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1.
Metabolically active gasotransmitters (nitric oxide, carbon monoxide and hydrogen sulfide) are important signalling molecules that show therapeutic utility in oxidative pathologies. The reduced form of selenium, hydrogen selenide (HSe/H2Se), shares some characteristics with these molecules. The simple selenide salt, sodium hydroselenide (NaHSe) showed significant metabolic activity, dose-dependently decreasing ex vivo O2 consumption (rat soleus muscle, liver) and transiently inhibiting mitochondrial cytochrome C oxidase (liver, heart). Pharmacological manipulation of selenoprotein expression in HepG2 human hepatocytes revealed that the oxidation status of selenium impacts on protein expression; reduced selenide (NaHSe) increased, whereas (oxidized) sodium selenite decreased the abundance of two ubiquitous selenoproteins. An inhibitor of endogenous sulfide production (DL-propargylglycine; PAG) also reduced selenoprotein expression; this was reversed by exogenous NaHSe, but not sodium hydrosulfide (NaHS). NaHSe also conferred cytoprotection against an oxidative challenge (H2O2), and this was associated with an increase in mitochondrial membrane potential. Anesthetized Wistar rats receiving intravenous NaHSe exhibited significant bradycardia, metabolic acidosis and hyperlactataemia. In summary, NaHSe modulates metabolism by inhibition of cytochrome C oxidase. Modification of selenoprotein expression revealed the importance of oxidation status of selenium therapies, with implications for current clinical practice. The utility of NaHSe as a research tool and putative therapeutic is discussed.  相似文献   
2.
Immunotherapy is an efficient approach to clinical oncology. However, the immune privilege of the central nervous system (CNS) limits the application of immunotherapeutic strategies for brain cancers, especially glioblastoma (GBM). Tumor resistance to immune checkpoint inhibitors is a further challenge in immunotherapies. To overcome the immunological tolerance of brain tumors, a novel multifunctional nanoparticle (NP) for highly efficient synergetic immunotherapy is reported. The NP contains an anti-PDL1 antibody (aPDL1), upconverting NPs, and the photosensitizer 5-ALA; the surface of the NP is conjugated with the B1R kinin ligand to facilitate transport across the blood-tumor-barrier. Upon irradiation with a 980 nm laser, 5-ALA is transformed into protoporphyrin IX, generating reactive oxygen species. Photodynamic therapy (PDT) further promotes intratumoral infiltration of cytotoxic T lymphocytes and sensitizes tumors to PDL1 blockade therapy. It is demonstrated that combining PDT and aPDL1 can effectively suppress GBM growth in mouse models. The proposed NPs provide a novel and effective strategy for boosting anti-GBM photoimmunotherapy.  相似文献   
3.
Recent advances provide evidence that the cellular signalling pathway comprising the ligand-receptor duo of thrombospondin-1 (TSP1) and CD47 is involved in mediating a range of diseases affecting renal, vascular, and metabolic function, as well as cancer. In several instances, research has barely progressed past pre-clinical animal models of disease and early phase 1 clinical trials, while for cancers, anti-CD47 therapy has emerged from phase 2 clinical trials in humans as a crucial adjuvant therapeutic agent. This has important implications for interventions that seek to capitalize on targeting this pathway in diseases where TSP1 and/or CD47 play a role. Despite substantial progress made in our understanding of this pathway in malignant and cardiovascular disease, knowledge and translational gaps remain regarding the role of this pathway in kidney and metabolic diseases, limiting identification of putative drug targets and development of effective treatments. This review considers recent advances reported in the field of TSP1-CD47 signalling, focusing on several aspects including enzymatic production, receptor function, interacting partners, localization of signalling, matrix-cellular and cell-to-cell cross talk. The potential impact that these newly described mechanisms have on health, with a particular focus on renal and metabolic disease, is also discussed.  相似文献   
4.
针对恶意安卓应用程序检测中存在的特征维度大、检测效率低的问题,结合卷积神经网络CNN良好的特征提取和降维能力以及catboost算法无需广泛数据训练即可产生较好分类结果的优点,构建一个CNN-catboost混合恶意安卓应用检测模型。通过逆向工程获取安卓应用的权限、API包、组件、intent、硬件特性和OpCode特征等静态特征并映射为特征向量,再在特征处理层使用卷积核对特征进行局部感知处理以增强信号。使用最大池化对处理后的特征进行下采样,降低维数并保持特征性质不变。将处理后的特征作为catboost分类层的输入向量,利用遗传算法的全局寻优能力对catboost模型进行调参,进一步提升分类准确率。对训练完成的模型,分别使用已知和未知类型的安卓应用程序数据集作实际应用测试。实验结果表明CNN-catboost模型调参用时较少,在预测精度和检测效率上也展示出较为良好的效果。  相似文献   
5.
