Abstract:Objective：This study aims to construct mitochondria-targeted ECSIT transgenic mice，identify the phenotype of the mice generated，and establish an animal model for ECSIT gene-related function. Methods：The expression vector pCAG-OTCL-ECSIT-3Xflag-BPA was constructed，and the linearized targeting vector was transferred into embryonic stem cells（ES cells）by electro transduction. The positive clones were injected into the blastocyst and transplanted into the surrogate mice to breed the chimeric mice. Chimeric mice and C57BL/6J mice then gave birth to potential heterozygote founders. The gene type of the mice was assayed by PCR. The cardiac function of mitochondria-targeted ECSIT mice was analyzed using small animal ultrasound. Results：Homologous recombinant vector pCAG-OTCL-ECSIT-3Xflag-BPA with mitochondrial targeted-overexpression of ECSIT was successfully constructed and identified correctly by PCR. Mitochondrial targeted-overexpression of ECSIT gene and blastocyst injection were completed and identified correctly by PCR. Mitochondrial and cytoplasmic proteins were isolated from transgenic mice，and ECSIT protein was specificly overexpressed in mitochondrion. Conclusion：Mitochondria-targeted ECSIT mice were successfully constructed；overexpression of ECSIT in mitochondrion had no significant effect on cardiac function in 8-week-age mice.

Abstract:Objective：This study aims to investigate the role and function of insulin-like growth factor-binding protein 7（IGFBP7）in the chondrogenic differentiation of human umbilical cord-derived mesenchymal stem cells（hUC-MSCs）. Methods：Human umbilical cord-derived mesenchymal stem cells（hUC-MSCs）were cultured in high-density pellets to establish a chondrogenic differentiation model. Differences in cartilage differentiation were detected by alcian blue staining. hUC-MSCs was transfected with pCMV3-IGFBP7 or si-IGFBP7 to change the expression level of IGFBP7. The expression level of IGFBP7 was detected in chondrogenesis by real-time PCR and Western blot. The chondrogenesis-related marker gene Sox9 was determined by real-time PCR and Western blot. Results：IGFBP7 mRNA and protein expression significantly increased after induction of chondrogenic differentiation. The level of IGFBP7 in hUC-MSCs transfected with pCMV3-IGFBP7 was significantly increased，while the level of IGFBP7 in the si-IGFBP7 group was significantly reduced. Over-expression of IGFBP7 increased mRNA and protein level of Sox9 and promoted the differentiation of hUC-MSCs into chondrocyte. On the contrary，suppression of IGFBP7 inhibited chondrogenic differentiation. Conclusion：IGFBP7 was a positive regulator in the chondrogenic differentiation of hUC-MSCs.

Abstract:Objective：This study aims to observe the changes of intestinal function in 11β- hydroxysteroid dehydrogenase（11β-HSD1）knockout mice. Methods：Six 11β-HSD1 knockout mice were paired with 6 control mice with C57/BL6 genetic background both fed standard chow ad libitum for a period of 6-8 weeks. The changes in mice characteristics and intestinal morphometry were observed. The intestinal function and inflammatory alterations were determined by PCR and immunohistochemistry. Results：11β-HSD1 gene abortion significantly decreased the intestinal inflammation. Intestinal mucosal permeability was altered，intestinal villus length was shortened，crypt depth became deeper，goblet cell number increased，and mucosal barrier function was enhanced. Conclusion：This study successfully established a 11β-HSD1 knockout mice model，which showed inflammation amelioration in intestinal tract after 11β-HSD1 gene knockout，providing a research foundation for further specific knockouting 11β-HSD1 in intestinal tissue.

