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991.
Flower-heads, herbivores, and their parasitoids: food web structure along a fertility gradient 总被引:1,自引:0,他引:1
Carlos Roberto Fonseca Paulo I. Prado Mário Almeida-Neto Umberto Kubota Thomas M. Lewinsohn 《Ecological Entomology》2005,30(1):36-46
Abstract. 1. The ways in which a soil fertility gradient affects three trophic level food webs defined by plants of the family Asteraceae, flower‐head herbivores, and their parasitoids was investigated. It was tested how the fertility gradient alters: (i) the abundance and richness of plants, herbivores, and their parasitoids, (ii) the herbivore–plant ratio, and (iii) the connectance of the plant–herbivore community matrix. 2. From April to May 2000, plants and insects were sampled in 16 Brazilian Cerrado (sensu stricto) sites along a physiognomic gradient varying from open shrublands (cerrado) to closed woodlands (cerradão). Sites were objectively positioned along the physiognomic gradient by a single index, tree density. Sixty‐seven per cent of the variation in tree density among sites was correlated to two principal components of a PCA, representing gradients of soil fertility. 3. Asteraceae abundance, richness, and flower‐head availability were negatively related to tree density due to their preference for sunny environments, despite the surplus of soil nutrients. The abundance and richness of Diptera and Lepidoptera, the most important flower‐head herbivores, were also negatively related to tree density. Parasitoid abundance decreased with tree density; however, the number of parasitoids per hosts was lower in cerrado, suggesting that top‐down forces are not getting stronger in more productive sites, as could be expected. 4. Community allometry analyses showed that the herbivore to plant ratio was independent of community richness and did not respond to tree density. 5. Connectance of the plant–herbivore matrix was dependent on the community matrix size. Proportionally, species‐rich cerrado sites had fewer interactions than their species‐poor counterparts. Nevertheless, after removing the effect of the matrix size, connectance was not related to tree density. 6. Soil fertility, as the primary cause of the cerrado–cerradão physiognomic gradient, strongly affected the abundance and richness of plants, herbivores and their parasitoids; however, it had little effect on important community attributes, such as the herbivore–plant ratio and the connectance of the plant–herbivore matrix. 相似文献
992.
Jong-Soo Kim Hisayo Kubota Toshio Sakai Kunio Doi Junzo Saegusa 《Experimental Animals》2005,54(1):107-110
Hyperplastic cells in subcapsular cell hyperplasia (SCH) lesion in adrenal glands of female IQI/Jic mice were examined by electron microscopy. These cells were small and polygonal, and had irregular nuclei, elongated mitochondria with lamellar cristae and dense lipid droplets. While these cells showed different features, some of them had desmosomes and basement membranes, and a few round mitochondria with tubular cristae as endocrine cells. These findings suggest that hyperplastic cells in SCH lesions might originate from endocrine blastemic cells. 相似文献
993.
Kyoko Wakamatsu Toshihiro Nanki Nobuyuki Miyasaka Kazuo Umezawa Tetsuo Kubota 《Arthritis research & therapy》2005,7(6):R1348
A small cell-permeable compound, dehydroxymethylepoxyquinomicin (DHMEQ), does not inhibit phosphorylation and degradation
of IκB (inhibitor of nuclear factor-κB [NF-κB]) but selectively inhibits nuclear translocation of activated NF-κB. This study
aimed to demonstrate the antiarthritic effect of this novel inhibitor of the NF-κB pathway in vivo in a murine arthritis model and in vitro in human synovial cells. Collagen-induced arthritis was induced in mice, and after onset of arthritis the mice were treated
with DHMEQ (5 mg/kg body weight per day). Using fibroblast-like synoviocyte (FLS) cell lines established from patients with
rheumatoid arthritis (RA), NF-κB activity was examined by electrophoretic mobility shift assays. The expression of molecules
involved in RA pathogenesis was determined by RT-PCR, ELISA, and flow cytometry. The proliferative activity of the cells was
estimated with tritiated thymidine incorporation. After 14 days of treatment with DHMEQ, mice with collagen-induced arthritis
exhibited decreased severity of arthritis, based on the degree of paw swelling, the number of swollen joints, and radiographic
and histopathologic scores, compared with the control mice treated with vehicle alone. In RA FLS stimulated with tumor necrosis
factor-α, activities of NF-κB components p65 and p50 were inhibited by DHMEQ, leading to suppressed expression of the key
inflammatory cytokine IL-6, CC chemokine ligand-2 and -5, matrix metalloproteinase-3, intercellular adhesion molecule-1, and
vascular cell adhesion molecule-1. The proliferative activity of the cells was also suppressed. This is the first demonstration
of an inhibitor of NF-κB nuclear translocation exhibiting a therapeutic effect on established murine arthritis, and suppression
of inflammatory mediators in FLS was thought to be among the mechanisms underlying such an effect. 相似文献
994.
