外植体采集时期与冷藏处理对马尾松愈伤组织诱导的影响

马尾松(Pinus massoniana)无性繁殖困难,研究常采用体细胞胚胎发生和器官发生的方式繁殖,外植体采集时期是实验成功的关键.本实验采用2011年10月至2012年10月期间(每周或每两周采集1次)采集的马尾松枝梢顶端分生组织为外植体,并将外植体置于4cC冰箱冷藏做不同冷藏时间处理(4 ～ 114天).处理后的外植体接种在添加不同激素浓度的改良GD培养基中,24 ～ 25℃条件下暗培养.实验结果表明:冷藏时间对马尾松愈伤组织诱导没有显著影响;2012年3月中旬至4月底采集的马尾松外植体,愈伤组织诱导率最高达89.8％,其平均诱导率达到80％以上;外植体经流水冲洗2～3h、75％的酒精处理20 ～30 s、0.1％的升汞处理9～ 10 min并去除鳞片和针叶,能有效降低外植体污染率;外植体经流水冲洗2～3h、去除鳞片和针叶后切成长约0.2 ～0.5 cm的薄片后接种,能大大降低培养过程中外植体的褐化率.     

玉米磷酸烯醇式丙酮酸羧化酶基因的研究进展

高等植物按照CO₂不同的同化途径,分为C₃、C₄和CAM植物。由于C₄植物具有高光效基因,使其在高温、高光照、高氧分压条件下具有比C₃植物更高的光合作用效率。目前,很多学者致力于研究玉米中的高光效基因-磷酸烯醇式丙酮酸羧化酶基因（PEPC）,并试图将此基因转入到C₃植物中,使C₃植物的光合特性得到一定改善,进而使其产量提高。本文综述将C₄高光效基因转入到C₃植物后,C₃植物的生理生化变化和对其光合作用的影响,对向C₃植物中导入pepc基因能否提高其光合作用效率和产量的潜在可能性进行探讨。     

野大麦耐盐性研究进展

野大麦是禾本科小麦族耐盐性最强的盐生植物之一,其耐盐机制的研究对提高作物的耐盐性具有重要意义。野大麦耐盐性的研究起步较晚,文章分别从耐盐生物学特性描述、耐盐性新品种选育、耐盐生理响应机制、筛选盐诱导差异表达的基因、克隆耐盐相关基因和编码蛋白、种属间遗传性几个方面对其耐盐性研究进行了综述,相关研究获得了很多有价值的结果,但其根本的耐盐生理机制和基因尚不清楚,仍待进一步研究。     

紫苏油微胶囊对夸克质构的影响

将紫苏油微胶囊产品加入夸克中,考察其对夸克质构的影响.结果表明：紫苏油微胶囊的添加对夸克质构的各项指标均有不同程度的影响.硬度随着紫苏油微胶囊添加量的增大而先上升后降低,紫苏油微胶囊后添加组在2％的添加量时,弹性出现大幅回升,达到显著水平（P＜0.05）.紫苏油微胶囊无论以何种方式加入夸克,对夸克凝聚性均没有显著影响.添加紫苏油微胶囊以后,夸克的回复性显著变差（P＜0.05）.紫苏油微胶囊的两种添加方式对夸克黏着性具有相似影响.     

水淹胁迫对紫穗槐生长及营养元素积累的影响

通过对不同水淹条件下紫穗槐(Amorpha fruticosa)植株营养生长及各组织中营养元素积累量的分析,发现紫穗槐在表面水淹条件下根系浅生化,半水淹条件下茎根生长不定根,近全淹条件下先生长茎后生出不定根来适应水淹胁迫。3个水淹处理组植株对氮、磷、钙、铁及锰的吸收表现为增益;对铜的吸收表现为降低;改变氮、磷、钙、锌和铜的分配以适应水淹逆境,均与对照组植株存在明显差异(P<0.05)。所有处理各营养元素的积累量均不低于植物正常生长水平,营养生长指标未见严重缺素症,表明紫穗槐可针对不同水淹条件选择最有效节能的适应机制,是优良的抗涝灌木种。     

Responses of energy balance, physiology, and production for transition dairy cows fed with a low-energy prepartum diet during hot season

Twenty multiparous Chinese Holstein dairy cows calving in hot summer (S group), were compared with 20 similar control cows calving in cool autumn (C group). Diets were the same for both groups; prepartum diets had relatively low energy density. Average temperature–humidity index was 76.5 and 53.0 in summer and autumn, respectively. S group cows had significantly higher rectal temperatures (39.6 vs. 39.0 °C) and respiration rates (79.0 vs. 31.3 breaths/min) than C group, and consumed less feed (prepartum 8.0 vs. 12.3 kg/day, postpartum 16.3 vs. 21.2 kg/day). Calculated energy balance (EB) was ?7.98 vs. ?5.15 Mcal/day for S group prepartum and postpartum, respectively. In contrast, EB was 1.36 vs. ?2.03 Mcal/day for C group prepartum and postpartum, respectively. S group produced significantly less milk than C group by 15.4 % (5.2 kg/day) and 26.8 % (10.2 kg/d) for milk yield and energy-corrected milk, respectively. Percentages of milk fat (3.28 vs. 4.29 %), protein (3.08 vs. 3.33 %), and solids-not-fat (8.46 vs. 8.78 %) were significantly lower for S group. Milk urea nitrogen (19.54 vs. 13.31 mg/dL) was significantly higher in S group. Significantly lower feed efficiency was observed in S group (1.56 vs. 1.66). During the entire transition period, S group had significantly lower circulating glucose levels. S group had significantly higher levels of nonesterified fatty acids (NEFA) prepartum, but after 14 days in milk, NEFA was significantly lower. We conclude that increasing dietary energy density during transition period (especially prepartum) is necessary to minimize adverse effects of hot season.     

