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71.
Makoto Tsuchiya 《Journal of experimental marine biology and ecology》1980,47(3):203-222
Seasonal changes in the amount of biodeposit (faeces and pseudofaeces) produced by the mussel Mytilus edulis L., which is one of the representative suspension-feeders in the rocky intertidal and shallow subtidal regions of Mutsu Bay, were studied in the laboratory. The effects of water temperature, light, food concentration, flow rate, body size, age, and spawning on biodeposit production were investigated. More biodeposit was produced in summer than in other seasons. Throughout the year, the amount of biodeposit was positively correlated with body size. Relatively more biodeposit was produced by smaller than by larger individuals. A M. edulis population living in one square meter was estimated to produce 9.20 kg of faeces and 2.71 kg of pseudofaeces per year (dry wt). More biodeposit was produced at water temperatures of 17.6–20.2° C than at 4.5–7.6° C and 25.2–26.0° C. The optimum temperature for biodeposit production was found to be ≈ 20.0 °C. When kept in the dark, M. edulis produced more biodeposit than in the light. When food concentration is increased, more psuedofaeces are produced; the amount of faeces, however, remains constant. With increasing flow rate, the amount o f biodeposit per h increased but the biodeposition rate decreased. Larger amounts of faeces and smaller amounts of pseudofaeces were produced by younger mussels than by older ones of a similar size. Spawning also affected biodeposit production. 相似文献
72.
Yoshikazu Inoh Yuuki Tsuchiya Yokiko Nakanishi Satoru Yokawa Tadahide Furuno 《Cell biology international》2020,44(4):1068-1075
Cationic liposomes are commonly used as vectors to effectively introduce foreign genes into target cells. In another function, we recently showed that cationic liposomes bound to the mast cell surface suppress the degranulation induced by the cross‐linking of high‐affinity immunoglobulin E receptor in a time‐ and dose‐dependent manner. This suppression is mediated by the impairment of the sustained level of intracellular Ca2+ concentration ([Ca2+]i) via the inhibition of store‐operated Ca2+ entry. Further, we revealed that the mechanism underlying an impaired [Ca2+]i increase is the inhibition of the activation of the phosphatidylinositol 3‐kinase (PI3K)‐Akt pathway. Yet, how cationic liposomes inhibit the PI3K‐Akt pathway is still unclear. Here, we focused on caveolin‐1, a major component of caveolae, which is reported to be involved in the activation of the PI3K‐Akt pathway in various cell lines. In this study, we showed that caveolin‐1 translocated from the cytoplasm to the plasma membrane after the activation of mast cells and colocalized with the p85 subunit of PI3K, which seemed to be essential for PI3K activity. Meanwhile, cationic liposomes suppressed the translocation of caveolin‐1 to the plasma membrane and the colocalization of caveolin‐1 with PI3K p85 also at the plasma membrane. This finding provides new information for the development of therapies using cationic liposomes against allergies. 相似文献
73.
Abstract The mechanisms of signal peptide cleavage has not been fully elucidated yet. In previous investigation, we have examined the effect of chicken lysozyme signal peptide mutations on the secretion of human lysozyme. During this study, we determined that the hydrophobic bulky amino acid Val at position ‐1 inhibited the function of signal peptide. To determine why the ‐1Val suppressed the function of signal peptide, turn‐promoting amino acids Pro and Gly were introduced after ‐lVal to prevent the signal peptide from forming α‐helix and induce β‐turn around the cleavage site. This mutation resulted in no processing of signal peptide and no secretion of human lysozyme. However, the replacement of ‐1Val with Ala permitted a functional signal. Based on these results, three dimensional models around the cleavage site of each signal peptide were made, which show that bulky side chain at ‐1 residue of signal peptide limits the reaction space for signal peptidase and suppresses cleavage by steric hindrance. We suggest that the bulky side chain at ‐1 residue suppresses the signal peptide cleavage by its local steric hindrance and not by a change in whole structure around the cleavage site. On the other hand, introduction of Pro at position +1 did not inhibit signal cleavage completely resulting in poor secretion and processing efficiency although Pro in position +1 has been recently reported to block cleavage of the prokaryotic signal peptide. The mechanism of cleavage of prokaryotic signal may be different than that of eukaryotic signal. 相似文献
74.
Zui Fujimoto Rintaro Suzuki Takahiro Shiotsuki Wataru Tsuchiya Akira Tase Mitsuru Momma Toshimasa Yamazaki 《PloS one》2013,8(2)
Juvenile hormones (JHs) control a diversity of crucial life events in insects. In Lepidoptera which major agricultural pests belong to, JH signaling is critically controlled by a species-specific high-affinity, low molecular weight JH-binding protein (JHBP) in hemolymph, which transports JH from the site of its synthesis to target tissues. Hence, JHBP is expected to be an excellent target for the development of novel specific insect growth regulators (IGRs) and insecticides. A better understanding of the structural biology of JHBP should pave the way for the structure-based drug design of such compounds. Here, we report the crystal structure of the silkworm Bombyx mori JHBP in complex with two molecules of 2-methyl-2,4-pentanediol (MPD), one molecule (MPD1) bound in the JH-binding pocket while the other (MPD2) in a second cavity. Detailed comparison with the apo-JHBP and JHBP-JH II complex structures previously reported by us led to a number of intriguing findings. First, the JH-binding pocket changes its size in a ligand-dependent manner due to flexibility of the gate α1 helix. Second, MPD1 mimics interactions of the epoxide moiety of JH previously observed in the JHBP-JH complex, and MPD can compete with JH in binding to the JH-binding pocket. We also confirmed that methoprene, which has an MPD-like structure, inhibits the complex formation between JHBP and JH while the unepoxydated JH III (methyl farnesoate) does not. These findings may open the door to the development of novel IGRs targeted against JHBP. Third, binding of MPD to the second cavity of JHBP induces significant conformational changes accompanied with a cavity expansion. This finding, together with MPD2-JHBP interaction mechanism identified in the JHBP-MPD complex, should provide important guidance in the search for the natural ligand of the second cavity. 相似文献
75.
