影响香芋不定芽增殖因素探讨

培养基中的６－ＢＡ、蔗糖浓度以及培养的光照强度等因素对香芋茎尖不定芽增殖的影响试验结果表明，６－ＢＡ浓度为５ｍｇ／Ｌ、蔗糖浓度为３％、光照强度为５００Ｌｘ时，不定芽的增殖倍数达到最大，为５．７倍。

荸荠茎尖组织培养增殖影响因素分析

以影响荸荠茎尖组织培养增殖的三要素6-BA、糖和pH值进行实验研究,分别对处理间和对照的芽苗增殖数进行统计和方差分析。实验结果表明:在MS液体培养基中,添加6-BA质量浓度为1.0 mg.L-1、NAA质量浓度为0.1 mg.L-1、糖质量浓度为65 g.L-1,pH值4.7～5.2,培养30 d荸荠茎尖增殖的芽苗数最多,叶状茎健壮。

影响扁桃组培快繁的因素研究

以扁桃品种莎车 2 4号为材料 ,研究了添加在培养基中的不同激素组成、糖源、糖浓度、培养条件等因子对扁桃增殖快繁的影响。结果表明 ,1 / 2MS +6 -BA 0 .5mg/L +IBA 0 .2mg/L +GA30 .0 5mg/L ,蔗糖2 0 g/L ,培养温度 2 4～ 2 6℃ ,光强 1 50 0～ 2 0 0 0lx ,每天光照 1 6小时 ,培养基pH值 6 .2 ,对增殖分化最有利 ,不定芽分化率 94 %。

Akt1/p27^(kip1) Pathway Mediates Inhibition of LXA_4 on TNF-α-induced Proliferation of Rat Mesangial Cells

Objective:To examine whether lipoxin A 4(LXA 4) has an inhibitory effect on tumor necrosis factor-α(TNF-α)-induced proliferation of glomerular mesangial cells of rat, and explore the molecular mechanisms of signal pathway in LXA 4 actions. Methods: Glomerular mesangial cells of rat were cultured and treated with TNF-α(10 ng/ml), with or without preincubation with LXA 4 at different concentrations. Cell proliferation was evaluated by monotetrazolium (MTT) colorimetric assay. The expression of cyclin E mRNA was measured by RT-PCR. Phosphorylated Akt1(Thr308) and p27 kip1 were analyzed by Western blotting. Results: TNF-α-stimulated proliferation of mesangial cells was inhibited by LXA 4 in a dose-dependent manner. The marked increments in cyclin E mRNA expression induced by TNF-α during proliferation of mesangial cells were down-regulated by LXA 4. Threonine phosphorylated Akt1 proteins at 308 site stimulated by TNF-α was reduced by LXA 4. TNF-α-induced decrements in expression of p27 kip1 proteins was ameliorated by LXA 4 in a dose-dependent manner. Conclusion: TNF-α-induced proliferation of rat mesangial cells can be inhibited by TXA 4 through the mechanism of Akt 1/p27 kip1 pathway-dependent signal transduction.

TSPAN1 protein expression:A significant prognostic indicator for patients with colorectal adenocarcinoma

AIM:To determine if TSPAN1 overexpression is associated with clinicopathological and prognostic factors in human colorectal adenocarcinoma.METHODS:Total RNA was extracted in 20 human adenocarcinoma tissues for TSPAN1 mRNA assay by RT-PCR.Eighty-eight specimens of human colorectal adenocarcinoma were surgically removed.TSPAN1 protein levels in cancer tissues were determined by immunohistochemistry using a polyclonal antibody against self-prepared TSPAN1.The correlation between TSPAN1 expression and the clinicopathological factors and the overall survival rate was analyzed by univariate and multivariate assay.RESULTS:TSPAN1 mRNA was detected in 90.0%(18/20) of cancerous tissues.The light density of TSPAN1 mRNA expression levels was 0.89 ± 0.30 in adenocarcinoma by gel-image system.TSPAN1 protein expression was detected in 78.41%(69/88) and weakly expressed in 40% normal colorectal tissues.There were significant differences between colorectal adenocarcinoma and normal control epithelium(P < 0.05).TSPAN1 protein expression in colorectal cancerous tissue was significantly correlated with the histological grade,cell expression PCNA,lymph nodal metastasis and TNM staging of the disease.Patients with TSPAN1 protein overexpression had a significantly shorter survival period than that in patients with TSPAN1 protein negative or weak expression,respectively(P < 0.05).Furthermore,by multivariate analysis,TSPAN1 protein expression demonstrated an independent prognostic factor for human colorectal cancers(P < 0.05,relative risk 0.755;95% confidence interval 0.302-1.208).CONCLUSION:The expression of TSPAN1 gene is increased in colorectal carcinoma,suggesting that TSPAN1 might serve as an independent prognostic factor for the colorectal adenocarcinoma patients.

