Objective To investigate the role of the pituitary tumor-transforming gene 3(PTTG3P)/microRNA-146a-3p(miR-146a-3p)/pituitary tumor-transforming gene 1(PTTG1)pathway in the castration-resistant transformation of prostate cancer(PCa).Methods Real-time quantitative PCR(qPCR)was used to detect the differences in PTTG3P mRNA expression between androgen-dependent PCa cells LNCaP and cas-tration-resistant PCa(CRPC)cells PC3 and DU145,as well as between primary PCa tissues and CRPC tis-sues.PTTG3P overexpression vectors and PTTG1 interference vectors(shPTTG1)were constructed and transfected into LNCaP cells.The cells were divided into the LNCaP group(control),LNCaP/PTTG3P group(transfected with PTTG3P overexpression vector),and LNCaP/PTTG3P/shPTTG group(transfected with PTTG3P overexpression vector and shPTTG).Under castrated conditions,qPCR was used to detect the ex-pression levels of PTTG3P mRNA and miR-146a-3p in each group of LNCaP cells.Cell viability assays in vitro were conducted to assess the growth status of each group of LNCaP cells,colony formation assays were performed to evaluate the tumorigenic ability of each group of LNCaP cells,and Western blotting was used to detect PTTG1 protein expression levels in each group of LNCaP cells.To investigate the role of miR-146a-3p in the PTTG3P/PTTG1 pathway,LNCaP cells were transfected with a miR-146a-3p mimic to establish a miR-146a-3p mimic cell line,and then transfected with the PTTG3P overexpression plasmid to create a miR-146a-3p mimic+PTTG3P cell line.A luciferase reporter assay was conducted to verify the relationship between miR-146a-3p and PTTG1.Results Compared with androgen-dependent PCa cells LNCaP and treatment-naive PCa tissues,PTTG3P mRNA expression was higher in CRPC cells PC3,DU145,and tissues(P<0.05).Un-der castration conditions,the cell viability and colony formation ability of the LNCaP/PTTG3P group were higher than those of the LNCaP group(P<0.05);cell viability and colony formation ability in the LNCaP/PTTG3P/shPTTG group were lower than those in the LNCaP/PTTG3P group(P<0.05);miR-146a-3p ex-pression was lower in CRPC than in treatment-naive PCa tissues(P<0.05).Overexpression of miR-146a-3p inhibited PTTG1 expression in LNCaP cells,and overexpression of PTTG3P reversed this effect(P<0.05).Conclusion Overexpression of PTTG3P promotes the progression of PCa to CRPC through the miR-146a-3p/PTTG1 pathway.The mechanism may involve PTTG3P competitively binding to miR-146a-3p,thereby upreg-ulating PTTG1 expression.

Objective : To investigate the effects of RO or incubation with cholesterol ( CH) on the differentiation and apoptosis of KCs. Methods : Ca2 + ( 1. 8 mmol/L) was added to KCs for 1 day after co - culture of RO alone or combined with CH in KCs for different time. The expression of Involucrin (INV) and Loricrin in KCs was analyzed by Western blot. After co⁃culture of RO alone or combination with CH in KCs for different time , the apoptotic changes of KCs cells were detected by flow cytometry and the expression of apoptotic proteins Bax and Bcl⁃2 were verified by Western blot. Results : RO down⁃regulated the expression of Ca2 + induced differentiation marker protein INV , but weakly inhibited the expression of Loricrin , while CH showed no antagonistic effect on RO. RO induced apoptosis of KCs cells in a time dependent manner. CH could antagonize the apoptotic effect of RO on KCs ; the expression of Bcl⁃2 and Bax was inhibited when RO was applied alone , CH could partially antagonize the inhibition effect of RO on Bcl⁃2 expression , but had no significant effect on Bax; however, RO reduced the ratio of Bcl⁃2/Bax in a time⁃dependent manner, and CH partially weakened the effect of RO on the ratio of Bcl⁃2/Bax. Conclusion RO may inhibit KCs differentiation and induce KCs cell apoptosis by down⁃regulating the expression of Loricrin and Bcl⁃2.

