南方红壤旱坡地花生植株对施用氮肥的响应

选用多年夏花生-冬蔬菜种植制度下的典型红壤旱坡地,通过田间试验,研究了5种氮肥水平下花生根系的形态特征、固氮能力、植株生物量以及荚果产量。结果表明:不同氮肥施用量对花生植株生物量及荚果产量影响均不显著(P=0.091);而不同处理的土壤固氮酶活性与氮肥施用量间呈极显著的负相关(R2=0.88,P=0.005);单株花生根系总长度、总表面积、总分叉数及根尖条数均随氮肥施用量的增加而减小,且与单株花生根瘤生物量呈极显著(P<0.001)正相关。     

解脂亚罗酵母菌体外降甘油三酯降胆固醇效果研究

筛选出高效降三酰甘油降胆固醇菌株,为新型药物、食品的制备提供优良菌株。从样品中筛选分离出酵母菌株,并测定菌株降三酰甘油能力,采用磷硫铁比色法测定菌株降胆固醇能力,通过耐酸、耐胆盐及毒性实验研究菌株各项性能,通过生理生化及26S rDNA法对菌株进行鉴定。结果显示,试验筛选出1株高效降脂降胆固醇酵母菌EAM-ZT003T,降三酰甘油能力高达80.2%,菌株具有很好的耐酸、耐胆盐能力,为期42 d的小鼠毒性试验发现,小鼠未出现异常体征,未发现异常死亡,且解剖观察各器官一切正常,菌株经26S rDNA鉴定为解脂亚罗酵母菌(Yarrowia lipolytica)。     

一种快速、无损大豆种子DNA提取方法的建立和应用

基因分型是进行植物基因功能的遗传分析和分子标记辅助育种的重要环节。该研究以大豆(Glycine max)成熟种子为材料, 建立了通过钻孔采集样品、快速提取DNA进行基因型鉴定的方法。用此方法, 一个熟练的工作人员可以在1个小时内完成120个样品的采集和DNA提取; 同时种子钻孔取样后, 不会对大豆种子的萌发造成影响。利用该方法获得的DNA可满足PCR扩增的要求。实验重复性好, 成功率在98%以上。这种快速且无损的大豆种子基因型鉴定方法可以用于鉴定杂交种子、品种纯度以及遗传分析等研究工作。     

Gene Discovery and Functional Analyses in the Model Plant Arabidopsis

The present mini-review describes newer methods and strategies, including transposon and T-DNA insertions, TILLING, Deleteagene, and RNA interference, to functionally analyze genes of interest in the model plant Arabidopsis. The relative advantages and disadvantages of the systems are also discussed.     

c-erbB-2单克隆抗体A18在乳腺癌中表达特性的研究

目的：研究一株自制的c-erbB-2单克隆抗体A18在乳腺癌中表达的特性。方法：应用免疫组织化学SP法、蛋白质印迹分析法和荧光激活的流式细胞分选检测技术检测A18在635例乳腺癌组织、100例癌旁乳腺组织、不表达c-erbB-2的NIH／3T3（鼠成纤维细胞）和NE91（转表皮生长因子受体基因的NR6鼠成纤维面积）细胞株及高表达c-erbB-2的T6－17（转c-erbB-2－基因的NIH／3T3细胞）和SKBR3（人乳腺癌细胞）细胞株中的表达状况,并与市售进口c-erbB-2抗体（MaximBiotech产品）进行了平行对照研究。A18系采用细胞表面区域表位包埋法免疫小鼠制备而成,,结果：A18阳性染色定位于细胞膜,部分伴微弱的细胞浆着色,无明显非特异性染色,A18和进口抗体对NIH／3T3、NE91细胞均呈阴性,T6－17、SKBR3细胞均呈阳性,在乳腺癌组织中,A18的阳性率为60．3％,明显高于癌旁乳腺组织的5．0％,A18与进口同类单抗的阴性、阳性及总符合率分别为84．0％、82．8％及83．2％,与进口同类多抗的阴性,阳性及总符合率分别为88．0％、90．2％和89．5％。A1和进口同类单抗与乳腺癌临床病理特征的关系一致。经反复冻融7次或4℃保存10个月A18效价仍保持在3μg/ml。结论：A18特异性强,定位准确,效价高而稳定、可用于临床乳腺癌的检测。     

湖南永顺县落叶木莲资源考察研究

首次报道湘西武陵山地永顺县发现国家一级保护植物落叶木莲。分布面积2000 hm2,多呈散生分布,稀有小面积群落,成年大树有5000余株,胸径5 cm以下幼树及小苗有20000余株。落叶木莲群落属常绿与落叶阔叶混交林,分布海拔400~900 m的山坡中下部,主要有枫香、野漆树、落叶木莲和甜槠、星毛石栎、落叶木莲等群落类型。此前,落叶木莲仅分布江西幕阜山地宜春市明月山,是木兰科木莲属极度濒危的唯一一个落叶树种,对探讨被子植物的起源和木兰科的系统演化有重要的科学意义。     

Pyrroloquinoline quinone inhibits oxygen/glucose deprivation-induced apoptosis by activating the PI3K/AKT pathway in cardiomyocytes

