Abstract:Objective:To research Sonic Hedgehog (Shh) signaling pathway effects on the cerebellum external granular layer (EGL layer) cell granule cell precursors (GCP cell) proliferation and migration in early development of cerebellum. Methods: Paraffin sections by immunofluorescence were performed to observe external granular layer of the cerebellum GCP cell proliferation. Mouse brain slices in vitro establish systems were performed to detect dynamic migration and proliferation of cerebellar external granular layer of GCP cells. Results: The number of granulosa cell proliferation precursors was reached the peak on the seventh days after birth in mice cerebellar external granular layer;Shh signaling pathway promoted proliferation of cerebellar external granular layer cells. After inhibition of the signaling pathway by cyclopamine (CPA), cell proliferation of cerebellar external granular layer was inhibited, but migration was unaffected. Conclusion: Shh signaling pathway is a part of promoting cell proliferation of cerebellar external granule layer and mitosis essential, and its function is only limited to the external granule layer.

Abstract:Objective:To investigate the mechanism of regulation of diacylglycerol kinase (DGK) on Hedgehog signaling pathway. Methods: The interaction between DGKs and IFT88 was analyzed through co-immunoprecipitation. The expression levels of Hedgehog signaling target gene Gli1 were detected after siRNA knockdown of DGKs. Ciliogenesis of MEF cells with DGKδ defeciency was observed under confocal microscope. The localization of IFT88 in primary cilia was detected as well in those DGKδ knockout MEFs. Results: The 7 members of DGK family were bound with IFT88 specifically. SiRNA knockdown of DGK decreased the transcriptional level of Gli1. DGKs regulated Hedgehog pathway between Ptch1 and Smo. Knockout of DGKδ inhibited growth of primary cilia and the distribution of IFT88 in cilia. Conclusion: Knockdown of DGK inhibits the activity of the Hedgehog signaling pathway, which is related to defect of ciliogenesis.

Abstract:Objective: To identify the potential biological function of hsa-miR-363. Methods: Firstly we analyzed hsa-miR-363 base sequence,chromosomalposition and conservation of the sequence through miRbase and UCSC databases. Secondly, we predicted the target genes by the miRNA databases, including Miranda, miRDB, PicTar, and TargetScan. Then the intersection of these predicted genes were done for further study. Finally, we clarified those cell functions and signaling pathways regulated by hsa-miR-363 target genes using GO and KEGG pathway analysis. Results: According to these bioinformatics data, we found that hsa-miR-363 might have a wide range of functions, and some potential target genes of this microRNA participated in the initiation and development of endometriosis. Conclusion: Hsa-miR-363 might be related to the pathogenesis of endometriosis, and it may provide a potential target for the clinical therapy to endometriosis.

Abstract:Objective:To investigate browning ability differences of adipose tissues in each part of mice (male C57BL/6J). Methods: We isolated adipose tissues from mice (male C57BL/6J). The expressions of browning, adipogenesis, adipokine and inflammation markers were examined by fluorescence quantitative PCR. The protein expression of uncoupling protein-1 (Ucp1) was detected by Western blotting. Results: The expression of browning genes in adipose tissues around the thyroid gland was the highest compared with those in the classic brown adipose tissues (interscapular and infrascapular brown adipose tissues). In mesenteric adipose tissues, perigonadal adipose tissues, and inguinal subcutaneous adipose tissues, browning genes showed the lowest expression. The expression of adipogenesis genes in subcutaneous adipose tissues was significantly higher than those in epididymis and mesenteric adipose tissues. The expression of adipocytokines in white adipocytes was significantly higher than that in brown adipocytes. The expression of inflammatory factor was significantly increased in perigonadal and mesenteric adipose tissues, while it was the lowest in subcutaneous adipose tissues. Conclusion: The browning ability in adipose tissues around the thyroid gland is close to that in interscapular and infrascapular brown adipose tissues. Adipose tissues around the thyroid gland, interscapular subcutaneous adipose tissues and adipose tissues from perirenal and axilla show brown-like abilities just like iBAT. Mesenteric adipose tissues, perigonadal adipose tissues, and inguinal subcutaneous adipose tissues showed strong abilities of adipogenesis and immune. The cytokine expression of mesenteric adipose tissues, perigonadal adipose tissues is lower, but inflammatory factor secretion is relatively higher, and lipolytic effect is stronger.