Abstract:Objective：This study aims to investigate the effect of IgG on activating signaling pathway of macrophages induced by CpG DNA. Methods：Bone - marrow derived macrophages were cultured in vitro and their surface markers and phagocytic functions were identified by flow cytometry and immunofluorescence technique. After the treatment of macrophages with IgG，CpG DNA and IgG plus CpG DNA，the activated molecules on the surface of macrophages were detected by flow cytometry，and the protein phosphorylation was detected by immuno-protein Western blot. Results：The expression rate of CD11b and F4/80 on the surface of macrophage in vitro was about 99.7 %，and the proportion of macrophage to FITC - IgG was about 70 %；IgG up-regulated the expression of CD40，CD80 and CD86 on the surface of macrophage induced by CpG DNA（P < 0.05）；IgG promotes the phosphorylation of JNK and p38 in macrophages induced by CpG DNA，but it has no effect on the phosphorylation of ERK and NF-κB；CpG DNA induces macrophages to secrete TNF-α，and combination of IgG with CpG DNA enhanced this process. Conclusion：CpG DNA activates macrophages and increases the phosphorylation of JNK and p38，and the combined treatment of CpG DNA and IgG highly induced this process；CpG DNA increased the co-stimulation molecule of CD40，CD80and CD86 on the surface of macrophages，while the co-therapy of IgG and CpG DNA highly up-regulates this expression.

Abstract:Objective：This study aims to investigate the effect of resveratrol（Res）on proliferation and collagen secretion in neonatal rat cardiac fibroblasts（CFs）and its possible mechanism. Methods：Neonatal rat CFs were isolated and identified by double enzyme digestion method，differential adhesion method and immunofluorescence from Sprague-Dawley rats born 1 day to 3 days. Two to three generations of CFs were randomly divided into four groups：Con（the normal control group），DMSO（the solvent control group），AngⅡ（the model group），AngⅡ+Res（the drug intervention group）. Then CCK8 and EdU staining kit were both used to detect cellular proliferation. Level of the cellular collagen secretion was measured by Hydroxyproline test kit. Moreover，the mRNA expression of AU-rich element RNA-binding factor 1（AUF1）and transforming growth factor-β1（TGF-β1）were examined by RT-qPCR，and the protein expression of AUF1 and TGF-β1 were detected by Western blot. Results：CFs were successfully extracted from SD rats and Vimentin was positive obviously. Compared with Con group，cellular proliferation and collagen secretion increased in AngⅡ group；the mRNA and protein expression of AUF1 and TGF-β1 increased as well. After the intervention of Res，AngⅡ+Res group had significantly lower cell proliferation and collagen secretion level than AngⅡ group；the mRNA and protein expression of AUF1 and TGF-β1 decreased as well. There was no statistically significant difference between the above indicators in the DMSO group and the Con group. Conclusion：Res can inhibit AngⅡ-induced proliferation and collagen secretion of cardiac fibroblasts，which may be related to the suppression of AUF1 and TGF-β1 expression.

Abstract:Objective：The present study was designed to investigate the protection of astragaloside Ⅳ（AS-Ⅳ）on human aortic endothelial cells（HAECs）after hypoxia injury and underlying mechanism. Methods：HAECs were cultured in 8% O2 to form hypoxic injury models. The cells were divided into control group（C），hypoxic group（H）and AS-IV treatment group（AS-Ⅳ，50 μg/mL）. The protective effect of AS-Ⅳ on HAECs after hypoxia was observed，and the migration，proliferation and tube formation of the cells were analyzed. Autophagy related proteins were also identified. Results：Compared with the C group，the cells with hypoxia presented increased supernatant lactic dehydrogenase（LDH）concentration（25.33 ± 1.70 U/L vs. 5.33 ± 1.25 U/L），decreased cell viability（81.12% ± 0.72% vs. 100.00% ± 3.07%），cellular migration and proliferation ability and tube formation（30.91 ± 3.78 vs. 62.1 ± 7.56）. Furthermore，the protein expression of Beclin and LC3-II of the injured cells were decreased. After AS-Ⅳ treatment，compared with the H group，decreased LDH release（18.33 ± 1.25 U/L），increased cell viability（85.71% ± 2.48%），cellular migration and proliferation ability，and tube formation（48.64 ± 4.80）were observed. And the protein expression of Beclin and LC3-II increased. Conclusion：AS-Ⅳ can alleviate hypoxia-induced damage and may promote angiogenesis of HAECs by the autophagy signaling pathway.

