丰城鸡血藤对小鼠造血系统损伤保护作用

目的 研究丰城鸡血藤对60Co-γ射线照射小鼠造血系统损伤保护作用。方法 连续动态观察不同剂量丰城鸡血藤对小鼠经60Co-γ射线照射后1、7、14、21 d外周血白细胞、红细胞、血红蛋白和血小板的影响,同时比较21 d小鼠脾脏指数、胸腺指数变化。结果 给丰城鸡血藤治疗后小鼠外周血白细胞、红细胞、血红蛋白和血小板计数下降趋势减缓,脾脏指数和胸腺指数高于模型组(P<0.05)。结论 丰城鸡血藤可在一定程度上促进辐射损伤小鼠外周血象的恢复,保护造血系统功能。     

灵芪扶正汤对辐射损伤小鼠的防护作用研究

目的研究灵芪扶正汤的抗辐射作用。方法采用60 Coγ射线照射造成辐射损伤模型,分别于照射后第3,7,14和25d检测小鼠外周血象,并测定胸腺、脾脏指数,HE染色观察脾脏的病理学变化。结果辐射损伤后小鼠外周血白细胞、红细胞、血小板计数降低,胸腺、脾脏指数下降。与模型组比较,灵芪扶正汤高剂量差异有统计学意义(P<0.05),可促进上述指标的恢复。结论灵芪扶正汤对辐射损伤小鼠的造血系统和免疫系统具有一定的保护作用。     

参力胶囊对辐射损伤小鼠的药效作用研究

目的:观察中药参力胶囊对60 Co-γ辐射损伤小鼠的防护效果。方法:将120只小鼠进行4Gy 60 Co-γ全身性照射,照射后不同剂量(0.175、0.350、0.700mg/g体重)参力胶囊连续灌胃给药14d,观察其不同时间点(0、3、6、9、14d)外周血白细胞数,血小板数,胸腺、脾脏的质量指数以及骨髓病理切片情况。结果:照射后小鼠白细胞数,血小板数,胸腺、脾脏的质量指数均较正常对照组明显降低,骨髓增殖情况极度不良。照射给药后,小鼠外周血白细胞数,血小板数,胸腺、脾脏质量指数均有所升高,骨髓增殖情况好转,参力胶囊高剂量组升高最为明显。结论:参力胶囊可改善辐射小鼠造血功能,减轻辐射对小鼠的损伤。     

生白饮对钴60照射小鼠造血系统损伤保护作用

目的：研究生白饮对^60Coγ射线照射小鼠造血系统损伤保护作用。方法：连续动态观察生白饮对小鼠经^60Coγ射线照射后7，14，21d外周血白细胞、骨髓有核细胞数、淋巴细胞转化指数、网织红细胞以及细胞肿瘤因子（TNF）、白细胞介素-6（IL6）活性的影响。结果：照射损伤后小鼠外周血白细胞、网织红细胞、骨髓有核细胞数明显减少，淋巴细胞转化指数下降。TNF、IL-6活性降低。生白饮可促进上述各造血指标的恢复及升高（P〈0．05或P〈0．01）。结论：生白饮对照射损伤小鼠造血系统具有保护作用。     

黄芪对急性辐射损伤小鼠预防作用的研究

目的 研究黄芪对急性辐射小鼠免疫器官损伤及外周血细胞减少预防作用的研究。方法：将30只SPF级雄性balb/c小鼠随机分为正常组、模型组、黄芪组（6.5 mL·kg^-1）,每组10只。正常组和模型组小鼠每天灌胃生理盐水,黄芪组小鼠每天灌胃浓缩的黄芪水煎液,1次/d,持续14d。第15d,除正常组外,其余各组小鼠均给予5Gy X射线一次性全身照射,建立急性辐射损伤模型。照射后第8d,处死小鼠取材,进行各项指标的检测,包括脾脏和胸腺指数、脾脏病理切片、红细胞计数、白细胞计数、血红蛋白浓度、血小板计数。结果 照射后第8d,与正常组相比,模型组小鼠外周血白细胞计数、红细胞计数及血红蛋白浓度及血小板计数、胸腺和脾脏指数均明显降低,脾脏红、白髓界限不清;与模型组相比,黄芪组小鼠外周血白细胞计数、红细胞计数及血红蛋白浓度均显著升高,血小板计数、脾脏和胸腺指数未见明显升高,脾脏红、白髓分界尚可。结论 5 Gy X射线致balb/c雄性小鼠的免疫器官损伤及外周血细胞减少,黄芪对急性辐射损伤小鼠具有一定的预防作用。     

