Objective MRI and MR hydrogen proton spectroscopy (1H-MRS) were used to detect the abnormal signal and alteration of metabolites, in order to explore the efficacy of these method in evaluating the damages of central nervous system (CNS) induced by occupational manganese exposure.Methods Eighteen workers exposed to manganese without any manganism symptoms, 12 workers with slightly chronic manganese poisoning, and 19 healthy workers were scanned using routine MRI sequence and 1H-MRS.The blood manganese concentration was also collected for each subject.On cerebral axial T1 WI,the signal intensities of ipsilateral globus pallidus and frontal white matter were measured in the visually brightest area (try to select the signal homogeneous region), and the globus pallidus index (PI) was then calculated.The 1H-MRS data was calculated to get the values of the peak height of N-acetylaspartate (NAA), choline (Cho), inositol (mI) and creatine (Cr) and the ratios of NAA/Cr, Cho/Cr, and mL/Cr were also calculated.One way ANOVA was used to compare the values of PI, NAA/Cr, Cho/Cr, mI/Cr and MnB among the three groups, and the correlations between PI and the time span of manganese exposure or blood manganese concentration were analyzed by Pearson correlation analysis.Eight workers exposed to manganese were followed up one year, and their PI , NAA/Cr before and after follow-up were compared by t test.Results Fourteen of 18 cases exposed to manganese without any manganism symptoms showed symmetrically high intensity signal on T1 WI, while the T2 WI were normal.No high signal intensity was observed on T1WI in any of the healthy workers or manganese poisoning workers.We found that the average PI in manganese exposed group (1.16 ±0.09) was significantly higher (F =24.79 ,P =0.O00)than those of the poisoning ( 1.05 ± 0.07 ) and control groups ( 1.01 ± 0.05 ).The blood manganese concentration in manganese exposed group, the poisoning group and the control group were (0.051 ±0.024), (0.047 ±0.018 ), ( 0.043 ± 0.020 ) μg/ml respectively, which was not significantly different ( F = O.623, P =0.541 ) and did not exceed the upper limit of normal reference value ( < 0.10 μg/ml ).There was a significantly correlation between PI and the time span of manganese exposure ( r = 0.67, P = 0.002 ),however, there was no correlation between PI and blood manganese concentration ( r = 0.20, P = 0.427 ).Furthermore, the NAA/Cr ratio decreased variously in the manganese poisoning group ( 1.22 ± 0.07 ) which was significantly lower( F = 4.120, P = 0.023 ) than those of the poisoning( 1.33 ± 0.13 ) and control groups ( 1.31 ±0.13).No statistical significanees were found in the ratios of Cho/Cr and mI/Cr among these three groups(P>0.05).No obvious changes of the PI and NAA/Cr were found in the 8 manganese exposed workers after 1 year follow-up.Conclusion Manganese exposure could lead to the high intensity signal on T1 WI, therefore the increased PI may be the biomarkers of central nerve system damages caused by the occupational manganese exposure.

AIM: To investigate the association of osteoprotegerin ( OPG) gene single nucleotide polymor-phisms (SNPs), 163A/G (rs3102735) and 245T/G (rs3134069), with susceptibility to rheumatoid arthritis (RA) in Chinese Han population .METHODS:A total of 205 patients with RA and 171 healthy control subjects were enrolled into this study.Genotyping was performed by polymerase chain reaction-based restriction fragment length polymorphism and subsequently confirmed by DNA sequencing .Odds ratio ( OR) and 95%confidence intervals ( CI) were calculated for the risk genotypes and alleles .RESULTS: OPG gene polymorphisms 163A/G and 245T/G were conformed to the Hardy-Weinberg equilibrium .The statistical differences in the genotypes of AA , AG and GG at 163A/G locus were found in RA and controls.The G allele was associated with an increased risk of RA , with OR of 1.219 (95%CI:1.066~2.339).No significant difference was observed between RA group and control group with respect to genotypic and allelic frequencies of OPG gene 245T/G (P>0.05).CONCLUSION:The OPG gene 163A/G SNP may be associated with RA susceptibility , and G allele may be the risk factor for developing RA .

Objective: To investigate the mechanism of resveratrol promoting fibronectin type Ⅲ domain-containing 5 (FNDC5) degradation in skeletal muscle of male obese mice． Methods: Six-week-old male C57BL /6 mice were randomly divided into three groups : standard control diet ( SCD) ，high-fat diet ( HFD) and high-fat diet treated with resveratrol (HFD + RES) ．HFD + RES group was intervened with resveratrol via gavage ［400 mg / kg · d) ］ while fed HFD for 20 weeks．The body mass，serum TG，TC，LDL-C and HDL-C levels were detected．The pathological changes in skeletal muscle were detected by HE staining．The expression of FNDC5，SIRT1，SIRT2，LC3， p62，Beclin-1，ATG5，ATG7 was assessed by immunohistochemistry，RT-PCR and Western blot respectively. Results: The body mass ，serum TG ，TC and LDL-C levels increased significantly ，meanwhile HDL-C levels decreased in HFD group．Lipid deposition between skeletal muscle fibers were obvious in HFD group．The immuno- histochemistry results showed that protein expression levels of SIRT1，SIRT2 and LC3 obviously decreased，while the protein levels of FNDC5 and p62 obviously increased．The expression levels of FNDC5 significantly increased， while the gene expression levels of SIRT1，SIRT2，LC3，Atg7 and Beclin-1 obviously decreased．All these responses were attenuated by treatment with RES． Conclusion RES has obvious effects of lipid-lowering and promoting FNDC5 degradation in skeletal muscle tissues，which may be related with SIRT1 and SIRT2-induced autophagy， thus resulting in degradation of FNDC5 .