst delivered a high C2+ Faradaic efficiency of 77.4% (56.6% for ethylene) during the CO2RR under an industrial current density of 500 mA/cm2. Spectroscopic characterizations and morphological evolution studies, together with in situ time-resolved attenuated total reflection-surface enhanced infrared absorption spectroscopy (ATR-SEIRAS) studies, established that the morphology and Cu0/Cu+ interfacial sites in the as-prepared Cu2O(CO) catalyst were preserved under high polarization and high current densities due to the nanograin-boundary-abundant structure. Furthermore, the abundant Cu0/Cu+ interfacial sites on the Cu2O(CO) catalyst acted to increase the *CO adsorption density, thereby increasing the opportunity for C-C coupling reactions, leading to a high C2+ selectivity.

NAT2 fast acetylator genotype and MGMT promoter methylation may contribute to gender difference in K-RAS mutation occurrence in Taiwanese colorectal cancer.

A recent study conducted by our group showed that the NAT2 fast acetylator genotype is associated with an increasing risk for the development of colorectal cancer (CRC), especially for females. We therefore examined whether a higher risk of CRC in females with the NAT2 fast acetylator genotype was associated with the occurrence of K-RAS mutation, and to further verify whether MGMT promoter methylation was linked to the occurrence of K-RAS mutation in patients with the NAT2 fast acetylator genotype. Herein, 151 CRC cases were examined for NAT2 genetic polymorphisms and MGMT promoter methylation by PCR-RFLP and methylation-specific PCR (MSP). The results of this study show that the NAT2 fast acetylator genotype is associated with the occurrence of K-RAS mutation in female cases (OR = 4.820, 95% CI = 1.113-20.873), but not associated with MGMT promoter methylation. Surprisingly, MGMT promoter methylation significantly deepens the impact of NAT2 fast acetylation on K-RAS mutation in the female cases (OR = 5.129, 95% CI = 1.092-24.105). In conclusion, Taiwanese women with the NAT2 fast acetylator genotype may exhibit a higher risk of CRC with increased occurrence of K-RAS mutation. Detection of NAT2 genotypes and MGMT promoter methylation may be useful in the risk assessment for CRC in Taiwanese women.

NAT2 fast acetylator genotype is associated with an increased risk of colorectal cancer in Taiwan.

In Taiwan, colorectal cancer has one of the highest rates of increased incidence in the past two decades. Heterocyclic amines from dietary cooked meats are metabolically activated by NAT2 (N-acetyltransferase 2), which are associated with colorectal cancer incidence. Thus, the NAT2 fast acetylator genotype may be associated with colorectal cancer risk. However, the association between the NAT2 genotype and colorectal cancer risk is not clearly understood. We conducted a study with 244 primary colorectal cancer cases and 299 cancer-free healthy control subjects to verify the association of NAT2 polymorphisms with the risk of Taiwanese colorectal cancer. Our data showed that subjects with the NAT2 W/W homozygous genotype had a 1.63-fold increased risk of colorectal cancer compared with those with the Mx/Mx slow acetylator genotype (95 percent confidence interval, 1.03-2.58); however, no risk was found in the W/Mx heterozygous and Mx/W+W/W fast acetylator genotypes. Being stratified by gender factors, the colorectal cancer risk in females with homozygous W/W or Mx/W+W/W fast acetylators increased 2.47-fold and 2.13-fold compared with those with the Mx/Mx slow acetylator genotype (95 percent confidence interval, 1.27-4.82 for W/W genotype; 95 percent confidence interval, 1.17-3.89 for Mx/W+W/W genotype); however, the risk of the NAT2 genotype and colorectal cancer was not observed in males. Collectively, patients with the NAT2 fast acetylator genotype were more prone to colorectal cancer and reflected the possibility that exposure to heterocyclic amines may contribute to colorectal cancer development in Taiwan, especially in Taiwanese females.

Different p53 mutation patterns in colorectal tumors from smokers and nonsmokers.

Epidemiological studies consistently find associations between colorectal cancer and cigarette smoking; however, there are little molecular data supporting the association. To examine the relationship between cigarette smoking and colorectal cancer, we compared p53 mutation patterns in colorectal tumors from smokers and nonsmokers. In this study, 153 tumor tissues from colorectal cancer patients, including 63 smokers and 90 nonsmokers, were examined for p53 mutation and p53 protein expression by direct sequencing and immunohistochemistry (IHC), respectively. p53 mutations were detected in 77 of 153 (50.3%) colorectal tumors, and no difference was observed in the p53 mutation frequencies in tumors from smokers and nonsmokers (33 of 63, 50.8% for smokers vs. 44 of 90, 48.9% for nonsmokers, P = 0.743). IHC showed that p53-immunoreactive tumors were positively correlated with p53-mutated tumors (P < 0.0001). G:C-->A:T transition and G:C-->T:A transversion were the predominant types of mutations detected in the tumor p53 genes. G:C-->A:T mutation was relatively more common in nonsmokers than in smokers (93.5% for nonsmokers vs. 77.3% for smokers), although this difference was not significant. The frequency of deletion mutation in smoker tumors, however, was significantly higher than that in nonsmoker tumors (7 of 33, 21.2% for smokers vs. 1 of 44, 2.3% for nonsmokers, P = 0.01). Although there were only a few cases of p53 deletion mutation in this study, the observation of a higher frequency of p53 deletion mutation in smoker tumors supports the association between cigarette smoking and the development of colorectal cancer.