Abstract:Objective:To deliver oxyntomodulin (OXM) to the food-grade strains of Lactctococcus Lactis (L.lactis), and identify its expression level in vivo and in vitro. Methods: L.lactis was transformed with recombinant plasmid pNZ8149-OXM by electroporation, and oxyntomodulin expression was detected by Western blot. Then, pNZ8149-OXM-transformed L.lactis was administered orally to mice, and OXM were detected by HPLC-MS from serum samples. Results: The expression of recombinant OXM from the pNZ8149-OXM-transformed L.lactis reached a maximum at 5 h after induction with nisin. The level of OXM in the serum of mice fed with pNZ8149-OXM-transformed L.lactis was 2.5 times higher than that in the control group. Conclusion: The recombinant L.lactis expressing oxyntomodulin is successfully constructed and expressed. It provides the basis for further study on the effect of reducing weight and lipid.

Abstract:Objective:To construct nucleic acid vaccine plasmid encoding severe fever with thrombocytopenia syndrome virus(SFTSV) nucleoprotein and to study its immunogenicity. Methods: SFTSV nucleoprotein gene was amplified by polymerase chain reaction (PCR). The PCR product was cloned into the expression vector pJW4303 to construct nucleic acid vaccine. The recombinant plasmid pJW4303-N was identified by sequencing and then transiently transformed into HEK293T cells to measure the nucleoprotein expression by Western blot. We immuned the BALB/c mice with pJW4303-N and used the blank vector pJW4303 as the control. The immunogenicity was detected by enzyme-linked immunosorbent method. Results: The recombinant SFTSV nucleoprotein expression vector pJW4303-N was successfully constructed and expressed in supernatants and cell lysates of HEK293T cells in vitro. Specific IgG antibodies and its subtype in mice were found by ELISA after immunization. IgG titer and its subsets in the serum of the BALB/c mice were significantly increased than those of the controls. IgG2a was significantly higher than IgG1. Conclusion: The nucleic acid vaccine of SFTSV nucleoprotein (pJW4303-N) has good immunogenicity. This research is the foundation for the further study of SFTSV nucleoprotein.

Abstract:Objective:To explore the regulation of angiogenic gene AGGF1 expression by miR-372. Methods: Bioinformatic prediction was performed to find the candidate microRNAs that may target AGGF1. Luciferase assays using AGGF1 3′-untranslational region (3′-UTR) reporters were performed to verify the binding of miR-372 to the AGGF1 3′-UTR; Real-time quantitative PCR (qPCR) and Western Blot assays were performed to measure the endogenous AGGF1 expression in 293T cells and HUVEC cells at mRNA and protein levels affected by overexpression of miR-372. In vitro angiogenesis assay was performed to verify the effects of miR-372 mediated downregulation of AGGF1 on angiogenesis. Results: Bioinformatic assays indicated that miR-372 targeted AGGF1. Luciferase assays confirmed that miR-372 downregulated AGGF1 expression directly through the miR-372 binding sites on 3′-UTR of AGGF1. qPCR and Western Blot assays revealed overexpression of miR-372 by mimic reduced AGGF1 expression at both mRNA and protein levels. In vitro matrigel based angiogenesis assay showed that overexpression of miR-372 reduced angiogenesis by downregulation of AGGF1. Conclusion: miR-372 downregulates AGGF1 expression and reduces angiogenesis.

