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101.
102.
Nigel A. Cunliffe Bimal K. Das Madhumati Ramachandran Maharaj K. Bhan Roger I. Glass Jon R. Gentsch 《Virus genes》1997,15(1):39-44
We have sequenced the genes encoding the inner capsid protein VP6 and the nonstructural proteins NSP1 and NSP4 of the Indian
neonatal serotype P8[11]G9 human/bovine reassortant candidate vaccine rotavirus strain 116E. These three genes share a high
degree of sequence and deduced amino acid homology with human prototype strain Wa. Our results confirm and extend those of
previous RNA-RNA hybridization studies which suggested that these genes are of human origin, and will facilitate examination
of the host immune response to 116E induced by natural infection and vaccination.
This revised version was published online in July 2006 with corrections to the Cover Date. 相似文献
103.
Kiyoshi Tanabayashi Kaoru Takeuchi Michiko Hishiyama Akio Yamada Akira Sugiura 《Virus genes》1990,3(4):361-365
The nucleotide sequence of the gene encoding the matrix (M) protein of mumps virus (MuV), Miyahara strain, has been determined from several overlapping cDNA clones. The M protein mRNA is 1248 nucleotides in length, exclusive of the poly(A) tail, and codes for a protein of 375 amino acids (Mr41,556). Comparison of the deduced amino acid sequence of the M protein of the Miyahara strain with that of the SBL-1 strain revealed that the M proteins of both strains are highly conserved. A significantly lower rate of nucleotide differences conducive to amino acid differences in the M gene compared with other genes appeared to indicate the importance of the conserved primary structure of the M protein for its function.Requests for reprints should be addressed to Kiyoshi Tanabayashi, Department of Measles Virus, National Institute of Health, 4-7-1 Gakuen, Musashimurayama, Tokyo 190-12, Japan. 相似文献
104.
Henriques C Sanchez MA Tryon R Landfear SM 《Molecular and biochemical parasitology》2003,130(2):101-110
African trypanosomes are unable to synthesize purines and depend upon purine nucleoside and nucleobase transporters to salvage these compounds from their hosts. To understand the crucial role of purine salvage in the survival of these parasites, a central objective is to identify and characterize all of the purine permeases that mediate uptake of these essential nutrients. We have cloned and functionally expressed in a purine nucleobase transport deficient strain of Saccharomyces cerevisiae a novel nucleobase transporter gene, TbNT8.1, from Trypanosoma brucei. The permease encoded by this gene mediates the uptake of hypoxanthine, adenine, guanine, and xanthine with Kms in the low micromolar range. The TbNT8.1 protein is a member of the equilibrative nucleoside transporter (ENT) family of permeases that occur in organisms as diverse as protozoa and mammals. TbNT8.1 is distinct from other ENT permeases that have been identified in trypanosomes in utilizing multiple purine nucleobases, rather than purine nucleosides, as substrates and is hence the first bona fide nucleobase permease identified in these parasites. Furthermore, unlike the mRNAs for other purine transporters, TbNT8.1 mRNA is significantly more abundant in insect stage procyclic forms than in mammalian stage bloodstream forms, and the TbNT8.1 permease thus may represent a major route for purine nucleobase uptake in procyclic trypanosomes. 相似文献
105.
We provide here 29 genetic variations, including 28 novel ones, in five genes that are potentially involved in the excitement
of cardiomyocytes: we found 4 in KCNA10, 2 in KCNK1, 8 in KCNK6, 11 in SLC18A1 (VMAT1), and 4 in SLC6A2 (norepinephrine transporter). We also examined their allelic frequencies in a Japanese population of long QT syndrome-affected
and nonaffected individuals. These data would be useful for genetic association studies designed to investigate acquired arrhythmias.
Received: May 22, 2001 / Accepted: June 8, 2001 相似文献
106.
Kai Aoki Takuji Suzuki Fang Hui Takuro Nakano Koki Yanazawa Masato Yonamine Shinichiro Fujita Takehito Sugasawa Yasuko Yoshida Naomi Omi Yasushi Kawakami Kazuhiro Takekoshi 《Nutrients》2021,13(5)
The effects of exercise on nutrient digestion and absorption in the intestinal tract are not well understood. A few studies have reported that exercise training increases the expression of molecules involved in carbohydrate digestion and absorption. Exercise was also shown to increase the blood concentration of glucagon-like peptide-2 (GLP-2), which regulates carbohydrate digestion and absorption in the small intestine. Therefore, we investigated the effects of exercise on the expression of molecules involved in intestinal digestion and absorption, including GLP-2. Six-week-old male mice were divided into a sedentary (SED) and low-intensity exercise (LEx) group. LEx mice were required to run on a treadmill (12.5 m/min, 1 h), whereas SED mice rested. All mice were euthanized 1 h after exercise or rest, and plasma, jejunum, ileum, and colon samples were collected, followed by analysis via IHC, EIA, and immunoblotting. The levels of plasma GLP-2 and the jejunum expression of the GLP-2 receptor, sucrase-isomaltase (SI), and glucose transporter 2 (GLUT2) were higher in LEx mice. Thus, we showed that acute low-intensity exercise affects the expression of molecules involved in intestinal carbohydrate digestion and absorption via GLP-2. Our results suggest that exercise might be beneficial for small intestine function in individuals with intestinal frailty. 相似文献
107.
