江河源区草地资源现状及其可持续发展

在分析青海省江河源区草地资源现状的基础上，进一步剖析了造成该区域草地生态环境恶化的综合因素，提出了合理利用和保护天然草地，优化草地生产结构，加强基础设施建设，建立饲草料生产基地，遏制草地退化，使草地生态进入良性演替，实现江河源区草地资源可持续利用和草地畜牧业可持续发展的对策。     

"黑土型"退化草地种植披碱草属牧草物候特征与分蘖动态的研究

在果洛地区“黑土型”退化草地上研究了2种披碱草属牧草(垂穗披碱草、短芒老芒麦)在1年内的物候期特点以及分蘖动态。     

肉仔鸡生长过程中行为与产热的变化

研究肉仔鸡成长过程中行为变化对产热量的影响 ,将 2日龄肉仔鸡 36只分为自由摄食、 50 %摄食和绝食 3组进行观测。立位行为集中在明期 ,特别是摄食 30min前后 ,暗期几乎没有出现立体行为。 2日龄时 ,每天约有 70 0min是立位的 ,其后 ,随着日龄的增加而减少。在自由采食区 ,公雏比母雏摄食时间长。 50 %摄食区较自由采食区的摄食时间少。在绝食区 ,随着日龄的增加 ,公母的立位时间呈现减少倾向。 2 1日龄之前随着日龄的增加其摄食时间也增加 ,其后呈现相反倾向。产热 (HP ,kJ/kg0 75)与摄食时间有相同倾向。在 2 1日龄前公雏的HP比母雏低 ,2 1日龄后母雏比公雏低。 1天中各个区的HP活动规律是摄食后 1h内最高 ,暗期降低 ;限制摄食量后 ,HP降低 ,明期和暗期的HP差也随之减小     

谷氨酰胺对肉仔鸡脾组织结构发育的影响

160只 1日龄艾维茵肉仔鸡随机分成 4组 ,分别饲喂添加 0 % ,0 2 % ,0 4%和 0 8%谷氨酰胺的饲粮 2 8d。每周末每组取 6只鸡 ,颈静脉放血致死 ,取脾脏 ,Bouin液固定 ,制作石蜡切片 ,HE染色 ,光镜观察 ,显微摄影 ,研究基础日粮中添加谷氨酰胺对肉仔鸡脾组织结构的影响。结果显示 :添加谷氨酰胺的各试验组脾小结增多、增大 ;动脉周围淋巴鞘增厚 ;椭球增多、增大 ,细胞排列疏松 ,鞘毛细血管内皮细胞增高、增多 ;红髓比例降低 ,脾索内浆细胞和巨噬细胞增多。添加 0 8%谷氨酰胺的脾小结变化明显 ,添加 0 4%谷氨酰胺的动脉周围淋巴鞘和椭球变化明显。说明日粮中适量添加谷氨酰胺可促进脾内淋巴细胞的增殖与分化 ,从组织学角度证明 ,谷氨酰胺可促进脾的免疫应答能力 ,提高机体的免疫功能     

9种除草剂对花生白绢病菌的影响

在实验室条件下测定了氟乐灵、乙草胺、异丙甲草胺、异恶草酮、乳氟禾草灵、乙氧氟草醚、三氟羧草醚、恶草酮、二甲戊乐灵等9种除草剂对花生白绢病菌Sclerotium rolfsi Sacc.的影响.结果表明:9种除草剂对花生白绢病病菌的毒力有较大差异,三氟羧草醚和乙氧氟草醚的毒力较高,IC50分别为7.88mg·L-1和18.91mg·L-1;9种除草剂对菌丝干重均有抑制作用,且随剂量的升高而升高,乙氧氟草醚和三氟羧草醚抑制作用最明显,在100mg·L-1和50mg·L-1时抑制率均达90%以上;除乙草胺和异丙甲草胺部分剂量外,其他除草剂对菌核数量均有不同程度的抑制作用,三氟羧草醚作用最为明显,在供试剂量下抑制率均达96%以上;除乙草胺、氟乐灵在供试剂量下对菌核单重有抑制作用外,其他除草剂在多数剂量下对菌核单重均有刺激作用,三氟羧草醚在50mg·L-1时,是对照菌核单重的8.34倍;而各种除草剂在供试剂量下,对菌核萌发均没有影响.     

