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目的研究绵萆藓中甾醇类的提取分离与鉴定方法。方法采用乙醇提取,递增极性溶剂逐步分离各组分,根据其结构和理化特性进行初步鉴定。结果提取物被分离为极性不等的六个组分,经鉴定只有一个组分中薯蓣皂甙元和甾醇的含量最高。结论本方法简单准确,可为进一步研究提供参考。 相似文献
153.
棠梨花化学成分研究 总被引:2,自引:0,他引:2
目的研究棠梨花的化学成分。方法采用硅胶柱层析,凝胶Pharmadex LH-20柱层析进行分离,采用光谱分析方法包括MS和1D-NMR鉴定化合物结构。结果从棠梨花中分离得到了13个化合物,分别鉴定为熊果醇(1),熊果醛(2),对羟基苄基甲基醚(3),对羟基苄基乙基醚(4),E-1-(4’-羟基苯基)-丁-1-烯-3-酮(5),5,6α-环氧-3β-醇-豆甾烷(6),5,6β-环氧-3β-醇-豆甾烷(7),豆甾-5-烯-3β,7α-二醇(8),棕榈酸胡萝卜苷(9),1,3-二亚油酸甘油酯(10),亚油酸(11),胡萝卜苷(12),β-谷甾醇(13)。结论化合物1~11首次从川梨中分离得到。 相似文献
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We determined the genomic structure of the human gene encoding 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase,
which catalyzes the conversion of HMG-CoA to mevalonate and is the rate-limiting and major regulatory enzyme in sterol biosynthesis.
The gene is more than 21 kb long, about five times the size of its corresponding cDNA. It consists of 20 exons, ranging in
size from 68 to 1809 bp. An amino-terminal hydrophobic membrane-bound domain is encoded by exons 2–10, a flexible linker domain
by exons 10 and 11, and the catalytic domain by exons 11–20. Exons 3–7 encode a sterol-sensing domain. We compared its genomic
structure in this region with the sterol-sensing domains of three related genes, sterol regulatory element binding protein
(SREBP) cleavage-activating protein (SCAP), Niemann-Pick type C1 protein (NPC1), and a morphogen receptor, Patched. Two of
the five positions of introns in the sterol-sensing domain of the HMG-CoA reductase gene were identical to the exon/intron organization of this domain in the related human genes, but these positions of introns
were not conserved in homologues from lower organisms, except in one instance. The data suggested that exon-shuffling may
have occurred during relatively recent evolution; this would account for the structural similarity of this domain in four
quite different human proteins.
Received: April 25, 2000 / Accepted: June 12, 2000 相似文献
158.
目的 探讨早期胰岛素治疗对糖尿病大鼠骨骼肌细胞内胆固醇调节元件结合蛋白-1c(SREBP-1c)表达的影响及可能的分子机制.方法 将7~8周龄高脂喂养联合小剂量链脲佐菌素诱导的雄性糖尿病SD大鼠24只按随机数字表法分为4组:正常对照组、未治疗糖尿病组、胰岛素组、格列齐特组,每组各6只.通过real-time PCR和Western blot法检测骨骼肌细胞SREBP-1c mRNA和核内成熟型蛋白表达水平、肿瘤坏死因子-α(TNF-α)蛋白表达、信号转导及转录活化子3磷酸化(Tyr705)(p-STAT3)蛋白表达水平.结果 与对照组(3.7±1.1)比较,糖尿病大鼠骨骼肌细胞SREBP-1c mRNA(7.3±2.6)和核内蛋白(3.3±0.4)、TNF-α(0.44±0.03)及P-STAT3蛋白(0.50 ±0.08)表达水平显著上调,早期胰岛素治疗则下调了SREBP-1c mRNA(4.1±1.8)和核内蛋白(2.7±0.3)表达、TNF-α(0.19±0.22)及P-STAT3蛋白(0.29±0.03)表达,差异有统计学意义(P<0.05).结论 早期胰岛素治疗抑制骨骼肌细胞内脂质合成通路中关键转录分子的表达,可能是骨骼肌内脂质沉积减少的机制之一. 相似文献
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《Annals of hepatology》2023,28(1):100762
Introduction and ObjectivesType 2 Diabetes Mellitus (T2DM) is comorbidity commonly presenting with fatty liver. A recently proposed definition of "metabolic associated fatty liver disease" (MAFLD) is thought to replace non-alcoholic fatty liver disease (NAFLD). Yet, despite the significant prevalence of T2DM among fatty liver, there remains limited evidence on the impact of the change in the definition of T2DM.Materials and MethodsThe current study uses data from the United States National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018. Survival analysis was conducted with a cox regression and sub-distribution hazard ratio for competing risk events.Results6727 patients had a diagnosis of T2DM. 4982 individuals with T2DM had MAFLD and 2032 were MAFLD(+)/NAFLD(-), while 2950 patients were MAFLD(+)/NAFLD(+). The new definition increased fatty liver diagnosis by 68.89%. Patients who were classified as MAFLD(+)/NAFLD(-) were at a higher risk of major adverse cardiovascular events, advanced fibrosis, all-cause and cardiovascular-related mortality compared to MAFLD(+)/NAFLD(+). In MAFLD(+)/NAFLD(-), viral hepatitis significantly increases the odds of advanced fibrosis (OR: 6.77, CI: 3.92 to 11.7, p < 0.001) and all-cause mortality (HR: 1.75, CI: 1.29 to 2.40, p < 0.001).ConclusionsThe identification and treatment of NAFLD in patients with T2DM is a major concern and the premature change to MAFLD results in an over-diagnosis of fatty liver, exaggerated mortality, and morbidity in patients with T2DM. The definition of MAFLD causes further heterogeneity in fatty liver disease/NAFLD. 相似文献