首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   51464篇
  免费   3714篇
  国内免费   24篇
  55202篇
  2023年   187篇
  2022年   591篇
  2021年   955篇
  2020年   598篇
  2019年   734篇
  2018年   1106篇
  2017年   980篇
  2016年   1617篇
  2015年   2485篇
  2014年   2879篇
  2013年   3211篇
  2012年   4268篇
  2011年   4029篇
  2010年   2576篇
  2009年   2352篇
  2008年   3237篇
  2007年   3101篇
  2006年   2741篇
  2005年   2525篇
  2004年   2345篇
  2003年   2031篇
  2002年   1765篇
  2001年   1377篇
  2000年   1318篇
  1999年   1070篇
  1998年   433篇
  1997年   386篇
  1996年   287篇
  1995年   248篇
  1994年   245篇
  1993年   207篇
  1992年   402篇
  1991年   351篇
  1990年   317篇
  1989年   271篇
  1988年   203篇
  1987年   195篇
  1986年   157篇
  1985年   141篇
  1984年   104篇
  1983年   102篇
  1982年   81篇
  1981年   71篇
  1980年   70篇
  1979年   91篇
  1978年   73篇
  1977年   61篇
  1976年   64篇
  1974年   80篇
  1973年   61篇
排序方式: 共有10000条查询结果,搜索用时 11 毫秒
101.
Mice with the CBA/N defect (xid) are unresponsive to phosphorylcholine (PC), To determine whether idiotype-specific suppressor T cells can also be generated in these defective mice, defective (CBA/N X BALB/c)F1 male and nondefective (CBA/N X BALB/c)F1 female or (BALB/c X CBA/N)F1 male mice were neonatally injected with antibodies specific for the major idiotype of anti-PC antibody, i.e., anti-TEPC-15 idiotype (T15id) antibody. Suppressor cell activity was examined by co-culturing spleen cells from neonatally treated F1 mice with spleen cells of normal nondefective F1 mice in the presence of antigen. Spleen cells from defective (CBA/NM X BALB/c)F1 mice treated with anti-T15id antibody demonstrated a level of suppressor activity (greater than 83% suppression) comparable to that of similarly treated nondefective F1 mice. This suppression was specific for the T15id of anti-PC response, and a Lyt-1-2+-bearing T cell population appeared to be responsible for the active suppression. These suppressor T cells recognized T15 but not PC, based on a functional absorption test. These results indicate that the CBA/N defects, including the deficiency in the anti-PC response by B lymphocytes and a possible T cell defect, do not influence the generation of T15id-specific suppressor T cells by neonatal injection with anti-T15id antibody.  相似文献   
102.
103.
αAIns, an elongated α-crystallin A chain previously observed in rat, was present beside the normal αA chain in mouse, gerbil and hamster, which places its origin at least 30 million years ago. Like in rat the sequences of golden hamster αAIns and αA were found to be identical, apart from the internal insertion of 22 residues in αAIns. The hamster chains only differed from the rat chains by a single substitution in the inserted sequence of αAIns. The origin of αAIns, by insertion of 22 residues in an otherwise unchanged αA chain, and its rigid evolutionary conservation are most easily explained by assuming the incomplete removal of a putative intervening sequence from the precursor mRNA of αA, leaving an intracistronic insert of 66 nucleotides in part of the eventually translated mRNA.  相似文献   
104.
105.
More than 300 reference strains representing 60 species and varieties ofFusarium cultures named according to different taxonomic systems are currently maintained at the American Type Culture Collection (ATCC). They have been preserved by freeze-drying and by freezing and subsequent storage in liquid nitrogen (–196°C) to insure their viability without contamination, variation, mutation, or deterioration. The materials and procedures used at the ATCC for the acquisition, accessioning, cataloguing, preservation and distribution are described. Longevity storage data for the strains available for distribution are presented and discussed.  相似文献   
106.
107.
