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六盘山典型森林伴随降水的总有机碳(TOC)通量变化特征   总被引:1,自引:0,他引:1  
杨丽丽  王彦辉  杜敏  于澎涛  郝佳  李振华 《生态学报》2014,34(21):6297-6308
在六盘山香水河小流域,选择6种典型森林样地,测定了2011年生长季的大气降水、穿透水、干流、枯落物渗漏水和主根系层(0—30 cm深)土壤渗漏水的总有机碳(TOC)浓度及其相应的通量变化。结果表明,在降水转化为由穿透雨和干流组成的林下降水中,所有样地的TOC浓度都不同程度地增大;虽然林冠截持使林下降水减小,但因雨水淋洗和与林冠发生碳交换,各样地林下降水携带的生长季TOC通量(kg/hm2)(华北落叶松人工林132.28、华山松次生林106.56、油松人工林94.10、灌木林79.49、桦木林66.52、辽东栎次生林63.01)都比林外降水(53.17)不同程度地明显增大,整体看来,林冠的TOC淋出作用在针叶林很大,在阔叶林较弱。在6种森林样地的枯落物层渗漏水中,其TOC浓度彼此相差不大,平均为24.51 mg/L,高于林冠穿透水的TOC浓度;受枯落物截持部分降水及与枯落物TOC交换的影响,4个样地枯落物渗漏水的TOC通量(kg/hm2)(桦木次生林84.35、野李子灌丛129.35、辽东栎次生林79.21、油松人工林114.93)都比其林下降水TOC通量增加了,但华北落叶松人工林和华山松次生林的TOC通量分别降至90.76和104.90 kg/hm2。在测定的华北落叶松人工林和华山松次生林的主根系层(0—30 cm)土壤渗漏水中,TOC浓度均低于枯落物渗漏水;由于水量减小和与土壤发生碳交换,土壤渗漏水的TOC通量均显著低于枯落物渗漏水,两个林分样地分别降至43.04和66.33 kg/hm2。整体来看,林外降水携带的TOC输入通量在林地TOC输入中占有重要地位,林冠的TOC淋洗使其程度不同地增加TOC通量,枯落物层具有增加或减少TOC通量的作用,但主根系层土壤会显著减少TOC输出通量,所以是固定TOC的重要场所。  相似文献   
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Cytokine storm and multi-organ failure are the main causes of SARS-CoV-2-related death. However, the origin of excessive damages caused by SARS-CoV-2 remains largely unknown. Here we show that the SARS-CoV-2 envelope (2-E) protein alone is able to cause acute respiratory distress syndrome (ARDS)-like damages in vitro and in vivo. 2-E proteins were found to form a type of pH-sensitive cation channels in bilayer lipid membranes. As observed in SARS-CoV-2-infected cells, heterologous expression of 2-E channels induced rapid cell death in various susceptible cell types and robust secretion of cytokines and chemokines in macrophages. Intravenous administration of purified 2-E protein into mice caused ARDS-like pathological damages in lung and spleen. A dominant negative mutation lowering 2-E channel activity attenuated cell death and SARS-CoV-2 production. Newly identified channel inhibitors exhibited potent anti-SARS-CoV-2 activity and excellent cell protective activity in vitro and these activities were positively correlated with inhibition of 2-E channel. Importantly, prophylactic and therapeutic administration of the channel inhibitor effectively reduced both the viral load and secretion of inflammation cytokines in lungs of SARS-CoV-2-infected transgenic mice expressing human angiotensin-converting enzyme 2 (hACE-2). Our study supports that 2-E is a promising drug target against SARS-CoV-2.Subject terms: Cell death, Molecular biology  相似文献   
54.
