Aim To observe the effects of the total fla-vonoids of scutellaria barbataon ( TFSB ) on high-fat
feeding ApoE gene deficiency mice in early atheroscle-rosis ( AS ) and its underlying mechanisms. Methods
40 ApoE-/ -male mice were divided into five groups:model group, SIM group and L-TFSB, M-TFSB, H-TFSB group, 5 C57BL/6J mice were selected as nor-mal control group. All mice in experimental group were fed with high-lipid diet for 4 weeks and all mice were killed after 8 weeks. H&E staining was used to observe morphology of aorta. Blood rheometer was used to ex-amine plasm viscosity and whole blood viscosity. Fully automatic biochemical analyser was used to detect the serum levels of TG, TC, LDL-C and HDL-C. The ex-pression levels of PLTP and VE in serum were meas-ured by ELISA. The expression levels of PLTP and FXR in liver were examined by Western blot. Results The model was established successfully. TFSB groups could improve the aorta AS morphology of model mice and significantly reduce the serum levels of TG, TC and LDL-C, while increase the level of HDL-C ( P<0. 05 or P<0. 01 ) . TFSB groups could decrease the
hematocrit value, plasma viscosity and whole blood vis-cosity of AS model mice significantly and had statistical significance when compared with model group ( P <0. 01 ) . The expression levels of PLTP of serum were reduced significantly when compared with model group ( P <0. 01 ) . We also found that the expression of PLTP was in negative correlation with VE ( r = -0. 675,P<0. 01). M-TFSB and H-TFSB group could decrease the expressions of PLTP and FXR of liver when compared with model group ( P <0. 01 ) . Con-clusion TFSB may exert its anti-AS effect partly through inhibiting the levels of FXR and PLTP of ApoE-/ -mice, increasing the level of VE, regulating blood lipids, improving blood rheology and reducing the damage of AS in mice.

Objective To evaluate the relationship between apoE gene polymorphisms and gallstone. Methods We included all the published studies on the association between apoE gene polymorphisms and gall-stone. A meta-analysis was employed to summarize all these studies, calculate the pooled OR and its 95% confidence interval (95% CI) , and test the overall effects. The Egger's publication bias analysis and sensitivity analysis were carried out to evaluate the reliability and stability of the meta-analysis. Results Eleven association studies between the apoE gene polymorphisms and gallstone fulfilled our inclusion criteria. There were 1248 patients with gallstones and 1660 controls. Remarkable heterogeneities were discovered in the allele ε4 and genotype E3/E4 of apoE between gallstone and control subjects in these studies (P<0. 05). Their ORs and 95%CIs were 1.32 (1.01, 1. 71), 1. 60 (1. 04, 2. 46), respectively (P<0. 05). The results of sensitivity analysis and publication bias analysis showed the reliability and stability of this meta-analysis. Conclusion apoE gene polymorphisms are associated with gallstone. Those with the alleleε4 or genotype E3 /E4 had a higher risk of suffering from gallstone.

BACKGROUND:MicroRNAs are widely involved in the regulation of protein expression, and play a critical role in many physiological and pathological processes in the body. But microRNA expression profile in degenerative lumbar scoliosis is rarely reported and understood. OBJECTIVE:To compare the microRNA expression profile in the normal intervertebral disc and degenerative lumbar scoliosis and to identify degenerative lumbar scoliosis-specific microRNAs, folowed by functional validation. METHODS: Total RNA samples were extracted from the nucleus pulposus tissues of 57 patients with degenerative lumbar scoliosis as experimental groups and the normal nucleus pulposus tissues of 42 patients with lumbar fractures as control group. An initial screening of differentialy expressed microRNAs in the nucleus pulposus tissues by microRNA microarray was performed in 10 samples from each group. Subsequently, differentialy expressed microRNAs were validated using real-time quantitative RCR. The level of differentialy expressed microRNAs in the degenerative nucleus pulposus tissues was investigated. Then, the functional analysis of microRNAs in regulating colagen II expression was carried out. Western blot and luciferase reporter assay were also used to detect target genes. RESULTS AND CONCLUSION:We identified 22 microRNAs that were differentialy expressed (17 upregulated and 5 downregulated) in degenerative lumbar scoliosis patients compared with the controls. Folowing real-time quantitative RCR confirmation, miR-491-5p was significantly down-regulated in degenerative nucleus pulposus tissues in comparison with the controls. Moreover, its level was closely correlated with the pathological grading of disc degeneration. Overexpression of miR-491-5p promoted type II colagen expression in nucleus pulposus cels. Bioinformatics target prediction identified matrix metaloproteinase-9 as a putative target of miR-491-5p. Furthermore, luciferase reporter assays demonstrated that miR-491-5p directly targeted matrix metaloproteinase-9 and affected its protein expression in nucleus pulposus cels. These results show that the downregulation of miR-491-5p induces type II colagen loss by directly targeting matrix metaloproteinase-9, thereby resulting in degeneration of the intervertebral disc and degenerative lumbar scoliosis. This study also underscores the potential of miR-491-5p as a novel therapeutic target in degenerative lumbar scoliosis.