Xiaoyu Wang Mingzhen Zhang Regina R. Woloshun Yang Yu Jennifer K. Lee Shireen R. L. Flores Didier Merlin James F. Collins 《Nutrients》2021,13(5)
Intestinal iron transport requires an iron importer (Dmt1) and an iron exporter (Fpn1). The hormone hepcidin regulates iron absorption by modulating Fpn1 protein levels on the basolateral surface of duodenal enterocytes. In the genetic, iron-loading disorder hereditary hemochromatosis (HH), hepcidin production is low and Fpn1 protein expression is elevated. High Fpn1-mediated iron export depletes intracellular iron, causing a paradoxical increase in Dmt1-mediated iron import. Increased activity of both transporters causes excessive iron absorption, thus initiating body iron loading. Logically then, silencing of intestinal Dmt1 or Fpn1 could be an effective therapeutic intervention in HH. It was previously established that Dmt1 knock down prevented iron-loading in weanling Hamp (encoding hepcidin) KO mice (modeling type 2B HH). Here, we tested the hypothesis that Dmt1 silencing combined with dietary iron restriction (which may be recommended for HH patients) will mitigate iron loading once already established. Accordingly, adult Hamp KO mice were switched to a low-iron (LFe) diet and (non-toxic) folic acid-coupled, ginger nanoparticle-derived lipid vectors (FA-GDLVs) were used to deliver negative-control (NC) or Dmt1 siRNA by oral, intragastric gavage daily for 21 days. The LFe diet reduced body iron burden, and experimental interventions potentiated iron losses. For example, Dmt1 siRNA treatment suppressed duodenal Dmt1 mRNA expression (by ~50%) and reduced serum and liver non-heme iron levels (by ~60% and >85%, respectively). Interestingly, some iron-related parameters were repressed similarly by FA-GDLVs carrying either siRNA, including 59Fe (as FeCl3) absorption (~20% lower), pancreatic non-heme iron (reduced by ~65%), and serum ferritin (decreased 40–50%). Ginger may thus contain bioactive lipids that also influence iron homeostasis. In conclusion, the combinatorial approach of FA-GDLV and Dmt1 siRNA treatment, with dietary iron restriction, mitigated pre-existing iron overload in a murine model of HH. 相似文献
108.
目的探讨ABCB4基因突变合并巨细胞病毒(CMV)感染致婴儿胆汁淤积症(IC)患儿的临床特征、基因检测结果和诊治方案。 方法选择2019年8月3日,于中山大学附属第七医院就诊并确诊为ABCB4基因突变合并CMV感染致IC的1例婴儿(女性,生后9个月)为研究对象。回顾性分析其临床病例资料,包括临床特征、实验室检查结果及基因检测结果。同时,检索国内外数据库中ABCB4基因突变所致IC患儿的相关文献,并进行文献复习。本研究遵循的程序符合2013年新修订的《世界医学协会赫尔辛基宣言》要求。 结果本例IC患儿在本院诊治结果如下。①病史采集:系G2P2,足月顺产,外观无异常,否认新生儿黄疸病史,生后2个月龄时出现皮肤及巩膜呈暗绿色,伴反复呕奶,当地医院治疗并诊断为胆汁淤积性肝病、CMV感染和泌尿系统感染,抗病毒治疗2周后好转出院。出院时,其血清总胆汁酸(sTBA)为152.8 μmol/L,CMV-DNA<4×102 copies/mL,口服熊去氧胆酸胶囊10 mg/(kg·d)治疗后,皮肤暗绿色逐渐消退,大、小便正常。出院后定期监测肝功能,sTBA、γ-谷氨酰转肽酶(GGT)仍然较正常值增高。②实验室检查:血清CMV免疫球蛋白(Ig)G抗体呈阳性、CMV IgM抗体呈阴性,CMV-DNA<55×102 copies/mL。基因检测结果:患儿及其父亲均携带ABCB4基因杂合变异。治疗结果:经口服熊去氧胆酸胶囊10 mg/(kg·d)及谷胱甘肽片0.1 g/次× 3次/d治疗后,对患儿定期复查sTBA、GGT。随访到18个月龄时,其各项指标逐渐恢复正常范围。③文献复习结果:共计检索到8篇国内外报道的因ABCB4基因突变引起IC相关文献,纳入14例IC患儿,均被诊断为进行性家族性肝内胆汁淤积3型(PFIC3),伴肝大,sTBA、GGT水平升高等。14例IC患儿中,共检测到ABCB4基因突变位点20个。其中,9例IC患儿接受熊去氧胆酸治疗,7例随访结果显示临床症状及实验室检查指标有所好转。 结论携带ABCB4基因突变,可引起IC。对于sTBA升高、肝酶异常的病因不明确、治疗效果不佳IC患儿,建议完善基因检测进一步排查ABCB4基因突变所致胆汁淤积症。 相似文献
109.
110.
YIN Yan-hui 《吉林大学学报(医学版)》2001,27(3):229-231
目的 :探讨编码人磷酸核糖焦磷酸合成酶亚单位 2的基因 PRPS2单核苷酸多态性与产生过剩型痛风患者的关系。方法 :利用聚合酶链反应扩增健康人和产生过剩型痛风患者 PRPS2基因全部外显 (包括外显子与内含子交界区 )的片段 ,采用多荧光标记的 PCR单链构象多态性分析技术对扩增的片段进行了筛选 ,对筛选到的片段进行序列测定 ,并与正常序列进行对照分析。结果 :在 PRPS2基因的第一个外显子区发现了一个 SNP( exon1+45A/G) ,第六个内含子区发现了一个 SNP ( intron6+12G/A) ,健康人与患者间的频率比较分别为 P =0 .0 96和 P =0 .2 73。结论 :提供了 PRPS2基因 SNP的数据库信息 ,为研究痛风发病机制提供了新的途径。 相似文献