PurposeThe electron beam melting (EBM) Ti-6Al-4V material technology has been developed over a short time period. It was introduced through a research to develop Ti-6Al-4V implants for patients, but EBM printed locking compression plates have not been used for clinical implants. The main purpose of this study is to find whether the EBM Ti-6Al-4V plate suit for clinical implants.MethodsFirst, we scanned an AO-locking compression plate (LCP) and printed LCP samples using EBM. Next, we evaluated the EBM plate surface roughness through optical microscopy as well as the LCP and EBM plates’ mechanical characteristics using the ASTM standard, which is commonly used to test the mechanical properties of bone plates subject to bending. Each sample was examined using a single-cycle four-point bending test and hardness testing to acquire data on bending stiffness, bending strength, bending structural stiffness, and hardness.ResultsThe results show significant differences in bending stiffness, bending strength, bending structural stiffness, and hardness between the samples using EBM and the original LCP plates. The EBM-printed samples’ surface roughness was 0.49 ± 0.02 μm. The mean hardness of the LCP sample was 266.67 HV10 ± 5.8, and the EBM-printed sample mean hardness was 341.1 HV10 ± 1.93. The EBM samples’ bending stiffness was 87.67%, which is greater than using the LCP plates’; and the bending strength was 190.7% greater, the bending structural stiffness was 73.2% greater, and the hardness was 27.9% greater.ConclusionsThe results show that the EBM plates’ general mechanical strength was significantly greater than the LCP plates. An EBM plate is advantageous for clinical implants because it can be customized with great potential for improvement.

The results from the published studies on the association between leptin (LEP) genetic polymorphism and cancer risk are conflicting. The common A19G (rs2167270) genetic polymorphism has been reported to be functional and may contribute to genetic susceptibility to cancers. However, the association between LEP A19G (rs2167270) genetic polymorphism and cancer risk remains inconclusive. To better understand the role of LEP A19G (rs2167270) genetic polymorphism in global cancer, we conducted this comprehensive meta-analysis encompassing 5,679 cases and 7,443 controls. Overall, the LEP A19G (rs2167270) genetic polymorphism was associated with lower cancer risk. In the stratified analysis, significant associations were found between the LEP A19G (rs2167270) genetic polymorphism and colorectal cancer and non-Hodgkin's lymphoma. For colorectal cancer, there was no significant association of LEP A19G (rs2167270) variant with this disease under heterozygous codominant model [odds ratio (OR) = 1.11 (0.97-1.27)], dominant genetic model [OR = 1.03 (0.91-1.17)], and additive genetic model [OR = 0.94 (0.86-1.03)]; however, there was a marginal association under homozygous codominant model [OR = 0.80 (0.66-0.97)] and recessive genetic model [OR = 0.75 (0.63-0.90)]. For non-Hodgkin's lymphoma, there was a significant association of LEP A19G (rs2167270) variant with the disease under homozygous codominant model [OR = 0.74 (0.59-0.94)], recessive genetic model [OR = 0.76 (0.61-0.94)], and additive genetic model [OR = 0.89 (0.80-0.99)], but not under heterozygous codominant model [OR = 0.95 (0.82-1.10)] and dominant genetic model [OR = 0.91 (0.79-1.04)]. Moreover, a significantly decreased cancer risk was found in recessive genetic model among Latin American population. When stratified by study design, significantly elevated susceptibility to cancer was not found among any studies. No significantly differences in genotype method and sample size in cases were found among genotypes. These findings suggest that the LEP A19G (rs2167270) genetic polymorphism may decrease the susceptibility to cancers in colorectal cancer and non-Hodgkin's lymphoma, when assuming a homozygote codominant model and a recessive genetic model among Latin American population. The phenomenon also indicates that the SNP functions as a recessive mutation, which needs to be verified or linked with functional studies.

Previous studies have shown conflicting results between the association of leptin receptor () genetic polymorphisms and cancer risk. The frequent Lys656Asn or Ser343Ser genetic polymorphism has been demonstrated to be functional and may promote genetic susceptibility to cancers. However, the association between the Lys656Asn or Ser343Ser genetic polymorphism and cancer risk remains to be determined. To improve the understanding of the Lys656Asn or Ser343Ser genetic polymorphism role in global cancer, a comprehensive meta-analysis was conducted that comprised 2,480 cases and 3,162 controls. The Lys656Asn or Ser343Ser genetic polymorphism did not significantly affect the cancer risk. In the stratified analysis, there was no significant association of the Lys656Asn or Ser343Ser variants with any type of cancer under any model. In addition, significantly increased risks were found in the Asian population in heterozygous codominant [odds ratio (OR), 1.24 (1.01-1.53)] and dominant [OR, 1.24 (1.02-1.50)] genetic models. A significantly increased susceptibility to cancer was not found when stratified by study design. There were no significant differences found in genotype method and sample size in cases among the genotypes. These findings indicated a lack of association between Lys656Asn or Ser343Ser polymorphisms and cancer susceptibility, however, these polymorphisms may increase the cancer susceptibility among the Asian population, particularly in the dominant genetic model. The single-nucleotide polymorphism is also suggested to function as a dominant mutation, which requires verification or association with functional studies.