Mast cell density and the context of clinicopathological parameters and expression of p185,estrogen receptor,and proliferating cell nuclear antigen in gastric carcinoma

AIM:To investigate the relationship between the mast cell density(MCD)and the context of clinicopathological parameters and expression of p185,estrogen receptor(ER), and proliferating cell nuclear antigen(PCNA)in gastric carcinoma. METHODS:Mast cell,p185,ER,and PCNA were detected using immunohistochemical S-P labeling method.Mast cell was counted in tissue of gastric carcinoma and regional lymph nodes respectively,and involved lymph nodes(ILN)were examined as usual. RESULTS:MCD was significantly related to both age and depth of penetration(x^2=4.688,P<0.05 for age and x^2=9.350, P<0.01 for depth of penetration)between MCD>21/0.03 mm^2 and MCD≤21/0.03 mm^2 in 100 patients;MCD in 1-6 ILN group patients was significantly higher than that in 7-15 ILN or>15 ILN group patients(u=6.881,8.055,P<0.01); There were significant differences intergroup in positive expression rate of p185,ER and PCNA between MCD>21/ 0.03 mm^2 and MCD≤21/0.03 mm^2 in 100 patients. CONCLUSION:Mast cell may have effect on inhibiting invasive growth of tumor,especially in the aged patients; The number of mast cells,in certain degree,may predicate the number of involved lymph nodes,which is valuable for assessment of prognosis;MCD was related to the expression of p185,ER,and PCNA in gastric carcinoma.It suggests that mast cell accumulation may inhibit the proliferation and the dissemination of the gastric carcinoma. INTRODUCTION Recently,many studies have reported on the association of mast cell with various tumorst.In several malignancies,mast cell has been found to correlate with growth,penetration and prognosis of tumor.Therefore,our study was undertaken to investigate the relationship between the mast cell density (MCD)and the context of clinicopathological parameters and expression of p 185,estrogen receptor(ER),and proliferating cell nuclear antigen(PCNA)in gastric carcinoma.

Effects of Bradykinin on the Expression of Interleukin-6 in C6 Glioma Cells

OBJECTIVE There is a close correlation between interleukin-6 （IL-6） and malignant proliferation of gliomas. We investigated the effect of bradykinin on the expression of IL-6 in C6 glioma cells. METHODS Semi-quantitive RT-PCR and radioimmunoassay were used to examine the effect of bradykinin on the expression of IL-6 in C6 glioma cells and on the level of IL-6 in the culture medium. RESULTS Using semi-quantitive RT-PCR, the expression of IL-6 mRNA was examined in C6 glioma cells at 0, 5, 10,15, 30, 60 rain following addition of 1μmol/L bradykinin. There was no statistical difference in expression of IL-6 mRNA between the treatment and control groups （P〉0.05） and IL-6 was not detected in the cell culture medium. CONCLUSION Within an hour, IL-6 expression in C6 glioma cells is not induced by bradykinin, suggesting that its clinical application may be useful as a potential therapeutic agent for tumors of the central nervous system .

Curcumin suppresses PPARδ expression and related genes in HT-29 cells

AIM:To investigate the effects of curcumin on the expression of peroxisome proliferator-activated receptorδ(PPARδ)and related genes in HT-29 cells. METHODS:HT-29 cells were treated with curcumin (0-80μmol/L)for 24 h.The effects of curcumin on the morphology of HT-29 cells were studied by Hoechst 33342 staining.The activity of caspase-3 was determined using DEVD-p NA as substrate.The levels of peroxisome PPARδ,14-3-3εand vascular endothelial growth factor(VEGF)in HT-29 cells were determined by Western blotting analysis and their mRNA expression was determined by real-time quantitative RT-PCR. RESULTS:Treatment with 10-80μmol/L curcumin induced typical features of apoptosis and activated the caspase-3 in HT-29 cells.The expression of PPARδ, 14-3-3εand VEGF was reduced and the activity of β-catenin/Tcf-4 signaling was inhibited by curcumin treatment. CONCLUSION:Curcumin can induce apoptosis of HT-29 cells and down-regulate the expression of PPARδ,14-3-3εand VEGF in HT-29.