CDH13 Genetic Polymorphisms, Adiponectin and Ischemic Stroke： a Chinese Family-based Sib-pair Study

Objective To understand the relationships between CDH13（T-cadherin） genetic polymorphisms, adiponectin levels and ischemic stroke, and possible interactions between CDH13 polymorphisms and other risk factors. Methods We recruited 342 Chinese ischemic stroke sib pairs. We genotyped rs4783244 and rs7193788 on CDH13 using time-of-flight mass spectrometry genotyping technology and measured total and high-molecular weight（HMW） adiponectin levels. We investigated associations between SNPs and ischemic stroke, and interactions between SNPs and other risk factors using multi-level mixed-effects regression model. Results In individuals without ischemic stroke, CDH13 rs4783244 was associated with total adiponectin levels（per T： Coef =-0.257, P = 0.001）. CDH13 rs7193788 was associated with total adiponectin levels（per A： Coef =-0.221, P = 0.001） and HMW adiponectin levels（per A： Coef =-0.163, P = 0.003）. rs7193788 was significantly associated with ischemic stroke（GA/AA vs. GG： OR = 1.55, 95% CI： 1.07 to 2.24, P = 0.020） after Bonferroni correction（α = 0.025）. There was an interaction between rs7193788 and diabetes（P = 0.036）. Compared to diabetes-free individuals with rs7193788 GG genotype, diabetes patients with rs7193788 GA/AA genotypes had higher risks for ischemic stroke（OR = 2.64, 95% CI： 1.58-4.40, P 〈 0.001）. Conclusion CDH13 genetic polymorphisms are associated with adiponectin levels and ischemic stroke. An interaction is found between CDH13 SNP and diabetes for ischemic stroke.

The Reduction Square Root and Perturbation for a Class of Strongly Continuous Operator Families

We introduce the concept of a times C-second resolvent families and present the rela- tionship between a times C-resolvent families and a times C-second resolvent families. Moreover, the perturbation and square root for a times C-resolvent families are considered in this paper which generalize the counterparts of C-Cosine operator functions.

Metabonomic study of the biochemical profiles of heterozygous myostatin knockout swine

Myostatin is a transforming growth factor-beta family member that normally acts to limit skeletal muscle growth. Myostatin gene (MSTN) knockout (KO) mice show possible effects for the prevention or treatment of metabolic disorders such as obesity and type 2 diabetes. We applied chromatography and mass spectrometry based metabonomics to assess system-wide metabolic response of heterozygous MSTN KO (MSTN+/-) swine. Most of the metabolic data for MSTN+/- swine were similar to the data for wild type (WT) control swine. There were, however, metabolic changes related to fatty acid metabolism, glucose utilization, lipid metabolism, as well as BCAA catabolism caused by monoallelic MSTN depletion. The statistical analyses suggested that: (1) most metabolic changes were not significant in MSTN+/- swine compared to WT swine; (2) only a few metabolic properties were significantly different between KO and WT swine, especially for lipid metabolism. Significantly, these minor changes were most evident in female KO swine and suggested differences in gender sensitivity to myostatin.