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目的:验证雪灵芝是否具有抑制大鼠肝癌的功效。方法:实验于2003—09/2004—08在广西疾病预防控制中心SPF级动物实验室完成。选用健康成年SD大鼠160只。按体质量分层随机分为5组:空白对照组、模型组、雪灵芝高剂量组、雪灵芝中剂量组和雪灵芝低剂量组,每组32只。雪灵芝高、中、低剂量组大鼠分别灌胃2.500,1.250,0.625mL/kg雪灵芝溶液,阴性对照组和模型组灌胃等量蒸馏水,1次/d,连续60d。第61天开始雪灵芝高、中、低剂量组和模型组灌胃二乙基亚硝胺溶液,对照组灌胃等量的生理盐水。于停止灌胃90d后各组处死一半受试大鼠(雌雄各半),检测血常规及血清主要生化指标,观察各脏器大体形态改变、脏器的癌变程度。1周后给剩余大鼠灌胃雪灵芝溶液(不含二乙基亚硝胺)。7周后处死余下的一半雄性大鼠,进行相同操作。8周后处死余下的全部大鼠,操作及检测方法同前。结果:纳入的160只SD大鼠,145只进入结果分析,15只脱落。①病理切片检查结果:除阴性对照组,其他各组大鼠肝组织均发生癌变或癌前病变。雪灵芝高、中、低剂量组的癌前病变发生率与模型组相近(P〉0.05);癌变的发生率均低于模型组,差异有显著性意义(P〈0.05,0.01)。②大体标本检查结果:阴性对照组大鼠肝脏的大体标本均无异常改变,其他各组大鼠的肝脏有些可见表面粗糙等病理改变。模型组大体标本病理改变的阳性率高于雪灵芝高、中、低剂量组,差异有显著性意义(P〈0.05)。肉眼观模型组癌变发生率高于其他各组。③其他脏器检查结果:模型组2只大鼠有肝癌肺转移。结论:以较大剂量的二乙基亚硝胺连续灌胃30d可以复制大鼠肝癌模型;雪灵芝对二乙基亚硝胺诱导的大鼠肝癌具有预防和抑制的作用。 相似文献
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A new frameshift mutation due to an insertion of G between codon 14/15 of the beta-globin gene was found in two unrelated Chinese patients with Cooley's anemia. The first patient (W.S.) was homozygous for haplotype 5 (Chinese) and carried a codon 41/42 (four base pair deletion) mutant, while the second patient (C.K.) was homozygous for haplotype 2 (Chinese), and also had a codon 17 (A----T) nonsense mutation. Molecular cloning and M13 sequencing of the beta gene in patient W.S. revealed that the new mutant was found in a beta-globin gene framework type 3 (Asian). Direct sequencing was performed on polymerase chain reaction-amplified genomic DNA from patient C.K. With the new mutation, an additional BstNI or EcoRII recognition site is generated and the abnormal restriction fragment (134 basepair) can be directly visualized on polyacrylamide gel electrophoresis of the amplified genomic DNA. 相似文献
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对睾酮及表睾酮的三甲基硅烷化进行了详细考察,找到了较好的抗氧剂巯基乙醇,确定了较好的衍生化条件,衍生化产物单一。并采用GC—MS法测定了尿中睾酮与表睾酮的比值。实验条件为:以氦为载气,SE—54熔融石英柔性毛细管柱、程序升温进行样品分离,多离子检测(MID),监测m/z432的离子。该法专属、灵敏、快速。睾酮与表睾酮比值在1:1~10:1(睾酮为20ng/μl)与相应峰面积比呈线性关系(r=0.998),最低检测限为1ng,最低检测尿药浓度为8ng/ml。 相似文献
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World Workshop on Oral Medicine VI: a systematic review of medication‐induced salivary gland dysfunction 下载免费PDF全文
A Villa A Wolff N Narayana C Dawes DJ Aframian AM Lynge Pedersen A Vissink A Aliko YW Sia RK Joshi R McGowan SB Jensen AR Kerr J Ekström G Proctor 《Oral diseases》2016,22(5):365-382
The aim of this paper was to perform a systematic review of the pathogenesis of medication‐induced salivary gland dysfunction (MISGD). Review of the identified papers was based on the standards regarding the methodology for systematic reviews set forth by the World Workshop on Oral Medicine IV and the PRISMA statement. Eligible papers were assessed for both the degree and strength of relevance to the pathogenesis of MISGD as well as on the appropriateness of the study design and sample size. A total of 99 papers were retained for the final analysis. MISGD in human studies was generally reported as xerostomia (the sensation of oral dryness) without measurements of salivary secretion rate. Medications may act on the central nervous system (CNS) and/or at the neuroglandular junction on muscarinic, α‐and β‐adrenergic receptors and certain peptidergic receptors. The types of medications that were most commonly implicated for inducing salivary gland dysfunction were those acting on the nervous, cardiovascular, genitourinary, musculoskeletal, respiratory, and alimentary systems. Although many medications may affect the salivary flow rate and composition, most of the studies considered only xerostomia. Thus, further human studies are necessary to improve our understanding of the association between MISGD and the underlying pathophysiology. 相似文献