Association between ADAM metallopeptidase domain 33 gene polymorphism and risk of childhood asthma: a meta-analysis.

This study aimed to investigate the association between ADAM metallopeptidase domain 33 (ADAM33) gene polymorphisms and the risk of childhood asthma. The relevant studies about the relationship between ADAM33 gene polymorphisms and childhood asthma were searched from electronic databases and the deadline of retrieval was May 2016. The single nucleotide polymorphisms (SNPs) of ADAM33 (rs511898, rs2280092, rs3918396, rs528557, rs2853209, rs44707, rs2280091 and rs2280089) were analyzed based on several models including the allele, codominant, recessive and dominant models. The results showed that the ADAM33 rs2280091 polymorphism in all four genetic models was associated with an increased risk of childhood asthma. Positive associations were also found between the polymorphisms rs2280090, rs2787094, rs44707 and rs528557 and childhood asthma in some genetic models. This meta-analysis suggested that ADAM33 polymorphisms rs2280091, rs2280090, rs2787094, rs44707 and rs528557 were significantly associated with a high risk of childhood asthma.

Cloning and sequence analysis of the LOC339524 gene in Sprague-Dawley rats.

We cloned the LOC339524 gene in Sprague-Dawley (SD) rats and analyzed the structure and function of the protein encoded by it. Based on the known human LOC339524 gene sequences, the full-length coding sequence of the LOC339524 gene in SD rats was cloned and amplified by the polymerase chain reaction using the complementary DNA of SD rats as a template. Bioinformatics analysis showed that the length of the cloned LOC339524 gene (GenBank accession No. KM224520) was 831 bp and it encoded a deduced protein of 276 amino acids. Sequence analysis revealed that the coded protein was identical to that produced in humans and its functional domain was located in the 138-236 amino acid fragments, a proline-rich region. Our results suggest that the encoded protein may be a significant regulator of the inflammatory response and may provide sufficient information to justify an in-depth investigation of the role of the LOC339524 gene.

Common polymorphisms in the HIF-1α gene confer susceptibility to digestive cancer: a meta-analysis.

Recent evidence suggests that common functional polymorphisms in the hypoxia inducible factor-1α (HIF-1α) gene may play an important role in the development and progression of digestive cancer, but individually published results are inconclusive. Our meta-analysis is aimed to derive a more precise estimation of the relationships between HIF-1α gene polymorphisms and digestive cancer risk. An extensive literature search for relevant studies was conducted on Pubmed, Embase, Web of Science, Cochrane Library, and CBM databases from their inception through May 1, 2013. This meta-analysis was performed using the STATA 12.0 software. The crude odds ratios (OR) with 95% confidence interval (CI) were calculated. Eight case-control studies were included with a total of 1276 digestive cancer patients and 3392 healthy controls. Our meta-analysis revealed that the A variant of HIF-1α G1790A polymorphism might be associated with increased risk of colorectal, esophageal, gastric, and liver cancers, especially among Asian populations. However, no statistically significant associations were found between HIF-1α C1772T polymorphism and susceptibility to digestive cancer. No publication bias was detected in this meta-analysis. The current meta-analysis suggests that the HIF-1α G1790A polymorphism may increase the risk of colorectal, esophageal, gastric, and liver cancers, especially among Asian populations.