During pathogenesis, effector proteins are secreted from the pathogen to the host plant to provide virulence activity for invasion of the host. However, once the host plant recognizes one of the delivered effectors, effector‐triggered immunity activates a robust immune and hypersensitive response (HR). In planta, the effector AvrRps4 is processed into the N‐terminus (AvrRps4N) and the C‐terminus (AvrRps4C). AvrRps4C is sufficient to trigger HR in turnip and activate AtRRS1/AtRPS4‐mediated immunity in Arabidopsis; on the other hand, AvrRps4N induces HR in lettuce. Furthermore, AvrRps4N‐mediated HR requires a conserved arginine at position 112 (R112), which is also important for full‐length AvrRps4 (AvrRps4F) processing. Here, we show that effector processing and effector recognition in lettuce are uncoupled for the AvrRps4 family. In addition, we compared effector recognition by lettuce of AvrRps4 and its homologues, HopK1 and XopO. Interestingly, unlike for AvrRps4 and HopK1, mutation of the conserved R111 in XopO by itself was insufficient to abolish recognition. The combination of amino acid substitutions arginine 111 to leucine with glutamate 114 to lysine abolished the XopO‐mediated HR, suggesting that AvrRps4 family members have distinct structural requirements for perception by lettuce. Together, our results provide an insight into the processing and recognition of AvrRps4 and its homologues.  相似文献   
108.
109.
Background:The tremendous global health burden related to COVID-19 means that identifying determinants of COVID-19 severity is important for prevention and intervention. We aimed to explore long-term exposure to ambient air pollution as a potential contributor to COVID-19 severity, given its known impact on the respiratory system.Methods:We used a cohort of all people with confirmed SARS-CoV-2 infection, aged 20 years and older and not residing in a long-term care facility in Ontario, Canada, during 2020. We evaluated the association between long-term exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2) and ground-level ozone (O3), and risk of COVID-19-related hospital admission, intensive care unit (ICU) admission and death. We ascertained individuals’ long-term exposures to each air pollutant based on their residence from 2015 to 2019. We used logistic regression and adjusted for confounders and selection bias using various individual and contextual covariates obtained through data linkage.Results:Among the 151 105 people with confirmed SARS-CoV-2 infection in Ontario in 2020, we observed 8630 hospital admissions, 1912 ICU admissions and 2137 deaths related to COVID-19. For each interquartile range increase in exposure to PM2.5 (1.70 μg/m3), we estimated odds ratios of 1.06 (95% confidence interval [CI] 1.01–1.12), 1.09 (95% CI 0.98–1.21) and 1.00 (95% CI 0.90–1.11) for hospital admission, ICU admission and death, respectively. Estimates were smaller for NO2. We also estimated odds ratios of 1.15 (95% CI 1.06–1.23), 1.30 (95% CI 1.12–1.50) and 1.18 (95% CI 1.02–1.36) per interquartile range increase of 5.14 ppb in O3 for hospital admission, ICU admission and death, respectively.Interpretation:Chronic exposure to air pollution may contribute to severe outcomes after SARS-CoV-2 infection, particularly exposure to O3.

