IL1RN Polymorphisms Are Associated with a Decreased Risk of Esophageal Cancer Susceptibility in a Chinese Population.

BACKGROUND: Recent evidence suggested that IL1RN (interleukin-1 receptor antagonist) polymorphisms increased the susceptibility to cancers. The present study aimed to evaluate whether IL1RN was related to esophageal cancer susceptibility in a Northwest Han Chinese population. METHODS: The case-control study was conducted on 384 esophageal cancer patients and 499 healthy controls. We successfully genotyped four SNPs distributed in IL1RN. The Gene Expression Profiling Interactive Analysis (GEPIA) database was used to observe the expression of IL1RN in esophageal cancer tissues and normal tissues. RegulomeDB and HaploReg v4.1 were used to calculate possible functional effects of the polymorphisms. We also used genetic models to detect any potential association between IL1RN variants and esophageal cancer risk. RESULTS: In our study, rs3181052 was associated with a reduced risk of esophageal cancer in the codominant (odds ratio [OR] = 0.70, 95% confidence interval [CI] 0.52-0.93, p = 0.040), the dominant (OR = 0.75, 95% CI 0.57-0.99, p = 0.041), and the overdominant (OR = 0.71, 95% CI 0.54-0.93, p = 0.012) model. The rs452204 was associated with a 0.76-fold (OR = 0.76, 95% CI 0.58-0.99; p = 0.043) decreased esophageal cancer risk under the overdominant model without adjustment. We also found that rs3181052 had a negative effect on esophageal cancer under the overdominant model (OR = 0.72, 95% CI 0.53-0.97, p = 0.033) adjusted for age and gender. In stratified analyses by age >55 years, rs3181052 reduced the risk of esophageal cancer in the dominant and overdominant models. In addition, rs315919 had a remarkable influence on esophageal cancer risk in females, while the association was not significant between rs3181052 and esophageal cancer risk in males. CONCLUSIONS: Our study provided the first evidence that IL1RN rs3181052, rs452204, and rs315919 are correlated with a decreased risk of esophageal cancer in a Northwest Han Chinese population. These findings may be useful for the development of early prognostics for esophageal cancer. However, further larger studies on different ethnic populations are warranted to verify these findings.

Microstructure and Properties of Nickel-Based Gradient Coatings Prepared Using Cold Spraying Combined with Laser Cladding Methods.

A cold spray-laser cladding composite gradient coating (CLGC) was successfully formed on a Cu substrate. In comparison with traditional laser cladding gradient coatings (LGC), cold spraying the pre-set Ni-Cu alloy's intermediate transition layer not only mitigates the negative impacts due to the high reflectivity of the copper substrate but also helps to minimize the difference in the coefficients of thermal expansion (CTE) between the substrate and coating. This reduces the overall crack sensitivity and improves the cladding quality of the coating. Besides this, the uniform distribution of hard phases in CLGC, such as Ni11Si12 and Mo5Si3, greatly increases its microhardness compared to the Cu substrate, thus resulting in the value of 478.8 HV0.5 being approximately 8 times that of the Cu substrate. The friction coefficient of CLGC is lowered compared to both the Cu substrate and LGC with respective values of 0.28, 0.54, and 0.43, and its wear rate is only one-third of the Cu substrate's. These results suggest CLGC has excellent anti-wear properties. In addition, the wear mechanism was determined from the microscopic morphology and element distribution and was found to be oxidative and abrasive. This approach combines cold spraying and laser cladding to form a nickel-based gradient coating on a Cu substrate without cracks, holes, or other faults, thus improving the wear resistance of the Cu substrate and improving its usability.

A Novel Superhard, Wear-Resistant, and Highly Conductive Cu-MoSi2 Coating Fabricated by High-Speed Laser Cladding Technique.