Abstract:Objective：To investigate the effect of histone deacetylation modification on early embryogenesis and three germ-layer diffierentiation of Xenopus laevis. Methods：Two-cell embryos were treated with 400 nmol/L Trichostation A（TSA）to observe early embryogenesis and expression of three germ layer marker genes by whole-mount in situ hybridization. Micro-injection of histone deacetylase 1（HDAC1）specific antisense oligonucleotide（HDAC1MO）was performed to knockdown HDAC1. The expression of three germ layer marker genes was detected by whole-mount in situ hybridization. Results：Embryos treated with 400 nmol/L TSA showed developmental defects. The expression of three germ layer marker genes were affected in embryos treated with TSA or knockdown of HDAC1. Conclusion：Histone deacetylase is involved in germ-layer differentiation during early embryogenesis.

Abstract:Objective：Evaluate the function of comprehensive analysis of Y-STRs and Y-SNPs，and apply network analysis in paternal lineage identification. Methods：Samples of 180 males from two pedigrees with different surnames were collected. Haplotypes at 26 Y-STRs loci were genotyped with YfilerTM Plus Kit. The genotypes of 42 Y-SNPs in 36 males selected from 180 males were obtained by mini-sequencing. The haplotypes were analyzed using direct counting method and network to discuss the variations of Y-STRs haplotypes within pedigree and the distribution of Y-SNPs haplogroups. Results：Eighteen Y-STRs haplotypes were found in 63 individuals of the P1 pedigree，and the 17 individuals selected all belonged to the N-M231 haplogroup；35 haplotypes were found in 117 samples of the P2 pedigree，and the 19 individuals selected all belonged to O1a1a1a1-F78 haplogroup. The network results showed that the P1 pedigree had a central tendency，while the P2 pedigree had two centers. Step-by-step mutation among Y-STR haplotypes within pedigree visually and clearly showed in the network. Conclusion：The Y-SNPs information and the network method integrated with the Y-STRs during pedigree investigation can largely broaden the scale in pedigree investigation，get more reliable paternal pedigree structure and increase the accuracy of paternal lineage identification.

Abstract:Objective：This study aims to investigate the relationship between chemokine C-X-C motif ligand 4（CXCL4） and gender differences in lung tissues of neonatal mice with hyperoxia-induced lung injury. Methods：Thirty-two mouse pups（16 animals per sex），were randomly and equally assigned to four groups：Hyperoxia-male group，Hyperoxia-female group，Room air-male group and Room air-female group，with 8 mice in each group. The mice in air group were exposed to room air（FiO2=21%）and those in hyperoxia group were exposed to hyperoxia（FiO2 ≥ 95%）for 7 days. All animals were sacrificed and lung tissues were excised for analysis via histological staining，tandem mass tags（TMT）technology and immunofluorescence staining. The levels of CXCL4 in tissue homogenates were measured. Results：The mouse pups exposed to hyperoxia had significant reductions in the degree of alveolarization，and radial alveolar count（RAC） in lung tissues（P < 0.001） was significantly decreased in hyperoxia-exposed animals and was decreased to a larger extent in males compared with females（P < 0.01）. Under hyperoxia intervention，CXCL4 upregulated was exclusively differentially regulated in hyperoxia exposed neonatal male mice compared to room air controls. M4 macrophage（MMP7+ S100A8+） infiltration was higher in male mice following postnatal hyperoxia exposure. Conclusion：These findings highlight sex-specific differences in hyperoxic lung injury，and male neonatal mice are more susceptible to hyperoxia-mediated lung injury and display larger arrest in lung alveolarization，which suggests the changes in M4 macrophages induced by CXCL4 may play a crucial role in sexual differences in neonatal hyperoxic lung injury.

