‘糯米糍’荔枝碳素营养储备动态与坐果的关系

 以10～12年生的‘糯米糍’荔枝(Litchi chinensis Sonn. ) 为材料, 研究了高产树(60～65 kg·株^{- 1} ) 和低产树(5～10 kg·株^{- 1} ) 不同部位(叶片、各级枝条和主干) 碳素营养储备(淀粉) 的差异及季节动态; 分析了不同果实发育阶段树体碳素营养水平与坐果率的关系。结果表明, 果实成熟时高产树各部位的淀粉含量均低于低产树, 而可溶性糖含量高于低产树。果实采收后, 低产树早于高产树抽发新梢。入冬季前(11月底前) , 低产树和高产树分别抽发了3次和2次秋梢。7～11月秋梢生长发育期间, 高产树和低产树均无显著淀粉积累, 11月中旬以后枝梢生长停滞期间, 各部位, 尤其是4 cm直径以内的枝条大量积累淀粉, 在花穗发育前达到高峰。之后, 随花穗发育、开花及坐果而持续降低。高产树和低产树各部位淀粉高峰并无明显差异, 表明坐果量对树体碳素营养储备的累积并无明显的长期影响。叶片、主枝和主干积累的淀粉含量较低, 总体相对稳定; 而4 cm直径以下的枝梢淀粉含量变化剧烈, 说明这些枝梢是更为活跃的碳素储备库。本研究还表明, 坐果早期(花后3周内) 枝条(2 cm直径) 的淀粉含量与该枝条上最终坐果率呈显著正相关, 而果实发育中期(花后8周) 枝条淀粉含量与坐果率无关, 说明早期果实发 育一定程度依赖树体碳素营养储备, 而中后期果实发育几乎不依赖树体储备。     

茄子离体叶片光系统Ⅱ的冷激胁迫效应及热力学分析

 以耐冷性较强的短把黑圆茄和耐热性较强的黑帅圆茄为试材,经冷激胁迫后采用植物效率仪PEA,进行快速叶绿素荧光参数测定,并利用最大光化学效率Fv/F m和活性中心RC/CSo的标准状态变性自由能变△GD进行PSⅡ冷稳定性的热力学分析。随着冷激胁迫温度的降低和时间的延长,PSⅡ的Fv/Fm、实际光化学效率ΔF/Fm′、RC/CSo呈"S"型下降趋势;单位反应中心DIo/RC和非光化学猝灭qN呈"S"型上升趋势;综合分析反映出冷激胁迫下PSⅡ反应中心的可逆失活和依赖于叶黄素循环的热耗散的双重机制在保护PSⅡ防止光抑制中起到重要作用。另外,通过两品种间PSⅡ行为差异,引入了两组新的参数作为便于直观比较冷胁迫的评价指标。黑帅圆茄Fv/Fm、ΔF/Fm＇的半衰温度T1/2和t1/2值分别高于短把黑圆茄1.4 ℃和0.8 ℃。茄子叶片Fv/Fm和RC/CSo的△GD随着冷激胁迫温度的降低而减少呈瀑布型的下降趋势。黑帅圆茄的△GD值和变性中点温度Tm都低于短把黑圆茄。它们均反映出黑帅圆茄的耐冷性低于短把黑圆茄。     

基于计算机视觉技术的番茄叶片叶绿素含量的检测

 研究利用计算机视觉技术快速测定叶绿素含量的方法,建立了根据番茄叶片颜色特征确定其叶绿素含量的一元二次拟合模型。在计算机视觉图像采集系统中采集番茄叶片图像,利用MATLAB图像处理工具提取图像的颜色特征参数,对颜色特征参数和番茄功能叶叶绿素含量做相关分析,建立回归模型。结果表明：RGB颜色系统的R/G、(G-R)/(G+R)、G-R、色度坐标r、r-g及HIS颜色系统的H值均与叶绿素含量呈极显著非线性相关性,可用于测定番茄叶片叶绿素含量。从建立的6组模型中筛选出拟合度较高的3组模型进行检验,预测误差在0～22.22%之间。用预测精度最高的G-R颜色特征预测叶绿素含量的模型为Chl.a = 0.0926 + 0.1208 (G-R) - 0.0009 (G-R)²,Chl b = - 0.0252 + 0.0397 (G-R) - 0.0003 (G-R)²和Chl.(a+b) = 0.1271 + 0.1600 (G-R) - 0.0011 (G-R)²。     

