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51.
Summary Anti-toxoplasma antibodies administered passively to mice may lead to suppression or enhancement (reported for the first time with Protozoan parasites) of subsequent antibody response when these animals are later infected withToxoplasma gondii. The outcome is dependent on infecting strain of Toxoplasma and the antigen-antibody ratio. 相似文献
52.
G. de Stevens L. H. Werner A. Halamandaris S. Ricca Jr. 《Cellular and molecular life sciences : CMLS》1958,14(12):463-463
Zusammenfassung Die Gewinnung eines neuen, tierexperimentell und klinisch hochwirksamen Diureticums der Formel III (6-Chlor-7-sulfamyl-3,4-dihydro-1,2,4-benzothiadiazin-1,1-dioxyd)
wird beschrieben.
相似文献
53.
Hoogenraad CC Koekkoek B Akhmanova A Krugers H Dortland B Miedema M van Alphen A Kistler WM Jaegle M Koutsourakis M Van Camp N Verhoye M van der Linden A Kaverina I Grosveld F De Zeeuw CI Galjart N 《Nature genetics》2002,32(1):116-127
Williams syndrome is a neurodevelopmental disorder caused by the hemizygous deletion of 1.6 Mb on human chromosome 7q11.23. This region comprises the gene CYLN2, encoding CLIP-115, a microtubule-binding protein of 115 kD. Using a gene-targeting approach, we provide evidence that mice with haploinsufficiency for Cyln2 have features reminiscent of Williams syndrome, including mild growth deficiency, brain abnormalities, hippocampal dysfunction and particular deficits in motor coordination. Absence of CLIP-115 also leads to increased levels of CLIP-170 (a closely related cytoplasmic linker protein) and dynactin at the tips of growing microtubules. This protein redistribution may affect dynein motor regulation and, together with the loss of CLIP-115-specific functions, underlie neurological alterations in Williams syndrome. 相似文献
54.
Patterns of subsurface wedges of ice that form along cooling-induced tension fractures, expressed at the ground surface by ridges or troughs spaced 10 30 m apart, are ubiquitous in polar lowlands. Fossilized ice wedges, which are widespread at lower latitudes, have been used to infer the duration and mean temperature of cold periods within Proterozoic and Quaternary climates, and recent climate trends have been inferred from fracture frequency in active ice wedges. Here we present simulations from a numerical model for the evolution of ice-wedge networks over a range of climate scenarios, based on the interactions between thermal tensile stress, fracture and ice wedges. We find that short-lived periods of severe cooling permanently alter the spacing between ice wedges as well as their fracture frequency. This affects the rate at which the widths of ice wedges increase as well as the network's response to subsequent climate change. We conclude that wedge spacing and width in ice-wedge networks mainly reflect infrequent episodes of rapidly falling ground temperatures rather than mean conditions. 相似文献
55.
56.
West AP Brodsky IE Rahner C Woo DK Erdjument-Bromage H Tempst P Walsh MC Choi Y Shadel GS Ghosh S 《Nature》2011,472(7344):476-480
Reactive oxygen species (ROS) are essential components of the innate immune response against intracellular bacteria and it is thought that professional phagocytes generate ROS primarily via the phagosomal NADPH oxidase machinery. However, recent studies have suggested that mitochondrial ROS (mROS) also contribute to mouse macrophage bactericidal activity, although the mechanisms linking innate immune signalling to mitochondria for mROS generation remain unclear. Here we demonstrate that engagement of a subset of Toll-like receptors (TLR1, TLR2 and TLR4) results in the recruitment of mitochondria to macrophage phagosomes and augments mROS production. This response involves translocation of a TLR signalling adaptor, tumour necrosis factor receptor-associated factor 6 (TRAF6), to mitochondria, where it engages the protein ECSIT (evolutionarily conserved signalling intermediate in Toll pathways), which is implicated in mitochondrial respiratory chain assembly. Interaction with TRAF6 leads to ECSIT ubiquitination and enrichment at the mitochondrial periphery, resulting in increased mitochondrial and cellular ROS generation. ECSIT- and TRAF6-depleted macrophages have decreased levels of TLR-induced ROS and are significantly impaired in their ability to kill intracellular bacteria. Additionally, reducing macrophage mROS levels by expressing catalase in mitochondria results in defective bacterial killing, confirming the role of mROS in bactericidal activity. These results reveal a novel pathway linking innate immune signalling to mitochondria, implicate mROS as an important component of antibacterial responses and further establish mitochondria as hubs for innate immune signalling. 相似文献
57.