Abstract:Objective:To explore whether and how the knockdown of Popdc2 with siRNA produced changes in the proliferative activity of neonatal rat cardiomyocytes. Methods:Postnatal of 0,7,14 day of Sprague Dawley rats cardiac tissue was prepared,qRT-PCR was performed to detect the Popdc2 relative mRNA expression level. Neonatal rat cardiomyocytes and fibroblast were prepared from the ventricles of Sprague Dawley rats aged 0~2 days,qRT-PCR was performed to detected Popdc family member mRNA expression level in cardiomyocytes and Popdc2 mRNA expression level in cardiomyocytes and fibroblast;negative control(NC)and Popdc2 small interference RNAs (si-Popdc2) were transferred into neonatal rat cardiomyocytes,EdU incorporation assay and Ki67 staining were used to detect cell proliferation,qRT-PCR was performed to detect the Popdc2,TBX20,TBX5,and Ki67 relative mRNA expression level,Western blot was used to test the total Akt and phosphorylation Akt protein expression level. Results:This study showed that Popdc2 mRNA expression level was the highest of Popdc family member in cardiomyocytes (P < 0.01). The expression was continuely increased after postnatal(P < 0.01),Popdc2 mRNA expression level was higher in cardiomyocytes compared with fibroblast(P < 0.05);EdU incorporation assay showed that knockdown of Popdc2 promoted cardiomyocytes DNA systhesis(P < 0.05),immune staining showed knockdown of Popdc2 increased the Ki67 position cardiomyocytes number (P < 0.05),qRT-PCR showed that knockdown of Popdc2 upregulated transcription factor TBX20(P < 0.01),TBX5(P < 0.05)),and proliferation protein Ki67(P < 0.05)mRNA expression level,Western blot showed that knockdown of Popdc2 significantly increased phosphorylation of Akt protein level,Akt308 (P < 0.05),Akt473 (P < 0.001). Conclusion:The present study demonstrated that knockdown of Popdc2 produced a significant increase in the proliferation of neonatal cardiomyocytes,and may via Akt phosphorylation and regulate cardiac transcription factor,suggesting that Popdc2 may become a therapeutic target for cardiac repair and heart regeneration.

Abstract:Objective:To detect the expression of miR-145 in non-small cell lung cancer(NSCLC) and explore it’s regulatory effect on N-cadherin in the invasion and metastasis of NSCLC. Methods:Real-Time PCR was performed to detect the expression of miR-145 and N-cadherin in 31 NSCLC tumor tissues. MiR-145 mimics was transiently transfected into SPC-A1 cells by lipofectamine method. RT-PCR and Western blot were used to detect the expression of N-cadherin. The invasion activity was detected using transwell assay. Results:MiR-145 expression was reduced significantly and N-cadherin expression was increased significantly in NSCLC tumor tissues,respectively. In addition,the expressions of miR-145 and N-cadherin were both closely correlated with lymph node metastasis. MiR-145 could significantly downregulate the expression of N-cadherin after transfection of mimics in SPC-A1 cells,and suppress invasion ability of cells. Conclusion:MiR-145 is downregulated in NSCLC,and may regulate the invasion and metastasis of NSCLC through targeting N-cadherin.

Abstract:Objective:To study the transfection and expression level of human NK4 gene in A549 cells by constructing NK4 of recombinant lentiviral vector, and observe the effect of NK4 on cell proliferation and apoptosis. Methods: The NK4 gene was cloned into lentiviral expression vector by recombining DNA technology. The recombinant plasmid was cotransfected with lentiviral packaged systems in 293T cells by lipofectin reagent to produce lentiviral particles. A549 cells were infected with the lentivirus, and the infection efficiency was observed under fluorescence microscope. Expression of NK4 gene and protein was identified by RT-PCR and Western blot, respectively. Three groups of cells were established, including the A549/NK4 group, the negative control group (A549/LV), and the blank control group (A549). Expression of c-met mRNA in the three groups of cells was examined by RT-PCR analysis. Through MTT colorimetric, we assayed the growth of the three groups of cells from the first day to the seventh day, and drew a growth curve to compare the proliferations of cells. The rates of apoptosis of the cells were detected by flow cytometry. Results: LV-NK4 transfected A549 cells expressed NK4, and the cells expressed less c-met than the blank and negative group. In MTT test, the A549/NK4 group cells grew slower than the other group from the fourth day (P < 0.05). With flow cytometry, the apoptosis rate of the A549/NK4 group was higher than the blank and negative control group. Conclusion: The NK4 recombinant lentiviral vector had been successfully constructed and effectively transfected A549 cells. NK4 can inhibit the proliferation and promote the apoptosis of A549 cells, the mechanism may be related to down-regulated c-met.