五麦党黄口服液对辐射损伤小鼠防护作用的初步研究

目的研究抗辐射复方中药五麦党黄口服液(WMDH)的辐射防护作用。方法将小鼠分为5组,即正常对照组、模型组、3个给药剂量组,连续给药14 d,末次给药后3 h采用60Coγ射线一次性全身照射(7.5 Gy),于照射后记录各给药组存活时间及30 d存活率;另分组及给药剂量同前,连续给药14 d,采用60Coγ射线一次性全身照射(3.0 Gy),测定各给药组动物外周血白细胞数、胸腺、脾脏指数。结果WMDH口服液可显著延长受照射小鼠的存活时间,升高外周血白细胞数、胸腺指数、脾脏指数。结论WMDH口服液对试验小鼠核辐射损伤具有明显的保护作用,值得进一步研究和开发。     

芪术口服液对环磷酰胺所致小鼠骨髓造血功能损伤的保护作用

目的:观察芪术口服液对环磷酰胺所致小鼠骨髓造血功能损伤的保护作用.方法:对小鼠腹腔注射100 mg/kg环磷酰胺后,观察芪术口服液对小鼠外周血象、骨髓有核细胞和胸腺、脾脏指数的影响.结果:芪术口服液能升高受损小鼠白细胞、红细胞、血小板、血红蛋白和骨髓有核细胞数量,并能使小鼠胸腺、脾脏指数升高.结论:芪术口服液对环磷酰胺引起的小鼠骨髓造血功能损伤有一定的保护作用.     

肉苁蓉总苷对~(60)Coγ射线照射小鼠造血系统损伤保护作用的研究

目的　研究肉苁蓉总苷 (GCs )对60 Coγ射线照射小鼠造血系统损伤的辐射防护作用 ,探讨其作用机制。方法　连续动态观察GCs对小鼠经60 Coγ射线照射后d 3,d 7,d14,d 2 1外周血血红蛋白、白细胞、网织红细胞、骨髓有核细胞数、脾集落数 (CFU S)以及骨髓细胞硒 谷胱甘肽过氧化物酶 (Se GSH Px)活性和丙二醛 (MDA)含量的影响。结果　辐射损伤后小鼠外周血白细胞、网织红细胞、骨髓有核细胞数、CFU S明显减少 ,骨髓细胞及脾Se GSH Px活性降低 ,MDA含量明显增加。GCs可促进上述各造血指标的恢复 ,提高Se GSH Px活性 ,降低MDA含量。结论　GCs对受照小鼠造血系统具有保护作用 ,其机制可能与抗氧化作用有关。     

灵芪红胶囊对放化疗所致小鼠白细胞减少症的治疗作用

目的 研究灵芪红胶囊对环磷酰胺和60Co-γ射线照射所致小鼠白细胞减少症的治疗作用,及其升高白细胞的作用机理.方法 采用环磷酰胺和60Co-γ射线造模,观察灵芪红胶囊对两个模型所致白细胞减少症的作用.分别测定骨骼造血干细胞脾脏节结(CFU-S)和人粒-巨噬系祖细胞集落(CFU-GM)及外周白细胞数和骨髓DNA.结果 环磷酰胺和60Co-γ射线照射能使小鼠骨髓白细胞生成减少,灵芪红胶囊能减少环磷酰胺和60Co-γ对小鼠造血系统的损伤作用.结论 灵芪红胶囊升白细胞的作用优于盐酸小檗胺 .     

香菇多糖对放化疗致动物白细胞减少症的影响

目的研究香菇多糖对放化疗致动物白细胞减少症的影响。方法通过制备小鼠和家兔白细胞减少实验动物模型,观察香菇多糖的升白作用。结果在所选择的剂量范围内,10、5、1 mg.kg-1剂量的香菇多糖不仅可以提升X射线照射和环磷酰胺致小鼠的外周血白细胞总数、血小板数量、血红蛋白含量和骨髓有核细胞总数,还可使外周血及骨髓白细胞分类趋于正常,减轻X射线照射和环磷酰胺注射所造成的骨髓抑制作用,并使胸腺、脾脏指数升高;3.7、1.9、0.9 mg.kg-1剂量香菇多糖可以提升盐酸阿糖胞苷致家兔的外周血白细胞、血小板数量和血红蛋白含量,并使外周血及骨髓白细胞分类趋于正常,减轻盐酸阿糖胞苷所造成的骨髓抑制,并使胸腺、脾脏指数升高。结论香菇多糖可以促进白细胞升高,减轻X射线照射、环磷酰胺、盐酸阿糖胞苷导致的骨髓抑制,明显改善骨髓的造血功能。     

Trichloroethylene. I. Carcinogenicity of trichloroethylene.

