Copper inks for printed electronics: a review.

Conductive inks have attracted tremendous attention owing to their adaptability and the convenient large-scale fabrication. As a new type of conductive ink, copper-based ink is considered to be one of the best candidate materials for the conductive layer in flexible printed electronics owing to its high conductivity and low price, and suitability for large-scale manufacturing processes. Recently, tremendous progress has been made in the preparation of cooper-based inks for electronic applications, but the antioxidation ability of copper-based nanomaterials within inks or films, that is, long-term reliability upon exposure to water and oxygen, still needs more exploration. In this review, we present a comprehensive overview of copper inks for printed electronics from ink preparation, printing methods and sintering, to antioxidation strategies and electronic applications. The review begins with an overview of the development of copper inks, followed by a demonstration of various preparation methods for copper inks. Then, the diverse printing techniques and post-annealing strategies used to fabricate conductive copper patterns are discussed. In addition, antioxidation strategies utilized to stabilize the mechanical and electrical properties of copper nanomaterials are summarized. Then the diverse applications of copper inks for electronic devices, such as transparent conductive electrodes, sensors, optoelectronic devices, and thin-film transistors, are discussed. Finally, the future development of copper-based inks and the challenges of their application in printed electronics are discussed.

CASC15 Gene Polymorphisms and Glioma Susceptibility in Chinese Children.

OBJECTIVE: Gliomas are the most common tumors in the central nervous system. The cancer susceptibility candidate 15 (CASC15) gene has been reported to be a susceptibility gene for several types of cancer. No studies have been carried out on the predisposing effect of CASC15 gene single nucleotide polymorphisms (SNPs) on glioma risk. METHODS: In order to determine whether CASC15 gene SNPs are involved in glioma susceptibility, the first association study in a relatively large sample, which consisted of 171 patients and 228 healthy controls recruited from China, was performed. The contribution of SNPs (rs6939340 A>G, rs4712653 T>C and rs9295536 C>A) to the risk of glioma was evaluated by multinomial logistic regression, based on the calculation of the odds ratio (OR) and 95% confidence interval (CI). RESULTS: In the single locus and combined analysis, it was revealed that the genetic risk score had no significant associations between CASC15 gene SNPs and glioma risk. However, in the stratified analysis, a significant decrease in risk of glioma was observed in subjects of <60 months old with the rs4712653 TT genotype, when compared to those with the CC/CT genotype (OR=0.12, 95% CI=0.02-0.91, P=0.041). CONCLUSION: The present study provides referential evidence on the association between the genetic predisposition of the CASC15 gene and glioma risk in Chinese children. However, more well-designed case-control studies and functional experiments are needed to further explore the role of CASC15 gene SNPs.

METTL14 gene polymorphisms influence hepatoblastoma predisposition in Chinese children: Evidences from a seven-center case-control study.

Hepatoblastoma as the most prevalent hepatic malignancy in children, its etiology remains unclear. N6-Methyladenosine (m6A) modification which can modify various physiological processes, plays a critical role in tumorigenesis. Methyltransferase-like 14 (METTL14), an important component of the m6A methyltransferase complex, remains elusive during hepatoblastoma occurrence and development. We explored the relationship between METTL14 gene polymorphisms (rs1064034 T > A, rs298982 G > A, rs62328061 A > G, rs9884978 G > A, and rs4834698 T > C) and hepatoblastoma susceptibility from 313 patients and 1446 controls. The role of METTL14 polymorphisms in hepatoblastoma was evaluated by odds ratios (ORs) and 95% confidence intervals (CIs). Of the included subjects, 308 patients and 1444 controls were successfully genotyped. We did not find any significant correlation between the risk of hepatoblastoma and the five potentially functional METTL14 polymorphisms individually. However, the presence of 4-5 risk genotypes exhibited a significant increased hepatoblastoma risk (adjusted OR = 1.32, 95% CI = 1.03-1.69, P = 0.031) compared to those carriers with 0-3 risk genotypes. Furthermore, the stratified analysis demonstrated that the rs1064034 AA genotype, rs62328061 AG/GG genotypes, rs4834698 TC/CC genotypes, and 4-5 risk genotypes were related to hepatoblastoma susceptibility in certain subgroups. The expression quantitative trait loci (eQTL) analysis revealed that rs1064034 T > A and rs4834698 T > C were correlated with the expression levels of METTL14 and its surrounding genes. Prospectively, these findings suggested that METTL14 polymorphisms may correlation with hepatoblastoma susceptibility and provide a fresh insight into the genetic underpinnings of m6A modification in hepatoblastoma.

