CIMMYT 273个小麦品种抗病基因Lr34/Yr18/Pm38的分子标记检测

【目的】明确CIMMYT观察圃273个小麦品种(系)在慢病基因Lr34/Yr18/Pm38位点的等位变异类型及其对条锈病、叶锈病和白粉病的抗性,进一步验证抗病基因功能标记的有效性。【方法】利用Lr34/Yr18/Pm38紧密连锁的STS标记csLV34和基于该基因第11外显子(exon11)等位变异开发的5对功能标记cssfr1-cssfr5检测新引进的273个CIMMYT小麦品种(系),同时在成都和北京分别对其进行田间条锈病和白粉病的抗性鉴定,并结合CIMMYT的田间条锈病和叶锈病抗性鉴定结果进行分析。【结果】STS标记csLV34与5对功能标记cssfr1-cssfr5检测结果的一致性为96.7%;在273份CIMMYT材料中有43份材料含有Lr34/Yr18/Pm38,在不同地点对条锈病、叶锈病和白粉病具有不同程度的抗病性。【结论】功能标记cssfr1-cssfr5可准确鉴定Lr34/Yr18/Pm38位点exon11中的等位变异,cssfr3、cssfr4、cssfr5可用于含有Lr34/Yr18/Pm38材料杂交后代的分子标记辅助选择。     

超甜玉米新品种正甜38的选育

正甜38是由3个超甜玉米自交系A6、B5和C4于2000年秋育成的超甜玉米三交种,杂交模式为(A6×B5)×C4.A6是利用普通玉米与优质甜玉米自交系杂交后,经过多代自交筛选出的遗传性状稳定,并具有抗病、抗倒伏等优良性状的自交系;B5、C4是利用甜玉米材料经过多代自交选育出的优质自交系.果穗长21 cm左右,粗5.0 cm左右,可溶性糖含量16.92%～18.31%,皮薄,品质优,抗病性和抗倒伏性与对照穗甜1号相当.广东春播生育期85 d(天)左右,秋播75 d(天)左右.平均单苞质量350 g,每667 m2产量900kg左右.适宜在我国玉米主栽地区栽培.     

CDA-2 induces differentiation and inhibits proliferation of human SWO-38 glioma cells

AIM: To investigate the differentiation-inducing effect of cell differentiation agent-2 (CDA-2) in human SWO-38 glioma cell line in vitro.METHODS: The inhibitory effect of CDA-2 on cell proliferation was assessed by MTT assay and colony formation assay.Cell morphology was determinded by light microscopy observation,and the expression of GFAP (glial fibrillary acidic protein) was detected by immunohistochemistry and Western blotting.Western blotting was also applied to explore the expression of PPARγ and COX-2.RESULTS: The data showed that CDA-2 inhibited proliferation and induced differentiation of SWO-38 cells.The inhibition efficiency was time-dependent and dose-dependent .The IC₅₀ of CDA-2 was (2.33±0.37) g/L and (0.51±0.01) g/L,respectively when cells were treated for 72 h and 10 days.CDA-2 caused differentiation of human glioma cells as indicated by outgrowth of long processes and expression of astrocyte marker GFAP.Simultaneously,the expression of PPARγ increased after 3 h of CDA-2 treatment，while the expression of COX-2 decreased after 48 h of CDA-2 treatment.CONCLUSION: CDA-2 inhibits proliferation and induces differentiation of SWO-38 cells.These effects may be through increasing cellular GFAP,PPARγ level and decreasing COX-2 expression induced by CDA-2.     

茶蚕颗粒体病毒AcMNPVORF38同源基因的克隆及序列分析

[目的]为利用昆虫病毒更好地防治害虫和进行分子生物学研究。[方法]从感病茶蚕幼虫的尸体中提取颗粒体病毒DNA后,进行酶切、克隆、测序和序列分析。[结果]成功克隆了茶蚕颗粒体病毒基因组中一个1 484 bp的片段。该片段含有1个完整的开放阅读框(ORF)和2个不完整ORF。完整ORF为666 bp,有典型Nudix结构域,其编码1个与苜蓿银纹夜蛾核多角体病毒AcMNPV的ORF38高度同源的基因,定名为AcORF38同源基因。2个不完整ORF分别编码p47蛋白基因的C-端和p24基因的N-端。[结论]茶蚕颗粒体病毒与卷蛾科宿主中颗粒体病毒亲源关系较近,而与夜蛾科宿主昆虫中颗粒体病毒较远。AcORF38同源基因与编码NTP焦磷酸水解酶的基因高度同源,可能与病毒的复制和DNA损伤的修复过程相关,也可能与入侵寄主的过程相关。     

