蜂王浆冻干粉对小鼠肿瘤的抑制作用

目的研究蜂王浆冻干粉对小鼠肿瘤的抑制作用.方法按每公斤体重0g、0.25g、0.50g、0.75g设对照及低、中、高3个剂量组,经口给予蜂王浆冻干粉30d后,接种小鼠肉瘤180(S180)和艾氏癌腹水型(EAC)两个瘤种.结果在两次重复的小鼠S180和EAC抑瘤试验中发现中剂量组瘤重明显低于阴性对照组(P<0.05),抑制率可达34%;中剂量组荷瘤小鼠平均生存时间均明显高于对照组(P<0.05).结论蜂王浆冻干粉具有抑制肿瘤的作用.     

Establishment of Germ-line Competent C57BL/6J Embryonic Stem Cell Lines

Objective To establish C57BL/6J embryonic stem （ES） cell lines with potential germ- line contribution Methods ES cells were isolated from blastocyst inner cell mass of C5 7BL/6J mice, and cultured for 15 passages, and then injected into blastococels of ICR mice blastocysts to establish chimeric mice. Results Three ES cell lines （mC57ES1,mC57ES3, mC57ES7） derived from the inner cell mass of C57BL/6J mice blastocysts were established. They were characteristic of undifferentiated state, including normal XY karyotype, expression of a specific cell surface marker “stage-specific embryonic antigen-I” and alkaline phosphatase in continuous passage. When injected into immunodeficient mice, mC57ES1 cells consistently differentiated into derivatives of all three embryonic germ layers. When mC57ES1 cells were transferred into ICR mice blastocysts, 4 chimeric mice have been obtained. One male of them revealed successful germ-line transmission. Conclussion We have obtained C57BL/6J ES cell lines with a potential germ-line contribution, which can be used to generate transgenic and gene knock-out mice.     

姬松茸多糖的抗炎作用

[目的 ]观察姬松茸多糖的抗炎作用 .[方法 ]制作二甲苯所致小鼠耳急性炎症模型、角叉菜胶所致大鼠关节肿胀模型、小鼠棉球肉芽肿亚急性炎症模型和大鼠佐剂关节炎模型 ,给予 4 0 ,80 ,16 0mg/kg的姬松茸多糖 .[结果 ]姬松茸多糖明显抑制上述各类型炎症反应 .[结论 ]姬松茸多糖具有抗炎作用 .     

The Lipid-regulating Effects of Atorvastatin on Type 2 Elder Diabetes Patients with Hyperlipidemia

Inthisstudy,theeffectofatorvastatinonlipidmetabolism ,especiallysLDL ,intype 2elderdiabetespatientswithhyperlipidemiawasstudy .Theresultswerepresentedasfollows.1　SUBJECTSANDMETHODS1 1　SubjectsThesubjectsincluded 2 6patientswithtype 2elderdiabetesandhyp…     

高脂血症患者血小板体积及有关参数的研究

本文报道242例高脂血症患者血小板(PLT)、平均血小板数(MPLT)及平均血小板体积(MPV)等参数的测定结果,其中高胆固醇并高甘油三酯患者,PLT、MPLT及巨大血小板比例(Macro-PLT)高于正常,MPV正常;而单纯高胆固醇或高甘油三酯患者,上述指标与正常人无显著性差异。提示高胆固醇并高甘油三酯患者,存在血小板生成动力学异常,其血小板的破坏增加,生成率加速、但处于一种高水平的动态平衡之中。这可能是高脂血症出现高凝状态的原因之一。同时表明此类患者使用抗血小板疗法具有一定的合理性和必要性。     

中药“附归参汤”修复混合菌所致小鼠输卵管炎性狭窄的病理改变

目的观察中药“附归参汤”灌胃给药后是否可改善混合菌导致的小鼠输卵管炎性狭窄的病理改变。为临床应用“附归参汤”治疗输卵管炎所致的不孕症提供实验依据。方法昆明小鼠随机分为对照组（n=10）、模型组（n=10）、模型组＋生理盐水处理组（n=10）、模型＋“附归参汤”处理组（n=20），输卵管炎性狭窄模型采用混合菌（溶血性链球菌、大肠埃希菌和金黄色葡萄球菌2：1：1）输卵管接种法制作，处理组分别胃饲生理盐水和“附归参汤”30天。应用组织学方法观察各组的病理学改变，评判各处理组病理学转归情况。结果在使用混合菌接种后，小鼠输卵管管壁结构发生改变，主要包括黏膜层水肿、上皮细胞顶端纤毛变短或消失、固有层炎性细胞浸润、毛细血管充血、管腔狭窄甚至闭塞。“附归参汤”长期给药后明显使上述病理改变向正常组织转归。结论中药“附归参汤”能够修复混合菌导致的小鼠输卵管炎性狭窄的病理改变，为临床应用该药治疗输卵管炎所致的不孕症提供了实验依据。     

