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91.
James W. Verbsky Mary K. Hintermeyer Pippa M. Simpson Mingen Feng Jody Barbeau Nagarjun Rao Carlyne D. Cool Luis A. Sosa-Lozano Dhiraj Baruah Erin Hammelev Alyssa Busalacchi Amy Rymaszewski Jeff Woodliff Shaoying Chen Mary Bausch-Jurken John M. Routes 《The Journal of allergy and clinical immunology》2021,147(2):704-712.e17
92.
M. C. DeRuiter A. C. Gittenberger-De Groot A. C. G. Wenink R. E. Poelmann M. M. T. Mentink 《Anatomical record (Hoboken, N.J. : 2007)》1995,243(1):84-92
Background: Classic theories descibe that the common pulmonary vein develops as an outgrowth from either the sinus venosus or atrial segment. Recent studies show that the pulmonary veins are connected to the sinu-atrial region before its differentiation into a sinus venosus and atrial segment. Methods: The development of the sinu-atrial region with regard to the developing common pulmonary vein and the growth of the atrial septum was investigated in avian embryos, using both scanning electron microscopy and immunohistochemistry. Embryos ranging between stage HH12 and HH28 were incubated with QH-1 that recognizes quail endothelial cells and precursors, HNK-1, that appears in this study to detect the myocardium of the sinus venosus, or with HHF-35, being specific for muscle actins. Also vascular casts of the heart were produced by injecting prepolymerized Mercox into the vascular system. Results: In preseptation stages the common pulmonary vein drains into the left part of the sinus venosus, that is clearly demarcated by the sinuatrial fold and HNK-1 expression. During atrial septation the left part of the sinus venosus, in contrast to the right part, loses its HNK-1 antigen from stage HH23 onwards, while at the same time the sinu-atrial fold in the left atrial dorsal wall flattens and disappears. From stage HH25 onwards HNK-1 expression is restricted to the right part of the sinus venosus, which contributes to the right atrium. The myocardial atrial septum never expresses the HNK-1 antigen, suggesting that the septum is of atrial origin. Discussion: It appeared that the sinus venosus does not only contribute to the sinus venarum of the right atrium, but also to the left atrium. © 1995 Wiley-Liss, Inc. 相似文献
93.
以博莱霉素A5造成大鼠肺间质纤维化动物模型,测定实验组和对照组鼠血浆及肺组织匀浆的内皮素(ET)含量。实验组大鼠血浆ET含量211.67±18.37ng/L,显著高于对照组的(183.91±23.86ng/L,P<0.05),而其肺组织匀浆的ET含量却显著低于对照组的(208.03±85.98ng/Lvs281.37±65.30ng/L,P<0.05)。同时检测两组动物的动脉血血气分析及肺组织的病理观察。提示内皮素在肺间质纤维化形成中有一定作用。 相似文献
94.
一氧化氮诱导大鼠肺动脉平滑肌细胞凋亡机制研究 总被引:3,自引:3,他引:3
目的:研究一氧化氮(NO)诱导大鼠肺动脉平滑肌细胞(PASMC)凋亡的作用机制。方法:体外培养Wistar大鼠PASMC,加入NO供体硝普钠(SNP)于常氧和低氧条件下孵育12h或24h,通过流式细胞术碘化丙啶染色法观察PASMC细胞周期时段及凋亡亚二倍体峰变化,应用细胞免疫化学法检测PASMCcaspase-3和NF-κB的表达,同时行DNA断裂琼脂糖凝胶电泳。结果:SNP作用后PASMC出现剂量-依赖性促凋亡作用(P<0.01),表现为凋亡指数与caspase-3表达的不同程度的增强。随凋亡的进展,出现PASMC凋亡核小体DNAladder,同时PASMCNF-κB阳性核表达较对照组少(P<0.01)。结论:外源性NO诱导大鼠PASMC凋亡,caspase-3与NF-κB可能涉及PASMC凋亡的调控信号途径。 相似文献
95.
96.
以6mg/kg体重皮下注射N-亚硝基-N-氨基甲酸乙酯诱发大鼠急性肺泡损伤,在注射后第2天,肺泡灌洗液(即肺泡空间成份)表面活性物质磷脂含量明显减少,而蛋白质含量明显增加。细胞内层状体和微粒体中磷脂及蛋白质含量未见明显改变。与此同时,各肺成份中磷脂的组成也发生了变化,即PG/PI的比率明显降低。分子种的检测显示,两种酸性磷脂(Po和PI)的分子种构成不同,其主要分子种在急性肺泡损伤时有所改变。 相似文献
97.