Associations between LMO1 gene polymorphisms and central nervous system tumor susceptibility.

IMPORTANCE: LIM domain only 1 (LMO1) gene polymorphisms were previously found to be implicated in the risk of several cancers. No available studies were performed regarding the predisposing effect of LMO1 gene single nucleotide polymorphisms (SNPs) on central nervous system (CNS) tumor risk. OBJECTIVE: We aimed to determine whether the LMO1 gene SNPs were associated with the risk of CNS tumor by applying a case-control study with 191 cases and 248 controls in China. METHODS: The contributions of LMO1 gene SNPs to the risk of CNS tumor was evaluated by multinomial logistic regression. RESULTS: Based on the calculations of odds ratio (OR) and 95% confidence interval (CI), we failed to detect a significant relationship between each LMO1 gene SNP (rs110419 A>G, rs4758051 G>A, rs10840002 A>G, rs204938 A>G, and rs2168101 G>T) and CNS tumor risk, respectively. A negative association was also found in the combined effects on these five SNPs and CNS tumor risk. The stratification analysis further demonstrated the individuals with rs204938 AG/GG genotype confer to increased risk of CNS tumor compared with those with an AA genotype in males (OR: 1.74, 95% CI: 1.01-2.98, P = 0.046). INTERPRETATION: We concluded that LMO1 gene SNPs may not strong enough to influence the risk of CNS tumor in Chinese children. More studies are required to verify this association.

The Genetic Changes of Hepatoblastoma.

Hepatoblastoma is the most common malignant liver cancer in childhood. The etiology of hepatoblastoma remains obscure. Hepatoblastoma is closely related to genetic syndromes, hinting that hepatoblastoma is a genetic predisposition disease. However, no precise exposures or genetic events are reported to hepatoblastoma occurrence. During the past decade, significant advances have been made in the understanding of etiology leading to hepatoblastoma, and several important genetic events that appear to be important for the development and progression of this tumor have been identified. Advances in our understanding of the genetic changes that underlie hepatoblastoma may translate into better patient outcomes. Single nucleotide polymorphisms (SNPs) have been generally applied in the research of etiology's exploration, disease treatment, and prognosis assessment. Here, we reviewed and discussed the molecular epidemiology, especially SNPs progresses in hepatoblastoma, to provide references for future studies and promote the study of hepatoblastoma's etiology.

Genetic variations in nucleotide excision repair pathway genes and hepatoblastoma susceptibility.

The etiology of hepatoblastoma is largely unknown due to the rarity of this disease. Nucleotide excision repair (NER), a versatile system in repairing DNA damage, is highly implicated in carcinogenesis. However, it remains unclear whether single nucleotide polymorphisms (SNPs) of genes in the NER pathway are related to hepatoblastoma risk. A total of 313 Chinese children diagnosed with hepatoblastoma and 1446 controls were recruited from seven hospitals across China. TaqMan assay was adopted to genotype 19 SNPs in NER pathway genes including ERCC1, XPA, XPC, XPD, XPF and XPG. Of them, only two SNPs in XPC gene predisposed to hepatoblastoma risk. The XPC rs2607775 polymorphism significantly contributed to hepatoblastoma risk (dominant model: adjusted OR = 1.44, 95% CI = 1.01-2.05, P = .046). However, XPC rs1870134 conferred a significantly decreased risk of hepatoblastoma in recessive model (adjusted OR = 0.50, 95% CI = 0.26-0.98, P = .042). Stratified analysis revealed that rs2607775 CG/GG genotype, rs1870134 CC genotype and four to five risk genotypes were associated with the risk of hepatoblastoma under certain subgroups. The significant relationships were confirmed by haplotype analyses and false-positive report probability analyses. In addition, expression quantitative trait locus analysis suggested that rs2607775 G increased expression of XPC mRNA. Collectively, our discover a promising candidate XPC gene as a biomarker for the risk of hepatoblastoma.