Yasuhiro Umemura Junko Yoshida Masashi Wada Yoshiki Tsuchiya Yoichi Minami Hitomi Watanabe Gen Kondoh Junji Takeda Hitoshi Inokawa Kyoji Horie Kazuhiro Yagita 《PloS one》2013,8(6)
We previously reported emergence and disappearance of circadian molecular oscillations during differentiation of mouse embryonic stem (ES) cells and reprogramming of differentiated cells, respectively. Here we present a robust and stringent in vitro circadian clock formation assay that recapitulates in vivo circadian phenotypes. This assay system first confirmed that a mutant ES cell line lacking Casein Kinase I delta (CKIδ) induced ∼3 hours longer period-length of circadian rhythm than the wild type, which was compatible with recently reported results using CKIδ null mice. In addition, this assay system also revealed that a Casein Kinase 2 alpha subunit (CK2α) homozygous mutant ES cell line developed significantly longer (about 2.5 hours) periods of circadian clock oscillations after in vitro or in vivo differentiation. Moreover, revertant ES cell lines in which mutagenic vector sequences were deleted showed nearly wild type periods after differentiation, indicating that the abnormal circadian period of the mutant ES cell line originated from the mutation in the CK2α gene. Since CK2α deficient mice are embryonic lethal, this in vitro assay system represents the genetic evidence showing an essential role of CK2α in the mammalian circadian clock. This assay was successfully applied for the phenotype analysis of homozygous mutant ES cells, demonstrating that an ES cell-based in vitro assay is available for circadian genetic screening. 相似文献
76.
Multidrug efflux pumps play an important role as a self-defense system in bacteria. Bacterial multidrug efflux pumps are classified into five families based on structure and coupling energy: resistance−nodulation−cell division (RND), small multidrug resistance (SMR), major facilitator (MF), ATP binding cassette (ABC), and multidrug and toxic compounds extrusion (MATE). We cloned a gene encoding a MATE-type multidrug efflux pump from Streptococcus pneumoniae R6, and designated it pdrM. PdrM showed sequence similarity with NorM from Vibrio parahaemolyticus, YdhE from Escherichia coli, and other bacterial MATE-type multidrug efflux pumps. Heterologous expression of PdrM let to elevated resistance to several antibacterial agents, norfloxacin, acriflavine, and 4′,6-diamidino-2-phenylindole (DAPI) in E. coli KAM32 cells. PdrM effluxes acriflavine and DAPI in a Na+- or Li+-dependent manner. Moreover, Na+ efflux via PdrM was observed when acriflavine was added to Na+-loaded cells expressing pdrM. Therefore, we conclude that PdrM is a Na+/drug antiporter in S. pneumoniae. In addition to pdrM, we found another two genes, spr1756 and spr1877,that met the criteria of MATE-type by searching the S. pneumoniae genome database. However, cloned spr1756 and spr1877 did not elevate the MIC of any of the investigated drugs. mRNA expression of spr1756, spr1877, and pdrM was detected in S. pneumoniae R6 under laboratory growth conditions. Therefore, spr1756 and spr1877 are supposed to play physiological roles in this growth condition, but they may be unrelated to drug resistance. 相似文献
77.
Mamunur Rashid Mahib Shoko Hosojima Hiroko Kushiyama Takeshi Kinoshita Toshihiko Shiroishi Takashi Suda Kohsuke Tsuchiya 《Microbiology and immunology》2020,64(2):143-152
Inflammasomes are innate immune mechanisms that activate caspase-1 in response to a variety of stimuli, including Salmonella infection. Active caspase-1 has a potential to induce two different types of cell death, depending on the expression of the pyroptosis mediator gasdermin D (GSDMD); following caspase-1 activation, GSDMD-sufficient and GSDMD-null/low cells undergo pyroptosis and apoptosis, respectively. Although Bid, a caspase-1 substrate, plays a critical role in caspase-1 induction of apoptosis in GSDMD-null/low cells, an additional mechanism that mediates this cell death independently of Bid has also been suggested. This study investigated the Bid-independent pathway of caspase-1-induced apoptosis. Caspase-1 has been reported to process caspase-6 and caspase-7. Silencing of caspase-7, but not caspase-6, significantly reduced the activation of caspase-3 induced by caspase-1, which was activated by chemical dimerization, in GSDMD/Bid-deficient cells. CRISPR/Cas9-mediated depletion of caspase-7 had the same effect on the caspase-3 activation. Moreover, in the absence of GSDMD and Bid, caspase-7 depletion reduced apoptosis induced by caspase-1 activation. Caspase-7 was activated following caspase-1 activation independently of caspase-3, suggesting that caspase-7 acts downstream of caspase-1 and upstream of caspase-3. Salmonella induced the activation of caspase-3 in GSDMD-deficient macrophages, which relied partly on Bid and largely on caspase-1. The caspase-3 activation and apoptotic morphological changes seen in Salmonella-infected GSDMD/Bid-deficient macrophages were attenuated by caspase-7 knockdown. These results suggest that in addition to Bid, caspase-7 can also mediate caspase-1-induced apoptosis and provide mechanistic insights into inflammasome-associated cell death that is one major effector mechanism of inflammasomes. 相似文献
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