By November 2021, COVID-19 had caused more than 5 million deaths globally1 and more than 29 400 in Canada.2 The clinical manifestations of SARS-CoV-2 infection range from being asymptomatic to multiple organ failure and death. Identifying risk factors for COVID-19 severity is important to better understand etiological mechanisms and identify populations to prioritize for screening, vaccination and medical treatment. Risk factors for severity of COVID-19 include male sex, older age, pre-existing medical conditions and being from racialized communities.35 More recently, ambient air pollution has been implicated as a potential driver of COVID-19 severity.610Long-term exposure to ambient air pollution, a major contributor to global disease burden,11 could increase the risk of severe COVID-19 outcomes by several mechanisms. Air pollutants can reduce individuals’ pulmonary immune responses and antimicrobial activities, boosting viral loads.8 Air pollution can also induce chronic inflammation and overexpression of the alveolar angiotensin-converting enzyme 2 (ACE) receptor,7 the key receptor that facilitates SARS-CoV-2 entry into cells.12,13 Exposure to air pollution contributes to chronic conditions, such as cardiovascular disease, that are associated with unfavourable COVID-19 prognosis, possibly owing to persistent immune activation and excessive amplification of cytokine development.10 Thus, greater exposure to long-term air pollution may lead to severe COVID-19 outcomes.Reports exist of positive associations between long-term exposure to particulate matter with diameters equal to or smaller than 2.5 or 10 μm (PM2.5 and PM10), ground-level ozone (O3) and nitrogen dioxide (NO2), and metrics of COVID-19 severity (e.g., mortality and case fatality rate).810 However, most studies to date have used ecological and cross-sectional designs, owing to limited access to individual data, which leads to ambiguity in interpreting the results, thus hindering their influence on policy. 6,14 Ecological designs do not allow for disentangling the relative impacts of air pollution on individual susceptibility to infection and disease severity.14 Residual confounding by factors such as population mobility and social interactions is also problematic. Therefore, a cohort study with data on individuals with SARS-CoV-2 is a more appropriate design.6,14 Studies that have used individual data were conducted in specific subpopulations15,16 or populations with few severe cases,17 or had limited data on individual exposure to air pollutants.18 In Canada, 1 ecological study found a positive association between long-term exposure to PM2.5 and COVID-19 incidence,19 but no published study has explored the association between air pollution and COVID-19 severity.We aimed to examine the associations between long-term exposure to 3 common air pollutants (PM2.5, NO2 and O3) and key indicators of COVID-19 severity, including hospital admission, intensive care unit (ICU) admission and death, using a large prospective cohort of people with confirmed SARS-CoV-2 infection in Ontario, Canada, in 2020. The air contaminants PM2.5, NO2 and O3 are regularly monitored by the Canadian government, and are key pollutants that are considered when setting air-quality policies. They originate from varying sources (NO2 is primarily emitted during combustion of fuel, O3 is primarily formed in air by chemical reactions of nitrogen oxides and volatile organic compounds, and PM2.5 can be emitted during combustion or formed by reactions of chemicals like sulphur dioxide and nitrogen oxides in air) and they may affect human health differently.20,21,22  相似文献   
110.
Budding cells of the yeast Saccharomyces cerevisiae possess a ring of 10-nm-diameter filaments, of unknown biochemical nature, that lies just inside the plasma membrane in the neck connecting the mother cell to its bud. Electron microscopic observations suggest that these filaments assemble at the budding site coincident with bud emergence and disassemble shortly before cytokinesis (Byers, B. and L. Goetsch. 1976. J. Cell Biol. 69:717-721). Mutants defective in any of four genes (CDC3, CDC10, CDC11, or CDC12) lack these filaments and display a pleiotropic phenotype that involves abnormal bud growth and an inability to complete cytokinesis. We showed previously by immunofluorescence that the CDC12 gene product is probably a constituent of the ring of 10-nm filaments (Haarer, B. and J. Pringle. 1987. Mol. Cell. Biol. 7:3678-3687). We now report the use of fusion proteins to generate polyclonal antibodies specific for the CDC3 gene product. In immunofluorescence experiments, these antibodies decorated the neck regions of wild-type and mutant cells in patterns suggesting that the CDC3 gene product is also a constituent of the ring of 10-nm filaments. We also used the CDC3-specific and CDC12-specific antibodies to investigate the timing of localization of these proteins to the budding site. The results suggest that the CDC3 protein is organized into a ring at the budding site well before bud emergence and remains so organized for some time after cytokinesis. The CDC12 product appears to behave similarly, but may arrive at the budding site closer to the time of bud emergence, and disappear from that site more quickly after cytokinesis, than does the CDC3 product. Examination of mating cells and cells responding to purified mating pheromone revealed novel arrangements of the CDC3 and CDC12 products in the regions of cell wall reorganization. Both proteins were present in normal-looking ring structures at the bases of the first zygotic buds.  相似文献   
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号