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961.
962.
Beata Anna Nowakowska Katarzyna Pankiewicz Urszula Nowacka Magdalena Niemiec Szymon Kozowski Tadeusz Issat 《International journal of molecular sciences》2022,23(1)
Fetal growth restriction (FGR) is one of the most formidable challenges in present-day antenatal care. Pathological fetal growth is a well-known factor of not only in utero demise in the third trimester, but also postnatal morbidity and unfavorable developmental outcomes, including long-term sequalae such as metabolic diseases, diabetic mellitus or hypertension. In this review, the authors present the current state of knowledge about the genetic disturbances responsible for FGR diagnosis, divided into fetal, placental and maternal causes (including preeclampsia), as well as their impact on prenatal diagnostics, with particular attention on chromosomal microarray (CMA) and noninvasive prenatal testing technique (NIPT). 相似文献
963.
964.
Asmaa Anwar Ismail Baraah Tariq Shaker Khalid Bajou 《International journal of molecular sciences》2022,23(1)
Angiogenesis is a process associated with the migration and proliferation of endothelial cells (EC) to form new blood vessels. It is involved in various physiological and pathophysiological conditions and is controlled by a wide range of proangiogenic and antiangiogenic molecules. The plasminogen activator–plasmin system plays a major role in the extracellular matrix remodeling process necessary for angiogenesis. Urokinase/tissue-type plasminogen activators (uPA/tPA) convert plasminogen into the active enzyme plasmin, which in turn activates matrix metalloproteinases and degrades the extracellular matrix releasing growth factors and proangiogenic molecules such as the vascular endothelial growth factor (VEGF-A). The plasminogen activator inhibitor-1 (PAI-1) is the main inhibitor of uPA and tPA, thereby an inhibitor of pericellular proteolysis and intravascular fibrinolysis, respectively. Paradoxically, PAI-1, which is expressed by EC during angiogenesis, is elevated in several cancers and is found to promote angiogenesis by regulating plasmin-mediated proteolysis and by promoting cellular migration through vitronectin. The urokinase-type plasminogen activator receptor (uPAR) also induces EC cellular migration during angiogenesis via interacting with signaling partners. Understanding the molecular functions of the plasminogen activator plasmin system and targeting angiogenesis via blocking serine proteases or their interactions with other molecules is one of the major therapeutic strategies scientists have been attracted to in controlling tumor growth and other pathological conditions characterized by neovascularization. 相似文献
965.
[目的]新型城镇化不断加快,城市所占土地资源扩张程度越发迅速,传统粗放的城市增长过程中呈现出生态系统结构与功能的破坏、城市无序扩张等问题,怎样合理控制城市规模、优化城市生态安全格局已成为当前中国国土资源管理的重点工作之一.探索中国城市增长边界划定的效益及现行方法,讨论未来发展驱动力和城市增长边界协调优化方法可能的研究方... 相似文献
966.
Gabriela Loscalzo Julia Scheel Jos Santiago Ibaez-Cabellos Eva García-Lopez Shailendra Gupta Jos Luis García-Gimenez Salvador Mena-Moll Alfredo Perales-Marín Jos Morales-Rosell 《International journal of molecular sciences》2022,23(1)
In a prospective study, 48 fetuses were evaluated with Doppler ultrasound after 34 weeks and classified, according to the cerebroplacental ratio (CPR) and estimated fetal weight (EFW), into fetuses with normal growth and fetuses with late-onset fetal growth restriction (LO-FGR). Overexpression of miRNAs from neonatal cord blood belonging to LO-FGR fetuses, was validated by real-time PCR. In addition, functional characterization of overexpressed miRNAs was performed by analyzing overrepresented pathways, gene ontologies, and prioritization of synergistically working miRNAs. Three miRNAs: miR-25-3p, miR-185-5p and miR-132-3p, were significantly overexpressed in cord blood of LO-FGR fetuses. Pathway and gene ontology analysis revealed over-representation of certain molecular pathways associated with cardiac development and neuron death. In addition, prioritization of synergistically working miRNAs highlighted the importance of miR-185-5p and miR-25-3p in cholesterol efflux and starvation responses associated with LO-FGR phenotypes. Evaluation of miR-25-3p; miR-132-3p and miR-185-5p might serve as molecular biomarkers for the diagnosis and management of LO-FGR; improving the understanding of its influence on adult disease. 相似文献
967.
安徽省产业结构与经济增长的相关性研究 总被引:8,自引:0,他引:8
徐宝英 《安徽工业大学学报》2006,23(2):217-220
通过相关性研究,分析和度量安徽省不同产业对地区经济增长的作用,探讨各产业是以何种方式影响经济增长的,旨在为今后安徽省制定产业政策提供决策依据. 相似文献
968.
HCFC141b气体水合物快速生成实验研究 总被引:2,自引:0,他引:2
制冷剂气体水合物快速均匀生成是气体水合物蓄冷技术实用化的关键.1~7℃内,实验中首次发现与试管壁面接触的铁丝对表面活性剂(十二烷基苯磺酸钠)水溶液与HCFC141b(CH3CC l2F,R141b)液体静态生成气体水合物有巨大影响:铁丝与壁面的接触位置改变了R141b气体水合物的成核点和生成区域,明显缩短了气体水合物的引导时间,大大加快了水合反应,相同条件下,穿过两相界面(十二烷基苯磺酸钠水溶液和R141b液体界面)与试管侧壁面接触的铁丝对R141b气体水合物生成的诱导作用最强;气体水合物不但可以在水和制冷剂液体两相界面上或水相中首先生成,而且也可以在制冷剂相中独立完成;水分子贴着玻璃壁面要比直接通过R141b液体容易扩散;水合率随恒温槽温度的变化表明环境温度仍然是决定水合反应快慢的基本因素之一. 相似文献
969.
Transforming growth factor-beta (TGF-β) is part of a family of molecules that is present in many body tissues and performs many different functions. Evidence has been obtained from mice and human cancer patients with bony metastases and non-metastatic disease, as well as pediatric burn patients, that inflammation leads to bone resorption and release of TGF-β from the bone matrix with paracrine effects on muscle protein balance, possibly mediated by the generation of reactive oxygen species. Whether immobilization, which confounds the etiology of bone resorption in burn injury, also leads to the release of TGF-β from bone contributing to muscle wasting in other conditions is unclear. The use of anti-resorptive therapy in both metastatic cancer patients and pediatric burn patients has been successful in the prevention of muscle wasting, thereby creating an additional therapeutic niche for this class of drugs. The liberation of TGF-β may be one way in which bone helps to control muscle mass, but further investigation will be necessary to assess whether the rate of bone resorption is the determining factor for the release of TGF-β. Moreover, whether different resorptive conditions, such as immobilization and hyperparathyroidism, also involve TGF-β release in the pathogenesis of muscle wasting needs to be investigated. 相似文献
970.