Abstract:Objective:To detect the expression and explore the role of miR-497/IGF-1R in hepatocelluar carcinoma (HCC) invasion and migration. Methods: The expressions of miR-497/IGF-1R in HCC samples and cell lines were detected by real-time PCR. Meanwhile, IGF-1R protein in HCC tissues and cell lines was assessed by immunohistochemistry and Western blot. In addition, the invasion and migration of HCC cells were analyzed by overexpressing or suppressing miR-497. Results: The expression of miR-497 was decreased in HCC samples compared with the adjacent non-cancer tissues, especially in HCC samples with vascular metastasis. The same results were observed in HCC cell line, the expression level of miR-497 decreased much more significantly in MHCC-97H than other cell lines. IGF-1R expression was significantly increased in HCC and HCC-derived cells. MiR-497 overexpression decreased the expression of IGF-1R and suppressed the invasion and migration of MHCC-97H. MiR-497 silenced SMMC-7721 cellular invasion and migration, which were enhanced with a boost in IGF-1R. Conclusion: This study indicates that miR-497 is downregulated in hepatocellular carcinoma, and miR-497 overexpression suppresses tumor cell invasion and migration with a decreased expression of IGF-1R. The study of miR-497 may provide a new therapeutic option for HCC.

Abstract:Objective:To investigate the signal pathway through which JMJD2B affected the malignant phenotype of human colorectal cancer cells. Methods: Human colorectal cancer cell lines HCT116 and SW1480 were interfered with siRNAs for silencing JMJD2B expression. The expression of ERK-MAPK signal pathway was detected by Western blotting, and cell proliferation was determined by CCK-8 assay, while cell cycle distribution and apoptosis were assessed by flow cytometry. Results: JMJD2B siRNA effectively and specifically inhibited the expression of JMJDB, which decreased ERK2 and its phosphorylation expression, and subsequently led to cell cycle arrest in G2/M or G0/G1 phase, increasing rates of cell apoptosis and significant cell proliferation inhibition (P < 0.05). Conclusion: Inhibition of histone demethylase JMJD2B restrained the malignant phenotype of human colorectal cancer cells via the inhibition of ERK-MAPK signal pathway transduction.

Abstract:Objective:To investigate whether lipopolysaccharide (LPS) combined with adenosine triphosphate (ATP) activates Nod-like receptor pyrin domain-containing protein 3(NLRP3) inflammasome in human pulmonary artery endothelial cells (HPAECs), and the underlying mechanism. Methods: HAPECs were stimulated by LPS with or without ATP to establish inflammation damage model. Cell vitality was assessed by cell counting kit-8. The levels of IL-1β and IL-18 in supernatant were analyzed by ELISA. The expressions of caspase-1, p-p38 and p-p65 were determined by Western blot. Reactive oxygen species (ROS) was detected by DCFH-DA fluorescent probe. Cell apoptosis was evaluated by annexin V and PI staining assay. Results: LPS alone had no effects on HPAECs. By combined with ATP, LPS significantly inhibited cell viability. The levels of IL-1β and IL-18 in supernatant, the expressions of caspase-1, p-p38 and p-p65 in cytoplasm, the concentrations of intracellular and extracellular ROS as well as cell apoptosis were up-regulated in HPAECs activated by LPS combined with ATP. These effects were inhibited by ROS scavenger N-acetylcysteine. Conclusion: High level ROS plays an important role in LPS combined with ATP-induced NLRP3 inflammasome activation as well as apoptosis of HPAECs.

Abstract:Objective:To investigate the reverse effect of astragaloside Ⅳ (As-Ⅳ) on angiotensin Ⅱ (Ang Ⅱ)-induced mitochondrial dysfunction of vascular smooth muscle cells (VSMCs) in rats. Methods: Cultured VSMCs were divided into the 24 h control group, the Ang Ⅱ treated for 24 h group, the 48 h control group, the Ang Ⅱ treated for 48 h group,and the As-Ⅳ treated group. After treatment, the 24 h control group and the Ang Ⅱ treated for 24 h group were tested for mitochondrial function by Extracellular Flux Analyzer and mitochondrial ATP production. The 48 h control group, the Ang Ⅱ treated for 48 h group,and the As-Ⅳ treated group were tested for mitochondrial function, mitochondrial ATP production, mitochondrial morphology by transmission electron microscope, and reactive oxygen species (ROS) production by confocal microscopy and Mn-SOD activity. Results: Compared with the 24 h controls group, oxygen consumption rates (OCRs) and mitochondrial ATP production decreased in the Ang Ⅱ treated for 24 h group (P ≤ 0.05); Compared with the 48 h controls group, the Ang Ⅱ treated for 48 h group showed a decrease of OCRs and mitochondrial ATP production (P ≤ 0.05), swollen and vacuolization of mitochondrial morphology with almost wash-out cristae, a decrease of Mn-SOD activity (P ≤ 0.05) and a increase of mtROS level (P ≤ 0.05). The As-Ⅳ treatment group showed significantly increased OCRs, mitochondrial ATP production (P ≤ 0.05) and Mn-SOD activity (P ≤ 0.05), decreased mtROS level (P ≤ 0.05), and reduced damage of mitochondrial morphology compared with the Ang Ⅱ treated for 24 h group. Conclusion: This study demonstrates that As-Ⅳ could reverse Ang Ⅱ induced mitochondrial dysfunction of VSMCs by enhancing Mn-SOD activity to decrease mtROS production, further alleviating the damage of mitochondrial morphology and increasing OCRs and mitochondrial ATP production.