The purposes of this study were to examine the protective effect of pyrroloquinoline quinone (PQQ) on oxygen/glucose deprivation (OGD)-induced injury to H9C2 rat cardiomyocytes and to investigate the mechanism. Using H9C2 cells cultured in vitro, we examined changes in cell viability with an MTT assay at 12, 24, and 48 h after injury induced by OGD. Various concentrations of PQQ (1, 10, and 100 μM) were added, and the effect of PQQ on cell viability after OGD was assessed using the MTT assay. Thus, the optimal concentration of PQQ for the protection of cardiomyocytes against oxygen and glucose deprivation injury was determined. We also used flow cytometry analysis to examine the effect of PQQ on H9C2 cells with OGD-induced injury. The molecular probe 2′,7′-dichlorofluorescin diacetate was used to label the H9C2 cells, and flow cytometry was used to detect the effect of PQQ on reactive oxygen species (ROS) content. After labeling the H9C2 cells using a mitochondrial green fluorescent probe (Mito-Tracker Green), we measured the change in the mitochondrial content of PQQ-treated H9C2 cells. Western blotting was used to examine the effect of PQQ on the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in the H9C2 cells. The results of the MTT assay showed that 48 h of OGD significantly injured the H9C2 cells (p < 0.01) and that treatment with 100 μM PQQ effectively decreased the level of OGD-induced injury (p < 0.01). The results of the flow cytometry analysis showed that PQQ significantly reduced apoptosis in H9C2 cells subjected to OGD (p < 0.05). In addition, OGD significantly increased the ROS level in H9C2 cells (p < 0.01), and PQQ significantly inhibited this increase (p < 0.05). The results of the Mito-Tracker Green staining suggested that PQQ effectively inhibited the decrease in mitochondrial content caused by OGD (p < 0.05). Western blot analysis showed that PQQ partially reversed the decrease in Akt phosphorylation that was caused by OGD (p < 0.05). PQQ treatment dose-dependently protects H9C2 cells from OGD-induced injury by reducing apoptosis, decreasing intracellular ROS levels, and rescuing the OGD-induced decrease in mitochondrial content. The protective effect of PQQ may be related to its effects on the PI3K/Akt pathway.     

The effect of HMGB1 A box on lung injury in mice with acute pancreatitis

The objective of this study is to observe the effect of high-mobility group protein B1 A Box (HMGB1 A) box on lung injury in mice with acute pancreatitis and its effect on the level of high-mobility group protein B1 (HMGB1) in lung, to explore the mechanism. A total of 60 male Institute of Cancer Research mice were randomly divided into control group (n = 30) and treatment group (n = 30). Severe acute pancreatitis mice model was induced by 20% L-Arg intraperitoneal injection. The recombination HMGB1 A box was used in treatment after modeling. All the mice were killed under anesthesia at 24 and 48 h after the modeling injection. The level of HMGB1 and activity of myeloperoxidase (MPO) in lung were measured. The pathological changes of lung were observed. The level of HMGB1 in lung of A box treatment group decreased more significantly 24 h and 48 h after modeling compared with control group. The activity of MPO in lung of A box treatment group decreased more significantly 24 h after modeling compared with control group. The lung tissue pathologic score of A box treatment group decreased more significantly 48 h after modeling compared with control group. HMGB1 expression levels in the lungs were positively related to histological score of injured lung in acute pancreatitis. It indicates that HMGB1 A box is remarkably protective to lung injury induced by acute pancreatitis.     

Meningitic Escherichia coli K1 penetration and neutrophil transmigration across the blood-brain barrier are modulated by alpha7 nicotinic receptor

Alpha7 nicotinic acetylcholine receptor (nAChR), an essential regulator of inflammation, is abundantly expressed in hippocampal neurons, which are vulnerable to bacterial meningitis. However, it is unknown whether α7 nAChR contributes to the regulation of these events. In this report, an aggravating role of α7 nAChR in host defense against meningitic E. coli infection was demonstrated by using α7-deficient (α7(-/-)) mouse brain microvascular endothelial cells (BMEC) and animal model systems. As shown in our in vitro and in vivo studies, E. coli K1 invasion and polymorphonuclear neutrophil (PMN) transmigration across the blood-brain barrier (BBB) were significantly reduced in α7(-/-) BMEC and α7(-/-) mice. Stimulation by nicotine was abolished in the α7(-/-) cells and animals. The same blocking effect was achieved by methyllycaconitine (α7 antagonist). The tight junction molecules occludin and ZO-1 were significantly reduced in the brain cortex of wildtype mice infected with E. coli and treated with nicotine, compared to α7(-/-) cells and animals. Decreased neuronal injury in the hippocampal dentate gyrus was observed in α7(-/-) mice with meningitis. Proinflammatory cytokines (IL-1β, IL-6, TNFα, MCP-1, MIP-1alpha, and RANTES) and adhesion molecules (CD44 and ICAM-1) were significantly reduced in the cerebrospinal fluids of the α7(-/-) mice with E. coli meningitis. Furthermore, α7 nAChR is the major calcium channel for nicotine- and E. coli K1-increased intracellular calcium concentrations of mouse BMEC. Taken together, our data suggest that α7 nAChR plays a detrimental role in the host defense against meningitic infection by modulation of pathogen invasion, PMN recruitment, calcium signaling and neuronal inflammation.