The pursuit of an advanced functional coating that simultaneously combines high hardness, wear resistance, and superior electrical conductivity has remained an elusive goal in the field of copper alloy surface enhancement. Traditional solid solution alloying methods often lead to a significant increase in electron scattering, resulting in a notable reduction in electrical conductivity, making it challenging to achieve a balance between high hardness, wear resistance, and high conductivity. The key lies in identifying a suitable microstructure where dislocation motion is effectively hindered while minimizing the scattering of conductive electrons. In this study, a novel Cu-MoSi2 coating was successfully fabricated on a CuCrZr alloy surface using the coaxial powder feeding high-speed laser cladding technique, with the addition of 10-30% MoSi2 particles. The coating significantly enhances the hardness and wear resistance of the copper substrate while maintaining favorable electrical conductivity. As the quantity of MoSi2 particles increases, the coating's hardness and wear resistance gradually improve, with minimal variance in conductivity. Among the coatings, the Cu-30%MoSi2 coating stands out with the highest hardness (974.5 HV0.5) and the lowest wear amount (0.062 mg/km), approximately 15 times the hardness of the copper base material (65 HV0.5) and only 0.45% of the wear amount (13.71 mg/km). Additionally, the coating exhibits a resistivity of 0.173 × 10-6 Ω·m. The extraordinary hardness and wear resistance of these coatings can be attributed to the dispersion strengthening effect of MoxSiy particles, while the high electrical conductivity is due to the low silicon content dissolved into the copper from the released MoSi2 particles, as well as the rapid cooling rates associated with the high-speed laser cladding process.

Association between ACYP2 polymorphisms and the risk of renal cell cancer.

BACKGROUND: Kidney cancer is the predominant form of malignancy of the kidney and accounts for approximately 3%-4% of all cancers. Renal cell cancer (RCC) represents more than 85% of kidney cancer. It has been reported that genetic factors may predispose individuals to RCC. This study evaluated the association between Acylphosphatase 2 (ACYP2) gene polymorphisms and RCC risk in the Han Chinese population. METHODS: Twelve single-nucleotide polymorphisms (SNPs) in ACYP2 were genotyped using the Agena MassARRAY platform from 293 RCC patients and 495 controls. The Chi-squared test, genetic models, haplotype, and stratification analyses were used to evaluate the association between SNPs and the risk of RCC. The relative risk was estimated using the odds ratio (OR) and 95% confidence interval (CI). RESULTS: We observed that the rs6713088 allele G (OR = 1.26, 95% CI: 1.03-1.53, p = .023) and rs843711 allele T (OR = 1.29, 95% CI: 1.06-1.57, p = .010) were associated with increased RCC risk. Genetic model analyses found that rs843711 was significantly associated with an increased RCC risk under the recessive model and log-additive model after adjusting for age and gender. Haplotype analysis showed that the haplotype "TTCTCGCC" (OR = 0.67, 95% CI: 0.48-0.94, p = .021) was associated with a decreased risk of RCC in the Han Chinese population. Stratification analysis also found that rs6713088 and rs843711 were significantly associated with increased RCC risk. CONCLUSION: In summary, the results suggested that ACYP2 polymorphisms could be used as a genetic marker for RCC. Additional functional and association studies are required to validate our results.

Overexpression of the BRIP1 ameliorates chemosensitivity to cisplatin by inhibiting Rac1 GTPase activity in cervical carcinoma HeLa cells.

BRCA1-interacting protein 1 (BRIP1), a DNA-dependent ATPase and a DNA helicase, is critical for BRCA-associated DNA damage repair functions and may be associated with the tumourigenesis and aggressiveness of various cancers. Here, we constructed a BRIP1 recombinant plasmid, overexpressed it in a cervical cancer cell line (HeLa) and found that ectopic expression of BRIP1 could remarkably enhance the antitumor activity of cisplatin, as demonstrated by decreased cell viability, colony formation and tumour xenografts' weight. Moreover, BRIP1 promoted cisplatin-mediated cell apoptosis and suppressed tumour angiogenesis. We also found that the synergistic inhibition effect of BRIP1 might be partially attributed to attenuation of Rac1 GTPase activation and that Rac1 GTPase re-activation could reverse the sensitizing effect induced by BRIP1. Our study suggested that up-regulation of BRIP1 could enhance chemosensitivity of HeLa cells to cisplatin through inhibiting Rac1 GTPase activation, and it provides a new insight into the essential role of BRIP1 in cervical cancer chemotherapy.