BACKGROUND:MicroRNAs (miRNAs) play an important role in a variety of diseases. Investigation of miRNA expression profile in degenerative lumbar scoliosis is beneficial for understanding its pathogenesis, providing a novel therapeutic target. Therefore, we tested the hypothesis that miRNAs promote intervertebral disc degeneration through the interleukin-10/STAT3 signaling pathway, a potential regulator of intervertebral disc degeneration.
OBJECTIVE:To compare the differentialy expressed miRNAs in the intervertebral disc tissues from patients with degenerative lumbar scoliosis and normal controls and to identify specific miRNAs in degenerative lumbar scoliosis folowed by functional validation.
METHODS: An initial screening of miRNA expression in nucleus pulposus tissues by miRNA Solexa Sequencing was performed in samples from 10 patients with degenerative lumbar scoliosis and 10 controls, respectively. Subsequently, differentialy expressed miRNAs were validated using qRT-PCR. The level of differentialy expressed miRNAs in degenerative nucleus pulposus tissues was investigated. Then, functional analysis of the miRNAs in regulating type II colagen expression was carried out. Western blot and luciferase reporter assay were used to further confirm the target gene.
RESULTS AND CONCLUSION: We identified 30 miRNAs that were differentialy expressed (16 upregulated and 14 downregulated) in patients with degenerative lumbar scoliosis compared with controls. Folowing qRT-PCR confirmation, Has-let-7f was significantly down-regulated in degenerative nucleus pulposus tissues as compared with controls. Moreover, its level was correlated with the severity of disc degeneration. Overexpression of Has-let-7f promoted type II colagen expression in nucleus pulposus cels. Knockout of interleukin-10 induced effects on nucleus pulposus cels similar to Has-let-7f. Bioinformatics target prediction identified interleukin-10 as a putative target of Has-let-7f. Furthermore, luciferase reporter assays demonstrated that Has-let-7f altered the expression of STAT3 and matrix metaloproteinase-2. These findings indicate that the downregulation of Has-let-7f induces type II colagen loss by directly targeting inleukin-10, thereby resulting in intervertebral disc degeneration and degenerative lumbar scoliosis. Has-let-7f is likely to be a novel therapeutic target for degenerative lumbar scoliosis.

The study on tumor metabolism has been gradually be-come a hot spot in recent years .A lot of proteins involved in the regulation of tumor metabolism especially the glucose transporter protein 1(GLUT1).As a key regulatory factor mediating energy metabolism within tumor cells , GLUT1 can regulate the glucose intake and maintain the basic level of metabolism in tumor cells . More importantly, the abnormal expression of GLUT1 was asso-ciated with many kinds of tumors , of which GLUT1 was used to meet the energy requirement for the fast growth of tumor .Thus GLUT1 also played a crucial role in growth , differentiation and metastasis of tumor cells and prognosis of tumors .Meanwhile , as three-dimensional crystal structure of GLUT 1 was determined , it is possible to design the small molecular inhibitors of GLUT 1, which can realize “starve to death” tumor cells.GLUT1 can be a particularly attractive target for tumor treatment and interfer-ence.The relationship between abnormal expression of GLUT 1 protein and tumor metabolism was reviewed . Moreover , the mechanism of tumor metabolism regulated by GLUT 1 protein ex-pression and treatment of cancers were discussed , which may provide references for future research and clinical treatment .