Objective To discuss the research status and hotspots related to breeding, planting, harvest, processing and storage of Lycium L. in China. Methods Relevant literature about breeding, planting, harvest, processing and storage of Lycium L. in CNKI from January 2004 to December 2013 was retrieved by computers. CiteSpaceⅡ was introduced to carry out key word analysis, high-frequency key word obtaining, co-occurrence network of high-frequency key words, and dendrogram of high-frequency words. Results Totally 759 articles were included. Key words about breeding were “genetic diversity”, “male sterile”, “its sequence”, “callus issue”, and“anther culture”. Key words about planting were“output”,“quality”,“hard twig cuttage”,“irrigation amount”. Key words about harvesting and processing were“picking machine of Lycium L.”,“drying kiln of Lycium L.”,“hot air drying”, and “combined drying”. Key words about storage were “pesticide residue”, “heavy metal”, and“organophosphorus pesticide”. Co-occurrence network of high-frequency key words showed that the research hotspots were pesticide residue, test of heavy metal and the storage of fresh fruits. Dendrogram of high-frequency key words showed that the high-frequency key words were “package”, “refreshment”, and “lycium barbarum polysaccharide”. Conclusion The research hotspots of planting of Lycium L. are planting skills effecting the output and quality of Lycium L.; In the field of harvesting and processing of Lycium L., design and research of picking machine has replaced traditional manual picking. Modern hot air drying has already replaced traditional drying in the sun or drying skills; In the aspect of storage of Lycium L., the study on the refreshment of Lycium L. has attached attention.

Objective_To explore the influence and mechanism of IL-31 on the expression of VEGF, EGF and EG-FR in 16HBE cells.Methods_16HBE cells were cultured and treated with IL-31 with or without SB203580 or SP600125, real-time PCR and Western blot were applied to determine the mRNA and protein expression of VEGF, EGF and EGFR respectively.Meanwhile, Western blot was used to examine the changes of P38 MAPK and JNK signaling pathways.Results_Compared with control group, the mRNA expression of VEGF, EGF and EGFR was increased markedly under the stimulation of IL-31 ( P<0.01 ) , the expression of p-P38 MAPK and p-JNK signifi-cantly increased ( P<0.01) .Compared with IL-31 group, the expression of p-P38 MAPK significantly decreased in IL-31 combined with SB203580 or SB203580 group ( P <0.01 ) , while the expression of p-JNK markedly decreased in IL-31 combined with SP600125 or SP600125 group( P<0.01) .Compared with IL-31 group, the expression of VEGF was significantly decreased in IL-31 combined with SB203580 or SP600125 group ( P <0.01 ) , while the expression of EGF and EGFR was markedly declined in IL-31 combined with SB203580 group ( P<0.01 ) .Conclusions_IL-31 may up-regulate the expression of VEGF through activating P38 MAPK and JNK signaling pathways and up-regulate the expression of EGF and EGFR through activating P38 MAPK signaling path-way in16 HBE cells.

Purpose To investigate the effect of interleukin-10(IL-10)on IL-15mRNA and IL-6mRNA in Hela cells induced by lipopolysaccharide(LPS)and to analyze their activiated signal transduction pathways.Methods Extracted total RNA and total proteins of cultured Hela cells,which were treated with different concentrations of LPS,or IL-10 alone or in combined use,were to analyze the levels of IL-15mRNA and IL-6mRNA using RT-PCR and to analyze the expression of signal transduction pathway proteins using Western blot.Results RT-PCR indicated that expression of IL-15mRNA and IL-6mRNA in Hela cells strikingly increased after 12 h using 1 ng-10μg LPS(P＜0.01 vs control),which had dose-dependence and achieved peak value using 100 ng/mL.During 0-24 h,expression of IL-15mRNA and IL-6mRNA strikingly increased with time changing(P＜0.01 vs control),which had time-dependence and achieved peak value at 12 h.Expression of IL-15mRNA and IL-6mRNA had no conspicuous difference in Hela cells treated with IL-10(10 ng/mL)alone(P＞0.05 vs control).Different concentrations of IL-10 1,10,100 ns/mL)markedly downregnlated expression of IL-15mRNA and IL-6mRNA in Hela cells induced by LPS.Furthermore,the effect of inhibition will be more obvious with dose increasing.Western blot indicated that LPS upregulated expression of IL-15mRNA and IL-6mRNA by phosphorylation of PI3K/AKT and ERK1/2.IL-10 blocked phosphorylation of AKT,but could not affect phosphorylation of ERK1/2.Conclusion IL-10 downregulated the expression of inflammatory cytokines IL-15 and 1L-6 induced by LPS,which may correlate with the fact that phosphorylation of AKT was blcoked by IL-10.Therefore,IL-10 may be used to prevent and treat some clincal infective diseases.

Objective To investigate the plasma level of SDF-1a in patients with breast cancer after modified radical mastectomy and chemotherapy, and to evaluate the value of serum SDF-1a half-life for predicting breast cancer recurrence and metastasis. The correlation of SDF-1 a half-life and breast cancer recurrence and metastasis after treatment were retrospectively analyzed. Methods Serum chemokine SDF-1a of 112 cases of breast cancer were detected before and after modified radical surgery, and 1 day beforeeach chemotherapy session. SDF-1a levels and the dynamic changes in the process were observed and calculated. Results In 85 cases with no recurrence and metastasis the plasma level of SDF-1 a decreased rapidly to normal level ,while that in 27 cases with recurrence and metastasis was on high level with the halflife of SDF-1a being longer than that in no recurrence group(P ＜0. 01 ). Taking SDF-1a half-life ≥14 d as cut off point to predict breast cancer recurrence and metastasis after treatment, the sensitivity is 81.5%,specificity is 70. 6 %, and accuracy is 73.2%. Conclusions Serum SDF-1a half-life is a valuable marker in predicting postoperative breast cancer recurrence and metastasis.

