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This article contributes first genome size assessments by flow cytometry for 16 species, 12 genera, and 3 tribes from family Asteraceae, mostly belonging to the Heliantheae alliance, an assembly of 13 tribes from subfamily Asteroideae with a large majority of its species in the New World. Most genome sizes are accompanied by their own chromosome counts, confirming in most cases, although not all, previous counts for the species, and revealing possible cases of unknown dysploidy or polyploidy for certain taxa. The data contribute to the pool of knowledge on genome size and chromosome numbers in the family Asteraceae and will further allow deeper studies and a better understanding on the role of dysploidy in the evolution of the Heliantheae alliance. However, we still lack data for tribes Chaenactideae, Neurolaeneae, Polymnieae, and Feddeeae (the latter, monospecific) to complete the alliance representation. 相似文献
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Samarjit Patnaik Dipanwita Basu Noel Southall Seameen Dehdashti Kanny K. Wan Wei Zheng Marc Ferrer Mercedes Taylor Daniel A. Engel Juan Jose Marugan 《Bioorganic & medicinal chemistry letters》2019,29(9):1113-1119
Nonstructural protein 1 (NS1) plays a crucial function in the replication, spread, and pathogenesis of influenza virus by inhibiting the host innate immune response. Here we report the discovery and optimization of novel pyrazolopyridine NS1 antagonists that can potently inhibit influenza A/PR/8/34 replication in MDCK cells, rescue MDCK cells from cytopathic effects of seasonal influenza A strains, reverse NS1-dependent inhibition of IFN-β gene expression, and suppress the slow growth phenotype in NS1-expressing yeast. These pyrazolopyridines will enable researchers to investigate NS1 function during infection and how antagonists can be utilized in the next generation of treatments for influenza infection. 相似文献
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Yih‐Ling Tzeng Zachary Berman Evelyn Toh Jose A. Bazan Abigail Norris Turner Adam C. Retchless Xin Wang David E. Nelson David S. Stephens 《Molecular microbiology》2019,111(1):254-268
Clusters of Neisseria meningitidis (Nm) urethritis among primarily heterosexual males in multiple US cities have been attributed to a unique non‐encapsulated meningococcal clade (the US Nm urethritis clade, US_NmUC) within the hypervirulent clonal complex 11. Resistance to antimicrobial peptides (AMPs) is a key feature of urogenital pathogenesis of the closely related species, Neisseria gonorrhoeae. The US_NmUC isolates were found to be highly resistant to the model AMP, polymyxin B (PmB, MICs 64–256 µg ml–1). The isolates also demonstrated stable subpopulations of heteroresistant colonies that showed near total resistant to PmB (MICs 384–1024 µg ml–1) and colistin (MIC 256 µg ml–1) as well as enhanced LL‐37 resistance. This is the first observation of heteroresistance in N. meningitidis. Consistent with previous findings, overall PmB resistance in US_NmUC isolates was due to active Mtr efflux and LptA‐mediated lipid A modification. However, whole genome sequencing, variant analyses and directed mutagenesis revealed that the heteroresistance phenotypes and very high‐level AMP resistance were the result of point mutations and IS1655 element movement in the pilMNOPQ operon, encoding the type IV pilin biogenesis apparatus. Cross‐resistance to other classes of antibiotics was also observed in the heteroresistant colonies. High‐level resistance to AMPs may contribute to the pathogenesis of US_NmUC. 相似文献
275.
Pacheco Nicolas Orellana-Saez Matias Pepczynska Marzena Enrione Javier Bassas-Galia Monica Borrero-de Acuña Jose M. Zacconi Flavia C. Marcoleta Andrés E. Poblete-Castro Ignacio 《Journal of industrial microbiology & biotechnology》2019,46(8):1139-1153
Journal of Industrial Microbiology & Biotechnology - Extreme environments are a unique source of microorganisms encoding metabolic capacities that remain largely unexplored. In this work, we... 相似文献
276.
Yalitza Lopez Corcino Shekina Gonzalez Ferrer Luz Eliana Mantilla Sophia Trikeriotis Jin‐Sang Yu Steven Kim Samuel Hansen Jose‐Andres C. Portillo Carlos S. Subauste 《Cellular microbiology》2019,21(10)
Toxoplasma gondii causes retinitis and encephalitis. Avoiding targeting by autophagosomes is key for its survival because T. gondii cannot withstand lysosomal degradation. During invasion of host cells, T. gondii triggers epidermal growth factor receptor (EGFR) signalling enabling the parasite to avoid initial autophagic targeting. However, autophagy is a constitutive process indicating that the parasite may also use a strategy operative beyond invasion to maintain blockade of autophagic targeting. Finding that such a strategy exists would be important because it could lead to inhibition of host cell signalling as a novel approach to kill the parasite in previously infected cells and treat toxoplasmosis. We report that T. gondii induced prolonged EGFR autophosphorylation. This effect was mediated by PKCα/PKCβ ? Src because T. gondii caused prolonged activation of these molecules and their knockdown or incubation with inhibitors of PKCα/PKCβ or Src after host cell invasion impaired sustained EGFR autophosphorylation. Addition of EGFR tyrosine kinase inhibitor (TKI) to previously infected cells led to parasite entrapment by LC3 and LAMP‐1 and pathogen killing dependent on the autophagy proteins ULK1 and Beclin 1 as well as lysosomal enzymes. Administration of gefitinib (EGFR TKI) to mice with ocular and cerebral toxoplasmosis resulted in disease control that was dependent on Beclin 1. Thus, T. gondii promotes its survival through sustained EGFR signalling driven by PKCα/β ? Src, and inhibition of EGFR controls pre‐established toxoplasmosis. 相似文献
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