Kei KAWAZU Akira OTUKA Tarô ADATI Hisako TONOGOUCHI Junya YASE 《Entomological Science》2008,11(3):315-322
This paper provides a list of moths captured in a region at latitudes 29–32°N and longitudes 127–130°E on the East China Sea on 14–28 June and 1–7 July 2005. Sixteen species of moths from the families Plutellidae, Crambidae, Sphingidae and Noctuidae were identified. Among these, three species were recorded on the East China Sea for the first time. The migration paths of the captured moths were analyzed using a three‐dimensional backward trajectory analysis method. Predicted migration sources for these moths are Taiwan and Fujian, Guangdong, Jiangxi, Zhejiang, Jiangsu, and Anhui provinces in China. 相似文献
995.
Uemura H Ishiguro H Ishiguro Y Hoshino K Takahashi S Kubota Y 《Molecular cancer research : MCR》2008,6(2):250-258
Angiotensin II has been shown to be a cytokine especially acting as a growth factor. A local renin-angiotensin system has been identified in the prostate gland, and the physiologic function of angiotensin II seems to be similar in prostate cancer, as we previously reported. In the present study, we explored the biological role of angiotensin II in oxidative stress of prostate cancer cells. Activated Akt was determined, and the expression of oxidative stress-related proteins (p47phox, manganese superoxide dismutase 2, glutathione peroxidase) was examined by Western blotting in LNCaP cells, which were stimulated with angiotensin II and/or an angiotensin II receptor type 1 blocker, candesartan. To examine DNA damage induced by angiotensin II, 8-hydroxy-2'-deoxyguanosine was determined, and Western blots were analyzed to detect checkpoint proteins including p53, Chk2, and cdc2. Immunocytochemical studies of inducible nitric oxide synthase and superoxide anion radical (O(2)(-)) were done in LNCaP cells stimulated with angiotensin II. The phosphorylation of Akt was induced by angiotensin II treatment and inhibited by candesartan, as well as by LY294002, an inhibitor of phosphoinositide 3-kinase. Oxidative stress-related proteins were up-regulated by angiotensin II and inhibited by pretreatment with candesartan or catalase. The level of 8-hydroxy-2'-deoxyguanosine was increased by angiotensin II and conversely decreased by candesartan. Immunocytochemical studies showed that angiotensin II enhanced an inflammatory marker, inducible nitric oxide synthase, and the production of O(2)(-) radical. The hypothesis that angiotensin II has the potential to induce oxidative stress, which may be implicated in carcinogenesis of the prostate gland through long-term exposure to chronic inflammation is proposed. 相似文献
996.
Dynamic functional relay between insulin receptor substrate 1 and 2 in hepatic insulin signaling during fasting and feeding 总被引:3,自引:0,他引:3
Kubota N Kubota T Itoh S Kumagai H Kozono H Takamoto I Mineyama T Ogata H Tokuyama K Ohsugi M Sasako T Moroi M Sugi K Kakuta S Iwakura Y Noda T Ohnishi S Nagai R Tobe K Terauchi Y Ueki K Kadowaki T 《Cell metabolism》2008,8(1):49-64
Insulin receptor substrate (Irs) mediates metabolic actions of insulin. Here, we show that hepatic Irs1 and Irs2 function in a distinct manner in the regulation of glucose homeostasis. The PI3K activity associated with Irs2 began to increase during fasting, reached its peak immediately after refeeding, and decreased rapidly thereafter. By contrast, the PI3K activity associated with Irs1 began to increase a few hours after refeeding and reached its peak thereafter. The data indicate that Irs2 mainly functions during fasting and immediately after refeeding, and Irs1 functions primarily after refeeding. In fact, liver-specific Irs1-knockout mice failed to exhibit insulin resistance during fasting, but showed insulin resistance after refeeding; conversely, liver-specific Irs2-knockout mice displayed insulin resistance during fasting but not after refeeding. We propose the concept of the existence of a dynamic relay between Irs1 and Irs2 in hepatic insulin signaling during fasting and feeding. 相似文献
997.