SH_(38)矮化中间砧嫁接对苹果实生苗叶片内源激素含量变化的影响

为明确矮化中间砧嫁接方式对苹果实生苗叶片中内源激素含量变化规律的影响,在河北省农林科学院石家庄果树研究所苹果标本试验园内,分别采集5-9月5个月的苹果实生苗国红×长富6的实生后代叶片,通过萃取、高效液相色谱等分离纯化方法对直接定植及SH38矮化中间砧嫁接2种处理下苹果叶片中内源激素含量进行分析比较。结果表明,SH38矮化中间砧嫁接方式下,苹果叶片中与成花相关的内源激素GA3、IAA、CTK含量均比直接定植的实生苗内源激素含量降低,但ABA含量显著提高。     

EM38探测复垦土壤厚度分布的可行性研究

该文采用EM38电磁感应电导率仪测量辽宁省阜新市海州露天矿场复垦区一块面积为5 000 m2的覆土层的表观电导率,试探性研究表观电导率（ECa）与矿区排土场覆土厚度（TSLT）的相关性。测定结果证实ECa与相同点位剖面挖掘所得的深度数据有很好的负相关性,而两层土壤的电导率差值与上层土壤深度之间存在一定的正相关性。结合地统计克里格插值,得到了该复垦区覆土深度分布的预测趋势图。研究结论指出,基于EM38测量的表观电导率预测矿区复垦区覆土层厚度具有良好的可行性,为废弃矿区复垦质量的客观评估,提供了一种实用、简捷的工程检测 手段。     

Effect of gonadotropin type II and 17-hydroxy-4-pregnene-3,20-dione on 17,20β-dihydroxy-4-pregnen-3-one production by rainbow trout testes at different developmental stages

Plasma levels of 17,20-dihydroxy-4-pregnen-3-one (17,20OHP), which is involved in the regulation of spermiation in male salmonid fish, increase dramatically at the time of spermiation. To advance the understanding of the regulation of 17,20OHP production during the spermatogenetic cycle in trout, we have studied the in vitro effect of gonadotropin type II (GtH II) and the precursor 17-hydroxy-4-pregnene-3,20-dione (17OHP) on the production of 17,20OHP. The sensitivity with which testes secreted 17,20OHP following stimulation with GtH II was maximum during spermatogenesis. The addition of 17OHP (10 to 1600 ng ml-1) to the culture medium of testes fragments induced a significant and dose-related increase in 17,20OHP secretion. Although the capacity to produce 17,20OHP was not saturated by the 17OHP concentrations used, the conversion rate was highest for tested at an immature stage. As to the regulation of 17OHP, in vivo, a single injection of partially purified salmon gonadotropin (50 ng g-1 body weight) induced a significant increase in the circulating levels of 17OHP of immature males. In conclusion, the maximum sensitivity to GtH II stimulation and the highest conversion rate of 17OHP to 17,20OHP in vitro, occurred before the dramatic increase in the 17,20OHP secretion observed in rainbow trout at the time of spermiation.     

Palmatine attenuates LPS-induced inflammatory response in mouse mammary epithelial cells through inhibiting ERK1/2, P38 and Akt/NF-кB signalling pathways

Palmatine has a wide range of pharmacological effects and anti-inflammatory function. However, the effect of palmatine on LPS-induced inflammatory response of mammary epithelial cells has not been reported. In this research, we studied the anti-inflammatory mechanism of palmatine in EpH4-Ev (mouse mammary epithelial cells). EpH4-Ev cells were pre-treated with palmatine and then incubated with LPS. Cells were collected for examining production of pro-inflammatory mediators by qRT-PCR, and the related inflammatory signalling pathway was detected through immunofluorescence and Western blot. The results found that palmatine could significantly reduce the expression of IL-6, TNF-α, IL-1β and COX-2 in EpH4-Ev cells. Research on mechanisms found that palmatine could significantly inhibit the protein levels of p-Akt, p-P65, p-ERK1/2 and p-P38 in EpH4-Ev cells. In conclusion, these data suggested that palmatine inhibits inflammatory response in LPS-induced EpH4-Ev cells via down-regulating Akt/ NF-кB, ERK1/2 and P38 signalling pathways.     

