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排序方式: 共有199条查询结果,搜索用时 31 毫秒
91.
Brameshuber M Weghuber J Ruprecht V Gombos I Horváth I Vigh L Eckerstorfer P Kiss E Stockinger H Schütz GJ 《The Journal of biological chemistry》2010,285(53):41765-41771
The plasma membrane has been hypothesized to contain nanoscopic lipid platforms, which are discussed in the context of "lipid rafts" or "membrane rafts." Based on biochemical and cell biological studies, rafts are believed to play a crucial role in many signaling processes. However, there is currently not much information on their size, shape, stability, surface density, composition, and heterogeneity. We present here a method that allows for the first time the direct imaging of nanoscopic long-lived platforms with raft-like properties diffusing in the live cell plasma membrane. Our method senses these platforms by their property to assemble a characteristic set of fluorescent marker proteins or lipids on a time scale of seconds. A special photobleaching protocol was used to reduce the surface density of labeled mobile platforms down to the level of well isolated diffraction-limited spots without altering the single spot brightness. The statistical distribution of probe molecules per platform was determined by single molecule brightness analysis. For demonstration, we used the consensus raft marker glycosylphosphatidylinositol-anchored monomeric GFP and the fluorescent lipid analog BODIPY-G(M1), which preferentially partitions into liquid-ordered phases. For both markers, we found cholesterol-dependent homo-association in the plasma membrane of living CHO and Jurkat T cells in the resting state, thereby demonstrating the existence of small, mobile, long-lived platforms containing these probes. We further applied the technology to address structural changes in the plasma membrane during fever-type heat shock: at elevated temperatures, the glycosylphosphatidylinositol-anchored monomeric GFP homo-association disappeared, accompanied by an increase in the expression of the small heat shock protein Hsp27. 相似文献
92.
Zsuzsa Bagoly Ferenc Sarkady Tünde Magyar János Kappelmayer Endre Pongrácz László Csiba László Muszbek 《PloS one》2013,8(7)
Background
Clinical studies suggest that 10-50% of patients are resistant to clopidogrel therapy. ADP induced platelet aggregation, a widely used test to monitor clopidogrel therapy, is affected by aspirin and is not specific for the P2Y12 receptor inhibited by clopidogrel.Objectives
To develop a P2Y12-specific platelet aggregation test and to compare it with other methods used for monitoring clopidogrel therapy.Patients/Methods
Study population included 111 patients with the history of ischemic stroke being on clopidogrel monotherapy and 140 controls. The effect of clopidogrel was tested by a newly developed ADP(PGE1) aggregation test in which prostaglandin E1 treated platelets are used. Results of conventional ADP induced platelet aggregation, VerifyNow P2Y12 assay and ADP(PGE1) aggregation were compared to those obtained by flow cytometric analysis of vasodilator stimulated phosphoprotein (VASP) phosphorylation. Reference intervals for all assays were determined according to the guidelines of Clinical Laboratory Standards Institute.Results
The P2Y12-specificity of ADP(PGE1) test was proven by comparing it with ADP aggregation in the presence of P2Y1 antagonist, adenosine 3’, 5’-diphosphate. The method was not influenced by aspirin treatment. Approximately 50% of patients were clopidogrel resistant by conventional ADP aggregation and VerifyNow tests. The ADP(PGE1) method and the VASP phosphorylation assay identified 25.9% and 11.7% of patients as non-responders, respectively. ADP(PGE1) aggregation showed good correlation with VASP phosphorylation and had high diagnostic efficiency.Conclusion
The new ADP(PGE1) method is a reliable test for monitoring P2Y12 receptor inhibition by platelet aggregation. As a subset of patients are non-responders, monitoring clopidogrel therapy by adequate methods is essential. 相似文献93.
Endre Aas Birgitta Liewenborg Bjørn Einar Grøsvik Lionel Camus Grete Jonsson Jan Fredrik Børseth 《Biomarkers》2013,18(6):445-460
In order to understand and apply DNA adduct formation in fish liver as a biomarker for aquatic pollution, information concerning the natural background levels in non-contaminated organisms, caused by endogenous compounds, is of fundamental importance. In this study, DNA adducts were analysed in liver of 11 fish species from arctic and sub-arctic areas in the northern Atlantic using the nuclease P1 version of the 32P-postlabelling technique. The collected fish were assumed not to have been influenced by anthropogenic pollution apart from possible long-range transported pollutants. As polycyclic aromatic hydrocarbons (PAHs) are thought to be fundamental in forming the type of DNA adducts detected by the method used, biliary PAH metabolite levels were measured in a selection of the investigated species. In all investigated individuals, the levels of PAH metabolites were undetectable. Controlled on-site exposure experiments with benzo[a]pyrene (polar cod) and laboratory experiments with crude oil (polar cod and Atlantic cod) were conducted. DNA adducts were formed in both these species. The field-sampled fish showed undetectable levels of DNA adducts or levels just above the detection limit. The present study supports the assumption that when DNA adducts are detected by the nuclease P1 version of the 32P-postlabelling method in fish liver, it can be interpreted as DNA damage caused by pollutants. 相似文献
94.