Abstract:Objective：This study aims to investigate the effect of experimental periodontitis on the expression of reactive oxygen species（ROS） in marrow of mice. Methods：A total of 20 eight-week-old C57BL/6 mice were used in the study，and-experimental periodontitis was induced in mice by thread ligature. After 4 weeks of experiment，the maxilla were undergone micro-CT scanning，HE staining，tartrate-resistant acid phosphatase（TRAP）staining. Flow cytometry was employed to study the expression of ROS in marrow. Results：After four weeks of experimental periodontitis，alveolar bone resorption and TRAP positive osteoclast number were all increased. There were significantly increases of the ROS level in marrow compared with controls. Conclusion：Experimental periodontitis can increase the expression of ROS in mice marrow，which may play regulatory roles in alveolar bone loss.

Abstract:Objective：This study aims to investigate how phosphorylation regulates the tumor-suppressive activity of Suppressor of fused（Sufu）in medulloblastoma（MB） cells and elucidate the potential mechanism. Methods：The expression and phosphorylation levels of Sufu in MB tissue microarrays were detected by immunohistochemistry. Wild type Sufu or its phosphorylation sites mutated plasmids were transfected into MB cell line DAOY. The cellular distribution of Sufu was detected by ICC and Western blot，and the cell proliferation and apoptosis were detected by CCK8，EdU labeling，and flow cytometry. Besides，the transcriptional activity of Glioma-associated oncogene homologue（Gli） at downstream of Hedgehog（Hh） signaling was analyzed by luciferase reporter assay，and the protein level of ornithine decarboxylase（ODC1）was detected by Western blot in transfected cells. Results：Sufu was highly expressed and phosphorylated in MB tissues，compared to normal cerebellum. Phosphorylated Sufu was mainly concentrated in the nucleus. Unphosphorylation dampened the inhibitory effect of Sufu on proliferation and its promotion of apoptosis in DAOY cells. It is known that Gli-mediated transcriptional activation and ODC1-mediated polyamine synthesis can promote MB cell growth at the downstream of Hh signaling. Phosphorylated Sufu inhibited the transcriptional activity of Gli. Unphosphorylated Sufu showed impaired repressor activity and promoted the expression of ODC1. Conclusion：Phosphorylation enhances the inhibitory effect of Sufu on MB cell growth，which may be related to inhibition of Gli-mediated Hh signaling transduction and the metabolism of polyamines.

Abstract:Objective：This study aims to explore the effects of paclitaxel on the differentiation of human lung fibroblasts（HLFs） into myofibroblasts induced by recombinant human transform growth factor-β1（rhTGF-β1） and potential mechanism. Methods：HLFs were cultured and divided into six groups：the control group，the TGF-β1-treated group（5 ng/mL），the TGF-β1 plus 0.01，0.10，1.00 nmmol/L paclitaxel group and the paclitaxel-only（1 nmol/L）group. Cell viability was measured by CCK8 assay. Cell morphology changes were observed and analyzed by microscope. Transwell assay was carried out to assess cell migration. Immunofluorescence was employed to detect the expression of α-SMA. The levels of α-SMA，fibronectin，collagenⅠ，collagen Ⅲ were detected by real-time PCR and Western blot. The protein levels of phospho-Smad3，Smad3，phospho-p38 and p38 in cells were determined by Western blot. Results：The results of CCK8 showed that 1 nmol/L PTX had no toxic effect on HLFs，0.01 nmol/L PTX could not inhibit the cell viability of HLFs induced by TGF-β1，and 0.1，1.0 nmol/L PTX could inhibit the cell viability of HLFs induced by TGF-β1；The results of cell morphology showed that 0.01 nmol/L PTX could not reduce the width of HLFs induced by TGF-β1，and 0.1，1.0 nmol/L PTX could reduce the width of HLFs induced by TGF-β1；The results of transwell assay showed that 0.01 nmol/L PTX could not inhibit the migration of HLFs induced by TGF-β，and 0.1，1.0 nmol/L PTX could inhibit the migration of HLFs induced by TGF-β1；The results of immunofluorescence showed that 0.01 nmol/L PTX could not decrease the fluorescence intensity of α-SMA induced by TGF-β1，and 0.1，1.0 nmol/L PTX could decrease the fluorescence intensity of α-SMA induced by TGF-β1；The results of Real-time PCR and Western blot showed that 0.01 nmol/L PTX could not decrease the content of phenotypic transformation markers such as α-SMA，fibronectin，collagen Ⅰ，collagen Ⅲ and down-regulated the phosphorylation p38，and 0.1，1.0 nmol/L PTX could decrease the content of phenotypic transformation markers such as α-SMA，fibronectin，collagen Ⅰ，collagen Ⅲ，and down-regulated the phosphorylation of Smad3 and p38. Conclusion：PTX inhibited the differentiation of human lung fibroblasts into myofibroblasts induced by TGF-β1 via TGF-β/Smad/MAPK signaling pathway.

