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71.
72.
同型半胱氨酸水平,MTHFR基因突变与原发性高血压的病例对照研究 总被引:3,自引:0,他引:3
从上海一个社区中随机选取127例35~75岁的原发性高血压病人和170例正常血压者。采用聚合酶链反应-限制性片段长度多态性分析MTHFR基因多态性。使用高效液相色谱结合电化学方法检测血清中同型半胱氨酸总浓度,使用放射免疫法同时测定血甭中叶酸和B12浓度。结果:调整年龄和性别后,病例和对照组同型半胱氨酸水平分别为10.56μmol/L和10.34μmol/L,差异无显著性(P=0.63)。在未服降压 相似文献
73.
对4’-去甲表鬼臼毒素的C_4位进行化学修饰,合成和筛选了10个4-烷硫基-4-脱氧-4’-去甲表鬼臼毒素衍生物以进一步研究C_4位不同的原子和取代基与活性之间的关系及寻找结构简单、活性更强的抗肿瘤新药。4’-去甲表鬼臼毒素与硫醇在三氟化硼·乙醚或三氟乙酸存在下生成相应的硫醚,也可用硫醇与4β-溴-4-脱氧-4’-去甲表鬼臼毒素反应生成相应的硫醚。在体外筛选中,化合物10和12抑制L1210白血病细胞的活性与依托泊甙相当或更强,化合物9,10,12和15抑制KB细胞的活性与依托泊甙相当或更强。 相似文献
74.
4-S-(5-酰氨基-1,3,4-噻二唑-2-基)-4-脱氧-4′-去甲基表鬼臼毒素衍生物的合成与抗肿瘤活性 总被引:3,自引:0,他引:3
基于在4′-去甲基表鬼臼毒素母核C4位上联结含有杂原子的芳香环取代基,以此考察其结构与活性关系的设想,设计并合成了10个标题化合物。体外L1210白血病细胞与KB细胞生长抑制试验结果表明,这类化合物有较强的抗肿瘤活性。其中化合物SIPI-92-1772,1774,1775,1776,1777与1779的活性超过临床用药依托泊甙。其余化合物活性与依托泊甙相当或略低。 相似文献
75.
Differentiation of hematopoietic precursor cells results in the formation of clonally related descendent cells. Using the mosaic expression of beta-galactosidase in female mouse fetuses heterozygous for an X-linked lacZ transgene, we analyzed the clonal relationship of the hematopoietic progeny. The proportion of beta-galactosidase positive cells for different T- and B-lymphoid and myeloid cell populations was determined at different stages of fetal development. We found excellent correlations of the proportion of beta-galactosidase expressing cells for all hematopoietic lineages confirming that they share a common ancestry. Therefore, it was possible to estimate the number of common precursor cells (PC) based on binomial distribution and covariance analysis of pairs of different hematopoietic cell populations. Our results obtained from hematopoietic cells at 15.5 to 18.5 days of gestation indicated the presence of 15 to 18 lymphoid and 18 to 22 myeloid/lymphoid specific precursor cells. Statistical analysis of the precursor cell numbers showed a trend of increasing numbers that was highly significant. The precursor cell number was inversely related to maturity of the cell populations analyzed; ie, the lowest number of lymphoid and lymphoid/myeloid precursors was calculated when the most mature CD3+ T-cell population was used for comparison. Determination of PC numbers can therefore be used to assess the relative maturity and developmental potential of individual cell populations. 相似文献
76.
WS Chung MB ChB MRCPsych YK Wing MRCP MRCPsych HFK Chiu MB BS MRPsych TS Lee MB ChB MRCPsych CN Chen FRCPsych FRANZCP 《International journal of clinical practice》1997,51(3):186-188
Narcolepsy is a chronic condition that usually afflicts the patient for decades. It is more common than is generally appreciated. However, it is likely to be misdiagnosed because doctors are unfamiliar with some of the symptoms. Its significant socioeconomic impact on the patient's quality of life warrants prompt medical attention. 相似文献
77.
Tears of the triangular fibrocartilage of the wrist: MR imaging 总被引:2,自引:0,他引:2
78.
79.
Long-range sequence analysis in Xq28: thirteen known and six candidate genes in 219.4 kb of high GC DNA between the RCP/GCP and G6PD loci 总被引:3,自引:0,他引:3
80.
Generalized CNS disease and massive GM1-ganglioside accumulation in mice defective in lysosomal acid beta-galactosidase 总被引:5,自引:1,他引:5
Hahn CN; del Pilar Martin M; Schroder M; Vanier MT; Hara Y; Suzuki K; Suzuki K; d'Azzo A 《Human molecular genetics》1997,6(2):205-211
Human GM1-gangliosidosis is caused by a genetic deficiency of lysosomal
acid beta-galactosidase (beta-gal). The disease manifests itself either as
an infantile, juvenile or adult form and is primarily a neurological
disorder with progressive brain dysfunction. A mouse model lacking a
functional beta-gal gene has been generated by homologous recombination and
embryonic stem cell technology. Tissues from affected mice are devoid of
beta-gal mRNA and totally deficient in GM1-ganglioside- hydrolyzing
capacity. Storage material was already conspicuous in the brain at 3 weeks.
By 5 weeks, extensive storage of periodic acid Schiff- positive material
was observed in neurons throughout the brain and spinal cord. Consistent
with the neuropathology, abnormal accumulation of GM1-ganglioside in the
brain progressed from twice to almost five times the normal amount during
the period from 3 weeks to 3.5 months. Despite the accumulation of brain
GM1-ganglioside at the level equal to or exceeding that seen in gravely ill
human patients, these mice show no overt clinical phenotype up to 4-5
months. However, tremor, ataxia and abnormal gait become apparent in older
mice. Thus, the beta-gal- deficient mice appear to mimic closely the
pathological, biochemical and clinical abnormalities of the human disease.
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