Endre Kristóf Gábor Zahuczky Klára Katona Zoltán Doró Éva Nagy László Fésüs 《Apoptosis : an international journal on programmed cell death》2013,18(10):1235-1251
Apoptotic cells express eat-me signals which are recognized by several receptors mainly on professional phagocytes of the mononuclear phagocyte system. This “engulfment synapse” can define a safe and effective clearance of apoptotic cells in order to maintain tissue homeostasis in the entire body. We show that the expression of four genes related to apoptotic cell clearance is strongly up-regulated in human macrophages 30 min after administration of apoptotic neutrophils. Out of these the significant role of the up-regulated intercellular adhesion molecule 3 (ICAM3) in phagocytosis of apoptotic neutrophils could be demonstrated in macrophages by gene silencing as well as treatment with blocking antibodies. Blocking ICAM3 on the surface of apoptotic neutrophils also resulted in their decreased uptake which confirmed its role as an eat-me signal expressed by apoptotic cells. In macrophages but not in neutrophils silencing and blocking integrin alphaL and beta2 components of lymphocyte function-associated antigen 1 (LFA-1), which can strongly bind ICAM3, resulted in a decreased phagocytosis of apoptotic cells indicating its possible role to recognize ICAM3 on the surface of apoptotic neutrophils. Finally, we report that engulfing portals formed in macrophages during phagocytosis are characterized by accumulation of ICAM3, integrin alphaL and beta2 which show co-localization on the surface of phagocytes. Furthermore, their simultaneous knock-down in macrophages resulted in a marked deficiency in phagocytosis and a slight decrease in the anti-inflammatory effect of apoptotic neutrophils. We propose that ICAM3 and LFA-1 act as recognition receptors in the phagocytosis portals of macrophages for engulfment of apoptotic neutrophils. 相似文献
95.
María Salazar Mar Lorente Elena García-Taboada Sonia Hernández-Tiedra David Davila Sheila E. Francis Manuel Guzmán Endre Kiss-Toth Guillermo Velasco 《Biochimica et Biophysica Acta (BBA)/Molecular and Cell Biology of Lipids》2013,1831(10):1573-1578
Δ9-Tetrahydrocannabinol (THC), the major active ingredient of marijuana, and other cannabinoids inhibit tumor growth in animal models of cancer. This effect relies, at least in part, on the up-regulation of several endoplasmic reticulum stress-related proteins including the pseudokinase tribbles homologue-3 (TRIB3), which leads in turn to the inhibition of the AKT/mTORC1 axis and the subsequent stimulation of autophagy-mediated apoptosis in tumor cells. Here, we took advantage of the use of cells derived from Trib3-deficient mice to investigate the precise mechanisms by which TRIB3 regulates the anti-cancer action of THC. Our data show that RasV12/E1A-transformed embryonic fibroblasts derived from Trib3-deficient mice are resistant to THC-induced cell death. We also show that genetic inactivation of this protein abolishes the ability of THC to inhibit the phosphorylation of AKT and several of its downstream targets, including those involved in the regulation of the AKT/mammalian target of rapamycin complex 1 (mTORC1) axis. Our data support the idea that THC-induced TRIB3 up-regulation inhibits AKT phosphorylation by regulating the accessibility of AKT to its upstream activatory kinase (the mammalian target of rapamycin complex 2; mTORC2). Finally, we found that tumors generated by inoculation of Trib3-deficient cells in nude mice are resistant to THC anticancer action. Altogether, the observations presented here strongly support that TRIB3 plays a crucial role on THC anti-neoplastic activity. This article is part of a Special Issue entitled Lipid Metabolism in Cancer. 相似文献
96.