Plant shoot phototropism is triggered by the formation of a light-driven auxin gradient leading to bending growth. The blue light receptor phototropin 1(phot1) senses light direction, but how this leads to auxin gradient formation and growth regulation remains poorly understood. Previous studies have suggested phot1’s role for regulated apoplastic acidification, but its relation to phototropin and hypocotyl phototropism is unclear. Herein, we show that blue light can cause phot1 to interact with...  相似文献   
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在实验室控制条件下,以转Bt基因棉花GK12、33B、SGK321上的烟粉虱为食料饲养龟纹瓢虫,研究转Bt基因棉花上的烟粉虱对龟纹瓢虫生长发育及捕食的影响,同时利用Y型嗅觉仪,观察龟纹瓢虫对来自不同类型棉花的棉叶及其烟粉虱的嗅觉反应和视觉反应。结果表明,转Bt基因棉花和对应的常规棉亲本上的烟粉虱对龟纹瓢虫的发育历期和存活率没有明显的影响。龟纹瓢虫对棉花叶片、烟粉虱若虫、蜜露、蜕等4种物质的视觉反应之间没有明显的差异。对4种嗅源物质的嗅觉选择性的大小依次为:烟粉虱若虫>蜕>棉花>蜜露;在两类不同的棉花之间,转基因棉花和常规棉,龟纹瓢虫对GK12、33B、SGK321等三种转基因棉花上的烟粉虱若虫的嗅觉选择性明显较对应的常规棉亲本SM3、33、SY321上的烟粉虱若虫小;对烟粉虱若虫的蜕,两种转单价基因棉花GK12、33B较对应的常规棉亲本上的小,而转双价基因的棉花SGK321上与对应的常规棉之间没有明显的差异。烟粉虱密度大于200头.皿-1时,龟纹瓢虫捕食转基因棉花上烟粉虱的数量大于对应的常规棉花亲本,但烟粉虱密度小于200头.皿-1时,龟纹瓢虫捕食转基因棉花上烟粉虱的数量小于对应的常规棉花亲本。龟纹瓢虫对烟粉虱的捕食符合HollingⅡ型反应。龟纹瓢虫取食转基因棉花上的烟粉虱的理论极限值、瞬间攻击率均大于常规棉花。  相似文献   
57.
In view of the important roles played by Kinetochore proteins in mitosis, we believed that they may contribute to the development and progression of human cancers, which has been reported recently elsewhere. Kinetochore-associated 1 (KNTC1) participates in the segregation of sister chromatids during mitosis, the effects of which on non-small-cell lung cancer (NSCLC) remain unclear. Here, we sought to identify the biological significance of KNTC1 in NSCLC. KNTC1 protein expression in NSCLC tissues was investigated by immunohistochemistry. Lentivirus delivered short hairpin RNA (shRNA) was utilized to establish KNTC1 silence NSCLC cell lines. The effects of KNTC1 depletion on NSCLC cell proliferation, migration, apoptosis, and tumor formation were analyzed by MTT assay, wound-healing assay, transwell assay, flow cytometry assay, and in nude mouse models in vivo. After KNTC1 reduction, NSCLC cell viability, proliferation, migration, and invasion were restrained. A xenograft tumor model was also provided to demonstrate the inhibited tumorigenesis in NSCLC. In addition, the downstream mechanism analysis indicated that KNTC1 depletion was positively associated with PSMB8. The findings of the present study suggested that KNTC1 may have a pivotal role in mediating NSCLC progression and may act as a novel therapeutic target for NSCLC.Subject terms: Non-small-cell lung cancer, Cell migration  相似文献   
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Keloid disorder is a tumour-like disease with invasive growth and a high recurrence rate. Genetic contribution is well expected due to the presence of autosomal dominant inheritance and various genetic mutations in keloid lesions. However, GWAS failed to reveal functional variants in exon regions but single nucleotide polymorphisms in the non-coding regions, suggesting the necessity of innovative genetic investigation. This study employed combined GWAS, RNA-sequence and Hi-C analyses to dissect keloid disorder genetic mechanisms using paired keloid tissues and normal skins. Differentially expressed genes, miRNAs and lncRNAs mined by RNA-sequence were identified to construct a network. From which, 8 significant pathways involved in keloid disorder pathogenesis were enriched and 6 of them were verified. Furthermore, topologically associated domains at susceptible loci were located via the Hi-C database and ten differentially expressed RNAs were identified. Among them, the functions of six molecules for cell proliferation, cell cycle and apoptosis were particularly examined and confirmed by overexpressing and knocking-down assays. This study firstly revealed unknown key biomarkers and pathways in keloid lesions using RNA-sequence and previously reported mutation loci, indicating a feasible approach to reveal the genetic contribution to keloid disorder and possibly to other diseases that are failed by GWAS analysis alone.  相似文献   
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