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961.
Sze‐Ying Ng Chi‐Hou Chin Yuen‐Ting Lau Jialie Luo Chun‐Kit Wong Zhao‐Xiang Bian Suk‐Ying Tsang 《Journal of cellular physiology》2010,224(1):165-177
Embryonic stem cells (ESCs) possess two unique characteristics: self‐renewal and pluripotency. In this study, roles of voltage‐gated potassium channels (Kv) in maintaining mouse (m) ESC characteristics were investigated. Tetraethylammonium (TEA+), a Kv blocker, attenuated cell proliferation in a concentration‐dependent manner. Possible reasons for this attenuation, including cytotoxicity, cell cycle arrest and differentiation, were examined. Blocking Kv did not change the viability of mESCs. Interestingly, Kv inhibition increased the proportion of cells in G0/G1 phase and decreased that in S phase. This change in cell cycle distribution can be attributed to cell cycle arrest or differentiation. Loss of pluripotency as determined at both molecular and functional levels was detected in mESCs with Kv blockade, indicating that Kv inhibition in undifferentiated mESCs directs cells to differentiate instead of to self‐renew and progress through the cell cycle. Membrane potential measurement revealed that Kv blockade led to depolarization, consistent with the role of Kv as the key determinant of membrane potential. The present results suggest that membrane potential changes may act as a “switch” for ESCs to decide whether to proliferate or to differentiate: hyperpolarization at G1 phase would favor ESCs to enter S phase while depolarization would favor ESCs to differentiate. Consistent with this notion, S‐phase‐synchronized mESCs were found to be more hyperpolarized than G0/G1‐phase‐synchronized mESCs. Moreover, when mESCs differentiated, the differentiation derivatives depolarized at the initial stage of differentiation. This investigation is the first study to provide evidence that Kv and membrane potential affect the fate determination of ESCs. J. Cell. Physiol. 224:165–177, 2010 © 2010 Wiley‐Liss, Inc. 相似文献
962.
Herman Tse Hoi Wah Tsoi Sze Pui Leung Susanna K. P. Lau Patrick C. Y. Woo Kwok Yung Yuen 《Journal of bacteriology》2010,192(5):1471-1472
Staphylococcus lugdunensis is a member of the coagulase-negative staphylococci and commonly found as part of the human skin flora. It is a significant cause of catheter-related bacteremia and also causes serious infections like native valve endocarditis in previously healthy individuals. We report the complete genome sequence of this medically important bacterium.Staphylococcus lugdunensis is a member of the coagulase-negative staphylococci (CoNS) commonly colonizing the human skin and mucosal membranes. While the genus Staphylococcus contains 48 named species currently, only a few species, notably S. aureus, are coagulase positive. Thus, the phenotypic characteristic is routinely tested in the medical microbiological laboratory for rapid differentiation of the highly pathogenic S. aureus from the other staphylococci. Among the CoNS, only a few species are known to cause human disease, usually in the form of opportunistic infections only (6). However, S. lugdunensis is an important exception (3). Besides causing catheter-related bacteremia similar to other CoNS, it causes a variety of severe nosocomial and community-acquired infections, including native valve endocarditis, a devastating and potentially fatal disease that can affect previously healthy individuals. Another unusual feature are the susceptibilities of S. lugdunensis isolates to multiple antimicrobial agents even when the incidence of multiple-drug-resistant CoNS and S. aureus occurrences are increasing in both hospital and community settings (4, 5).The genome sequence of S. lugdunensis strain HKU09-01 was determined by high-throughput sequencing performed on a GS FLX system (Roche Diagnostics, Basel, Switzerland), with approximately 45-fold coverage of the genome. This clinical strain was previously isolated from the culture of pus from a skin swab. Genome assembly was performed using the Newbler assembler, resulting in 30 large contigs (>500 bp in size). The contigs were then ordered and oriented into one scaffold using OSLay (11). The genome-finishing strategy for S. lugdunensis was similar to that employed for our previously sequenced Laribacter hongkongensis genome (12). Briefly, gap closures were performed by genomic PCR followed by DNA sequencing of amplification products on an ABI 3130xl sequencer (Applied Biosystems, CA). The finished sequence was validated by genome macrorestriction analysis using multiple rare-cutting enzymes and visualization by pulsed-field gel electrophoresis. Protein coding regions were predicted with Glimmer3 (2), and automatic genome annotation was performed on the RAST server (1). Additionally, annotation of tRNA and transfer-messenger RNA (tmRNA) genes was performed using tRNAScan-SE (10) and ARAGORN (9). Identification of rRNA genes was performed using RNAmmer (8).The genome of S. lugdunensis strain HKU09-01 consists of a circular 2,658,366-bp chromosome with G+C content of 33.87%, similar to those of other staphylococci. No plasmids are present in the sequenced strain. The genome contains 61 tRNA genes for all amino acids and 2,489 predicted protein-coding genes. Eight putative genomic islands were identified, and one actually consists of a pair of duplicated 32-kb genomic regions. Similar to Staphylococcus saprophyticus (7), but different from the other staphylococci, the genome contains 6 rRNA operons, one of them having the unusual organization 5S-16S-23S-5S.With the availability of the present genome sequence, S. lugdunensis now joins other staphylococcal species with human pathogenic potential, like S. aureus, S. epidermidis, S. haemolyticus, and S. saprophyticus, to have at least one reference genome available. Further in-depth analysis will be necessary to fully elucidate the genomic differences that may explain the variation in virulence of the staphylococcal species. 相似文献
963.
