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951.
Lack of Viral Escape and Defective In Vivo Activation of Human Immunodeficiency Virus Type 1-Specific Cytotoxic T Lymphocytes in Rapidly Progressive Infection 下载免费PDF全文
Christine M. Hay Debbie J. Ruhl Nesli O. Basgoz Cara C. Wilson James M. Billingsley Maria Pia DePasquale Richard T. DAquila Steven M. Wolinsky John M. Crawford David C. Montefiori Bruce D. Walker 《Journal of virology》1999,73(7):5509-5519
Human immunodeficiency virus type 1 (HIV-1)-specific immune responses over the course of rapidly progressive infection are not well defined. Detailed longitudinal analyses of neutralizing antibodies, lymphocyte proliferation, in vivo-activated and memory cytotoxic T-lymphocyte (CTL) responses, and viral sequence variation were performed on a patient who presented with acute HIV-1 infection, developed an AIDS-defining illness 13 months later, and died 45 months after presentation. Neutralizing-antibody responses remained weak throughout, and no HIV-1-specific lymphocyte proliferative responses were seen even early in the disease course. Strong in vivo-activated CTL directed against Env and Pol epitopes were present at the time of the initial drop in viremia but were quickly lost. Memory CTL against Env and Pol epitopes were detected throughout the course of infection; however, these CTL were not activated in vivo. Despite an initially narrow CTL response, new epitopes were not targeted as the disease progressed. Viral sequencing showed the emergence of variants within the two targeted CTL epitopes; however, viral variants within the immunodominant Env epitope were well recognized by CTL, and there was no evidence of viral escape from immune system detection within this epitope. These data demonstrate a narrowly directed, static CTL response in a patient with rapidly progressive disease. We also show that disease progression can occur in the presence of persistent memory CTL recognition of autologous epitopes and in the absence of detectable escape from CTL responses, consistent with an in vivo defect in activation of CTL. 相似文献
952.
Soil pCO2, soil respiration,and root activity in CO2-fumigated and nitrogen-fertilized ponderosa pine 总被引:2,自引:0,他引:2
Dale Johnson Donn Geisinger Roger Walker John Newman James Vose Katherine Elliot Timothy Ball 《Plant and Soil》1994,165(1):129-138
The purpose of this paper is to describe the effects of CO2 and N treatments on soil pCO2, calculated CO2 efflux, root biomass and soil carbon in open-top chambers planted with Pinus ponderosa seedlings. Based upon the literature, it was hypothesized that both elevated CO2 and N would cause increased root biomass which would in turn cause increases in both total soil CO2 efflux and microbial respiration. This hypothesis was only supported in part: both CO2 and N treatments caused significant increases in root biomass, soil pCO2, and calculated CO2 efflux, but there were no differences in soil microbial respiration measured in the laboratory. Both correlative and quantitative
comparisons of CO2 efflux rates indicated that microbial respiration contributes little to total soil CO2 efflux in the field. Measurements of soil pCO2 and calculated CO2 efflux provided inexpensive, non-invasive, and relatively sensitive indices of belowground response to CO2 and N treatments. 相似文献
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The current world-wide epidemic of diabetes has prompted attempts to generate new sources of insulin-producing cells for cell replacement therapy. An inherent challenge in many of these strategies is the lack of cell-surface markers permitting isolation and characterization of specific cell types from differentiating stem cell populations. Here we introduce an iterative proteomics procedure allowing tag-free isolation of cell types based on their function. Our method detects and associates specific cell-surface markers with particular cell functionality by coupling cell capture on antibody arrays with immunofluorescent labeling. Using this approach in an iterative manner, we discovered marker combinations capable of enriching for discrete pancreatic cell subtypes from human islets of Langerhans: insulin-producing beta cells (CD9high/CD56+), glucagon-producing alpha cells (CD9- /CD56+) and trypsin-producing acinar cells (CD9- /CD56-). This strategy may assist future beta cell research and the development of diagnostic tools for diabetes. It can also be applied more generally for function-based purification of desired cell types from other limited and heterogeneous biological samples. 相似文献
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In allergic asthma Beta 2 adrenergic receptors (β2ARs) are important mediators of bronchorelaxation and, paradoxically, asthma development. This contradiction is likely due to the activation of dual signaling pathways that are downstream of G proteins or β-arrestins. Our group has recently shown that β-arrestin-2 acts in its classical role to desensitize and constrain β2AR-induced relaxation of both human and murine airway smooth muscle. To assess the role of β-arrestins in regulating β2AR function in asthma, we and others have utilized β-arrestin-1 and -2 knockout mice. However, it is unknown if genetic deletion of β-arrestins in these mice influences β2AR expression in the airways. Furthermore, there is lack of data on compensatory expression of βAR subtypes when either of the β-arrestins is genetically deleted, thus necessitating a detailed βAR subtype expression study in these β-arrestin knockout mice. Here we standardized a radioligand binding methodology to characterize and quantitate βAR subtype distribution in the airway smooth muscle of wild-type C57BL/6J and β-arrestin-1 and β-arrestin-2 knockout mice. Using complementary competition and single-point saturation binding assays we found that β2ARs predominate over β1ARs in the whole lung and epithelium-denuded tracheobronchial smooth muscle of C57BL/6J mice. Quantification of βAR subtypes in β-arrestin-1 and β-arrestin-2 knockout mouse lung and epithelium-denuded tracheobronchial tissue showed that, similar to the C57BL/6J mice, both knockouts display a predominance of β2AR expression. These data provide further evidence that β2ARs are expressed in greater abundance than β1ARs in the tracheobronchial smooth muscle and that loss of either β-arrestin does not significantly affect the expression or relative proportions of βAR subtypes. As β-arrestins are known to modulate β2AR function, our analysis of βAR subtype expression in β-arrestin knockout mice airways sets a reference point for future studies exploiting these knockout mice in various disease models including asthma. 相似文献
960.
Caryn S. Ross-Innes Irene Debiram-Beecham Maria O'Donovan Elaine Walker Sibu Varghese Pierre Lao-Sirieix Laurence Lovat Michael Griffin Krish Ragunath Rehan Haidry Sarmed S. Sami Philip Kaye Marco Novelli Babett Disep Richard Ostler Benoit Aigret Bernard V. North Pradeep Bhandari Adam Haycock Danielle Morris Stephen Attwood Anjan Dhar Colin Rees Matthew D. D. Rutter Peter D. Sasieni Rebecca C. Fitzgerald 《PLoS medicine》2015,12(1)
BackgroundBarrett''s esophagus (BE) is a commonly undiagnosed condition that predisposes to esophageal adenocarcinoma. Routine endoscopic screening for BE is not recommended because of the burden this would impose on the health care system. The objective of this study was to determine whether a novel approach using a minimally invasive cell sampling device, the Cytosponge, coupled with immunohistochemical staining for the biomarker Trefoil Factor 3 (TFF3), could be used to identify patients who warrant endoscopy to diagnose BE.ConclusionsThe Cytosponge-TFF3 test is safe and acceptable, and has accuracy comparable to other screening tests. This test may be a simple and inexpensive approach to identify patients with reflux symptoms who warrant endoscopy to diagnose BE. 相似文献