Abstract:Objective:To investigate the inhibitory effects of mesenchymal stem cells (MSC) on hepatic fibrosis and activation degree of hepatic stellate cells (HSC) after transplantation. Methods: Ficoll-Hypaque density gradient centrifugation and adherent culture were performed to separate and purify bone marrow mesenchymal stem cells (BM-MSCs) from 4 months old SD rats. Liver fibrosis model of SD rats was induced by long-term intraperitoneal injection of low-dose of CCl4 for 8 weeks. A total of 18 rats were performed to make model, since 4 weeks after the modeling process, 9 of them were taken out to receive treatment of 6×106 MSCs for 4 weeks by tail vein injection, the remains were injected the same volume of saline without MSCs. The normal control group containing 9 rats were only given the same volume of saline injection for 4 weeks. ALT, AST, TBIL,and ALB levels of serum were determined by automatic biochemical analyzer every week from the start to the end of research in a total of 8. The localization and expression of alpha-smooth muscle actin (α-SMA), transforming growth factor beta 1 (TGF-β1), and collagen type Ⅰ (COL-Ⅰ) in liver tissues were analyzed by the immunohistochemical method. Density gradient centrifugation after situ perfusion and 326 nm of ultraviolet excitation together with α-SMA immunofluorescence staining were performed to isolate and identify HSC, respectively. The mRNA and protein expression levels of α-SMA and TGF-β1 in HSC were detected by qRT-PCR and Western blot, respectively. All above experiments were done at the end of the experiment at 8 weeks. Results: Compared with the model group, ALT, AST,and TBIL levels of serum; fibrosis and inflammation degree; α-SMA, TGF-β1,and COLⅠ expression levels in liver; the mRNA and protein expression levels of α-SMA and TGF-β1 in HSC were significantly reduced in the treatment group after MSCs transplantation. Conclusion: Liver fibrosis degree and liver function of SD rat were significantly reduced and improved after BM-MSC transplantation, respectively, which may be related to its inhibition of the activation level of HSC.

Abstract:Objective:To observe the effect of metformin on urinary nephrin excretion in type 2 diabetic model rats and investigate its protection of glomerular podocytes. Methods: Type 2 diabetes SD rats induced by high fat diet/ streptozotocin (HFD-STZ) were randomly divided into 3 groups: the diabetic model group, the metformin group, the glibenclamide group,and the normal control group. Blood glucose (BG), urine albumin (UALB) and nephrin excretion were monitored before and after the intervention, and glycosylated hemoglobin (HbA1c) was measured at the end of the study. Results: (1)BG and HbA1c levels of diabetic rats were significantly higher than those of normal group (P < 0.05); BG and HbA1c levels of the metformin and glyburide group were significantly lower than those of the type 2 diabetic model group (P < 0.05) at the end of the 4th and 8th week, but there were no significant differences between the two intervention groups. (2)At the end of the 4th and 8th week, UACR in all diabetic rats was significantly higher than that of the normal group (P < 0.05), which was significantly decreased in the metformin and glyburide group when compared with the type 2 diabetic model group (P < 0.05). There were no significant differences between the two intervention groups (P > 0.05) at the 4th week, but statistically differences were found at the 8th weeks (P < 0.05). (3)There were no significant differences of UNER among the 4 groups at the end of the 0th and 2nd weekend. At the end of the 4th and 8th week, UNER in the diabetic groups was significantly higher than that of the normal group (P < 0.05). UNER was significantly decreased in the metformin and glyburide group compared with the diabetic model group. The level of UNER in the metformin group was obviously lower than that of the glyburide group (P < 0.05). (4)Pearson correlation analysis showed that UNER was positively correlated with UACR(r = 0.846, P < 0.05). Conclusion: Metformin can decrease the excretion of urinary nephrin and provide some protection for glomerular podocyte in diabetic rats, which is not completely dependent on its hypoglycemic effect.

