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61.
This mini-review aims to compare the differences in the kinetics of the induction of micronucleated polychromatic erythrocytes (MN-PCE) and cytotoxicity by distinct antineoplastic and genotoxic agents in murine peripheral blood in vivo and to correlate these kinetics with the underlying processes. Comparisons were carried out using our previously obtained data with nominal doses causing similar levels of cytotoxicity, as measured in terms reduction of PCE. The aneuploidogens caused the most rapid induction of MN-PCEs and had the highest rates of cytotoxicity and genotoxicity. The promutagens cyclophosphamide and dimethylnitrosamine showed the most delayed responses and had the lowest genotoxic and cytotoxic efficiencies. DNA crosslinking agents had a similar delay of 4–5 h, greater than those of aneuploidogens, but differed in their cytotoxic and genotoxic efficiencies. Methylnitrosourea and 5-aza-cytidine caused greater delays than crosslinking agents. These delays can be due to the methylnitrosourea-mediated induction of formation of mono alkyl adducts which are interpreted as mismatches during DNA duplication, whereas 5-aza-cytidine requires incorporation into the DNA to induce breakage. This review allows us to conclude that the requirement for metabolic activation and the mechanisms of DNA breakage and of micronucleus induction are the main factors that affect the time of maximal MN-PCE induction.  相似文献   
62.
目的观察益气活血解毒化痰方对二甲基亚硝胺(DMN)诱导的大鼠肝纤维化预防和治疗作用.方法 DMN诱导大鼠肝纤维化,分别于造模初及结束时灌服益气活血解毒化痰方,以重组人干扰素α2b肌肉注射对照.90d后测定血清谷草转氨酶(AST)、谷丙转氨酶(ALT)活性,总胆红素(TBil)、总蛋白(TP)、白蛋白(Alb)含量,放射免疫分析法测定层粘连蛋白(Laminin,LN)、Ⅳ型胶原(collagen TypeⅣ,Ⅳ-C)、透明质酸(Hyaluronic Acid,HA)、Ⅲ型前胶原(Procollagen Type Ⅲ,PC Ⅲ)含量,同时苏木素-伊红(HE)染色及苦味酸-天狼星红染色,光镜下观察肝细胞损伤及胶原纤维增生程度.结果益气活血解毒化痰方预防性给药,能明显降低DMN诱导肝纤维化大鼠AST、ALT活性及TBil含量(P<0.05),提高TP、Alb含量(P<0.05),降低LN含量(P<0.05);造模结束后治疗性给药,明显降低Ⅳ-C、HA含量(P<0.05);预防及治疗给药均改善肝细胞损伤及胶原纤维增生程度,预防性给药明显降低纤维化计分(P<0.05).结论预防性及治疗性服用益气活血解毒化痰方,均抑制DMN诱导的大鼠肝纤维化,而预防性给药能更好地阻止肝纤维化的形成和发展.  相似文献   
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64.
目的:观察大鼠肝纤维化形成过程中成纤维细胞激活蛋白(fibroblast activation protein, FAP)的动态表达变化特点。方法:Wistar雄性大鼠分为正常对照组和模型组。模型组ip 0.5%二甲基亚硝胺复制肝纤维化模型, 于造模1、2、3周分别收集肝组织标本, 造模4周后处死大鼠, 收集血清和肝组织标本。全自动生化仪测定丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、总胆红素(TBIL)、谷氨酰转肽酶(GGT)和白蛋白(ALB), HE、天狼猩红染色观察病理形态, 试剂盒测定肝组织羟脯氨酸;real-time PCR和western blotting法检测肝组织FAP基因和蛋白表达。结果:模型组肝功能较正常组明显下降, 组织病理形态学和羟脯氨酸测定显示模型组肝损伤明显, 纤维化形成。real-time PCR和western blotting显示FAP基因和蛋白随造模时间延长表达逐渐增高。结论:FAP伴随大鼠肝纤维化模型形成逐渐增加, 与肝纤维化形成密切相关。  相似文献   
65.
积雪草总苷抗DMN诱导大鼠肝纤维化的作用   总被引:5,自引:0,他引:5       下载免费PDF全文
目的 研究积雪草总苷抗实验性大鼠肝纤维化的作用。方法 采用二甲基亚硝氨(dimethylni-trosamine,DMN)腹腔注射6周,制备大鼠肝纤维化模型。动物随机分为6组(正常组、模型组、秋水仙碱组、积雪草总苷大、中、小剂量组)。于造模开始时同时给予积雪草总苷灌胃,实验结束后分别检测血清总蛋白(TP)、白蛋白(ALB)、谷丙转氨酶(ALT)、谷草转氨酶(AST)、透明质酸(HA)、层粘连蛋白(LN)含量,并作肝组织病理学观察。结果 积雪草总苷能改善肝功能,与模型组相比可明显降低血清ALT、AST、HA的含量(P<0.05)。肝组织病理学检查显示具有抗肝纤维化作用。结论 积雪草总苷对DMN诱导的大鼠慢性肝纤维化具有良好的治疗作用。  相似文献   
66.
