复合天然添加剂对鹌鹑蛋品质影响的研究

用300只10月龄产蛋鹌鹑随机分成3组,对照组A饲喂全价基础日粮,试验组B添加0.5%的含有红椒粉和油菜花粉的天然添加剂,试验组C添加0.5%的含有红椒粉和甜茶粉的天然添加剂,试验期15天。测定第0、5、10、15天的蛋重、蛋形指数、蛋壳厚度、蛋黄指数及蛋黄色泽度(RCF)。结果表明:B和C蛋黄色泽度明显高于A(P<0.01),同时B高于C(P<0.05);B和C蛋黄指数显著高于A(P<0.05,P<0.01),且第15天时B显著高于C(P<0.05);蛋重、蛋形指数和蛋壳厚度组间差异不显著(P>0.05)。试验说明:该两种复合天然添加剂能够明显提高鹌鹑蛋黄色泽度和蛋黄指数。     

吉林省主要粮食作物比较优势分析

根据比较优势理论，应用综合比较优势指数法对吉林省玉米、水稻、大豆三种主要粮食作物在1997-2005年间的比较优势变动趋势进行了分析，其结果表明：三种作物中，玉米具有明显的比较优势，大豆次之，水稻则处于劣势，但呈现出稳步上升的趋势；并在此基础上提出了吉林省主要粮食作物结构调整的建议。     

BMY牛的选育进展

总结了经历20多年选育的BMY牛所取得的进展,再通过3～5年的努力将完成BMY牛的培育,届时BMY牛将是一个适应我国南方炎热地区的热带肉牛新品种.     

氮肥对保水剂吸水保肥性能的影响

测定保水剂在不同氮肥(尿素、碳酸氢铵、硝酸铵、硫酸铵、氯化铵)溶液中的吸水倍率和对肥料养分的吸持量,分析不同氮肥对保水剂吸水、保肥性能的影响。结果表明:保水剂在各种氮肥溶液中吸水倍率显著下降,并随肥料浓度的增加下降幅度增加;受影响程度聚丙烯酸钠盐型保水剂大于聚丙烯酰胺-丙烯酸盐型保水剂;不同氮肥对保水剂吸水倍率的影响按尿素、碳酸氢铵、硝酸铵、硫酸铵、氯化铵顺序递增。保水剂在大量吸水的同时,也对溶液中的肥料分子或者离子有吸持作用,吸持量均随肥料浓度的增加而增加;保水剂和肥料品种不同,吸持量也不同;除尿素外,保水剂对肥料的吸持率随肥料浓度的增加而降低,最高浓度下,吸持率按硝酸铵、碳酸氢铵、氯化铵、硫酸铵、尿素次序依次增大。     

猪附红细胞体可溶性抗原的分析

为了解附红细胞体可溶性抗原的特性,本试验对解离下的猪附红细胞体,经超声波裂解制备粗抗原,再经SephadexG-200分离提纯后,应用对流免疫电泳(CIEP)定位特异性抗原蛋白峰,再进行十二烷基硫酸钠-聚丙烯酰胺凝胶电泳(SDS-PAGE)及免疫印迹(Westernblot),对猪附红细胞体粗提及纯化的可溶性抗原进行了分析。结果表明,猪附红细胞体可溶性抗原的电泳图谱上有四条蛋白带,其分子量分别为77Ku、62Ku、58Ku、29Ku,其中特异性抗原分子量为58Ku和29Ku。从而为附红细胞体抗原成分的进一步分析及该病的免疫学诊断等研究奠定了基础。     

浙东白鹅肉用性能测定

为研究浙东白鹅的种质特性和生产性能,笔者曾于2006年5月对浙东白鹅(10周龄未经肥育肉鹅)的屠宰性能、鹅肉的常规营养成分及肉质性状进行测定分析,现将结果报告如下。1材料与方法试验从浙东白鹅原种场随机选择10周龄未经肥育的浙东白鹅12只(公5只,母7只),空腹12h后按常规方法屠     

喷施KH_2PO_4对胡萝卜采种的影响

通过叶面喷施磷酸二氢钾(KH2PO4)溶液,对胡萝卜种株生长势、种子产量、质量和种子活力进行了研究。结果表明,种株抽薹后喷施2g·L-1KH2PO4溶液不仅可提高叶片光合速率和蒸腾速率,而且可显著提高种株的茎粗、节长、花盘横径及生物产量,可使种子产量和千粒重显著增加,种子的发芽活力显著提高。     

设施栽培中桃树14C同化物分配特性的研究

 利用放射性同位素¹⁴C - 示踪方法研究了设施桃树果实不同发育时期¹⁴ C同化物的运转分配特性。结果表明: 在果实膨大期和果实成熟期, 分配到果实中的¹⁴C同化物最多, 随着果实生长, 分配到果实中的¹⁴C同化物比例增加。叶片的自留量小于果实获得的¹⁴C同化物量, 且随着果实的生长, 叶片的自留量逐渐减少。在各器官中果实的放射比活性最强, 其次为叶片与根系。说明果实膨大期和果实成熟期是设施桃树对碳素同化物需求和竞争最大的时期。     

Effects of tetramethylpyrazine on calcinerin and proliferating cell nuclear antigen gene expression in the proliferation of vascular smooth muscle cells

AIM：To evaluate the effects of tetramethylpyrazine (TMP) on calcineurin (CaN) and proliferating cell nuclear antigen (PCNA) gene expression in the proliferation of vascular smooth muscle cells (VSMCs) treated by angiotensin Ⅱ (AngⅡ).METHODS：A cell proliferating model of VSMCs induced by AngⅡ was established.PCNA gene exprersion was observed by immunocytochemical staining and image analysis technique;Calcineurin (CaN) activity was detected by enzyme reaction phosphorus measurement.RESULTS：AngⅡ significantly stimulated the proliferation of VSMCs,cell proliferation activity,CaN activity and the expression levels of PCAN were higher than those in control (P<0.01).While treated with TMP,the CaN activity and PCNA expression were obviously lower than those in AngⅡ group (P<0.01).CONCLUSION：The VSMCs proliferation induced by AngII can be inhibited by tetramethylpyrazine significantly,and the inhibiting mechanism of TMP may be related to inhibiting CaN activity and restraining the expression of PCNA in a dose and time-dependent manner.     

Effect of TLR4 activation on endothelium adhesion function and atorvastatin intervention

AIM：To investigate the modulation of LOX-1 and monocyte-endothelium adhesion by TLR4 activation in human umbilical vein endothelial cells (HUVECs),and explore LOX-1’s role in mediating monocyte-endothelium adhesion,and the effect of atorvastatin.METHODS：TLR4 and LOX-1 mRNA were measured by RT-PCR.The expression percentage of TLR4 and LOX-1 positive cells were detected by flow cytometry.The adhesive percentage between monocytes and HUVECs were determined by counting.RESULTS：Incubation by LPS (1 mg/L) for 24 hours upregulated TLR4,LOX-1 mRNA and protein expression in HUVECs，and increased the percentage of monocyte adhesion to endothelium.Pretreatment of cell with anti-LOX-1 partly abolished the increase of monocyte adhesion to endothelium.Atorvastatin (10 μmol/L) inhibited LPS-mediated effects above.CONCLUSION：TLR4 activation upregulates LOX-1 expression and increases monocyte-endothelium adhesion.LOX-1 partly involves in LPS-induced monocyte-endothelium adhesion,atorvastatin may have protective effects on endothelium by inhibiting TLR4 and TLR4-induced LOX-1 expression.