检测砂梨潜隐病毒的IC-RT-PCR和TC-RT-PCR的研究

以砂梨为试材,在生物学和血清学检测的基础上,采用免疫捕作RT-PCR穴IC-RT-PCR雪和试管捕作RT-PCR穴TC-RT-PCR雪技术,对苹果褪绿叶斑病毒(Applechloroticleafspotvirus,ACLSV)和苹果茎沟病毒(Applestemgroovingvirus,ASGV)进行了检测分析。结果表明,TC/IC-RT-PCR均能有效检测梨粗提液中的ACLSV和ASGV,分别获得了大小约358bp和499bp的目标扩增片段;但IC-RT-PCR检测ACLSV的效果受到病毒分离株间血清学关系影响。与传统的RT-PCR相比,IC/TC-RT-PCR不仅灵敏度更高,而且不需提取总RNA,可以简化操作程序和减少苯酚、氯仿类有机试剂对人体的伤害和对环境的污染,适合于大量梨样品的病毒快速灵敏检测。     

Model establishment and biological behaviour observation of mouse blastocyst co-cultured with hepatocarcinoma cell lines with differently invasive and metastatic potential in vitro

AIM: To explore interaction and biological behaviour changes of two kinds of cells-blastocysts and hepatocarcinoma cells in the same microenvironment. METHODS:The models of mouse blastocysts co-cultured with human hepatocarcinoma cell lines were established, then biological behaviours and mutual effects of the two kinds of cells in co-culture system were observed. RESULTS: Compared with control group, hepatocarcinoma cells with differently invasive and metastatic potential significantly enhanced the rates of blastocyst hatchment , attachment and outgrowth(P＜0.05). There was no significant difference in those among hepatocarcinoma cells co-cultured groups (P＞0.05). The blastocyst hatched and attached to hepatocarcinoma cells with differently invasive and metastatic potential. Then, differential trophoblasts invaded hepatocarcinoma cells. The clear-cut interfaces were gradually formed between both sides. Hepatocarcinoma cells on interface showed changes of growth direction and cell shapes and did not invade blastocysts. CONCLUSIONS: Hepatocarcinoma cells promoted blastocyst development. Blastocysts implanted and invaded hepatocarcinoma cells with differently invasive and metastatic potential in vitro, which indicate that blastocyst implantation in vitro does not relate with the kinds and differential level of interactional cells and the low selectivity maybe relate with high adaptability of early life.     

除草剂靶标酮醇酸还原异构酶(KARI)研究进展

酮醇酸还原异构酶(KARI)是植物和微生物体内支链氨基酸生物合成的关键酶之一,可以作为设计除草剂的靶标,通过抑制酶的活性中断支链氨基酸的合成使植物死亡,达到除草目的。文章综述了KARI的催化性质、晶体结构以及作为除草剂靶标的研究现状。     

Proteomic analysis of the effects of tumor necrosis factor-α on endothelial cells

AIM: To investigate the affected proteins by tumor necrosis factor (TNF)-α in endothelial cells, and further explore the potential molecular mechanism of TNF-α on endothelial cells. METHODS: Nitric oxide (NO) production in the cultured human umbilical vein endothelial cells (HUVECs) was measured by a NO assay kit. Proteomic alterations were analyzed using two-dimensional electrophoresis, and peptide mass fingerprinting with matrix-assisted laser desorption/ionization-time of flight mass spectrometry. RESULTS: NO production in HUVECs decreased significantly after TNF-α treatement. Proteomics analysis showed 21 protein spots were changed including 9 spots that were increased and 11 spots that were decreased after TNF-α stimulation, and 1 spot was only detected in TNF-α activated cell gels. CONCLUSIONS: Decreased the expression of ecNOS by TNF-α might result in decreased NO production. Up-regulated MAP/ERK kinase 3 expression might imply that TNF-α activates the expression of adhesion molecules. Cytoskeletal protein actin is also involved in TNF-α injuried HUVECs. Proteomic analysis can find some clues for identifying new potential target of TNF-α.     

Astrocyte proliferation in the rat hippocampus after middle cerebral artery occlusion

AIM: To study rat astrocyte proliferation in ipsilateral hippocampus following focal cerebral ischemia. METHODS: Ischemia was induced by temporary middle cerebral artery occlusion (MCAO). In hippocampus of rats at 3, 7 and 30 days after MCAO, the numbers and anatomic distribution of glial fibrillary acidic protein (GFAP) were detected by immunohistochemistry. The protein expression of GFAP and proliferating cell nuclear antigen (PCNA) in the ipsilateral hippocampus were analyzed by Western blot analysis. RESULTS: Astrocytes appeared hypertrophic, with increased process thickness and numbers at 7 days after MCAO, and the highest density of astrocytes were seen at 30 days in the CA1, CA2 regions of the ipsilateral hippocampus. Western blot analysis revealed that GFAP levels were normal at 3 days, but increased by 7 days and remained elevation at 30 days. Western blot analysis of PCNA protein also revealed identified upregulation PCNA at 3 days after MCAO and the expression peaked at 7 days. CONCLUSION: This study demonstrates that focal cerebral ischemia in the rat results in a rapid response, a process often referred to as reactive astrogliosis or glial scarring, from resident astrocytes of the ipsilateral hippocampus to the side of ischemia.