964.
Using serum from guinea-pigs immunized with a DeltaAFMP1DeltaAFMP2 deletion mutant of Aspergillus fumigatus to screen a cDNA library of A. fumigatus, we cloned a novel immunogenic 57-kDa protein in A. fumigatus. We also cloned its 55-kDa homologue in Penicillium marneffei, which was possibly related to amino acid biosynthesis and metabolism, with homologues present only in the subphylum Pezizomycotina of Ascomycota. The recombinant 55-kDa protein of P. marneffei reacted strongly with guinea-pig serum immunized with P. marneffei and with the sera of patients with P. marneffei infection. A similar approach could be applied to immunogenic protein screening in other microorganisms for serological diagnosis, epidemiological studies and the study of vaccines. 相似文献
965.
966.
967.
多效唑对大花高代组培苗生长的效应 总被引:7,自引:0,他引:7
以MS0、MS+PP3330.5mg·L-1、MS+PP3331mg·L-1和MS+PP3332mg·L-14种培养基研究多效唑(PP333)对大花高代组培苗生长影响的结果表明,PP333对大花高代组培苗有明显的矮化效应,在0.5 ̄2mg·L-1PP333范围内,浓度越高,植株越矮,节间越短,叶形指数越小。根据组培苗的真叶和根的发生动态、矮化和黄化程度综合考虑,认为MS+PP3331mg·L-1是较理想的矮化大花高代苗的培养基。 相似文献
968.
969.
970.
Ghosh S Kewalramani G Yuen G Pulinilkunnil T An D Innis SM Allard MF Wambolt RB Qi D Abrahani A Rodrigues B 《Free radical biology & medicine》2006,41(9):1413-1424
Increased awareness of obesity has led to a dietary shift toward "heart-friendly" vegetable oils containing omega-6 polyunsaturated fatty acid (omega-6 PUFA). In addition to its beneficial effects, omega-6 PUFA also exhibits proinflammatory and prooxidative properties. We hypothesized that chronic dietary omega-6 PUFA can induce free radical generation, predisposing the cardiac mitochondria to oxidative damage. Male Wistar rats were fed a diet supplemented with 20% w/w sunflower oil, rich in omega-6 PUFA (HP) or normal laboratory chow (LP) for 4 weeks. HP feeding augmented phospholipase A(2) activity and breakdown of cardiolipin, a mitochondrial phospholipid. HP hearts also demonstrated elevated inducible nitric oxide synthase expression, loss of Mn superoxide dismutase, and increased mitochondrial nitrotyrosine levels. In these hearts, oxidative damage to mitochondrial DNA (mDNA) was demonstrated by 8-hydroxyguanosine immunopositivity, overexpression of DNA repair enzymes, and a decrease in the mRNA expression of specific respiratory subunits encoded by the mDNA. Functionally, at higher workloads, HP hearts also demonstrated a greater decline in cardiac work than LP, suggesting a compromised mitochondrial reserve. Our study, for the first time, demonstrates that consumption of a high fat diet rich in omega-6 PUFA for only 4 weeks instigates mitochondrial nitrosative damage and causes cardiac dysfunction at high afterloads. 相似文献