Flow diagram of search strategy and study selection.

<p>Flow diagram of search strategy and study selection.</p

A Meta-Analysis of Apolipoprotein E Gene ε2/ε3/ε4 Polymorphism for Gallbladder Stone Disease

<div><h3>Background</h3><p>Numerous studies have investigated the relationship between apolipoprotein (Apo) E gene polymorphisms and gallbladder stone disease (GSD) across ethnic populations; however, the results are often inconsistent. This meta-analysis aims to comprehensively evaluate the influence of a common ε2/ε3/ε4 polymorphism in Apo E gene on the risk of gallbladder stone disease.</p> <h3>Method</h3><p>Data were analyzed using the RevMan software (V5.1) and a random-effects model was applied irrespective of between-study heterogeneity. Publication bias was weighed using the fail-safe number.</p> <h3>Results</h3><p>There were 17 study populations totaling 1773 cases and 2751 controls for ε2/ε3/ε4 polymorphism of Apo E gene. Overall comparison of alleles ε2 with ε3 in all study populations yielded a 16% decreased risk for GSD (95% confidence interval [95% CI]: 0.68–1.05; P = 0.31; <em>I²</em> = 13%), and comparison of alleles ε4 with ε3 yielded a 25% increased risk (95% confidence interval [95% CI]: 0.97–1.61; P = 0.0003; <em>I²</em> = 63%). Subgroup analysis by study design indicated that the magnitude of association in hospital-based studies was largely significantly strengthened for ε4 allelic model (odds ratio [OR]  = 1.46; 95% CI: 1.05–2.02; p = 0.0007; <em>I²</em> = 65%). Subgroup analysis by age of controls indicated a remarkably significant elevation in the magnitude of association in age >50 subgroups in ε4 allelic model (OR = 1.50; 95% CI: 1.03–2.19; p = 0.0009; <em>I²</em> = 72%). Moreover, subgroup analysis by cases gender indicated a reduction in the magnitude of association in male<30% studies for E2/2 genotypic model (OR = 0.32; 95% CI: 0.07–1.49; p = 0.16; <em>I²</em> = 45%).</p> <h3>Conclusions</h3><p>Our results reveal that Apo E gene ε4 allele is a risk factor of gallbladder stone disease, especially in elder people and Chinese population.</p> </div

Comparisons of E4 vs E3 in allele, genotype dominant and recessive models for GSD risk.

<p>Abbreviations: OR, odds ratio; CI, confidence interval.</p

Pooled random-effects-based odds ratio of developing GSD for ε4 versus ε3.

<p>Pooled random-effects-based odds ratio of developing GSD for ε4 versus ε3.</p

Fail-safe number.

<p>Fail-safe number.</p

Comparisons of E2 vs E3 in allele, genotype dominant and recessive models for GSD risk.

<p>Abbreviations: OR, odds ratio; CI, confidence interval.</p

Pooled random-effects-based odds ratio of developing GSD for ε2 versus ε3.

<p>Pooled random-effects-based odds ratio of developing GSD for ε2 versus ε3.</p

Overexpression of Parkin Ameliorates Dopaminergic Neurodegeneration Induced by 1- Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine in Mice

<div><p>Mutations in the <em>parkin</em> gene are currently thought to be the most common cause of recessive familial Parkinsonism. Parkin functions as an E3 ligase to regulate protein turnover, and its function in mitochondrial quality control has been reported recently. Overexpression of parkin has been found to prevent neuronal degeneration under various conditions both in vivo and in vitro. Here, we generated a transgenic mouse model in which expression of wild type parkin was driven by neuron-specific enolase (NSE) promoter. We reported that both young and old parkin transgenic mice exhibited less reduction of striatal TH protein and number of TH positive neurons in the substantia nigra induced by 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP), compared to wild type littermates. MPTP-induced mitochondrial impairment in the substantia nigra was improved in young parkin transgenic mice. Decreased striatal α-synuclein was demonstrated in old parkin transgenic mice. These results provide reliable evidence from the transgenic mouse model for parkin that overexpression of parkin may attenuate dopaminergic neurodegeneration induced by MPTP through protection of mitochondria and reduction of α-synuclein in the nigrostriatal pathway.</p> </div

Comparison of mRNA expression of hepatic <i>ABCG5</i>, <i>ABCG8</i> and <i>NPC1L1</i> genes among genotypes of NPC1L1 gene polymorphisms.

<p>(A) g-762T>C polymorphism and (B) g1679C>G polymorphism. ‘a’ vs ‘b’: P<0.01 by ANOVA, post-hoc LSD analysis.</p

Sleep-wake profiles of the WT and GAT1 KO mice under baseline conditions.

<p>(A) Time-course changes in each stage. Each circle represents the hourly mean amount of each stage. Open and filled circles stand for the values of the WT and KO mice, respectively. The horizontal open and filled bars on the χ-axis indicate the 12-h light and 12-h dark periods. (B) Total time spent in each stage for 12-h light/dark periods and 24 h all day. Open and filled columns represent the profiles for the WT (n = 7) and KO (n = 8) mice, respectively. Values are expressed as means ± SEM. * P<0.05 and ** P<0.01, compared with the corresponding WT control, assessed by unpaired <i>t</i>-test.</p