全文获取类型
收费全文 | 179篇 |
免费 | 16篇 |
国内免费 | 18篇 |
出版年
2023年 | 4篇 |
2022年 | 3篇 |
2021年 | 1篇 |
2020年 | 6篇 |
2019年 | 10篇 |
2018年 | 7篇 |
2017年 | 4篇 |
2016年 | 5篇 |
2015年 | 8篇 |
2014年 | 8篇 |
2013年 | 15篇 |
2012年 | 6篇 |
2011年 | 6篇 |
2010年 | 8篇 |
2009年 | 5篇 |
2008年 | 12篇 |
2007年 | 14篇 |
2006年 | 13篇 |
2005年 | 9篇 |
2004年 | 12篇 |
2003年 | 11篇 |
2002年 | 2篇 |
2001年 | 1篇 |
2000年 | 4篇 |
1999年 | 9篇 |
1998年 | 4篇 |
1997年 | 3篇 |
1996年 | 7篇 |
1995年 | 5篇 |
1994年 | 4篇 |
1993年 | 1篇 |
1991年 | 2篇 |
1989年 | 1篇 |
1983年 | 1篇 |
1981年 | 1篇 |
1977年 | 1篇 |
排序方式: 共有213条查询结果,搜索用时 15 毫秒
1.
Variation in mitochondrial DNA and post-glacial colonization of north western Europe by brown trout 总被引:1,自引:0,他引:1
A purified mitochondrial DNA (mtDNA) probe was used to examine restriction fragment length polymorphisms produced by six restriction enzymes ( Xba I, Eco RV, Ava II, Hinf I, Hae III, Mbo I) in 915 brown trout from western Europe. A total of 20 composite haplotypes were found with one to seven haplotypes in individual populations. Icelandic trout samples from north, south, east, and west coast drainages showed only a single common haplotype in contrast to the high level of polymorphism found in Irish and Scottish populations. The phylogeny of mtDNA haplotypes and the pattern of haplotype distribution suggests that post-glacial colonization of brown trout in NW Europe was more complex than the dual colonization model which has been proposed on the basis of differential LDH-5* allele distribution. For example, Lough Melvin (Ireland) appears to have been independently 相似文献
2.
硒对培养人胚肝细胞Ⅲ型前胶原,羟脯氨酸合成的影响 总被引:7,自引:0,他引:7
原代培养人胚肝细胞经1.156×10 ̄(-7)mol/L硒预处理4h,加入20mmol/L四氟化碳作用20h,观察硒对其Ⅲ型前胶原(PCⅢ)和羟脯氨酸(Hyp)生成的影响。结果培养液中PCⅢ水平、细胞内Hyp含量及细胞内外丙二醛(MDA)水平均降低,与未加硒对照组比较差别有显著性(P<0.01)。而硒谷腕甘肽过氧化物酶(Se-GSH-PX)活性则较对照组显著增高(P<0.001),且PCⅢ水平与Se-GSH-P_X/MDA比值呈负相关(r=-0.9156,P<0.01)。提示硒可提高Se-GSH-P_X/MDA比值,抑制脂质过氧化激发的肝细胞胶原合成。 相似文献
3.
4.
使用FLOW-SSO、PCR-SSP以及测序等分型技术, 发现一个与HLA-B*270401基因相关的未知基因。设计基因特异性引物单独扩增B*27基因的外显子2-5, 包括内含子2-4, 并进行双向测序, 分析与B*270401基因序列的差异。该基因的扩增产物为1 815 bp。与B*270401相比在外显子3和4共有10个碱基的改变, 从而使相应氨基酸发生错义或同义突变。碱基634 A→C (密码子130丝氨酸→精氨酸); 670 A→T (密码子142苏氨酸→丝氨酸); 683 G→T (密码子146色氨酸→亮氨酸); 698 A→T (密码子151谷氨酸→缬氨酸); 774 G→C (密码子176谷氨酸→天冬氨酸); 776 C→A (密码子177苏氨酸→赖氨酸); 781 C→G (密码子179谷氨酰胺→谷氨酸); 789 G→T (密码子181丙氨酸同义突变); 1 438 C→T (密码子206甘氨酸同义突变); 1 449 G→C (密码子210甘氨酸→丙氨酸)。在IMGT/HLA数据库中B*27组只有3个基因(B*270502 / 2706 / 2732)提交了内含子序列。该未知基因的内含子2序列与B*2706相同, 显示了与B*27组基因的同源性, 但其同源性在内含子3、4均未得到支持, 与B*27组基因相比, 内含子3的第106个碱基C→G, 碱基168缺失, 碱基179 G→A, 碱基536 G→A; 内含子4中碱基82 T→C。但其内含子3、4序列却与B*070201完全相同。该基因序列已提交GenBank, 编号为被DQ915176, 被WHO确认为HLA-B*2736等位基因。 相似文献
5.
