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      • Comparison of Gadobenate Dimeglumine and Gadopentetate Dimeglumine for Breast MRI Screening: a Meta-analysis

        Yang, Xiao-Ping,Han, Yue-Dong,Ye, Jian-Jun,Chen, Gang,Luo, Ying,Ma, Hong-Xia,Yu, Xue-Wen,Niu, Juan-Qin,Ren, Fang-Yuan,Guo, You-Ming Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.12

        Background: As a common and essential contrast medium at present, gadobenate dimeglumine has shown better performance than some other agents when applied to Breast Magnetic Resonance Imaging Screening (Breast MRI Screening). Nevertheless, reports on the diagnostic performance of these two mediums (gadobenate dimeglumine and gadopentetate dimeglumine) are not completely consistent. Objective: To assess the diagnostic value of gadobenate dimeglumine and gadopentetate dimeglumine for Breast MRI Screening in patients suffering from breast cancer and to provide more convinced evidence to guide clinical practice in terms of appropriate contrast agents. Data Sources and Review Methods: Original articles in English and Chinese published before January 2013 were selected from available databases (The Cochrane Library, PUBMED, EMBASE, Chinese Biomedical Literature Database, Chinese Scientific Journals Full-text Database, Chinese Journal Full-text). The criteria for inclusion and exclusion were based on the standard for diagnosis tests. Meta-Disc software (Version 1.4) was used for data analysis. Then, the area under curve (AUC) of SROC and the spearman rank correlation of sensitivity against (1-specificity) were calculated. Results: Total of 17 researches involving 1934 patients were included. The pooled sensitivity of gadobenate dimeglumine and gadopentetate dimeglumine were 0.99 (0.97, 1.00) and 0.93 (0.88, 1.00) respectively. The pooled specificity for these two contrast agents were 0.924 (0.902, 0.943) and 0.838 (0.817, 0.858) respectively, and the AUC of SROC curve were 0.9781 and 0.9215 respectively. Conclusions: Gadobenate dimeglumine can be regarded as a more effective and feasible contrast medium for Breast MRI Screening. At least 5% differences in diagnostic performance are usually considered as clinically relevant.

      • SCOPUSKCI등재

        Glucosamine induces cell death $via$ proteasome inhibition in human ALVA41 prostate cancer cell

        Liu, Bao-Qin,Meng, Xin,Li, Chao,Gao, Yan-Yan,Li, Ning,Niu, Xiao-Fang,Guan, Yifu,Wang, Hua-Qin Korean Society for Biochemistry and Molecular Bion 2011 Experimental and molecular medicine Vol.43 No.9

        Glucosamine, a naturally occurring amino monosaccharide, has been reported to play a role in the regulation of apoptosis more than half century. However the effect of glucosamine on tumor cells and the involved molecular mechanisms have not been thoroughly investigated. Glucosamine enters the hexosamine biosynthetic pathway (HBP) downstream of the rate-limiting step catalyzed by the GFAT (glutamine:fluctose- 6-phosphate amidotransferase), providing UDP-GlcNAc substrates for O-linked ${\beta}$-N-acetylglucosamine (O-GlcNAc) protein modification. Considering that O-GlcNAc modification of proteasome subunits inhibits its activity, we examined whether glucosamine induces growth inhibition $via$ affecting proteasomal activity. In the present study, we found glucosamine inhibited proteasomal activity and the proliferation of ALVA41 prostate cancer cells. The inhibition of proteasomal activity results in the accumulation of ubiquitinated proteins, followed by induction of apoptosis. In addition, we demonstrated that glucosamine downregulated proteasome activator $PA28{\gamma}$ and overexpression of $PA28{\gamma}$ rescued the proteasomal activity and growth inhibition mediated by glucosamine. We further demonstrated that inhibition of O-GlcNAc abrogated $PA28{\gamma}$ suppression induced by glucosamine. These findings suggest that glucosamine may inhibit growth of ALVA41 cancer cells through downregulation of $PA28{\gamma}$ and inhibition of proteasomal activity via O-GlcNAc modification.