Hirayama S Yamazaki Y Kitamura A Oda Y Morito D Okawa K Kimura H Cyr DM Kubota H Nagata K 《Molecular biology of the cell》2008,19(3):899-911
McKusick–Kaufman syndrome (MKKS) is a recessively inherited human genetic disease characterized by several developmental anomalies. Mutations in the MKKS gene also cause Bardet–Biedl syndrome (BBS), a genetically heterogeneous disorder with pleiotropic symptoms. However, little is known about how MKKS mutations lead to disease. Here, we show that disease-causing mutants of MKKS are rapidly degraded via the ubiquitin–proteasome pathway in a manner dependent on HSC70 interacting protein (CHIP), a chaperone-dependent ubiquitin ligase. Although wild-type MKKS quickly shuttles between the centrosome and cytosol in living cells, the rapidly degraded mutants often fail to localize to the centrosome. Inhibition of proteasome functions causes MKKS mutants to form insoluble structures at the centrosome. CHIP and partner chaperones, including heat-shock protein (HSP)70/heat-shock cognate 70 and HSP90, strongly recognize MKKS mutants. Modest knockdown of CHIP by RNA interference moderately inhibited the degradation of MKKS mutants. These results indicate that the MKKS mutants have an abnormal conformation and that chaperone-dependent degradation mediated by CHIP is a key feature of MKKS/BBS diseases. 相似文献
998.
Tada Y Koarada S Morito F Mitamura M Inoue H Suematsu R Ohta A Miyake K Nagasawa K 《Arthritis research & therapy》2008,10(5):R121-11
Introduction
RP105 is a Toll-like receptor homolog expressed on B cells, dendritic cells (DCs), and macrophages. We investigated the role of RP105 in the development of collagen-induced arthritis (CIA).Methods
CIA was induced in RP105-deficient DBA/1 mice and the incidence and arthritis index were analyzed. The cytokine production by spleen cells was determined. The functions of the DCs and regulatory T cells (Tregs) from RP105-deficient or control mice were determined by adding these cells to the lymph node cell culture. Arthritis was also induced by incomplete Freund's adjuvant (IFA) plus collagen or by injecting anti-collagen antibody and lipopolysaccharide.Results
RP105-deficient mice showed accelerated onset of arthritis and increased severity. Interferon-gamma (IFN-γ) and tumor necrosis factor-alpha production by spleen cells from RP105-deficient mice was increased in comparison with that from wild-type mice. The DCs from RP105-deficient mice induced more IFN-γ production, whereas Tregs from those mice showed less inhibitory effect against IFN-γ production. RP105-deficient mice also showed more severe arthritis induced by collagen with IFA.Conclusions
These results indicate that RP105 regulates the antigen-presenting cell function and Treg development, which induced the attenuation of the cell-mediated immune responses and, as a result, suppressed the development of CIA. 相似文献999.
1000.
Sayako Miura‐Takeda Junko Tashiro‐Yamaji Hidehiro Oku Takeshi Takahashi Tetsunosuke Shimizu Tetsuya Sugiyama Tsunehiko Ikeda Takahiro Kubota Ryotaro Yoshida 《Microbiology and immunology》2008,52(12):601-610
EAU in mice is a model of human posterior uveitis. EAU is a Th1‐dependent disease that has been assumed to target the neural retina and related tissues; however, in situ effector cells and the target have not yet been clearly demonstrated. In the present study, we induced EAU in B10R mice by immunizing them with human interphotoreceptor retinoid‐binding protein peptide 161–180. Histological examinations revealed that EAU occurred approximately 11 days after the immunization and reached a peak on day 14. Retinae from normal or EAU mice were treated with proteases to obtain mono‐dispersed cells. The mono‐dispersed cells thus obtained were separated into three to four fractions by discontinuous Percoll density‐gradient (e.g. PBS/40/60) centrifugation. In normal mice, 94% of the total cells were recovered in two fractions (i.e. PBS/40 and pellet); and these fractions mainly contained inner and outer segments and cell bodies of photoreceptor cells and RPE cells, respectively. In EAU mice, additional cells (i.e. inflammatory cells) were obtained at the 40/60 interface. Electron microscopic examination showed that tissue damage during EAU was initiated by non‐phagocytic destruction of inner segments by Mac‐1+ mononuclear cells on day 11, followed by phagocytic activity of macrophages against outer segments and RPE cells on day 14. In vitro culturing of normal retinal cells with EAU infiltrates suggested the involvement of TNF‐α and NO in the tissue damage. These results indicate that EAU was initiated by non‐phagocytic destruction of inner segments of photoreceptor cells by Mac‐1+ mononuclear cells. 相似文献