Abstract:Objective：This study aims to explore the effect of exosome of prostate cancer cells on the osteoblast differentiation. Methods：The ExoQuick-TC kit and ultrafiltration are adopted to isolate and purify exosomes from prostate cancer cell lines. The exosomes will be characterized by marker CD63，and observed through electron microscopy. Extract total RNA from pre-osteoblasts treated by exosomes of prostate cancer cells；then expressions of Osx，Runx2 and Alp were detected by real-time PCR. Osx and Runx2 are the biomarker of early osteogenic differentiation and Alp is the biomarker of metaphase osteogenic differentiation. Furthermore，osteogenic differentiation were ohserved by using ALP and ARS staining. Results：Prostate cancer cell exosomes can enter pre-osteoblasts. Compared to control cells，the expression of Osx，Runx2 and Alp are decreased in pre-osteoblasts cells treated with prostate cancer cell exosomes（P < 0.05）. The staining results showed that osteogenic differentiation was inhibited. Conclusion： Prostate cancer cells secrete exosomes that can act on pro-osteoblasts and inhibit osteoblast differentiation.

Abstract:Objective：To investigate the role and possible molecular mechanism of microRNA（miR）-558 in liver cancer. Methods：RT-PCR was used to detect the expression of miR-558 in 35 liver cancer tissues and 35 paracancerous tissues. The effects of miR-558 and TNFAIP1 on the growth and cycle of hepatoma cell were detected by cell counting kit-8（CCK-8），plate clone and flow cytometry. Luciferase assays were performed to analyze the relationship between miR-558 and TNFAIP1. The expression of protein level was detected by Western blot. Results：The expression of miR-558 in the liver cancer tissues was significantly higher than that in the paracancerous tissue（P < 0.01）. Knock down of miR-558 significantly inhibited the proliferation of hepatoma cells，while overexpression of miR-558 could significantly promote the growth of hepatoma cells（P < 0.01）. MiR-558 functioned in hepatoma cells through targeting TNFAIP1 directly. TNFAIP1 overexpression could significantly reverse the effect of miR-558 on hepatoma cell. Conclusion：MiR-558 was highly expressed in liver cancer tissue，and miR-558 can promote the proliferation of hepatoma cells by targeting TNFAIP1. MiR-558 had a certain value of target therapy in liver cancer patients.

Abstract:Objective：This study aims to explore the transformation of Kupffer cells（KCs）in the process of liver ischemia and reperusion and its role in liver ischemia-reperfusion injury. Methods：Mice models of liver ischemia at different time were established. Flow cytometry was used to analyze the number of KCs after ischemia. qPCR was used to analyze the expression of inflammatory cytokines and surface markers of macrophages. Western blotting was used to analyze PI3K/p-Akt2 signaling pathway. After using Akt2 inhibitor before ischemia，the cells were extracted for cell culture in vitro. The expression of inflammatory cytokines and surface markers of macrophages were analyzed by qPCR. In addition，liver injury was analyzed by HE staining of liver slices and serum alanine aminotransferase（ALT） after 6 hours of liver ischemia reperfusion in mice. Results：The number of KCs decreased after ischemia in liver，and the expression of pro-inflammatory cytokines in surviving cells stimulated by LPS was significantly higher than that in control group（P < 0.05），and the expression level of iNOS，a surface marker of M1 macrophages，was also higher than that in control group（P < 0.05）. The PI3K/p-Akt2 signaling pathway in the cells was activated，thus promoting the transformation of KCs to M1 macrophages after ischemia. The transformation can be blocked by Akt2 inhibitor，and it protects liver from ischemia-reperfusion injury. Conclusion：Liver ischemia in mice promotes the transformation of KCs to M1 macrophages through activating PI3K/p-Akt2 signaling pathway and aggravates liver ischemia-reperfusion injury.