Trichloroethylene (TCE) as an industrial pollutant may damage human health and can be considered as carcinogen. TCE has been detected in the environment and in various human organs, e.g., liver, kidney and brain etc. There are histological alterations such as depletion of glycogen and hydropic degeneration in the liver, however, other signs of TCE effects can be found in various organs as well. TCE and its metabolites, e.g., trichlorethanol, trichloro-acetic acid and epoxides were recently identified as strong mutagens in Ames mutagenicity test inducing frameshift and base-substitution mutations. TCE induced predominantly hepatocellular carcinoma after long term administration in mice. In these animals, kidneys and liver were supposed to be primary target organs with low epoxy-hydrolase activity. A high level of mitotic gene conversion (or gene rearrangement) was indicated by the metabolism of TCE after repeated administration. Purified TCE by was a weak mutagen in the presence of S9 microsomal fraction of rats and as a consequence, the carcinogenic activity was low in the kidney of rats. However, a dose related increase of Leydig cell tumors was found in male rats.     

Trichloroethylene. II. Mechanism of carcinogenicity of trichloroethylene.

The cancer inducing effect of trichloroethylene (TCE) was studied by various methods. DNA complexing activity and apoptosis inhibition were found to be the key elements of the carcinogenicity of TCE and its metabolites. The ability of TCE to interact with DNA was low, but its incorporation into the RNA and DNA of the brain, testis, pancreas, kidney, liver, lung and spleen, cannot be excluded. Exposure to TCE and its metabolites provides a selective growth advantage to spontaneously occurring mutations in some K- and H-ras oncogenes (as non specific results of secondary DNA or RNA damage). The amount of DNA-TCE adducts was higher in mouse hepatocytes than in rat hepatocytes. These differences may explain the species difference in carcinogenicity of TCE, which was dose dependent (due to metabolism) in mice but independent in rats. The blood level kinetics of TCE confirmed the faster metabolic rate in mice, including peroxisome proliferation and induction in hepatocytes. Dichloroacetic- and trichloroacetic acid were found to be hepatic carcinogens in mice, and the specificity depends on peroxisome proliferation induction. Possibly, TCE and related compounds down regulated apoptosis in mouse liver, and the reduced ability to remove initiated cells by apoptosis could be responsible for liver cancer induction by TCE.     

Studies in antifertility agents. 11. Secosteroids. 5. Synthesis of 9,11-secoestradiol.

9,11-Secoestradiol (9) and 11-hydroxy-9,11-secoestradiol (12) have been synthesized starting from 17-acetoxyestradiol 3-methyl ether (1) and found to possess significant antifertility activity in rats. 3-Methoxy-9,11-seco-9-oxo-17beta-acetoxyestra-1,3,5(10)-trien-11-oic acid (2), prepared by CrO3 oxidation of 1, on hydrogenolysis gave methyl 17beta-hydroxy-3-methoxy-9,11-secoestra-1,3,5(10)-triene-11-carboxylate (3). The 17-O-THP derivative of 3 was treated with LiAlH4 to give 17beta-(O-tetrahydropyranyl)-3-methoxy-11-hydroxy-9,11-secoestra-1,3,5(10)-triene (5). The 11-O-mesylate of 5 on LiAlH4 reduction followed by mild acid treatment and demethylation under alkaline conditions gave 9. LiAlH4 reduction of 3 gave 9,11-seco-11-hydroxyestradiol 3-methyl ether (11) which on demethylation gave 9,11-seco-11-hydroxyestradiol (12).     

Metabolism of benzothiazole. I. Identification of ring-cleavage products.

1. The metabolic fate of benzothiazole in guinea pig has been investigated following i.p. administration at a dose of 30 mg/kg. 2. Five ring-cleavage products were identified in urinary extracts by g.l.c.-mass spectra. By reference to authentic compounds the three major metabolites were shown to be 2-methylmercaptoaniline (I), 2-methylsulphinylaniline (II) and 2-methylsulphonylaniline (III). On the basis of the mass spectrometric evidence the remaining two metabolites were postulated to be 2-methylsulphinylphenylhydroxylamine (IV) and 2-methylsulphonylphenylhydroxylamine (V). 3. I, II and III were present in conjugated and unconjugated forms; IV and V were identified only after hydrolysis with sulphatase.     

Discussion of S.G. Donald et al. and R. Davidson

Summary This paper discusses aspects of the papers by S.G. Donald et al. and R. Davidson, which were presented at The Econometrics Journal sponsored special session on the econometrics of inequality measurement, held at the Royal Economics Society Meeting in Surrey in 2010.