Xa21转基因大米对大鼠致畸作用的实验研究

目的　观察Xa2 1转基因大米对大鼠胚胎生长、发育的影响。方法　将初断乳Wistar大鼠按雌雄分别随机分为 4组 :转基因大米组、非转基因大米组、AIN93G对照组和敌枯双阳性对照组。单笼喂养 ,饲相应鼠料 ,喂满 90天 ,雌雄合笼。观察母鼠和胎鼠的生长发育情况。结果　转基因大米组孕鼠增重、活胎体重、身长、尾长均显著高于阳性对照组 ,而死胎数、吸收胎数、畸形率 (外观、内脏、骨骼 )均显著低于阳性对照组。转基因大米组与非转基因大米组、AIN93G对照组相比 ,所有观察指标均无统计学差异。结论　转Xa2 1基因大米与非转基因大米相比 ,对大鼠受孕率、胚胎生长发育无显著性差异。     

转基因大米的免疫毒理学评价

目的　评价转基因大米和非转基因大米对小鼠免疫功能的异同。方法　以转豇豆胰蛋白酶抑制剂 (cowpeatrypsininhibitor ,CpTI)基因大米和母系非转基因大米喂养BALB C小鼠 30天 (均配成AIN 93G的全价营养饲料 ,并且含有最大量的转基因大米或非转基因大米 ) ,比较各组小鼠的各项免疫毒理指标 :体重、脏器指数、血常规、淋巴细胞分类、血清抗体滴度、空斑试验 (PFC)、迟发型皮肤过敏反应 (DTH)、腹腔巨噬细胞吞噬鸡红细胞试验。结果　发现转基因大米和非转基因大米喂养的小鼠各项免疫毒理指标无差异。结论　转基因大米对小鼠的免疫功能的影响与非转基因大米基本相同 ,转基因大米与非转基因大米在免疫毒理学方面的评价具有“实质等同性”。     

转豇豆胰蛋白酶抑制剂大米的致畸作用研究

目的　用表达杀虫蛋白CpTI(豇豆胰蛋白酶抑制剂 )的大米喂养Wistar大鼠 ,研究其是否具有致畸作用。方法　将断乳的Wistar大鼠随机分为 4组 ,转基因大米组、非转基因大米组、阴性对照组和阳性对照组 ,敌枯双为阳性对照物。转基因大米组含 78 3%转基因大米 ,非转基因大米组含 74 7%与转基因大米同品系的非转基因大米 ,两个对照组的饲料为AIN93G ,三种饲料的宏量及微量营养素的含量相同。大鼠性成熟后 ,进行传统的致畸实验 ,观察母鼠及胎鼠的情况。结果　转基因大米组的孕鼠增重、胎鼠体重、身长和尾长显著高阳性对照组 ,畸形率 (包括外观畸形、骨骼畸形和内脏畸形 )显著低于阳性对照组 (P <0 0 1) ,转基因大米组、非转基因大米组及阴性对照组间的所有指标均无显著性差异 (P >0 0 5 )。结论　此种转CpTI基因的大米对大鼠无母体毒性、胚胎毒性和致畸作用。     

水中微量甲胺磷农药的检验

目的选择检出水中微量甲胺磷农药的最佳方案。方法分别使用液-液萃取法、固相萃取法、活性炭富集法提取甲胺磷含量极低的液体检材，提取液经MS／GC检验。结果液-液萃取法为阴性结果，固相萃取法、活性炭富集法为阳性结果。结论实验表明对于常规液-液萃取方法效果欠佳的甲胺磷含量极低的液体检材，采取固相萃取法或活性炭富集法进行萃取，可提高检出率。     

甘草体外抑制呼吸道合胞病毒作用研究

目的:开发安全有效的抗呼吸道合胞病毒的新药.方法:采用细胞病变抑制实验观察甘草在Hela细胞中对呼吸道合胞病毒的抑制作用.结果:甘草半数中毒浓度(TC50)为3.43g/L;抑制呼吸道合胞病毒的半数有效浓度(EC50)为0.2535g/L,治疗指数(TI)为13.53;甘草对呼吸道合胞病毒的抑制作用存在量效反应关系;在感染后0 h、2 h、4 h、6 h、8 h,甘草均有抑制呼吸道合胞病毒的作用.结论:甘草在Hela细胞中对呼吸道合胞病毒有明显的抑制作用,其作用机制是多途径的.     

鹿茸口服液对抗氧化酶的影响

目的:研究鹿茸口服液对青年及老年小鼠的抗氧化作用.方法:灌服鹿茸口服液后,测定小鼠SOD、CAT和GSHpx活性及MDA含量.结果:鹿茸口服液对老年小鼠SOD活性增强和MDA含量降低作用均明显强于对青年小鼠,并能增强老年小鼠肝CAT和GSHpx活性.结论:鹿茸口服液对老年小鼠具有抗氧化作用.     

Hb Alesha [β67(E11)Val→Met (GTG>ATG); HBB: c.202G > A] Found in a Chinese Girl

Mutations that cause destabilization of the hemoglobin (Hb) tetramer are a rare cause of hemolytic anemia. In contrast to the hemolytic anemia caused by enzyme deficiencies, a dominant mode of inheritance characterizes the unstable Hbs. Hb Alesha [β67(E11)Val→Met; HBB: c.202G>A] is caused by a G>A mutation at codon 67 of the β-globin gene, resulting in a valine to methionine substitution at helix E11. This replacement disrupts the apolar bonds between valine and the heme group, producing an unstable Hb and severe hemolysis. We report this rare hemoglobinopathy in a Chinese girl with severe hemolytic anemia, splenomegaly and frequent requirement for red blood cell (RBC) transfusions.     

Mechanism underlying treatment of diabetic kidney disease using Traditional Chinese Medicine based on theory of Yin and Yang balance

The pathogenic mechanism of diabetic kidney disease(DKD) is complex. The development of DKD cannot be fully explained by a single mechanism.Traditional Chinese Medicine(TCM) has been applied extensively for the treatment of DKD in China.However, studying the mechanism of DKD using theories and methods that are appropriate for TCM characteristics and searching for theoretical bases for TCM clinical application are topics that still need to be explored and researched. Activation of the transforming growth factor(TGF)-β1/Smad and PI3 K/Akt/mTOR signaling pathways functions as a self-protection mechanism against renal microinflammation in DKD. However, the persistent abnormal overactivation of reactions causes secondary cell dysfunction, cell apoptosis, increased extracellular matrix(ECM) secretion, and eventually renal fibrosis. During this process, the dysregulation of self-balance among a variety of signaling pathways and the loss of self-feedback regulatory mecha-nisms downstream of these signaling pathways are critical causes of the occurrence and development of DKD. TCM may both inhibit the expression or activation of "hyperactive" signaling pathways(NFB, Smad3, and PI3 K/Akt/mTOR) and increase the expression or activation of "deficient" signaling pathways(Smad7 and PTEN) to restore balance to cells with an abnormal pathophysiological status and achieve the goal of DKD treatment.