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81.
Emi Kunitake Shuji Tani Jun-ichi Sumitani Takashi Kawaguchi 《Applied microbiology and biotechnology》2013,97(5):2017-2028
82.
Sogawa K Numayama-Tsuruta K Takahashi T Matsushita N Miura C Nikawa J Gotoh O Kikuchi Y Fujii-Kuriyama Y 《Biochemical and biophysical research communications》2004,318(3):746-755
We have identified an enhancer responsible for induction by 3-methylcholanthrene in the upstream region of the CYP1A2 gene. The enhancer does not contain the invariant core sequence of XREs that are binding sites for the Ah receptor (AhR) and Arnt heterodimer. The enhancer did not show any inducible expression in Hepa-1-derived cell lines, C4 and C12, deficient of Arnt and AhR, respectively. On the other hand, bacterially expressed AhR-Arnt heterodimer could not bind to the enhancer. Mutational analysis of the enhancer revealed that a repeated sequence separated by six nucleotides is important for expression. A factor binding specifically to the enhancer was found by using gel shift assays. Bacterially expressed AhR-Arnt heterodimer interacted with the factor. A dominant negative mutant of the AhR to XRE activated the enhancer. Collectively, these results demonstrate that a novel induction mechanism is present in which the AhR-Arnt heterodimer functions as a coactivator. 相似文献
83.
Chihiro Nishimura Seitaro Ohkuma Jun-ichi Tamura Kinya Kuriyama 《Neurochemistry international》1982,4(5):413-418
The specific binding of GABA (γ-aminobutyric acid) agonist 3H-muscimol, to synaptic membranes from the rat brain showed a significant increase, when the membranous preparations were treated with a low concentration (10?4–10?5M) of mercurial sulfhydryl reagents such as p-chloromercuribenzoate and mercuric chloride. This activation in GABA receptor binding was bicuculline-sensitive, and was partially restored by subsequent treatments with 10 mM cysteine, penicillamine, or mercaptoethanol. Scatchard analysis of the binding revealed that this activation was due to the increase in the affinity of both high and low affinity bindings sites but not in the Bmax values. On the other hand, the treatment of synaptic membranes with hydrophilic sulfhydryl reagents such as N-ethylmaleimide and iodoacetate had no effect on the binding. These hydrophilic sulfhydryl reagents, however, induced an increase of the binding following the pretreatment of synaptic membranes with 0.01% Triton X-100 or 0.5 U/mg prot. of phospholipase A2 (EC 3.1.1.4.). These results suggest that mercurials-sensitive sulfhydryl groups, which are normally masked by membrane lipids, may play a modulating role in GABA receptor binding at central synapses. 相似文献
84.
85.
Nishiyama Misa Nakamichi Noritaka Yoshimura Tomoyuki Masuo Yusuke Komori Tomoe Ishimoto Takahiro Matsuo Jun-ichi Kato Yukio 《Neurochemical research》2020,45(11):2664-2678
Neurochemical Research - Understanding of the underlying mechanism of epilepsy is desired since some patients fail to control their seizures. The carnitine/organic cation transporter OCTN1/SLC22A4... 相似文献
86.
Kohei Yuyama Hui Sun Shota Sakai Susumu Mitsutake Megumi Okada Hidetoshi Tahara Jun-ichi Furukawa Naoki Fujitani Yasuro Shinohara Yasuyuki Igarashi 《The Journal of biological chemistry》2014,289(35):24488-24498
Elevated levels of amyloid-β peptide (Aβ) in the human brain are linked to the pathogenesis of Alzheimer disease. Recent in vitro studies have demonstrated that extracellular Aβ can bind to exosomes, which are cell-secreted nanovesicles with lipid membranes that are known to transport their cargos intercellularly. Such findings suggest that the exosomes are involved in Aβ metabolism in brain. Here, we found that neuroblastoma-derived exosomes exogenously injected into mouse brains trapped Aβ and with the associated Aβ were internalized into brain-resident phagocyte microglia. Accordingly, continuous intracerebral administration of the exosomes into amyloid-β precursor protein transgenic mice resulted in marked reductions in Aβ levels, amyloid depositions, and Aβ-mediated synaptotoxicity in the hippocampus. In addition, we determined that glycosphingolipids (GSLs), a group of membrane glycolipids, are highly abundant in the exosomes, and the enriched glycans of the GSLs are essential for Aβ binding and assembly on the exosomes both in vitro and in vivo. Our data demonstrate that intracerebrally administered exosomes can act as potent scavengers for Aβ by carrying it on the exosome surface GSLs and suggest a role of exosomes in Aβ clearance in the central nervous system. Improving Aβ clearance by exosome administration would provide a novel therapeutic intervention for Alzheimer disease. 相似文献
87.
The concentrations of cadmium and other metal ions in selected organs, urine, and blood of female rats were measured after
exposure to cadmium chloride through their diet or by oral or intravenous administration. The hematological and urinary variations
were followed for 4 wk.
Body weight gain and the weights of livers and kidneys from all treated groups were not significantly different from the controls.
No gross morphological changes were observed in any of the tissues studied at necropsy.