黄金树花器官发生及发育的形态观察

利用普通光学显微镜和扫描电镜技术对黄金树花器官的发生及发育过程进行了观察.结果显示:(1)黄金树花器官的形态发生及发育过程集中于3月下旬-5月上旬;(2)花原基分化形成花的整个过程符合一般的分化顺序:花萼原基-花冠原基-雄蕊原基-雌蕊原基,且各原基在分化顺序上存在交叉;(3)花药及胚珠的发育与花器官的形态发生之间有明显的连续性,当花蕾直径为3.0 mm左右时花粉母细胞及完整的花粉囊壁形成,直径达到3.5 mm左右时胚珠中出现孢原细胞的分化,它直接起大孢子母细胞的功能.     

Impact of serial activation of embryonic pax2 and WT1 genes on transdifferentiation of renal tubular epithelial cells

AIM: To investigate the mechanisms of transdifferentiation of renal tubular epithelial cells by the observation of serial activation of embryonic pax2 and WT1 genes in chronic renal failure model of 5/6 nephrectomized injury. METHODS: Embryo of mice, cultured renal tubule cells and chronic renal failure rat model of 5/6 nephrectomized injury were established. The expressions of paired Box gene (pax2) and Willm’s tumor gene (WT1), as well as α-smooth muscle actin (α-SMA), a phenotype of mesenchymal cells, were detected by RT-PCR and immunohistochemistry techniques. RESULTS: (1) Expressions of pax2 and WT1 mRNA began at 11.5 d and 14 d of embryo and increased gradually, and expression in trace quantity at 2 weeks after birth. Immunohistochemistry analysis revealed that WT1 only expressed in the glomerular podocytes and expressions of pax2 and WT1 in adult renal tubular cells were negative. (2) Deno-expression of pax2 and WT1 in some tubular cells appeared at week 2 and peaked at week 4 in 5/6 nephrectomized rats, both showing a same trend of expression. However, pax2 showed another peak at week 10 afterwards. (3) Re-expressions of pax2 and WT1 in TEC at 0.5 and 24 h after treated with IL-1α (10 μg/L) or AngII (10-9 mol/L) were observed respectively, followed by upregulation of α-SMA expression, and mesenchymal cells characters were shown. The effects were inhibited by Ang II receptor 2 antagonist and WT1 antibody, respectively. CONCLUSION: Adult renal tubule cells acquire re-activation of embryonic pax2 and WT1 genes and phenotypes of mesenchymes when challenge with certain injuries. Deno-expression of pax2 and WT1 genes closely relates with high concentration of bioactive facors, such as AngII and IL-1, which are involved in the mechanisms of renal tubule cells transdifferentiation.     

Abnormalities of miR-21 expression in human breast cancer is associated with distinctive pathologic features and shortened postoperative survival

AIM: To investigate the potential relevance of miR-21 expression level to clinicopathological characteristics and patient survival. METHODS: 113 BRCA cases with more then 5 years fallow-up data were selected. Total RNA from formalin-fixed paraffin-embedded (FFPE) tissues of 113 breast cancer (BRCA) and normal adjacent tissues (NATs) were isolated for miR-21 quantitative analysis by real-time RT-PCR. RESULTS: The miR-21 expression levels in BRCA were significantly higher than those in NATs (P<0.01) with average up-regulated level of 1.74 ± 0.48. Interestingly, high level expression of miR-21 was significantly correlated with advanced clinical stage (P<0.01), lymph node metastasis (P<0.01), and shorter survival of the patients ［hazard ratio (HR)=5.476, P<0.01］. Multivariate Cox regression analysis revealed that miR-21 was one of independent prognostic impacts (HR=4.133, P<0.01) on BRCA. CONCLUSION: Over-expression of miR-21 is associated with poor prognosis of BRCA and may serve as an independent prognostic marker for BRCA.     