Lhcb1-2 and PsbS proteins of photosystem II (PSII) have important roles in photoprotective thermal energy dissipation of the
absorbed excess light energy. The light responses of chlorophyll fluorescence parameters were analyzed to examine how the
absence of Lhcb1-2 or PsbS proteins can modify the energy allocation patterns of absorbed light energy in PSII using an antisense
construct of lhcb2 and a psbS deletion (npq4-1) mutant of Arabidopsis thaliana. Both mutants exhibit reduced Stern–Volmer non-photochemical chlorophyll fluorescence quenching (NPQ). Here, we have adopted
an approach, presented by Hendrickson et al. (Photosynth Res 82:73–81, 2004), to gain a better insight into the mechanism of the NPQ in these mutants. We have found no significant differences in the
quantum yields of photochemical energy conversion (ΦPSII) between the mutants and the wild type. Nevertheless, as it was expected, the fraction of the energy, which is dissipated
as heat via regulated pathways in PSII (ΦNPQ) for both mutants, were reduced as compared to the wild type. In a complementary way, the extent of non-regulated non-photochemical
energy loss in PSII (ΦNO) for both mutants was significantly higher than that in the wild type. This reflects, together with the lower ΦNPQ (or NPQ) values, suboptimal capacity of photoprotective reactions at higher light intensities. 相似文献
97.
Endre Aas Birgitta Liewenborg Bj rn Einar Gr svik Lionel Camus Grete Jonsson Jan Fredrik B rseth Lennart Balk 《Biomarkers》2003,8(6):445-460
In order to understand and apply DNA adduct formation in fish liver as a biomarker for aquatic pollution, information concerning the natural background levels in non-contaminated organisms, caused by endogenous compounds, is of fundamental importance. In this study, DNA adducts were analysed in liver of 11 fish species from arctic and sub-arctic areas in the northern Atlantic using the nuclease P1 version of the 332P-postlabelling technique. The collected fish were assumed not to have been influenced by anthropogenic pollution apart from possible long-range transported pollutants. As polycyclic aromatic hydrocarbons (PAHs) are thought to be fundamental in forming the type of DNA adducts detected by the method used, biliary PAH metabolite levels were measured in a selection of the investigated species. In all investigated individuals, the levels of PAH metabolites were undetectable. Controlled on-site exposure experiments with benzo[a]pyrene (polar cod) and laboratory experiments with crude oil (polar cod and Atlantic cod) were conducted. DNA adducts were formed in both these species. The field-sampled fish showed undetectable levels of DNA adducts or levels just above the detection limit. The present study supports the assumption that when DNA adducts are detected by the nuclease P1 version of the 3ng method in fish liver, it can be interpreted as DNA damage caused by pollutants. 相似文献
98.
Sverre Kobro Linda Søreide Endre Djønne Trond Rafoss Gunnhild Jaastad Peter Witzgall 《Population Ecology》2003,45(1):25-30
Masting of rowan Sorbus aucuparia L. has been studied in 45 sites in southern Norway for 22 years. We present data on the year-to-year variation in fruit setting
of rowan, and show that masting is spatially synchronous in Norway and probably all over Fennoscandia. The apple fruit moth
Argyresthia conjugella Zeller is an important seed predator on rowan. We present data on the abundance of apple fruit moth in rowanberries during
these years and discuss the consequences of masting and intermasting of rowan for apple fruit moth as a pest of apple. We
conclude that growth and climate have little impact on flowering intensity and suggest that masting of rowan is an adaptive
defense against seed predation and a new example of predator satiation: intermast years inhibit predators and prepare the
rowan for the subsequent mast.
Received: September 3, 2001 / Accepted: February 24, 2003 相似文献
99.
The Pin2 genes encode potato type II proteinase inhibitors that act against pathogenic attack. The first examples were found only in the Solanaceae family, but, using new EST and genomic data, we have found 11 homologous genes dispersed through almost the whole range of mono- and di-cotyledonous plants. In contrast to the repetitive precursor sequences of the Solanaceae Pin2 genes, the new homologs have only a single repeat unit. The gene family appears to have evolved from a single-domain ancestral gene through a series of gene-duplication and domain-duplication steps. A number of unequal cross-over and gene conversion events could explain the current gene and domain pattern of the Solanaceae Pin2 subfamily. 相似文献
100.
Oluf Dimitri R?e Endre Anderssen Eli Helge Caroline Hild Pettersen Karina Standahl Olsen Helmut Sandeck Rune Haaverstad Steinar Lundgren Erik Larsson 《PloS one》2009,4(8)