全文获取类型
收费全文 | 242篇 |
免费 | 28篇 |
专业分类
270篇 |
出版年
2022年 | 2篇 |
2021年 | 3篇 |
2016年 | 4篇 |
2015年 | 6篇 |
2014年 | 10篇 |
2013年 | 8篇 |
2012年 | 8篇 |
2011年 | 8篇 |
2010年 | 4篇 |
2009年 | 2篇 |
2008年 | 4篇 |
2007年 | 10篇 |
2006年 | 12篇 |
2005年 | 4篇 |
2004年 | 11篇 |
2003年 | 9篇 |
2002年 | 4篇 |
2001年 | 7篇 |
2000年 | 10篇 |
1999年 | 7篇 |
1998年 | 7篇 |
1994年 | 2篇 |
1993年 | 3篇 |
1992年 | 8篇 |
1991年 | 12篇 |
1990年 | 5篇 |
1989年 | 9篇 |
1988年 | 8篇 |
1987年 | 5篇 |
1986年 | 10篇 |
1985年 | 5篇 |
1984年 | 6篇 |
1983年 | 4篇 |
1982年 | 4篇 |
1979年 | 3篇 |
1975年 | 5篇 |
1974年 | 8篇 |
1973年 | 3篇 |
1972年 | 2篇 |
1968年 | 2篇 |
1937年 | 1篇 |
1932年 | 1篇 |
1931年 | 1篇 |
1930年 | 1篇 |
1928年 | 1篇 |
1913年 | 1篇 |
1910年 | 1篇 |
1907年 | 1篇 |
1906年 | 1篇 |
1905年 | 1篇 |
排序方式: 共有270条查询结果,搜索用时 15 毫秒
81.
82.
83.
84.
Background
The determination of structural haplotypes at copy number variable regions can indicate the mechanisms responsible for changes in copy number, as well as explain the relationship between gene copy number and expression. However, obtaining spatial information at regions displaying extensive copy number variation, such as the DEFA1A3 locus, is complex, because of the difficulty in the phasing and assembly of these regions. The DEFA1A3 locus is intriguing in that it falls within a region of high linkage disequilibrium, despite its high variability in copy number (n = 3–16); hence, the mechanisms responsible for changes in copy number at this locus are unclear.Results
In this study, a region flanking the DEFA1A3 locus was sequenced across 120 independent haplotypes with European ancestry, identifying five common classes of DEFA1A3 haplotype. Assigning DEFA1A3 class to haplotypes within the 1000 Genomes project highlights a significant difference in DEFA1A3 class frequencies between populations with different ancestry. The features of each DEFA1A3 class, for example, the associated DEFA1A3 copy numbers, were initially assessed in a European cohort (n = 599) and replicated in the 1000 Genomes samples, showing within-class similarity, but between-class and between-population differences in the features of the DEFA1A3 locus. Emulsion haplotype fusion-PCR was used to generate 61 structural haplotypes at the DEFA1A3 locus, showing a high within-class similarity in structure.Conclusions
Structural haplotypes across the DEFA1A3 locus indicate that intra-allelic rearrangement is the predominant mechanism responsible for changes in DEFA1A3 copy number, explaining the conservation of linkage disequilibrium across the locus. The identification of common structural haplotypes at the DEFA1A3 locus could aid studies into how DEFA1A3 copy number influences expression, which is currently unclear.Electronic supplementary material
The online version of this article (doi:10.1186/1471-2164-15-614) contains supplementary material, which is available to authorized users. 相似文献85.
TDP‐1, the Caenorhabditis elegans ortholog of TDP‐43, limits the accumulation of double‐stranded RNA
86.
Hankes GH Ardell JL Tallaj J Wei CC Aban I Holland M Rynders P Dillon R Cardinal R Hoover DB Armour JA Husain A Dell'Italia LJ 《American journal of physiology. Heart and circulatory physiology》2006,291(1):H147-H151
Mitral regurgitation (MR) is associated with increased neuronal release of norepinephrine (NE) and epinephrine (EP) into myocardial interstitial fluid (ISF) that may be necessary in sustaining left ventricular (LV) function via activation of cardiomyocyte beta-adrenergic receptors (ARs). However, activation of neuronal beta-ARs on cardiac neurons may lead to further catecholamine release, with an attendant risk of functional deterioration. We hypothesize that a beneficial effect of beta-AR blockade may therefore mitigate excessive catecholamine release from cardiac adrenergic neurons in dogs with MR. We measured the effects of chronic beta-receptor blockade (beta-RB) on ISF NE and EP release using in vivo microdialysis in open-chest anesthetized dogs after 4 wk of MR with or without extended release of metoprolol succinate (100 mg/day) as well as in control dogs. Fractional shortening increased by 30% in both MR and MR + beta-RB dogs after 4 wk of MR. In MR + beta-RB dogs, stellate-stimulated heart rate change was attenuated compared with control and MR dogs, whereas peak change of LV pressure over time (+dP/dt) increased equally in all groups. Stellate-stimulated ISF NE increased fivefold over baseline in MR versus twofold in control dogs (< 0.05), but the NE release was significantly attenuated in MR + beta-RB dogs. In contrast, stellate-stimulated increases in ISF EP did not differ in control, MR, and MR + beta-RB dogs. This study demonstrates that beta-RB attenuates ISF NE release from cardiac neurons and that the LV functional response to MR is not dependent on an excess increase in ISF NE. Thus beta1-RB may exert a beneficial effect by attenuating untoward effects of excessive sympathetic efferent neural NE release while sustaining early LV functional adaptation to MR. 相似文献
87.