磁性远红外寝具对高脂血症患者血脂、血糖及抗氧化作用的影响

目的 观察磁性远红外寝具对高脂血症患者血脂、血糖及抗氧化作用的影响。方法 60例高脂血症患者，按随机数字表法分为实验组（30例）和对照组（30例）。实验组每晚（6～8h）均使用磁性远红外寝具，连续2个月。对照组用普通寝具。两组均于实验前后取全血，测定血脂、血糖及抗氧化指标等。结果 实验组实验后血清总胆固醇，甘油三酯含量明显低于实验前；实验前后血清高密度脂蛋白胆固醇（HDL-ch）含量及血糖无明显变化（P〉0．05）。实验组实验后MDA含量较实验前显著下降（P〈0．05），而血清超氧化物歧化酶（SOD）活性较实验前显著提高（P〈0．01）；实验前后血清中NO含量无明显变化（P〉0．05）。对照组实验前后以上各项指标较实验前均无明显变化，差异均无显著性（P〉0．05）。结论 磁性远红外寝具对高脂血症患者具有降血脂作用及抗氧化作用。     

久泻宁动物毒性试验研究

目的 （1）观察久泻宁一日内小鼠灌胃1～3次后的毒性反应和死亡情况，测定最大耐受量；（2）观察久泻宁给大鼠连续灌胃3个月，对机体产生的毒性反应、严重程度及可逆性，确定无毒剂量。为人拟用量提供参考。方法 （1）久泻宁小鼠灌胃，一日2～3次，观察急性毒性反应．测定最大耐受量；（2）久泻宁高、中、低三个剂量组和一个对照组，大鼠连续灌胃3个月，观察外观行为和体质量变化。试验期结束。每组取1/2动物活杀。检测血常规、血液生化、病理组织；1／2动物停药进行3周的恢复期观察后。同法检测上述指标。结果 久泻宁小鼠灌胃给药的最大耐受药量为750g／kg（含生药）。相当临床日拟用量（2．5g／kg）的300倍；大鼠连续3个月灌胃给药的无毒剂量为125g／kg（含生药）．相当临床拟用量50倍。结论 久泻宁无明显毒性，安全范围大。临床日拟用量2.5g／kg、疗程1个月是安全的。     

Interleukin-18 Affects Local Cytokine Expression But Does Not Impact on the Development of Kidney Allograft Rejection

Interleukin-18 is predominantly a macrophage-derived cytokine with a key role in inflammation and cell-mediated immunity. Having previously demonstrated IL-18 upregulation in a rat model of kidney rejection, here we examined IL-18 in a fully MHC-mismatched murine model of acute kidney rejection using IL-18-deficient recipients (IL-18-/-) and animals administered neutralizing IL-18 binding protein (IL-18BP). Gene expression of IL-18 and its receptor were significantly upregulated in allografts compared to isografts, as was the cellular infiltrate (T cells and macrophages) (p < 0.001). Allografts developed kidney dysfunction (p < 0.05) and tubulitis (p < 0.01) not observed in controls. There was a significant reduction in gene expression of IL-18 downstream pro-inflammatory molecules (iNOS, TNFalpha and IFNgamma) in IL-18-/- recipients (p < 0.01), and IL-18BP-treated animals. The CD4+ infiltrate and IL-4 mRNA expression was greater in the IL-18-/- recipients than wild-type (WT) allografts and IL-18BP-treated animals (p < 0.05), suggesting a Th2-bias which was supported by IFNgamma and IL-4 ELISPOT data and an increased eosinophil accumulation (p < 0.001). Neither IL-18 deficiency nor neutralization prevented renal dysfunction or tubulitis. This study demonstrates increased production of IL-18 in murine kidney allograft rejection and provides evidence that IL-18-induced pathways of inflammation are active. However, neither IL-18 deficiency nor neutralization was protective against the development of allograft rejection.