基于描述文本的网络攻击自动化分类是实现APT攻击知识智能抽取的重要基础。针对网络攻击文本专业词汇多、难识别,语义上下文依赖强、难判断等问题提出一种基于上下文语义分析的文本词句特征自动抽取方法,通过构建BERT与BiLSTM的混合神经网络模型BBNN(BERT and BiLSTM Neural Network),计算得到网络攻击文本的初步分类结果,再利用方差过滤器对分类结果进行自动筛选。在CAPEC(Common Attack Pattern Enumeration and Classification)攻击知识库上的实验结果显示,该方法的准确率达到了79.17%,相较于单一的BERT模型和BiLSTM模型的分类结果分别提高了7.29%和3.00%,实现了更好的网络攻击文本自动化分类。  相似文献   
6.
引入句法依存信息到原方面术语,提出一种新的方面术语表示方法,利用Glove词向量表示单词以及单词与单词之间的依存关系,构造出包含句法依存信息的依存关系邻接矩阵和依存关系表示矩阵,利用图卷积神经网络和多头注意力机制将句法依存信息融入到方面术语中,使得方面术语表达与上下文结构高度相关。将改进后的方面词术语表示替换到现有模型后,模型泛化能力得到有效提升。对比试验和分析结果表明:该方法具有有效性和泛化性。  相似文献   
7.
提出一种对膨胀土进行判别和分类的新指标——最大面积收缩率(SCR),其定义为最大面积收缩率试验中试样干燥后收缩裂隙的总面积与试样初始面积的比值。通过对不同地区土样开展试验,研究了制样初始含水率、初始厚度、接触面粗糙度以及环境温度对试验结果的影响,并对SCR作为膨胀土判别与分类指标的可信度与可靠度进行了分析,最终提出了利用SCR对膨胀土进行分类的界限指标。试验结果表明:初始含水率和界面粗糙度对SCR用于膨胀土的判别和分类没有影响;当初始厚度限制在8 mm以内时,可以忽略厚度对试验结果的影响;建议烘干温度为105℃。SCR与蒙脱石含量、阳离子交换量线性相关,能较好地反应膨胀土的胀缩特性;SCR与标准吸湿含水率和塑性指数线性相关,体现出利用SCR对膨胀土进行判别与分类具有较高的可信度。最大面积收缩率试验操作简单、周期短且可重复性高。  相似文献   
8.
The peroxisome is a single-membrane subcellular compartment present in almost all eukaryotic cells from simple protists and fungi to complex organisms such as higher plants and animals. Historically, the name of the peroxisome came from a subcellular structure that contained high levels of hydrogen peroxide (H2O2) and the antioxidant enzyme catalase, which indicated that this organelle had basically an oxidative metabolism. During the last 20 years, it has been shown that plant peroxisomes also contain nitric oxide (NO), a radical molecule than leads to a family of derived molecules designated as reactive nitrogen species (RNS). These reactive species can mediate post-translational modifications (PTMs) of proteins, such as S-nitrosation and tyrosine nitration, thus affecting their function. This review aims to provide a comprehensive overview of how NO could affect peroxisomal metabolism and its internal protein-protein interactions (PPIs). Remarkably, many of the identified NO-target proteins in plant peroxisomes are involved in the metabolism of reactive oxygen species (ROS), either in its generation or its scavenging. Therefore, it is proposed that NO is a molecule with signaling properties with the capacity to modulate the peroxisomal protein-protein network and consequently the peroxisomal functions, especially under adverse environmental conditions.  相似文献   
9.
日本是垃圾分类水平最高、资源循环利用率最高的国家之一。对日本生活垃圾长效治理机制进行分析与介绍,有助于我国破解生活垃圾“运动式”治理所面临的可持续性难题,推进源头分类,实现从“新时尚”到“好习惯”到“绿色循环低碳发展的转变”。  相似文献   
10.
Doxorubicin increases endothelial permeability, hence increasing cardiomyocytes’ exposure to doxorubicin (DOX) and exposing myocytes to more immediate damage. Reactive oxygen species are major effector molecules of doxorubicin’s activity. Mangiferin (MGN) is a xanthone derivative that consists of C-glucosylxanthone with additional antioxidant properties. This particular study assessed the effects of MGN on DOX-induced cytotoxicity in human umbilical vein endothelial cells’ (HUVECs’) signaling networks. Mechanistically, MGN dramatically elevated Nrf2 expression at both the messenger RNA and protein levels through the upregulation of the PI3K/AKT pathway, leading to an increase in Nrf2-downstream genes. Cell apoptosis was assessed with a caspase-3 activity assay, transferase-mediated dUTP-fluorescein nick end labeling (TUNEL) staining was performed to assess DNA fragmentation, and protein expression was determined by Western blot analysis. DOX markedly increased the generation of reactive oxygen species, PARP, caspase-3, and TUNEL-positive cell numbers, but reduced the expression of Bcl-2 and antioxidants’ intracellular concentrations. These were effectively antagonized with MGN (20 μM), which led to HUVECs being protected against DOX-induced apoptosis, partly through the PI3K/AKT-mediated NRF2/HO-1 signaling pathway, which could theoretically protect the vessels from severe DOX toxicity.  相似文献   
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