The complete nucleotide sequence of RNA beta from the type strain of barley stripe mosaic virus. 总被引:5,自引:5,他引:5 下载免费PDF全文
The complete nucleotide sequence of RNA beta from the type strain of barley stripe mosaic virus (BSMV) has been determined. The sequence is 3289 nucleotides in length and contains four open reading frames (ORFs) which code for proteins of Mr 22,147 (ORF1), Mr 58,098 (ORF2), Mr 17,378 (ORF3), and Mr 14,119 (ORF4). The predicted N-terminal amino acid sequence of the polypeptide encoded by the ORF nearest the 5'-end of the RNA (ORF1) is identical (after the initiator methionine) to the published N-terminal amino acid sequence of BSMV coat protein for 29 of the first 30 amino acids. ORF2 occupies the central portion of the coding region of RNA beta and ORF3 is located at the 3'-end. The ORF4 sequence overlaps the 3'-region of ORF2 and the 5'-region of ORF3 and differs in codon usage from the other three RNA beta ORFs. The coding region of RNA beta is followed by a poly(A) tract and a 238 nucleotide tRNA-like structure which are common to all three BSMV genomic RNAs. 相似文献
88.
Influence of a natural and a synthetic inhibitor of factor XIIIa on fibrin clot rheology 总被引:2,自引:0,他引:2 下载免费PDF全文
We investigated the origins of greater clot rigidity associated with FXIIIa-dependent cross-linking. Fibrin clots were examined in which cross-linking was controlled through the use of two inhibitors: a highly specific active-center-directed synthetic inhibitor of FXIIIa, 1,3-dimethyl-4,5-diphenyl-2[2(oxopropyl)thio]imidazolium trifluoromethylsulfonate, and a patient-derived immunoglobulin directed mainly against the thrombin-activated catalytic A subunits of thrombin-activated FXIII. Cross-linked fibrin chains were identified and quantified by one- and two-dimensional gel electrophoresis and immunostaining with antibodies specific for the alpha- and gamma-chains of fibrin. Gamma-dimers, gamma-multimers, alpha(n)-polymers, and alpha(p)gamma(q)-hybrids were detected. The synthetic inhibitor was highly effective in preventing the production of all cross-linked species. In contrast, the autoimmune antibody of the patient caused primarily an inhibition of alpha-chain cross-linking. Clot rigidities (storage moduli, G') were measured with a cone and plate rheometer and correlated with the distributions of the various cross-linked species found in the clots. Our findings indicate that the FXIIIa-induced dimeric cross-linking of gamma-chains by itself is not sufficient to stiffen the fibrin networks. Instead, the augmentation of clot rigidity was more strongly correlated with the formation of gamma-multimers, alpha(n)-polymers, and alpha(p)gamma(q)-hybrid cross-links. A mechanism is proposed to explain how these cross-linked species may enhance clot rigidity. 相似文献
89.
J A Armour 《Canadian journal of physiology and pharmacology》1985,63(6):704-716
Neuronal activity in the in situ middle cervical ganglion of dogs was investigated using extracellular recording techniques. The recorded action potentials were frequently active during specific phases of the cardiac cycle, particularly during systole, and this activity persisted following acute decentralization of the ganglion. The activity of these action potentials was modified when systemic arterial pressure was altered by isoproterenol, noradrenaline, adrenaline, or partial occlusion of the aorta, whether in the intact or acutely decentralized preparation. These neurons were active between systolic pressures of 70 and 180 mmHg (1 mmHg = 133.322 Pa). Action potentials were frequently modified by mechanical distortion of the superior vena cava, ventricular epicardium, or adventitia of the aorta, whether the preparation was acutely decentralized or not. Seventy percent of these action potentials were unaffected by stimulation (1 ms, 4 V, 0.5 Hz) of a cardiopulmonary nerve and 27% were suppressed by such stimulation. Five of the neurons were activated by such stimulation. It is presumed that the latter neurons had axons in a cardiopulmonary nerve and most likely were efferent sympathetic postganglionic neurons. Sixty-three percent of these spontaneously active phase-locked units were modified by stimulation of a ramus or an ansa. It is postulated that some of the neurons in the middle cervical ganglia can be modified by afferent axons arising from receptors in thoracic organs, in particular from the great vessels and heart, whether in an intact or acutely decentralized preparation. The majority of these neurons are presumed not to be afferent neurons or efferent postganglionic neurons, as they are not activated directly by electrical stimulation of axons in cardiopulmonary nerves. Rather they are presumed to be interneurons. These results lend support to the thesis that considerable integration of neuronal activity related to thoracic cardiovascular dynamics occurs within the middle cervical ganglia of dogs. 相似文献
90.