The stimulatory effect of TLRs ligands on maturation of chicken bone marrow-derived dendritic cells

Dendritic cells (DCs) are crucial for initiation of both innate and adaptive immune responses. TLR ligands combine with Toll-like receptors (TLRs) expressed on the DC surface and induce DC maturation. The potential effect of three types of TLR ligands (Bacillus subtilis (B. subtilis) spores, polyinosinic–polycytidylic acid and CpG oligodeoxynucleotides) on chicken bone marrow-derived DCs (chBM-DCs) maturation was studied. The chBM-DCs cultured in presence of recombinant chicken granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL)-4 displayed the typical morphology of DCs after 7 days of culture. These immature chBM-DCs up-regulated the expression of MHC-II and of the putative CD11c, but had yet low to moderate levels of the CD40 and CD86 co-stimulatory molecules. After stimulation by the TLR ligands, the chBM-DCs displayed a more mature morphologic phenotype, significantly increased the CD40 and CD86 cell surface expression levels and gained the ability to stimulate proliferation of naive T cells in the allogeneic mixed lymphocyte reaction, compared to the immature chBM-DCs. In conclusion, our data demonstrated that all three TLR ligands were strong stimuli for driving chBM-DCs maturation in vitro, with B. subtilis spores being the most efficient.     

Expression kinetics of chicken β2-microglobulin and Class I MHC in vitro and in vivo during Marek’s disease viral infections

Marek’s disease virus (MDV) is a highly cell-associated herpesvirus that causes a disease in chickens characterized by tumor formation and immunosuppression. The changes of major histocompatibility complex (MHC) expression in different MDV-infected cells are not completely understood. In this study, we investigated the expression of the Class I MHC and β2-microglobulin (β2m) genes in response to MDV infection at different time points by real-time PCR. In both in vitro and in vivo, the expression levels of Class I MHC and β2m genes were upregulated during early MDV infections in comparison to control cells; We also found that the expression of Class I MHC gene was downregulated in BudR (5-bromo-2′-deoxyuridine)-treated MSB1 cells at 48 h and MDV-infected chicken embryo fibroblast cells (CEF) at 120 and 168 h post infection (hpi); Furthermore, compared to control groups, Class I MHC and β2m expression levels were downregulated in peripheral blood lymphocytes (PBLC) from MDV-infected chickens at 14 and 28 days post infection (dpi); Interestingly, both Class I MHC and β2m gene expression levels increased again in PBLC from MDV RB1B-infected chickens at 35 dpi, in which MDV was in the latent or transformed infection stages. In addition, Class I MHC expression was clearly decreased in MDV-infected CEF at 120 hpi although β2m expression was significantly increased. These changes in Class I MHC and β2m gene expression might provide more insights into host-virus interaction.     

分析解读欧盟关于转基因蜂蜜的检测要求和手段

欧盟是我国蜂蜜出口重要的市场,2011年下半年以来,欧盟要求检测蜂蜜中的转基因成分,我国转基因作物种植的品种和数量不断增加,转基因成分在蜂蜜中存在的风险性也不断加大。欧盟官方推荐在食品中如果使用经批准的转基因花粉含量占总花粉含量超过0.9%的蜂蜜时应当予以标识,在0.9%限量界定方面,目前倾向的鉴定方法是用PCR方法与显微镜检验相结合的方法。欧盟官方认可的QSI实验室和intertek实验室目前检测蜂蜜中转基因花粉成分时,选择的三个筛选基因为P-35S、T-NOS和FMV基因。     

Lactogenic hormones stimulate expression of lipogenic genes but not glucose transporters in bovine mammary gland

During the onset of lactation, there is a dramatic increase in the expression of glucose transporters (GLUT) and a group of enzymes involved in milk fat synthesis in the bovine mammary gland. The objective of this study was to investigate whether the lactogenic hormones mediate both of these increases. Bovine mammary explants were cultured for 48, 72, or 96 h with the following hormone treatments: no hormone (control), IGF-I, insulin (Ins), Ins + hydrocortisone + ovine prolactin (InsHPrl), or Ins + hydrocortisone + prolactin + 17β-estradiol (InsHPrlE). The relative expression of β-casein, α-lactalbumin, sterol regulatory element binding factor 1 (SREBF1), fatty acid synthase (FASN), acetyl-CoA carboxylase α (ACACA), stearyol-CoA desaturase (SCD), GLUT1, GLUT8, and GLUT12 were measured by real-time PCR. Exposure to the lactogenic hormone combinations InsHPrl and InsHPrlE for 96 h stimulated expression of β-casein and α-lactalbumin mRNA by several hundred-fold and also increased the expression of SREBF1, FASN, ACACA, and SCD genes in mammary explants (P < 0.01). However, those hormone combinations had no effect on GLUT1 or GLUT8 expression and inhibited GLUT12 expression by 50% after 72 h of treatment (P < 0.05). In separate experiments, the expression of GLUTs in the mouse mammary epithelial cell line HC11 or in bovine primary mammary epithelial cells was not increased by lactogenic hormone treatments. Moreover, treatment of dairy cows with bovine prolactin had no effect on GLUT expression in the mammary gland. In conclusion, lactogenic hormones clearly stimulate expression of milk protein and lipogenic genes, but they do not appear to mediate the marked up-regulation of GLUT expression in the mammary gland during the onset of lactation.