Abstract:Objective：To investigate effects and mechanisms of PKM2 on hepatocellular carcinoma（HCC）cell. Methods：PKM2 expression was detected in liver cancer tissues and liver cancer cell lines（HepG2，Hep3B，HuH7 and smmc-7721）by quantitative PCR（qPCR），Western blot（WB）and immunohistochemistry（IHC）. PKM2 expression was inhibited by small interfering RNA（siRNA）in HCC cell lines. Effects of siRNA on the proliferation，invasion and migration was analyzed in HCC cell lines. In addition，we studied the effect of PKM2 siRNA on Hippo signaling pathway. Results：qPCR，WB and IHC showed PKM2 expression was significantly higher in HCC tissues than paracancer tissue，and in HCC cell lines than normal liver cell line（L02）. PKM2 siRNA effectively inhibited the proliferation，invasion and migration of HCC cells. Further study confirmed that Hippo signaling activity was inhibited in HCC cell lines compared with L02，and was enhanced in PKM2 siRNA-treated HCC cell lines. Inhibition of Hippo signaling activity significantly reversed inhibition of proliferation，invasion and migration in PKM2 siRNA-mediated HCC cell lines. Conclusion：PKM2 may inhibit phosphorylation of LAST1 and YAP，decrease Hippo signaling pathway，and promote HCC cell proliferation，invasion and migration.

Abstract:Objective：This study aims to invesigate the effects of metformin combined pemetrexed on proliferation and apoptosis of human lung adenocarcinoma A549 cells. Methods：The A549 cells were treated with different doses of metformin（0，2.5，5.0，10.0，20.0，40.0 mmol/L）and pemetrexed（0，0.5，1.0，2.0，4.0，8.0 μmol/L）for 48 h，CCK8 assay to assess the antiproliferative of the differently treated A549 cell lines and detect the half maximal inhibitory concentration（IC50）of metformin and pemetrexed；The A549 cells were treated with metformin at IC50，pemetrexed at IC50，and metformin combined pemetrexed to assess the antiproliferative of the differently treated A549 cell lines by the CCK8 assay；The apoptosis of A549 cells was detected by the flow cytometry；The protein expressions of Bcl-2，Bax，Mcl-1 and Noxa were detected by Western blot. Results：The proliferation of A549 cells was inhibited by metformin and pemetrexed monotherapy in a dose-dependent manner compared with the control groups（P < 0.05）；The combination of metformin and pemetrexed induced higher percentage of cell proliferation than that of metformin and pemetrexed used alone（P < 0.05）in a time-dependent manner（P < 0.05）；Apoptosis rate of metformin combining pemetrexed［（30.6 ± 0.4）%］was significantly higher than that of metformin［（13.3 ± 0.3）%］ and pemetrexed［（12.9 ± 0.1）%］group，respectively（P < 0.05），The combination of metformin and pemetrexed down regulated the protein expression of Bcl-2 and Mcl-1，up-regulated the protein expression of Bax and Noxa compared with metformin and pemetrexed monotherapy. Conclusion：metformin combined with pemetrexed can inhibit in vitro human lung adenocarcinoma A549 cells proliferation and apoptosis，the mechanism may be connected with down-regulation of Bcl-2 and Mcl-1，up-regulation of Bax and Noxa expression.