Polymorphisms in METTL3 gene and hepatoblastoma risk in Chinese children: A seven-center case-control study.

Hepatoblastoma is the most common malignant liver cancer in childhood, yet its etiology remains unclear. As an m6A methylation modifier, methyltransferase like 3 (METTL3) has an active methyltransferase domain that functionally participates in various tumor occurrence and development. However, little is known about how METTL3 polymorphisms affect the occurrence of hepatoblastoma. Here, we attempted to investigate the associations between METTL3 gene polymorphisms and hepatoblastoma risk in a seven-center case-control study. We genotyped four METTL3 polymorphisms (rs1061026 T > G, rs1061027 C > A, rs1139130 A > G, rs1263801 G > C) by TaqMan technique in 313 cases and 1446 controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to evaluate the contributions of these four single nucleotide polymorphisms (SNPs) to hepatoblastoma susceptibility. In single genotype analysis, we detected no significant correlation between these four polymorphisms in METTL3 and hepatoblastoma risk. However, in the combined analysis, the presence of 2-4 risk genotypes of METTL3 was associated with an increased risk of hepatoblastoma compared with that of 0-1 risk genotypes (adjusted OR = 1.48, 95% CI = 1.03-2.12, P = 0.035). The stratified analysis further revealed that carriers of 2-4 risk genotypes are more susceptible to hepatoblastoma in the subgroups of subjects aged under 17 months (adjusted OR = 1.88, 95% CI = 1.12-3.16, P = 0.016) and females (adjusted OR = 1.79, 95% CI = 1.06-3.05, P = 0.031). Overall, our results revealed that none of these four SNPs could increase susceptibility to hepatoblastoma individually. Carriers with 2-4 risk genotypes in the combined analysis tend to increase the risk of hepatoblastoma.

Genetic variations in base excision repair pathway genes and risk of hepatoblastoma: a seven-center case-control study.

Hepatoblastoma is a rare childhood liver cancer without known explicit etiology. Base excision repair (BER) pathway genes have been implicated in the pathophysiology of cancer, yet the role of BER pathway gene single nucleotide polymorphisms (SNPs) on hepatoblastoma risk still awaits to be explored. This study aims to determine whether hepatoblastoma risk be modulated by polymorphisms in the BER pathway genes based on genotyped data from 313 cases and 1446 controls. We applied TaqMan assay to genotype these included samples. We comprehensively genotyped 20 SNPs across six genes of BER, and estimated odds ratio (ORs), 95% confidence intervals (CIs), and P-values of the selected SNPs' contribution to the risk of hepatoblastoma using logistic regression models. Only SNP rs293795 in the hOGG1 gene could significantly enhance hepatoblastoma risk under recessive model (adjusted OR=3.78, 95% CI=1.01-14.17, P=0.047). Stratified analysis revealed that rs159153 TC/CC genotype decreased hepatoblastoma risk in male subgroup. Moreover, rs293795 GG and 1-3 risk genotypes could increase hepatoblastoma risk in clinical stages I+II and male subgroups, respectively. False-positive report probability validated the reliability of the significant results. Our findings provide some clues of a potential risk effect of BER pathway gene hOGG1 SNPs on hepatoblastoma. Further investigation is warranted to confirm these findings and to better elucidate the biological pathways involved.

Genetic variants in m6A modification core genes are associated with glioma risk in Chinese children.