Abstract:Objective:To explore the effects and mechanisms of E2 on cognitive disorder induced by chronic mild stress (CMS) of depressive female ovariectomized (OVX) mice. Methods:We used CMS as the animal model for stress-induced depression,and detected plasma corticosterone of normal and depressive mice. Then,we examined whether 7 days treatment using E2 could ameliorate the effects of CMS on plasma E2 in female OVX mice. Morris water maze was performed to test spatial learning and memory ability of mice after last treatment. At the same time,we analyzed the mRNA and protein expression of nitric oxide synthase (nNOS) in hippocampus as well as positive nNOS neurons of dentate gyrus. Primary cultured hippocampal neurons from female embryo were adopted,the mRNA and protein expressions of nNOS were detected in neurons exposed to corticosterone (CORT) or CORT combined with E2 for 24 h. In addition,we detected the level of extracellular signal-regulated kinase (ERK) phosphorylation in neurons exposed to E2 for 24 h. Results:Plasma CORT of female and male mice was significantly increased after CMS. Ectogenic supplement of E2 reversed the decrease of plasma E2 and spatial learning and memory deficit,as well as the decrease of hippocampal nNOS mRNA and protein expression induced by CMS in female OVX mice. In vitro,E2 reversed nNOS mRNA and protein expression induced by corticosterone in primary cultured cortical hippocampal neurons from female embryo. In addition,E2 significantly up-regulated ERK phosphorylation in the hippocampal neurons from female embryo. Conclusion:E2 could reverse the spatial learning and memory deficits and abnormal hippocampal nNOS expression induced by chronic stress in female OVX mice. The hippocampal neuronal ERK phosphorylation is involved in the effects of E2.

Abstract:Objective:To investigate the expression of miR-155 in papillary thyroid cancer(PTC) tissue and plasma,and to evaluate the significance of plasma miR-155 level as a biomarker for PTC patients. Methods:Real-time fluorescence quantitative polymerase chain reaction was used to detect the change of miR-155 in tumor tissues and plasma of 52 PTC cases and 32 nodular goiter cases,as well as in plasma of 30 controls. Receiver operating characteristic(ROC) curves were drawn to evaluate the diagnostic threshold as well as the correlation between plasma miR-155 expression and tumorous tissue in PTC patients. Results:The average of miR-155 expression in PTC tumorous tissues and nodular goiter tissues was 8.43 ± 6.14 and 1.14 ± 0.41 respectively. The relative level of miR-155 in plasma of PTC and nodular goiter was 3.35 ± 1.85 and 1.41 ± 0.24,respectively. ROC curves for miR-155 to distinguish PTC and the control group yielded an AUC of 0.932(95%CI:0.851~0.970)(P < 0.001)and nodular goiter yielded an AUC of 0.887 (95%CI:0.811~0.961)(P < 0.001). There was a positive correlation of miR-155 expression between plasma and tumorous tissue in PTC patients (r=0.589,P < 0.000 1). However,there was no relevance between the expression of plasma miR-155 and the clinical characteristics of the study population(P > 0.05). Conclusion:miR-155 expression is upregulated in patients with PTC. Plasma miR-155 may be used as a noninvasive biomarker for the prediction of papillary thyroid cancer.

Abstract:Objective:To investigate the expression of CD90 and its clinical significance in gastric cancer tissues. Methods: The expressions of CD90 in gastric cancer tissues, adjacent tissues and chronic gastritis tissues were detected by immunohistochemical staining to analyze their relationship with clinical pathological features and prognosis in gastric cancer. Result: The positive expression rate of CD90 was 66.7%(64/96)in gastric cancer tissues, 15.6%(15/96)in adjacent normal tissues, and 15.0% (3/20) in chronic gastritis tissues, with a statistically significant difference (P < 0.01). The expression of CD90 in gastric cancer was associated with the TNM stage (P=0.014, P T=0.02,PN=0.017 and PM =0.045). Multivariate survival analysis indicated that patients with high expression of CD90 had poorer 5-year overall survival (P < 0.05). Conclusion: CD90 is associated with the invasion and metastasis of gastric cancer, and may be helpful in providing a novel molecular therapeutictarget and evaluating prognosis of gastric cancer.