L. B. Kim 《Bulletin of experimental biology and medicine》2008,146(6):680-681
We studied enzyme systems (lactate dehydrogenase) of mitochondria in cerebral nerve cells in experimental encephalopathy developing
after thermal injury. In animals receiving neuromedin at the early terms after injury, the ratio of forward to reverse lactate
dehydrogenase reactions significantly increased over the first day after injury and returned to normal on day 7.
__________
Translated from Byulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 145, No. 6, pp. 626–627, June, 2008 相似文献
98.
Double nondisjunction during karyotypic progression of chemically induced Syrian hamster cell lines 总被引:1,自引:0,他引:1
The karyotypic evolution of three chemically induced cell lines of Syrian hamster embryo in culture are described. The only karyotypic alteration of one clone was a trisomy of chromosome #11, which presumably arose by nondisjunction after carcinogen treatment. A pure population of cells with the trisomy was observed repeatedly upon karyotyping of cells at the first three passages after cloning. However, at a late passage, apparently normal diploid cells appeared in the culture, which we propose resulted from a second nondisjunction of one chromosome #11, reverting the cells from trisomy 11 to disomy 11. The karyotypic evolution of two other cell lines also involved double nondisjunction, which resulted in duplication of a translocated chromosome and concurrent loss of the normal nonrearranged chromosome. Taken together with the reported findings of others, the results indicate that double nondisjunction is a mechanism in karyotypic progression during neoplastic development. 相似文献
99.
压力超负荷大鼠心、肺、肾血管重构的动态研究 总被引:3,自引:1,他引:3
目的 探讨压力超负荷与大鼠心、肺、肾内小动脉形态学重建的关系。方法 采用缩窄腹主动脉造成大鼠压力负荷模型,将大鼠随机分为两组:假手术组(SOG)和手术组(OG)。每组分为术后1、2、4、7、14、21、30、45、60d 9个时间点,对大鼠心、肺、肾组织连续切片,采用光镜配合计算机图像分析技术检测三个脏器小动脉几何形态的动态改变。结果 (1)随着压力负荷的增加,心、肺、肾小动脉的形态学重建可能存在时间顺序。(2)平均动脉压和造模时间与小冠状动脉和肾小动脉的壁腔比显著相关,而对小冠状动脉的管壁面积无影响;收缩压和造模时间与肾小动脉的管壁面积显著相关;造模时间与肺小动脉的壁腔比和管壁面积显著相关。结论 压力超负荷与心、肺、肾小血管的动态重构关系密切。小冠状动脉的重建以中膜平滑肌细胞的重排为主,肺、肾内小动脉的重建则可能存在中膜平滑肌细胞的肥大和增殖。 相似文献
100.
Mutation analysis of the TSC1 and TSC2 genes in Japanese patients with pulmonary lymphangioleiomyomatosis 总被引:2,自引:0,他引:2
Sato T Seyama K Fujii H Maruyama H Setoguchi Y Iwakami S Fukuchi Y Hino O 《Journal of human genetics》2002,47(1):20-28
Pulmonary lymphangioleiomyomatosis (LAM) is a destructive lung disease characterized by a diffuse hamartomatous proliferation
of smooth muscle cells (LAM cells) in the lungs. Pulmonary LAM can occur as an isolated form (sporadic LAM) or in association
with tuberous sclerosis complex (TSC) (TSC-LAM), a genetic disorder with autosomal dominant inheritance with various expressivity
resulting from mutations of either the TSC1 or TSC2 gene. We examined mutations of both TSC genes in 6 Japanese patients with TSC-LAM and 22 patients with sporadic LAM and identified six unique and novel mutations.
TSC2 germline mutations were detected in 2 (33.3%) of 6 patients with TSC-LAM and TSC1 germline mutation in 1 (4.5%) of 22 sporadic LAM patients. In accordance with the tumor-suppressor model, loss of heterozygosity
(LOH) was detected in LAM cells from 3 of 4 patients with TSC-LAM and from 4 of 8 patients with sporadic LAM. Furthermore,
an identical LOH or two identical somatic mutations were demonstrated in LAM cells microdissected from several tissues, suggesting
LAM cells can spread from one lesion to another. Our results from Japanese patients with LAM confirmed the current concept
of pathogenesis of LAM: TSC-LAM has a germline mutation but sporadic LAM does not; sporadic LAM is a TSC2 disease with two somatic mutations; and a variety of TSC mutations causes LAM. However, our study indicates that a fraction of sporadic LAM can be a TSC1 disease; therefore, both TSC genes should be examined, even for patients with sporadic LAM.
Received: August 30, 2001 / Accepted: November 2, 2001 相似文献