      • KCI등재

        Beneficial effects of natural Jeju groundwaters on lipid metabolism in high-fat diet-induced hyperlipidemic rats

        Yan-chao Wang,Jin-miao Lu,Hui-zi Jin,Ai-niu Ma,Jin-yang Zhang,Nian Gong,Qi Xiao,Bin Zhu,Ying-fang Lv,Na Yu,Wei-dong Zhang,Yong-xiang Wang 한국영양학회 2014 Nutrition Research and Practice Vol.8 No.2

        BACKGROUND: Groundwater is believed to possess many beneficial effects due to its natural source of various minerals. In this study, we examined the effects of natural Jeju groundwater S1 (SamdasooTM), S2 and S3 pumped up from different locations of Jeju Island, Korea, along with local tap water, on body weight gain, serum lipids and lipoproteins, and liver histopathology in high-fat diet-induced hyperlipidemic rats. MATERIALS/METHODS: Rats were randomly and equally divided into 6 groups. Different water samples were supplied to the hyperlipidemic rats as their daily drinking water and the widely-used anti-hyperlipidemic drug simvastatin was used as a positive control. Body weight, serum lipids and lipoproteins were measured weekly. Liver weight, liver index and liver histopathology were examined after the execution of the rats. RESULTS: After drinking Jeju groundwaters for two months, S2 but not S3 significantly reduced weight growth and serum triglycerides levels and increased high density lipoprotein-C (HDL-C) without affecting total cholesterol or LDL-C. S1 and particularly S2 significantly reduced the severity of liver hypertrophy and steatosis. All Groundwaters had much higher contents of vanadium (S3>S2>S1>>tap water) whereas S1 and S2 but not S3 markedly blocked autoxidation of ferrous ions. CONCLUSION: Jeju Groundwater S1 and particularly S2 exhibit protective effects against hyperlipidemia and fatty liver and hypothesize that the beneficial effect of Jeju Groundwaters may be contributed from blockade of autoxidation of ferrous ions rather than their high contents of vanadium.

      • KCI등재

        Glucosamine induces cell death via proteasome inhibition in human ALVA41 prostate cancer cell

        Bao-Qin Liu,Hua-Qin Wang,Xin Meng,Chao Li,Yan-Yan Gao,Ning Li,Xiao-Fang Niu,Yifu Guan 생화학분자생물학회 2011 Experimental and molecular medicine Vol.43 No.9

        Glucosamine, a naturally occurring amino monosaccharide,has been reported to play a role in the regulation of apoptosis more than half century. However the effect of glucosamine on tumor cells and the involved molecular mechanisms have not been thoroughly investigated. Glucosamine enters the hexosamine biosynthetic pathway (HBP) downstream of the rate-limiting step catalyzed by the GFAT (glutamine:fluctose-6-phosphate amidotransferase), providing UDPGlcNAc substrates for O-linked β-N-acetylglucosamine (O-GlcNAc) protein modification. Considering that O-GlcNAc modification of proteasome subunits inhibits its activity, we examined whether glucosamine induces growth inhibition via affecting proteasomal activity. In the present study, we found glucosamine inhibited proteasomal activity and the proliferation of ALVA41 prostate cancer cells. The inhibition of proteasomal activity results in the accumulation of ubiquitinated proteins, followed by induction of apoptosis. In addition, we demonstrated that glucosamine downregulated proteasome activator PA28γ and overexpression of PA28γ rescued the proteasomal activity and growth inhibition mediated by glucosamine. We further demonstrated that inhibition of O-GlcNAc abrogated PA28γ suppression induced by glucosamine. These findings suggest that glucosamine may inhibit growth of ALVA41 cancer cells through downregulation of PA28γ and inhibition of proteasomal activity via O-GlcNAc modification.

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