棚室专用薄皮甜瓜新品种‘永甜4号’的选育

‘永甜4号’薄皮甜瓜是用地方薄皮甜瓜品种自交系‘白B10’为母本、‘郑引55’自交系‘A97-I-14-63’为父本配制的杂交一代新品种。该品种早熟,全生育期93d,果实发育期31d。在棚室种植坐瓜率高,产量稳定,果皮浅黄色,梨形,单果质量450⁴80g,极少裂瓜,畸形瓜少,中心可溶性固形物含量12%480g,极少裂瓜,畸形瓜少,中心可溶性固形物含量12%¹3%。货架期长,耐运输。2006年通过黑龙江农作物品种审定委员会审定。     

早花忍冬离体快繁技术

以东北地区早春植物早花忍冬的幼嫩茎段为外植体,MS培养基为基本培养基,添加不同的植物生长调节物质,进行了离体快速繁殖技术研究。结果表明:采用2.0%NaClO处理20min的灭菌效果好;诱导早花忍冬侧芽分化的适宜培养基为MS+1.0mg/L 6-BA+0.05mg/L NAA+3.0%蔗糖+0.7%琼脂;增殖培养基为MS+2.0mg/L 6-BA+0.05mg/L NAA+3.0%蔗糖+0.7%琼脂,30d的增殖系数为8;最佳的生根培养基为1/2MS+0.3mg/L IBA+0.3mg/L NAA+1.5%蔗糖+0.7%琼脂,生根率达100%。     

薄皮甜瓜新品种京玉绿宝的选育

京玉绿宝是以白沙蜜5代自交系357为母本,以地方品种240提纯系选后代397为父本配制而成的薄皮甜瓜一代杂种。果实扁卵圆形,单果质量200~400g,果面光滑无棱,果皮深绿色,果肉白绿色,可溶性固形物含量11%~15%,早熟,抗逆性较强,适合保护地及少雨露地栽培,每667m2产量1600kg。已在北京、河北、辽宁、吉林、内蒙古等地示范推广3000hm2。     

瓠瓜新品种浙蒲8号的选育

浙蒲8号是以自交系G7-4-3-1-2-1为母本、自交系J63-1-6-3-2-1为父本配制而成的耐热瓠瓜一代杂种。植株生长势较强,早中熟,以侧蔓结瓜为主,坐瓜性较好。商品瓜中棒形,上下粗细较均匀,平均瓜长约30cm,横径约5cm,瓜皮绿色,具光泽,单瓜质量0.4~0.5kg。耐高温性较强,高温期商品瓜率较对照杭州长瓜高6个百分点;品质佳,游离氨基酸总量1304.193μg·g-1,其中谷氨酸含量85.663μg·g-1;田间对枯萎病和白粉病的抗性强于对照杭州长瓜。适宜作露地栽培和夏秋季设施避雨栽培,夏秋季栽培每667m2产量2600kg以上。     

Mycoplasma pneumoniae induces IL-1β production through activating NLRP3 inflammasome by ROS in RAW264.7 cells

AIM: To investigate whether Mycoplasma pneumoniae (Mp)-induced interleukin-1β (IL-1β) production in RAW264.7 cells is through the activation of NLRP3 inflammasome via reactive oxygen species (ROS). ME-THODS: RAW264.7 cells were randomly divided into 3 groups. In normal group, RAW264.7 cells were treated without Mp. In model group, RAW264.7 cells were treated with 1∶ 10 multiplicity of infection (MOI) of Mp. In NAC group, RAW264.7 cells were pretreated with N- acetylcysteine (NAC) at a concentration of 5 mmol/L for 30 min before infection with Mp. The RAW264.7cells were infected with Mp (1∶ 10 MOI) for 4, 8, 16 and 24 h in model group and NAC group, respectively. The intracellular ROS level was analyzed by flow cytometry. The mRNA expressions of NLRP3, ASC and caspase-1 were detected by real-time PCR. The protein levels of NLRP3, ASC and caspase-1 p20 were determined by Western blot. The levels of pro-inflammatory cytokine IL-1β in the supernatant were measured by ELISA. RESULTS: Compared with normal group, the production of ROS were significantly increased at 4, 8, 16 and 24 h after infection, the mRNA expression of NLRP3, ASC and caspase-1 were increased at 8, 16 and 24 h after infection, the protein levels of NLRP3, ASC and caspase-1 p20 were increased at 16 and 24 h after infection, and the releases of IL-1β were increased at 24 h after infection in model group (P<0.01). Compared with the model group, the level of ROS in NAC group decreased, so as the expression of NLRP3, ASC and caspase-1 at mRNA and protein levels and the releases of IL-1β in the supernatant at the corresponding time points. CONCLUSION: Mp may stimulate the ROS production to activate NLRP3 inflammasome in RAW264.7 cells.     