6.
摘要 目的:研究3.0 T磁共振T2×mapping成像技术定量评估膝关节骨性关节炎(OA)的临床价值及与西安大略和麦克马斯特大学骨关节炎指数(WOMAC)评分的相关性。方法:将我院于2017年4月~2019年12月期间收治的膝关节OA患者80例纳入研究。根据K-L分级标准将膝关节OA患者分成轻度组(K-L分级为Ⅰ~Ⅱ级)32例,重度组(K-L分级为Ⅲ~Ⅴ级)48例。另取同期于我院进行体检的健康者30例作为对照组。所有受试者均接受3.0 T磁共振T2×mapping扫描,比较各组膝关节不同部位软骨T2值、WOMAC评分以及血清炎症因子水平,以Pearson相关性分析膝关节OA患者膝关节不同部位软骨T2值和WOMAC评分的关系。结果:重度组膝关节不同部位软骨T2值均高于轻度组以及对照组,且轻度组膝关节不同部位软骨T2值均高于对照组(均P<0.05)。重度组各项WOMAC评分及总分均高于轻度组以及对照组,且轻度组各项WOMAC评分及总分均高于对照组(均P<0.05)。经Pearson相关性分析发现:膝关节OA患者膝关节不同部位软骨T2值和各项WOMAC评分及总分均呈正相关(均P<0.05)。重度组血清白介素-1β(IL-1β)、白介素-18(IL-18)、肿瘤坏死因子α(TNF-α)均高于轻度组以及对照组,且轻度组血清IL-1β、IL-18、TNF-α均高于对照组(均P<0.05)。结论:3.0 T磁共振T2×mapping成像技术定量评估膝关节OA的临床价值较高,且患者膝关节不同部位软骨T2值与WOMAC评分密切相关。 相似文献
7.
JIANHONG CHEN AGRIPINA G. DEACIUC LINDA P. DWOSKIN PETER A. CROOKS DONGLU BAI 《Journal of enzyme inhibition and medicinal chemistry》2013,28(6):667-680
A series of N, N– disubstituted piperazines and homopiperazines were prepared and evaluated for binding to natural α4β2* and α7* neuronal nicotinic acetylcholine receptors (nAChRs) using whole brain membrane. Some compounds exhibited good selectivity for α4β2* nAChRs and did not interact with the α7* nAChRs subtype. The most potent analogs were compounds 8-19 (Ki = 10.4 μM), 8–13 (Ki = 12.0 μM), and 8–24 (Ki = 12.8 μM). Thus, linking together a pyridine π-system and a cyclic amine moiety via a homopiperazine ring affords compounds with low affinity but with good selectivity for α4β2* nAChRs. 相似文献
8.
Chiara Ciaccio Alessandra Pesce Grazia R. Tundo Lesley Tilleman Laura Bertolacci Sylvia Dewilde Luc Moens Paolo Ascenzi Martino Bolognesi Marco Nardini Massimo Coletta 《Biochimica et Biophysica Acta - Proteins and Proteomics》2013,1834(9):1813-1823
Functional and structural properties of protoglobin from Methanosarcina acetivorans, whose Cys(101)E20 residue was mutated to Ser (MaPgb*), and of mutants missing either the first 20 N-terminal amino acids (MaPgb*-ΔN20 mutant), or the first 33 N-terminal amino acids [N-terminal loop of 20 amino acids and a 13-residue Z-helix, preceding the globin fold A-helix; (MaPgb*-ΔN20Z mutant)] have been investigated. In keeping with the MaPgb*-ΔN20 mutant crystal structure, here reported at 2.0 Å resolution, which shows an increased exposure of the haem propionates to the solvent, the analysis of ligand binding kinetics highlights high accessibility of ligands to the haem pocket in ferric MaPgb*-ΔN20. CO binding to ferrous MaPgb*-ΔN20 displays a marked biphasic behavior, with a fast binding process close to that observed in MaPgb* and a slow carbonylation process, characterized by a rate-limiting step. Conversely, removal of the first 33 residues induces a substantial perturbation of the overall MaPgb* structure, with loss of α-helical content and potential partial collapse of the protein chain. As such, ligand binding kinetics are characterized by very slow rates that are independent of ligand concentration, this being indicative of a high energy barrier for ligand access to the haem, possibly due to localized misfolding. This article is part of a Special Issue entitled: Oxygen Binding and Sensing Proteins. 相似文献
9.
10.
《Molecular & cellular proteomics : MCP》2019,18(11):2298-2309
- Download : Download high-res image (115KB)
- Download : Download full-size image
- •HLA-B*40:02 and ERAP2 are risk factors for ankylosing spondylitis.
- •The effects of ERAP2 on the B*40:02 peptidome are defined.
- •ERAP2 has a major influence mainly due to alterations of N-terminal residues.
- •These effects provide a basis for the association of ERAP2 with disease.