Abstract:[Abstract] Objective:To investigate the relation between mRNA expression of CCAT-1 in the peripheral blood, clinicopathological features and prognosis of patients with colorectal carcinoma. Methods: Real-time quantitative polymerase chain reaction (qPCR) was performed to detect CCAT-1 mRNA expression levels in patients with colorectal carcinoma (60 cases) and colorectal adenoma (30 cases) as well as healthy volunteers (30 cases). The value of CCAT-1 in diagnosis of colorectal carcinoma was evaluated by ROC curve, diagnosis threshold of CCAT-1 mRNA level in colorectal carcinoma was determined by Youden index. Bivariate correlation analysis was performed to analyze the correlation of the expression levels of CCAT-1 and clinicopathological features in patients with colorectal carcinoma. Kaplan-Meier survival curve was performed to analyze the correlation between CCAT-1 expression and survival of patients with colorectal carcinoma. Results: CCAT-1 mRNA expression levels in patients with colorectal carcinoma were significantly higher than those in patients with adenoma (P < 0.01) and healthy volunteers (P < 0.01). CCAT-1 mRNA expression levels were positively correlated with the diameters of tumor, grade of differentiation, invasion depth of primary tumor, the number of lymph node and distant metastasis (P < 0.05) and TNM stage (P < 0.01), and were negatively correlated with survival time (P < 0.05). The survival time of patients with colorectal carcinoma with higher-level CCAT-1 expression was significantly shorter than that of the lower-level group. Conclusion: CCAT-1 can be considered as a valuable marker for early screening and prognosis assessment of colorectal carcinoma.

Abstract:Objective:To compare the expression of serum lipid among ovarian benign epithelial tumor,early and late malignant epithelial tumor,and explore the possible role of blood lipids changes in the occurrence and development of epithelial ovarian tumor. Methods:Total of 200 patients with ovarian epithelial tumor was randomly collected. According to the pathological results after operation,these patients were divided into the benign group with 100 cases,early malignant group and advanced malignant group with 50 cases in each group. Serum lipids were collected,and total cholesterol (TC),triglyceride (TG),high density lipoprotein cholesterol (HDL-c),low density lipoprotein cholesterol (LDL-c),lipoprotein (a) were detected. Results:TC and HDL-c levels of malignant group were significantly lower than those in benign group(both P < 0.05). The LP (a) levels of malignant group preferred to be lower than the benign group increased (P=0.061) while the LDL-c showed a decreasing trend than those of the benign group (P=0.061). One-Way ANOVA analysis showed that LP,TC,HDL-c,and LDL-c among the three groups had significant difference(P < 0.05). Furthermore,HDL-c level of benign group was lower than that of the early group significantly (P < 0.001). TC,HDL-c,LDL-c in advanced group decreased significantly than thoses in benign group (P < 0.05),while the LP (a) level of advanced group was higher than that of the benign group (P=0.013). The advanced group and early group had no significant difference on the indicators,and only LP (a) were increased potentially (P=0.052). Logistic regression analysis showed that the level of HDL-c,LDL-c,and LP (a) was related with the development of ovarian tumor. Conclusion:HDL-c,LDL-c,and LP (a) were associated with the degree of development of ovarian epithelial tumors,the more advanced the tumor was,the lower level of HDL-c and LDL-c while the higher level of LP (a) was.

Abstract:Objective:To explore the incubation period and the influencing factors of HIV infection among men who have sex with men(MSM) in Jiangsu. Methods:An ambispective cohort study was conducted to collect a HIV infection and AIDS cases in two cities in Jiangsu Province with certain time mark of infected and onset. The average incubation period was calculated by Kaplan-Meier product-limited method. Cox regression model was used to explore the influencing factors. Results:The average incubation period of HIV infection was(46.129 ± 2.795) months,95%CI was 40.651-51.606 months,among MSM with HIV/AIDS through homosexual transmission in Jiangsu. COX proportional hazards regression model showed that higher CD4 counts at baseline and 6 months after diagnosis were the protective factors of incubation period. Conclusion:Incubation period of homosexual transmission AIDS may be lower than that of other previously reported data. The present study suggested that it was important for public halth service institutes to provide proper service for the early treatment of MSM infectors to prolong their survival time and to improve their survival quality.