Ultrastructural impairment of islet microvascular endothelial cells in STZ-induced type 1 diabetic mice

AIM: To investigate the ultrastructural changes of islet microvascular endothelial cells in STZ-induced type 1 diabetic mice. METHODS: BALB/c mice were randomly divided into diabetic group and control group. The expression of insulin and platelet-endothelial cell adhesion molecule-1 (CD31) in islet microvessels was detected by immunohistochemical staining. The ultrastructural changes of islet β cells and islet microvessels were observed under transmission electron microscope. RESULTS: Compared with control group, the number of islet β cells, ratio of β cells/α cells, average number of secretory granules in β cells and insulin expression area per islet in diabetic group were significantly decreased (P<0.01). Besides, diabetic group had fewer microvessels with lower expression of CD31 (P<0.01). Mitochondria in islet microvascular endothelial cells and pericytes in diabetic group were swelling. The basement membrane of islet microvessels became thicker in diabetic group (P<0.01). CONCLUSION: Islet microvascular endothelial cells were impaired in type 1 diabetic mice.     

泛素/26S蛋白酶体途径调节非生物胁迫的研究进展

随着环境的恶化和资源的匮乏,非生物胁迫已成为制约植物生长和发育的重要因素,严重影响农作物的产量和农产品的品质。泛素/26S蛋白酶体途径(ubiquitin/26Sproteasome pathway,UPP)通过特异性地降解泛素化修饰的蛋白质,介导了植物生长发育的诸多方面,并在植物应对非生物胁迫过程中起关键的调控作用。该文主要概述了泛素/26S蛋白酶体途径及其调控植物响应非生物胁迫机制的研究进展。     

秸杆栽培食用菌拮抗菌株的鉴定及混菌发酵条件的优化

从海洋泥样和食用菌发酵料中分离出了32个菌株,从中筛选出了既具有较高的纤维素酶活性又具有对青霉(Penicillium spp)、木霉(Trichoderma spp.)、根霉(Rhizopus)、曲霉(Aspergillus spp)、毛霉(Mucro)较强拮抗能力的W-4、W-10、N-14三个菌株。经鉴定W-4、W-10分别属于放线菌中黄色节杆菌(Arthrobacter flavescens)和石灰壤诺卡氏菌(Nocardia calcarea),N-14属于细菌中的乳酸乳杆菌(Lactobacillus lactis)。通过正交试验对上述3个菌株混合发酵条件进行优化,确定在温度35℃、时间36h、pH7.5、装液量60ml/250ml时为最适发酵条件。在此条件下3个菌株混合发酵液纤维素酶活力仍然很高。同时混合发酵液对青霉、曲霉、毛霉、木霉、根霉的拮抗能力分别为单菌株发酵液的1.79倍、1.36倍、1.29倍、1.04倍、1.07倍。     

哺乳动物卵母细胞非整倍体产生机制的研究进展

雌性生殖细胞进行减数分裂时易发生染色体分离错误而产生非整倍体卵母细胞,其受精后会产生非整倍体胚胎,导致出生缺陷或胚胎致死,是影响哺乳动物繁殖的重要因素。卵母细胞在第一次减数分裂前期发生同源染色体联会,此时DNA双链断裂引发重组。重组时缺乏交叉、重组事件数量的减少及交叉靠近端粒或着丝粒导致染色体发生同向分离或不分离,从而产生非整倍体卵母细胞。减数分裂期间,当染色体的端粒共向于同一极或没有完全附着在纺锤体微管上时,纺锤体组装检查点（spindle assembly checkpoint,SAC）被激活,E3泛素连接酶APC/Cyclome （APC/C）沉默,保护分离酶抑制蛋白（securin）和细胞周期蛋白B （cyclin B）不被降解,从而抑制分离酶和染色体的分离。直到所有染色体与纺锤体实现稳定的双极定向并正确排列到赤道板上,SAC关闭,染色体正确分离。卵母细胞中SAC蛋白缺失,导致SAC不能有效地监测端粒在纺锤体上的正确附着,发生染色体分离错误,从而产生非整倍体卵母细胞。因此,通过现代分子技术手段解析非整倍体卵母细胞所涉及的机制是保护哺乳动物生育的重要目标。作者主要介绍了卵母细胞减数分裂的特点,详细阐述了卵母细胞非整倍体发生的染色体分离错误的分子机制,以期为开发卵母细胞非整倍体的治疗手段提供参考。