全文获取类型
收费全文 | 73873篇 |
免费 | 4994篇 |
国内免费 | 1519篇 |
专业分类
耳鼻咽喉 | 560篇 |
儿科学 | 1275篇 |
妇产科学 | 1104篇 |
基础医学 | 10140篇 |
口腔科学 | 1617篇 |
临床医学 | 4925篇 |
内科学 | 10007篇 |
皮肤病学 | 1230篇 |
神经病学 | 5323篇 |
特种医学 | 2429篇 |
外国民族医学 | 1篇 |
外科学 | 6216篇 |
综合类 | 8400篇 |
现状与发展 | 8篇 |
一般理论 | 1篇 |
预防医学 | 5341篇 |
眼科学 | 902篇 |
药学 | 11835篇 |
15篇 | |
中国医学 | 4268篇 |
肿瘤学 | 4789篇 |
出版年
2023年 | 765篇 |
2022年 | 1026篇 |
2021年 | 2604篇 |
2020年 | 1993篇 |
2019年 | 2470篇 |
2018年 | 2336篇 |
2017年 | 2510篇 |
2016年 | 2249篇 |
2015年 | 2243篇 |
2014年 | 2621篇 |
2013年 | 4170篇 |
2012年 | 3290篇 |
2011年 | 3185篇 |
2010年 | 2427篇 |
2009年 | 3005篇 |
2008年 | 3354篇 |
2007年 | 3911篇 |
2006年 | 3726篇 |
2005年 | 3529篇 |
2004年 | 2984篇 |
2003年 | 2832篇 |
2002年 | 2381篇 |
2001年 | 2245篇 |
2000年 | 2045篇 |
1999年 | 1871篇 |
1998年 | 1341篇 |
1997年 | 1393篇 |
1996年 | 1226篇 |
1995年 | 1040篇 |
1994年 | 1048篇 |
1993年 | 891篇 |
1992年 | 799篇 |
1991年 | 795篇 |
1990年 | 707篇 |
1989年 | 553篇 |
1988年 | 553篇 |
1987年 | 460篇 |
1986年 | 406篇 |
1985年 | 524篇 |
1984年 | 450篇 |
1983年 | 353篇 |
1982年 | 342篇 |
1981年 | 274篇 |
1980年 | 292篇 |
1979年 | 190篇 |
1978年 | 124篇 |
1977年 | 129篇 |
1976年 | 112篇 |
1975年 | 93篇 |
1970年 | 84篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
991.
支气管肺炎患儿治疗前后血清SIL-2R和白三烯测定的临床意义 总被引:1,自引:0,他引:1
目的:探讨了血清可溶性白细胞介素-2受体(SIL-2R)和半胱氨酰白三烯(LTS)水平在支气管肺炎患儿治疗前后的变化及意义。方法:应用ELISA对35例支气管肺炎患儿进行了血清SIL-2R和LTS测定,并与30例正常儿作比较。结果:支气管肺炎患儿在治疗前血清SIL-2R和LTS水平非常显著地高于正常儿组(P〈0.01)。治疗后2周后血清SIL-2R和LTS水平与正常儿比较无显著性差异(P〉0.05)。结论:检测支气管肺炎患儿血清中SIL-2R和LTS水平可作为病情预后判断的重要指标。 相似文献
992.
目的 了解IL-7对中国HIV/AIDS患者病程的影响。方法应用超敏感酶免法对66例中国HIV/AIDS感染者及8例健康对照者血浆IL-7水平进行定量检测,分析其与CD^+T细胞绝对值、血浆病毒载量及HIV表型的相关性;并且在体外研究rhIL-7对人PBMC中T淋巴细胞增殖及CXCR4表达的影响。结果中国HIV/AIDS患者血浆IL-7水平高于健康对照(P〈0.05),与CD4^+T细胞绝对值负相关(P〈0.01),与血浆病毒载量正相关(P〈0.05)。rhIL-7可在体外促进T淋巴细胞增殖反应及CXCR4表达。结论中国HIV/AIDS患者血浆IL-7水平升高,且与疾病进展密切相关,可作为疾病进展的相关标志之一。 相似文献
993.
目的:探讨了NO、NOS和血浆C-型利钠多肽(CNP)水平在急性颅脑损伤早期的病理、生理作用。方法:分别应用放免法测定血浆CNP水平,生化法测定NO、NOS水平。结果:在治疗前急性颅脑损伤患者血浆CNP水平和NO水平非常显著地低于正常人组水平(P<0.01),而NOS水平显著地高于正常人组水平(P<0.01),经治疗后一个月则与正常人组比较无显著性差异(P>0.05)。结论:观察血浆CNP、NO和NOS水平的变化对研究急性早期颅脑损伤的病理生理变化,判断疗效及预后观察是具有十分重要的临床意义。 相似文献
994.
995.
It is well known that prolonged exposure to morphine results in tolerance to morphine-induced antinociception. In the present study, we found that mice that were tolerant to morphine-induced antinociception exhibited an increase in immunoreactivity for the neural cell adhesion molecule in the dorsal horn of the spinal cord, which was highly overlapped with immunoreactivity for the increased metabotropic glutamate receptor 5 induced by morphine. These findings support the idea that repeated stimulation of μ-opioid receptors increases the expression of neural cell adhesion molecule and metabotropic glutamate receptor 5. This phenomenon leads to the enhanced excitatory synaptic transmission in the dorsal horn of the spinal cord, and in turn suppresses the morphine-induced antinociception. 相似文献
996.