Effect of p38 MAPK on cisplatin-induced renal tubular cell apoptosis

AIM:To investigate the role of p38 MAPK in cisplatin-induced rat renal proximal tubular cell (RPTC) apoptosis. METHODS:To determine the optimal concentration of cisplatin to induce RPTC apoptosis, the cells were treated with 0, 5, 10 and 20 μmol/L cisplatin for 24 h, and then the cell lysates were collected for Western blot analysis of cleaved PARP, p38 and phosphor ylated p38 (p-p38). To determine the role of p38 MAPK in cisplatin-induced RPTC apoptosis, the cells were divided into control group, cisplatin group (the cells were treated with cisplatin for 24 h) and cisplatin+p38 MAPK inhibitor group (the cells were treated with p38 MAPK inhibitor SB203580 for 1 h, and then treated with cisplatin for another 24 h). The morphological changes of apoptotic cells were observed under phase-contrast fluorescence microscope. The apoptotic rate of the cells were analyzed by flow cytometry. The caspase activity of RPTC lysates was examined using Ac-DEVD-AFC kit. The protein levels of p-p38, p38, cleaved PARP and cleaved caspase-3 were determined by Western blot. The pH value of extracellular environment of the cells was measured by pH meter. RESULTS:Cisplatin at 20 μmol/L obviously induced apoptosis of RPTC. The p38 MAPK was phosphorylated and its phosphorylation peaked at 15 min after cisplatin treatment. The apoptotic rate of RPTC was 12.08% after cisplatin induction. Cisplatin treatment also enhanced caspase activity, and increased cleavage of PARP and caspase-3 proteins (P<0.05). The p38 MAPK inhibitor SB203580 effectively inhibited the phosphorylation of p38 MAPK, down-regulated the RPTC apoptosis rate and caspase activity, and reduced the cleavage of PARP and caspase-3 proteins. The pH value change in RPTC culture medium was also inverted by SB203580. CONCLUSION:The phosphorylation of p38 MAPK is involved in cisplatin-induced apoptosis of RPTC. The apoptosis induced by cisplatin results in the change of acidic extracellular environment, which is inhibited by p38 MAPK inhibitor SB203580.     

Asiaticoside attenuates hypoxic pulmonary hypertension in mice by inhibiting NF-κB/p38 signaling pathway

AIM: To investigate whether asiaticoside attenuates hypoxic pulmonary hypertension by inhibiting p38/NF-κB signaling pathway. METHODS: BALB/c mice (n=30) were randomly divided into normoxia (N) group, hypoxia (H) group, and hypoxia+asiaticoside group. Right ventricular systolic pressure (RVSP), mean carotid artery pressure (mCAP), the weight ratio of right ventricle/(left ventricle+ventricular septum)[RV/(LV+S)], the ratio of right ventricle/body weight (RV/BW), vessel wall area/vessel total area (WA/TA) and vessel wall diameter/vessel wall total diameter (WT/TT) were determined after the model was established. The protein levels of p38, p-p38, NF-κB and p-NF-κB in the lung tissues were detected by Western blot. The fluorescence intensity of p-p38 and p-NF-κB were measured by immunofluorescence method. The serum levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured by ELISA. RESULTS: Compared with N group, the levels of RVSP, RV/(LV+S), RV/BW, WA/TA and WT/TT were significantly increased in H group, while administration of asiaticoside decreased the levels of RVSP, RV/(LV+S), RV/BW, WA/TA and WT/TT (P<0.05). Compared with N group, the relative protein levels of p-p38 and p-NF-κB in H group were significantly increased (P<0.05), and the concentrations of IL-6 and TNF-α were significantly increased, which were apparently attenuated by asiaticoside injection. CONCLUSION: Inhibition of p38/NF-κB signaling pathway and reduction of inflammatory responses may be the important mechanisms of asiaticoside in the prevention and treatment of hypoxic pulmonary hypertension.