Glioma is a highly heritable disease with a strong genetic component. The N6-methyladenosine (m6A) modification core genes play important roles in the context of cancer. However, the effects of polymorphisms in the m6A modification core genes on the risk of pediatric glioma remain undefined. Here, we intended to demonstrate the relationship between 24 functional single-nucleotide polymorphisms (SNPs) in eight m6A modification core genes and glioma risk. Case-control design and multinomial logistic regression were used to develop models to estimate the risk of glioma while accounting for the subtypes of glioma. A total of 171 glioma cases and 228 controls from South China were genotyped using a TaqMan assay. The WTAP rs7766006, YTHDF2 rs3738067, and FTO rs9939609 variants conferred a statistically significant increased risk of glioma, respectively. YTHDC1 rs2293595, YTHDC1 rs3813832, and FTO rs8047395 were associated with a significant inverse association with risk of glioma, respectively. The significant associations were more predominant in stratification analyses of certain subgroups. Functional annotations revealed that WTAP rs7766006 and YTHDF2 rs3738067 could be potential functional variants by increasing expression of WTAP and YTHDF2 mRNA, respectively. Overall, these findings implicate variants in the m6A modification core genes as playing a role in pediatric glioma etiology.

YTHDC1 gene polymorphisms and hepatoblastoma susceptibility in Chinese children: A seven-center case-control study.

BACKGROUND: Hepatoblastoma is a commonly occurring embryonal tumors in children. N6-methyladenosine (m6 A) plays a critical role in gene expression, thus contributing to the occurrence and progression of cancer. RNA splicing is regulated by the nuclear m6 A reader YTHDC1, yet the roles of YTHDC1 polymorphisms in hepatoblastoma remain unclear. METHODS: We conducted a seven-center case-control study to determine the association between YTHDC1 gene polymorphisms (rs2293596 T>C, rs2293595 T>C and rs3813832 T>C) and hepatoblastoma susceptibility. We recruited 313 hepatoblastoma patients and 1446 healthy controls. RESULTS: There was no significant association between all of these polymorphisms and hepatoblastoma susceptibility in single locus or combined analysis. Stratification analysis revealed that rs2293596 TC/CC genotype carriers had a higher risk of developing hepatoblastoma in the subgroup of clinical stages III + IV [adjusted odds ratio (OR) = 1.80, 95% confidence interval (CI) = 1.18-2.76, p = 0.007]. In addition, 3 risk genotype carriers are more likely to develop hepatoblastoma in the subgroup of clinical stages III + IV (adjusted OR = 1.80, 95% CI = 1.18-2.76, p = 0.007). Furthermore, false-positive probability analysis was used to notarize our findings. Haplotype analysis indicated that there was no significant association between inferred haplotypes of YTHDC1 gene based on observed genotypes and hepatoblastoma risk. CONCLUSIONS: In conclusion, our findings suggest that the rs2293596 T>C polymorphism may contribute to hepatoblastoma susceptibly and YTHDC1 gene polymorphisms may have a cumulative effect on hepatoblastoma risk.

Redox-sensitive lipophilic prodrugs: delivering unstable chemotherapeutant for improved cancer therapy.

Therapeutic application of unmodified camptothecin (CPT) is severely restricted by its extremely low water solubility and the instability of active lactone ring. In this study, a redox-sensitive CPT-OA conjugate containing the disulfide bond (CPT-SS-OA) was used to deliver the lactone-stabilized CPT for the improved antitumor efficacy. A non-sensitive CPT-OA was used as control to illuminate the role of disulfide bond. Both CPT-SS-OA and CPT-OA formulated in cremophor EL micelles (CM) displayed multiple therapeutic advantages: small diameter (∼14 nm), efficient cellular internalization, prolonged blood circulation, and favorable biodistribution. However, only CPT-SS-OA/CM achieved the superior chemotherapeutic efficacy over CPT solution in the Lewis lung carcinoma (LLC) cancer xenograft, which was ascribed to the accelerated release of the active lactone CPT responding to the elevated reductive glutathione in tumor cells. Such redox-sensitive lipophilic prodrugs represent an effective alternative strategy for the delivery of CPT in the active lactone form. This strategy can be used for other chemically unstable chemotherapeutant for the improved therapeutic efficacies.