B. Shannon Danes Paula De Angelis Frank Traganos Ulrik Ringborg Lars Holme Nielsen Myron R. Melamed 《Clinical genetics》1990,37(3):188-193
The anatomical location of the squamous cell carcinoma (SCCA) within the oral cavity and oropharynx influenced the association of SCCA with the biomarker in vitro hyperdiploidy in human dermal fibroblast cultures (IVH). There was a strong association of IVH with the occurrence of SCCA in the anterior 2/3 of the tongue, floor of the mouth and lower alveolar ridge of the oral cavity and in the base of the tongue and pharyngeal wall of the oropharynx. There was a lower association of SCCA with IVH in the tonsillar region of the oropharynx. IVH showed no association with SCCA located in other anatomical parts of the oral region. The patient group whose diagnosis of SCCA in the anterior 2/3 of the tongue occurred prior to the age of 50 years were invariably IVH-, whereas those diagnosed after the age of 50 years were IVH+, providing evidence for heterogeneity. There was no such correlation of biomarker subgrouping with age of diagnosis demonstrated for SCCA at any other anatomical location within the oral cavity or oropharynx. 相似文献
997.
Boldogköi Zsolt Braun Attila Medveczky István Glávits Róbert Gyúró Bence Fodor István 《Virus genes》1998,17(1):89-98
A recombinant pseudorabies (Aujeszky’s disease) virus (PrV) designated as vE16lac was constructed by deleting a 3-kbp DNA
segment spanning the junction of long and short components of the viral genome, and by replacing the deleted segment with
a lacZ-expression cassette. The aim of constructing this mutant was (a) to determine whether the terminal repeat (Tr) can
serve as a template for the regeneration of the internal repeat (Ir), and (b) whether this deletion causes a reduction in
the neuroinvasiveness of the virus. To analyze the mechanism of equalization, revertant viruses were selected and structurally
characterized from vE16lac infection of PK-15 cells, mice and pigs. Because all revertants acquired Ir sequences identical
to that of the wild-type virus, the equalization process occurred using the Tr as a template to reconstitute the Ir. We also
found that the recombinant virus vE16lac was virulent in both pigs and mice. The data are discussed in view of studies performed
with similar PrV mutants by other authors (Rall et al., 1992, Dean and Cheung, 1995 and Dean et al., 1996).
This revised version was published online in July 2006 with corrections to the Cover Date. 相似文献
998.
999.
Lida Bruni Barbara Angeletti Esterina Pascale Maria Cristina Tozzi Paola Giammaria Roberto Verna Ettore D'Ambrosio 《Clinical genetics》1996,50(2):89-92
Genotyping with flanking DNA markers was used to ascertain Treacher Collins Franceschetti syndrome (TCOF1) in a subject affected by tetralogy of Fallot and cryptorchidism. The proband's family consisted of a father and sister who were affected by the disease, and a healthy mother. Since cardiac malformation and cryptorchidism have been associated with the TCOF1 syndrome, the proband was suspected to be a carrier of the mutated gene. Microsatellite markers D5S527, SPARC and D5S519, which previously mapped the TCOF1 gene within a 2.1-cM interval on chromosome 5 (5q32–33.1), were used to follow the transmission of the TCOf 1 mutated locus. Flanking markers D5S519 and D5S527 were informative and enabled us to exclude inheritance of a TCOF1 mutation to the proband, while showing that cardiac malformation and cryptorchidism were unrelated in mis patient. 相似文献
1000.
Shichi D Kikkawa EF Ota M Katsuyama Y Kimura A Matsumori A Kulski JK Naruse TK Inoko H 《Tissue antigens》2005,66(3):200-208
Cardiomyopathy is a heart muscle disease with impaired stretch response that can result in severe heart failure and sudden death. A small proportion of hepatitis C virus (HCV)-infected patients may be predisposed to develop dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM). The molecular mechanisms involved in the predisposition remain unknown due in part to the lack of information on their genetic background. Because the human leukocyte antigen (HLA) region has a pivotal role in controlling the susceptibility to HCV-induced liver disease, we hypothesized that particular HLA alleles and/or non-HLA gene alleles within the human major histocompatibility complex (MHC) genomic region might control the predisposition to HCV-associated DCM (HCV-DCM) and/or HCV-associated HCM (HCV-HCM). Here, we present mapping results of the MHC-related susceptibility gene locus for HCV-associated cardiomyopathy by analyzing microsatellite and single nucleotide polymorphism markers. To delineate the susceptibility locus, we genotyped 44 polymorphic markers scattered across the entire MHC region in a total of 59 patients (21 HCV-DCM and 38 HCV-HCM) and 120 controls. We mapped HCV-DCM susceptibility to a non-HLA gene locus spanning from NFKBIL1 to MICA gene loci within the MHC class III-class I boundary region. Our results showed that HCV-DCM was more strongly associated with alleles of the non-HLA genes rather than the HLA genes themselves. In addition, no significant association was found between the MHC markers and HCV-HCM. This marked difference in the MHC-related disease susceptibility for HCV- associated cardiomyopathy strongly suggests that the development of HCV- DCM and HCV-HCM is under the control of different pathogenic mechanisms. 相似文献