The accumulation of cadmium occurred in the liver and kidney. The zinc levels in these organs were elevated relative to controls,
in all treated groups regardless of dose and exposure route. Copper was elevated in the liver, kidney, bone, and blood of
animals subject to intravenous administration of cadmium. Hepatic iron was decreased in the dietary and orally treated groups,
but was not affected in the intravenous study group. The level of magnesium in kidney was increased for all exposure routes,
but that of liver was increased only in the intravenously injected groups. The changes in the concentrations of sodium, potassium,
calcium, and phosphorus did not follow a specific pattern and varied from organ to organ, depending on the exposure route.
The discussion includes a relationship between tissue injury and the alteration of tissue essential element concentrations. 相似文献
88.
Nalidixic acid-resistant mutations of the gyrB gene of Escherichia coli 总被引:41,自引:0,他引:41
Jun-ichi Yamagishi Hiroaki Yoshida Michiko Yamayoshi Shinichi Nakamura 《Molecular & general genetics : MGG》1986,204(3):367-373
Summary DNA fragments of 3.4 kb containing the gyrB gene were cloned from Escherichia coli KL-16 and from spontaneous nalidixic acid-resistant mutants. The mutations (nal-24 and nal-31) had been determined to be in the gyrB gene by transduction analysis. Nucleotide sequence analysis of the cloned DNA fragments revealed that nal-24 was a G to A transition at the first base of the 426th codon of the gyrB gene, resulting in an amino acid change from aspartic acid to asparagine, and nal-31 was an A to G transition at the first base of the 447th codon, resulting in an amino acid change from lysine to glutamic acid. This indicates that mutations in the gyrB gene are responsible for nalidixic acid resistance. 相似文献
89.
Kawahata K Misaki Y Yamauchi M Tsunekawa S Setoguchi K Miyazaki J Yamamoto K 《Journal of immunology (Baltimore, Md. : 1950)》2002,168(9):4399-4405
Normal T cell repertoire contains regulatory T cells that control autoimmune responses in the periphery. One recent study demonstrated that CD4(+)CD25(+) T cells were generated from autoreactive T cells without negative selection. However, it is unclear whether, in general, positive selection and negative selection of autoreactive T cells are mutually exclusive processes in the thymus. To investigate the ontogeny of CD4(+)CD25(+) regulatory T cells, neo-autoantigen-bearing transgenic mice expressing chicken egg OVA systemically in the nuclei (Ld-nOVA) were crossed with transgenic mice expressing an OVA-specific TCR (DO11.10). Ld-nOVA x DO11.10 mice had increased numbers of CD4(+)CD25(+) regulatory T cells in the thymus and the periphery despite clonal deletion. In Ld-nOVA x DO11.10 mice, T cells expressing endogenous TCR alpha beta chains were CD4(+)CD25(-) T cells, whereas T cells expressing autoreactive TCR were selected as CD4(+)CD25(+) T cells, which were exclusively dominant in recombination-activating gene 2-deficient Ld-nOVA x DO11.10 mice. In contrast, in DO11.10 mice, CD4(+)CD25(+) T cells expressed endogenous TCR alpha beta chains, which disappeared in recombination-activating gene 2-deficient DO11.10 mice. These results indicate that part of autoreactive T cells that have a high affinity TCR enough to cause clonal deletion could be positively selected as CD4(+)CD25(+) T cells in the thymus. Furthermore, it is suggested that endogenous TCR gene rearrangement might critically contribute to the generation of CD4(+)CD25(+) T cells from nonautoreactive T cell repertoire, at least under the limited conditions such as TCR-transgenic models, as well as the generation of CD4(+)CD25(-) T cells from autoreactive T cell repertoire. 相似文献
90.
Shusuke Numata Kazuo Ishii Atsushi Tajima Jun-ichi Iga Makoto Kinoshita Shinya Watanabe Hidehiro Umehara Manabu Fuchikami Satoshi Okada Shuken Boku Akitoyo Hishimoto Shinji Shimodera Issei Imoto Shigeru Morinobu Tetsuro Ohmori 《Epigenetics》2015,10(2):135-141
Aberrant DNA methylation in the blood of patients with major depressive disorder (MDD) has been reported in several previous studies. However, no comprehensive studies using medication-free subjects with MDD have been conducted. Furthermore, the majority of these previous studies has been limited to the analysis of the CpG sites in CpG islands (CGIs) in the gene promoter regions. The main aim of the present study is to identify DNA methylation markers that distinguish patients with MDD from non-psychiatric controls. Genome-wide DNA methylation profiling of peripheral leukocytes was conducted in two set of samples, a discovery set (20 medication-free patients with MDD and 19 controls) and a replication set (12 medication-free patients with MDD and 12 controls), using Infinium HumanMethylation450 BeadChips. Significant diagnostic differences in DNA methylation were observed at 363 CpG sites in the discovery set. All of these loci demonstrated lower DNA methylation in patients with MDD than in the controls, and most of them (85.7%) were located in the CGIs in the gene promoter regions. We were able to distinguish patients with MDD from the control subjects with high accuracy in the discriminant analysis using the top DNA methylation markers. We also validated these selected DNA methylation markers in the replication set. Our results indicate that multiplex DNA methylation markers may be useful for distinguishing patients with MDD from non-psychiatric controls. 相似文献