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991.
同源四倍体皇家嘎拉苹果的生长结果特性 总被引:2,自引:1,他引:2
皇家嘎拉苹果四倍体是一个由皇家嘎拉苹果二倍体经诱变处理获得的品系。为了解皇家嘎拉苹果四倍体与二倍体对照植株在生长结果特性方面的差异,取2种果树的接穗高接到10年生大树上,在植株结果后进行了调查研究。结果表明,由皇家嘎拉苹果二倍体诱变成的同源四倍体植株在高接后第3年开始结果,其花萼、花瓣、雌蕊、雄蕊及花药比对照大;叶片变宽,叶柄和果柄变短粗;单果大,种子数少,果形指数小,果实可溶性固形物、总糖和可滴定酸含量增高;其节间长、叶长及果肉硬度与二倍体则无显著差异。 相似文献
992.
用改进的Ellman方法测定了河北省昌黎、涿州、卢龙和抚宁四个不同地理种群甘薯茎线虫Ditylenchus destructor的乙酰胆碱酯酶(AChE)的生化特性及其对抑制剂涕灭威和毒扁豆碱的敏感性差异。结果表明:甘薯茎线虫AChE至少存在两种类型,一种类型对毒扁豆碱的IC50值小于10^-6mol/L,另一种类型大于10^-4mol/L。当抑制剂毒扁豆碱浓度为10^-6~10^10mol/L、涕灭威浓度为10^-5~10^10mol/L时,甘薯茎线虫昌黎种群AChE的敏感性抑制率明显高于涿州、抚宁、卢龙三地的甘薯茎线虫种群AChE的抑制率。各地种群AChE对抑制剂敏感性差异是由于甘薯茎线虫AChE的多态性和各分子型综合性改变的结果。 相似文献
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Gencheng Zhang Yanqing Wang Hongmei Zhang Shuhe Tang Weihua Tao 《Pesticide biochemistry and physiology》2007,87(1):23-29
The interaction between herbicide paraquat and human serum albumin (HSA) was investigated by fluorescence and UV/Vis absorption spectroscopy. Paraquat can strongly quench the intrinsic fluorescence of HSA by static quenching and nonradiative energy transferring; The hydrophobic and electrostatic interactions play a major role in stabilizing the complex. The binding site number n and apparent binding constant KA, corresponding thermodynamic parameters ΔG, ΔH, ΔS at different temperatures, were calculated. The distance r between donor (HSA) and acceptor (paraquat) was obtained according to fluorescence resonance energy transfer. The effect of paraquat on the conformation of HSA was analyzed using synchronous fluorescence spectroscopy. 相似文献
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对60头大约克夏从70~190日龄,每隔15d测定体重和背膘厚,分析其生长发育规律。结果表明:①大约克夏生长肥育期的各阶段日龄与体重间的相关系数r≥0.67(P<0.0001)。②Logistic模型和Compertz模型均可拟合大约克夏在生长肥育期的生长曲线(P<0.0001),但Logistic模型(R2=0.9967)优于Compertz模型(R2=0.9694)。③大约克夏130 ̄160日龄间的背膘厚度与体重保持极小的比值(约0.11),160日龄前背膘厚的分化生长率小于1(0.2653 ̄0.7711);大约克夏190日龄时体重为119.31kg,背膘厚为14.59mm。 相似文献
1000.
ZHANG Hao-qing ZOU Peng WANG Hua-dong LU Da-xiang LI Mei-ai QI Ren-bin WANG Yan-ping FU Yong-mei 《园艺学报》2007,23(3):495-499
AIM:To investigate the mechanisms by which berberine attenuates LPS-induced acute lung injury, and provide a new strategy for the treatment of the lung injury due to LPS. METHODS:BALB/c mice were randomly assigned into three groups (control, LPS group, and berberine treatment group). Mice were administered intragastrically with distilled water (0.1 mL/10 g) or neutral sulfate berberine (50 mg/kg) once a day for 3 days, 1 h after intragastrical treatment on day 3, LPS (20 mg/kg) or normal saline was injected intraperitoneally (ip). All animals were sacrificed 12 h after LPS injection, the left lung tissue sections were prepared for histology analysis and the right lung were used to determine the ratio of wet to dry lung tissue weight (W/D). In another experiment, bronchoalveolar lavage fluid (BALF) was collected, and then the total protein content, and the amounts of white blood cells (WBC) and polymorphonuclear neutrophils (PMN) in BALF were determined. Furthermore, the phosphorylation of cytosolic phospholipase A2 (cPLA2) was detected with immunohistochemical analysis by using phospho-cPLA2(Ser505) antibody, and the contents of thromboxane B2 (TXB2) in BALF, malondialdehyde (MDA) in the lungs, and activity of superoxide dismutase (SOD) in lung tissues were also determined.RESULTS:LPS induced acute lung injury, activated cPLA2, and increased TXB2 content in the BALF and MDA level in the lung tissue. The pretreatment with berberine significantly attenuated lung injury, lung edema and protein leakage induced by intraperitoneal injection of LPS. The expression of phospho-cPLA2 in the lung tissues and TXB2 content in the BALF in the berberine treatment group were lower than those in LPS group (P<0.05). In addition, the content of MDA in the lung tissue was lower in the berberine treatment group than LPS group (P<0.05), but there was no significant difference in activity of lung SOD between the berberine treatment and LPS group (P>0.05). CONCLUSION:Pretreatment with berberine remarkably reduces the LPS-induced lung injury, which is, at least in part, through inhibiting phosphorylation of cPLA2 and decreasing lipid peroxidation. These findings provide a new strategy for the prevention and treatment of LPS-induced acute lung injury. 相似文献