Objective To investigate the clinical and laboratory characteristics of anticentromere antibody (ACA)and anti-SSA antibody expressions in patients with Primary Sj(o)gren's Syndrome (PSS). Methods Twelve PSS patients with ACA positive but SSA negative(ACA PSS)and 19 PSS patients with SSA positive but ACA negative(SSA PSS)were enrolled into the study and classified into two groups. We compared the age,laboratory data,occurrence of Raynaud's phenomenon(RP),and histological changes in minor labial salivary glands biopsies of the patients from two group. Results The mean age of the ACA PSS group(68.4 ± 7.9)years was significantly higher than that of the SSA PSS(54. 6 ± 16. 2)years group(P ＜ 0. 05). Serum IgG level of ACA PSS group(17. 89 ±4. 08)g/L was close to the normal range,which was significantly lower than that of SSA PSS(27.90 ±6. 72)(P ＜0. 01). Leukocytopenia was less frequently observed in ACA PSS than in SSA PSS(P ＜ 0. 05),the difference between two groups was statistically significant. We also found more frequent RP in the ACA PSS group than SSA PSS group(P ＜ 0. 05). Conclusions Our data confirm that ACA positive PSS differs from SSA positive PSS at several clinical respects and laboratorial examinations.

Purpose To explore the antiviral effect of interleukin 29(IL-29) on hepatitis B virus in vitro.Methods To study the antiviral effect of IL-29 against hepatitis B virus by the amount of HBV mRNA detected .Through the quantity of mRNA translated from genes of MxA,2′,5′-OAS,PKR and RNase L as well as the signal pathway induced by IL-29,we used RT-PCR and Western blot to discuss the anti-hepatitis B virus mechanism which was stimulated by IL-29.Results The amount of HBV mRNA in HepG2.2.15 cells was reduced by stimulation of IL-29.The expression of MxA and 2′,5′-OAS was up-regulated,as well as P-ERK and P-AKT were activated by IL-29.Conclusion These findings showed that IL-29 had obvious antiviral activity towards HBV in HepG2.2.15 cells.

In ischemic hypertrophic myocardium, contractile dysfunction can be attributed to the decreased calcium induced calcium release (CICR) in cytoplasm. This study aimed to investigate the electrophysiological properties and the expression of L calcium channel subunits in post-MI myocardium. The ischemic heart remodeling model was established in SD rats. The expressions of calcium channel subunits were determined by realtime RT-PCR. Whole cell patch clamp was used to record the electrophysiological properties of L calcium channel. The results showed that the L calcium channel agonist Bayk 8644 induced the significantly decreased CICR in the rat cardiomyocyte 6weeks after myocardial infarction (MI). In the post-MI cardiomyocytes, the amplitude of ICaL decreased dramatically and the inactivation curve of the current shifted to more negative potential. At mRNA level, the expression of the calcium channel alphalc, beta2c subunits decreased dramatically in the ventricle of post-MI rats. The expression of alpha2/delta subunit, however, remained constant.It is concluded that the abnormal expression of the L calcium channel subunits in post-MI cardiomyocytes contributes to the ICaL decrease at early stage of the ischemic remodeling in cardiomyocytes,which leads to the decreased CICR in the cell and contractile dysfunction of myocardium.

In ischemic hypertrophic myocardium, contractile dysfunction can be attributed to the decreased calcium induced calcium release (CICR) in cytoplasm. This study aimed to investigate the electrophysiological properties and the expression of L calcium channel subunits in post-MI myocardium. The ischemic heart remodeling model was established in SD rats. The expressions of calcium channel subunits were determined by realtime RT-PCR. Whole cell patch clamp was used to record the electrophysiological properties of L calcium channel. The results showed that the L calcium channel agonist Bayk 8644 induced the significantly decreased CICR in the rat cardiomyocyte 6 weeks after myocardial infarction (MI). In the post-MI cardiomyocytes, the amplitude of I(CaL) decreased dramatically and the inactivation curve of the current shifted to more negative potential. At mRNA level, the expression of the calcium channel alpha1c, beta2c subunits decreased dramatically in the ventricle of post-MI rats. The expression of alpha2/delta subunit, however, remained constant. It is concluded that the abnormal expression of the L calcium channel subunits in post-MI cardiomyocytes contributes to the ICaL decrease at early stage of the ischemic remodeling in cardiomyocytes, which leads to the decreased CICR in the cell and contractile dysfunction of myocardium.