目的:观察柴胡皂苷d抗实验大鼠肝纤维化的作用和可能的作用机理。方法:本实验将18只雄性SD大鼠随机分为正常组,模型组和柴胡皂苷d(saikosaponin d,SSd)预防组。模型组和SSd预防组大鼠均腹腔注射二甲基亚硝胺(DMN),建立大鼠肝纤维化模型。在造模的同时予以SSd腹腔注射预防,1次/d,共4周。正常组大鼠只相应注射生理盐水。检测肝功和血清肝纤维化指标Ⅳ型胶原(IV—C)水平。病理学观察HE和天狼星红染色切片。免疫组化法测定α—SMA和TGF—β,在肝组织中的表达。结果:和模型组相比SSd预防组大鼠血清ALT和肝纤维化标志物IV—C的水平显著下降(P〈0.01),表明SSd对肝脏具有保护作用;HE和天狼星红染色观察到肝纤维化程度改善,胶原沉积面积明显减少(P〈0.01);免疫组化结果表明SSd显著抑制α—SMA和TGF—β在大鼠肝组织中的表达(P〈0、01)。结论:SSd具有预防DMN诱导的肝纤维化作用,能够预防肝纤维化的发展,可能和它调节胶原沉积,抑制肝星状细胞活化作用有关。  相似文献   
67.
The cytotoxicity and mutagenicity of dimethylnitrosamine (DMN) was determined in the CHO/HGPRT system. Metabolic activation of the promutagen was achieved by use of a liver homogenate supernatant (S9) prepared from Aroclor 1254-induced Sprague-Dawley rats. The cytotoxic and mutagenic effects of DMN were enhanced by the inclusion of calcium chloride in the incubation mix, and this enhancement was dependent on the presence of sodium phosphate. Under conditions that yielded maximal activity (10 mM calcium chloride, 10 mM magnesium chloride, 50 mM sodium phosphate), an apparent calcium phospate precipitate was observed. DMN activity increased with increasing amounts of S9 protein over the range 0.3–3.0 mg/ml in the S9 mix and appeared to plateau at higher concentrations. The mutagenicity of DMN can be described as 110 mutants/106 cells per mM DMN per mg/ml S9 protein per hour.  相似文献   
68.
Transplacental administration of 200 mg/kg of 3,4-benzpyrene (Bp) by intraperitoneal injection caused marked increase in 8-azaguanine (8AG)-resistant mutations in lung (75.2107 cells) and total body cells. Morphological transformations and chromosome aberrations were also observed in lung and total body cells. On transplacental administration of 200 200 mg/kg of dimethylnitrosamine (DMN), the highest rates of morphological transformation (6.53%) and 8AG-resistant mutation (128107 cells) were induced in cells of liver origin, and chromosome abnormalities were also detected in liver and total body cells. Transplacental administration of 100 mg/kg of nitrosomethylurea (NMU) caused a marked increase in transformed colonies (4.08–4.40%) and 8AG-resistant mutations (134.8 and 79.9107 cells) of brain and total body cells. The cells from mice and rats that were most affected by transplacental administration of these chemicals were derived from the respective target organs of these chemicals in vivo.  相似文献   
69.
Cultures of adult rabbit hepatocytes have been used to study the early toxic effects of 2 model hepatotoxins, dimethylnitrosamine and allyl alcohol. Leakage of glutamate oxaloacetate transaminase and glutamate pyruvate transaminase into the cell culture medium was a sensitive indicator of plasma membrane damage by these compounds and a dose-response relationship was observed. By contrast, γ-glutamyltranspeptidase and alkaline phosphatase were insensitive markers. The effects of dimethylnitrosamine were slower to develop. Dimethylnitrosamine also produced a dose-related inhibition of protein synthesis after 4 h, a decrease in NADPH diaphorase and an increase in non-specific esterase after 20 h. Dimethylnitrosamine, unlike allyl alcohol, caused extensive disruption of ribosome association with the endoplasmic reticulum.  相似文献   
70.
C3H strain male mice were treated with dimethylnitrosamine (DMN) during 8 successive weeks at dose levels of 0.05 and 0.1 mg/kg per day: chromosomal translocations were not produced.  相似文献   
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