Autophagy is a common phenomenon which widely ex-ists in eukaryotic cells. Researches have shown that autophagy plays a critical role in maintaining cellular hemostasis, cell com-ponents update and keeping a normal physiological state. In re-cent years, the study has found that autophagy is closely related to the growth, the development of cardiovascular diseases and tumors. Further studies show that in different pathological condi-tions, autophagy could both promote angiogenesis and inhibit the formation of blood vessels. Therefore, it is particularly critical to elucidate the mechanisms of autophagy in the regulation of angio-genesis in different pathological conditions. The role of autophagy in cardiovascular diseases especially in the regulation of angio-genesis is discussed in this paper. Besides, the paper also in-cludes the discussion about the mechanisms of autophagy in the regulation angiogenesis, which may provide references for follow-up research and clinical treatment.

Objective To study the whole-genome evolution of influenza B viruses prevalent in Qingdao from 2006 to 2011 .Methods RNA was extracted from influenza B viruses isolated in Qingdao from 2006 to 2011 .Each gene segment was amplified by reverse transcription polymerase chain reaction ( RT-PCR) and then sequenced .Gene sequences of each virus were determined and assembled by using Sequench -er software .A phylogenetic analysis for each gene segment was conducted by using MEGA 5.0 software pack-age.Results The phylogenetic tree of hemagglutinin ( HA) gene showed that 13 strains from 2006 to 2009 belonging to V1 clade of Victoria lineage were B/Malaysia/2506/2004-like viruses,and 12 strains from 2009 to 2011 belonging to the V2 clade of Victoria lineage were B/Brisbane/60/2008-like viruses.Moreover, strains of Yamagata lineage were all B/Florida/4/2006-like viruses including 5 strains of Y1 clade circulated from 2006 to 2008 and 7 strains of Y2 clade circulated from 2010 to 2011, respectively.The analysis of whole-genome evolution showed that 3 viruses of V2 clade presented 5+3 reassortment and 1 virus presented 1+7 reassortment.All reassortant strains matched with the vaccine strains of the present and previous season . The Yamagata and Victoria lineage strains belonged to genotype 2 and genotype 15,respectively.Compared with vaccine strains , the HA1 protein of Victoria lineage strains showed mutations at amino acid sites of H14Q, L58P, N129S, I146V, N171D and R279K, while R48K, K88R, P108A, N116K, S150I, N165Y, D196N,N202S and S229G amino acid mutations were mainly detected in Yamagata lineage strains .The sites 116 and 129,150,165,196 and 202 located in the 120,150,160 and 190 loops,respectively,which had been previously determined to be the hotspots under positive selection .Conclusion Both Yamagata and Victoria lineages of influenza B viruses were prevalent in Qingdao and evolved continuously from 2006 to 2011 .The selective pressure that a vaccine would provide was only to virus strains belonging to the same lineage ,sug-gesting a bivalent vaccine may be better for the induction of protective immunity .

Tumor metastasis is one of the important biological characteristics of malignant tumor,which is closely related with the prognosis of the cancer patients.High expression of ADAM8 in varieties of tumors was revealed in many recent studies,and such aberrant expression played a crucial role in regulating of tumor metastasis.Studies showed that overexpression of ADAM8 attenuated the intercellular adhesion effect,promoted tumor angiogenesis,and enhanced the degradation of ECM as well as the releasing of cytokines.Therefore,suppression of ADAM8 may lead to inhibition of tumor metastasis,which makes ADAM8 a particular attractive target as it can be used as a prognostic indicator and a potential therapeutic target of malignant tumor.A review about the relations between ADAM8 protein′s abnormal expression and tumor occurrence was discussed in this paper,also include discussion about the mechanisms of ADAM8 protein′s disorder-induced tumor formation,as well as therapeutic strategies based on ADAM8-targeted,which may provide references for follow-up research and clinical treatment.