Alternariol induces DNA polymerase β expression via the PKA-CREB pathway in NIH3T3 cells

AIM: To investigate the signal transduction induced DNA polymerase β expression by alternariol(AOH) in NIH3T3 cells. METHODS: The NIH3T3 cells were treated with 15 μmol/L AOH for 16 h or the cells were pretreated with an inhibitor of PKA (H89) for 1 h, and then exposed to AOH. The changes of DNA polβ expression and phospho-CREB in the cells with different treatments were determined by Western blotting and immunocytochemistry analysis. RESULTS: The expression of DNA polymerase β and phospho-CREB in NIH3T3 cells induced by AOH were significantly higher than that in control group (P<0.05). However, H89 partly blocked the AOH-induced phospho-CREB and DNA polβ expression. CONCLUSION: Alternariol up-regulates DNA polymerase β expression via the PKA-CREB pathway in NIH3T3 cells.     

13-MTD induces apoptosis of MCF-7 breast cancer cells by activating MAPK pathway and inhibiting Akt signaling

［ABSTRACT］AIM: To study the effect of 13-methyltetradecanoic acid (13-MTD), a saturated branched-chain fatty acid, on apoptotic induction in breast carcinoma cell line MCF-7 and its underlying mechanisms. METHODS: Breast carcinoma cell line MCF-7 and normal breast epithelial cells MaEC were treated with solvent or 13-MTD at concentration of 140 mg/L. Apoptosis was analyzed by flow cytometry. Phosphorylation of JNK, p38, FADD and Akt after treated with 13-MTD were detected by Western blotting. RESULTS: 13-MTD effectively induced apoptosis of breast carcinoma cell line MCF-7 and no influence to normal breast epithelial cells MaEC, which were confirmed by flow cytometry analysis, was observed. The results of Western blotting showed that obvious increase in p38 and JNK phosphorylation. No significant difference of FADD phosphorylation was observed. However, evidently decrease in Akt phosphorylation was found after treated with 13-MTD. CONCLUSION: 13-MTD was a new safe, effective chemotherapeutic drug. Its underlying mechanisms are through activating MAPK pathway and inhibiting Akt pathway to induce the cancer cells apoptosis.     

Effects of salvianolic acid B on neurons during oxygen/glucose deprivation and reintroduction

AIM: To observe the damage induced in the primary cultured rat cortical neurons by oxygen/glucose deprivation and reintroduction, and to investigate the neuroprotective mechanism of salvianolic acid B (SalB). METHODS: Primary cultured rat cortical neurons were randomly divided into the control group, the model group and the SalB group. The cell model was established by oxygen/glucose deprivation for 3 h followed oxygen/glucose reintroduction for 24 h. The cortical neurons viability was determined by MTT assay. The leakage rate of lactate dehydrogenase (LDH) was measured by chromatometry. The mitochondrial membrane potentials (MMP) and the apoptosis rate were quantitatively analyzed by flow cytometry. The cytosolic free calcium was assessed using LSCM. The morphologic changes of neuronal nuclei were observed by Hoechst 33342 fluorescence staining. RESULTS: Compared to the model group, the cortical neurons viability, the survival rate and the fluorescence value of MMP in the SalB group were obviously increased (P<0.05,P<0.01). In addition, in the SalB group, the leakage rate of LDH, the fluorescence intensity of cytosolic free calcium and the apoptosis rate were significantly lower than those in the model group (P<0.01). CONCLUSION: The neuroprotective mechanism of SalB in the oxygen/glucose deprivation and reintroduction neurons would be due to the fact that SalB maintains the MMP and the calcium homeostasis.