Gavin C. Higgins Philip M. Beart Phillip Nagley 《Cellular and molecular life sciences : CMLS》2009,66(16):2773-2787
To characterize neuronal death, primary cortical neurons (C57/Black 6 J mice) were exposed to hydrogen peroxide (H2O2) and staurosporine. Both caused cell shrinkage, nuclear condensation, DNA fragmentation and loss of plasma membrane integrity.
Neither treatment induced caspase-7 activity, but caspase-3 was activated by staurosporine but not H2O2. Each treatment caused redistribution from mitochondria of both endonuclease G (Endo G) and cytochrome c. Neurons knocked down for Endo G expression using siRNA showed reduction in both nuclear condensation and DNA fragmentation
after treatment with H2O2, but not staurosporine. Endo G suppression protected cells against H2O2-induced cell death, while staurosporine-induced death was merely delayed. We conclude that staurosporine induces apoptosis
in these neurons, but severe oxidative stress leads to Endo G-dependent death, in the absence of caspase activation (programmed
cell death-type III). Therefore, oxidative stress triggers in neurons a form of necrosis that is a systematic cellular response
subject to molecular regulation.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. 相似文献
58.
59.
Chemical reduction of three-dimensional silica micro-assemblies into microporous silicon replicas 总被引:1,自引:0,他引:1
Bao Z Weatherspoon MR Shian S Cai Y Graham PD Allan SM Ahmad G Dickerson MB Church BC Kang Z Abernathy HW Summers CJ Liu M Sandhage KH 《Nature》2007,446(7132):172-175
The carbothermal reduction of silica into silicon requires the use of temperatures well above the silicon melting point (> or =2,000 degrees C). Solid silicon has recently been generated directly from silica at much lower temperatures (< or =850 degrees C) via electrochemical reduction in molten salts. However, the silicon products of such electrochemical reduction did not retain the microscale morphology of the starting silica reactants. Here we demonstrate a low-temperature (650 degrees C) magnesiothermic reduction process for converting three-dimensional nanostructured silica micro-assemblies into microporous nanocrystalline silicon replicas. The intricate nanostructured silica microshells (frustules) of diatoms (unicellular algae) were converted into co-continuous, nanocrystalline mixtures of silicon and magnesia by reaction with magnesium gas. Selective magnesia dissolution then yielded an interconnected network of silicon nanocrystals that retained the starting three-dimensional frustule morphology. The silicon replicas possessed a high specific surface area (>500 m(2) g(-1)), and contained a significant population of micropores (< or =20 A). The silicon replicas were photoluminescent, and exhibited rapid changes in impedance upon exposure to gaseous nitric oxide (suggesting a possible application in microscale gas sensing). This process enables the syntheses of microporous nanocrystalline silicon micro-assemblies with multifarious three-dimensional shapes inherited from biological or synthetic silica templates for sensor, electronic, optical or biomedical applications. 相似文献
60.
AA Pezzulo XX Tang MJ Hoegger MH Alaiwa S Ramachandran TO Moninger PH Karp CL Wohlford-Lenane HP Haagsman M van Eijk B Bánfi AR Horswill DA Stoltz PB McCray MJ Welsh J Zabner 《Nature》2012,487(7405):109-113
Cystic fibrosis (CF) is a life-shortening disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Although bacterial lung infection and the resulting inflammation cause most of the morbidity and mortality, how the loss of CFTR function first disrupts airway host defence has remained uncertain. To investigate the abnormalities that impair elimination when a bacterium lands on the pristine surface of a newborn CF airway, we interrogated the viability of individual bacteria immobilized on solid grids and placed onto the airway surface. As a model, we studied CF pigs, which spontaneously develop hallmark features of CF lung disease. At birth, their lungs lack infection and inflammation, but have a reduced ability to eradicate bacteria. Here we show that in newborn wild-type pigs, the thin layer of airway surface liquid (ASL) rapidly kills bacteria in vivo, when removed from the lung and in primary epithelial cultures. Lack of CFTR reduces bacterial killing. We found that the ASL pH was more acidic in CF pigs, and reducing pH inhibited the antimicrobial activity of ASL. Reducing ASL pH diminished bacterial killing in wild-type pigs, and, conversely, increasing ASL pH rescued killing in CF pigs. These results directly link the initial host defence defect to the loss of CFTR, an anion channel that facilitates HCO(3)(-) transport. Without CFTR, airway epithelial HCO(3)(-) secretion is defective, the ASL pH falls and inhibits antimicrobial function, and thereby impairs the killing of bacteria that enter the newborn lung. These findings suggest that increasing ASL pH might prevent the initial infection in patients with CF, and that assaying bacterial killing could report on the benefit of therapeutic interventions. 相似文献