Abstract:Objective：To evaluate the clinical efficacy and safety of flexible ureteroscopic lithotripsy using 365 μm holmium laser for nephrolithiasis in this study. Methods：Patients who were diagnosed as nephrolithiasis and submitted in our center between July 2017 and July 2018，were randomized into two groups：60 cases for 365 μm group treated by flexible ureteroscopic lithotripsy using 365 μm holmium laser，and 60 cases for 200 μm group treated by conventional flexible ureteroscopic lithotripsy. The surgery-related indexes，the complications and biochemistry examinations between two groups were compared. Results：Compared with 200 μm group，the operation time for cases in 365 μm group were significantly shortened. No significance was observed in the length of hospitalization and the stone free rate between two groups. For safety，the complication rate was significantly low and biochemistry examinations were significantly improved in 365 μm group. In addition，the damage of flexible ureteroscopy and fiber were less in 365 μm group than in 200 μm group. Conclusion：Our study firstly reported the highly efficientcy of flexible ureteroscopic lithotripsy using 365 μm holmium laser for nephrolithiasis in this cohort，which significantly shortened the operation time for the stones larger than 2 cm. Moreover，the comparable safety and higher cost-effectiveness were observed in 365 μm group.

Abstract:Objective：This study aims to explore the efficacy and safety of imatinib（IM）or nilotinib（NIL）as the first-line treatment in elderly chronic phase of chronic myeloid leukemia（CML-CP）. Methods：A retrospective analysis of 75 elderly CML patients receiving IM or NIL as first-line treatment. The clinical efficacy and safety indexes were compared between IM（43 cases）and NIL（32 cases）group. Results：No difference was found between the two groups when comparing 3 month-，6 month-，9 month- and 12 month- major molecular response（MMR）（23.07% vs. 15.00 %，52.38% vs. 52.38%，57.89% vs. 59.09%，54.17% vs. 57.14%，P＞0.05）and MR4.0（11.53% vs. 10.00 %，52.38% vs. 47.62%，57.89% vs. 50.00%，54.17% vs. 42.86%，P＞0.05）. There was no significantly difference of 3 month-，6 month-，12 month- and 18 month- optimal response between the two groups（60.47% vs. 75.00 %，60.47% vs. 71.88%，62.79% vs. 75.00%，72.09% vs. 90.63%，P＞0.05），as well as overall survival（OS），progression-free survival（PFS）and event-free survival（EFS）during the therapies（90.70% vs. 93.75%，79.07% vs. 90.62%，34.88% vs. 65.63%，P＞0.05）. More failure happened in IM group（15.63% vs. 44.19%，P=0.009）. More cardiovascular or hematologic adverse events（AEs） happened in NIL group（31.25% vs. 6.78%，P=0.006）. Conclusion：No difference was found between IM and NIL when comparing molecular response and optimal response. Less failure but more cardiovascular or hematologic AEs happened in NIL group.

Abstract:Gynecomastia，the most common benign disease of the breast in men，is a primary disease in most case，mainly due to the imbalance of endogenous estrogen and androgen，resulting in hyperplasia of glands and hypertrophy of adipose tissue. The clinical feature of the disease is the enlargement of the bilateral or unilateral breast tissue. Simon’s classification is the most commonly used grading method，and the main treatment methods are drug treatment and surgical treatment. This is a review about the cause，type and treatment of gynecomastia，especially the advantages and disadvantages of the common treatment methods.

Abstract:AMP-activated protein kinase is the cellular energy sensor. It has the function of regulating and maintaining energy dynamic balance. Activated AMPK inhibits the synthesis and metabolism of triglycerides，gluconeogenesis，cholesterol and fatty acids in the liver. Nonalcoholic fatty liver disease has become one of the most common chronic liver diseases in China. Its pathogenesis is complicated，insulin resistance and oxidative stress may account for a key factor. Other factors may involve leptin，adiponectin，resistin，tumor necrosis factor，etc. The activation of AMPK may affect these risk factors and improve NAFLD. We aim to describe how AMPK plays a role in the occurrence of NAFLD.