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151.
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153.
在粗粒料三轴试验中,橡皮膜嵌入量可造成显著的体积变形量测误差。本文针对颗粒材料的接触特点,利用Nagata Patch方法重建颗粒表面,基于重建曲面进行接触状态的判断和接触几何信息的计算,开发了高效的颗粒接触算法。该法采用dual mortar有限元方法处理颗粒与橡皮膜间的接触模拟,针对橡皮膜变形较大的特点,采用更新坐标的大变形计算格式,并根据重建的颗粒表面对颗粒-橡皮膜的距离进行几何修正,实现了颗粒-橡皮膜接触的精细化模拟,可较好地模拟计算“柔性”橡皮膜嵌入颗粒孔隙的过程。进行了Kramer钢球试验以及粗颗粒料和标准粗砂三轴试验橡皮膜嵌入过程的模拟计算,计算结果符合一般规律,与相应的试验结果吻合较好,验证了本文方法对于粗粒料膜嵌入问题的适用性。 相似文献
154.
Florian A. Schmid J. Koudy Williams Thomas M. Kessler Arnulf Stenzl Wilhelm K. Aicher Karl-Erik Andersson Daniel Eberli 《International journal of molecular sciences》2021,22(8)
Urinary incontinence (UI) is a major problem in health care and more than 400 million people worldwide suffer from involuntary loss of urine. With an increase in the aging population, UI is likely to become even more prominent over the next decades and the economic burden is substantial. Among the different subtypes of UI, stress urinary incontinence (SUI) is the most prevalent and focus of this review. The main underlying causes for SUI are pregnancy and childbirth, accidents with direct trauma to the pelvis or medical treatments that affect the pelvic floor, such as surgery or irradiation. Conservative approaches for the treatment of SUI are pelvic physiotherapy, behavioral and lifestyle changes, and the use of pessaries. Current surgical treatment options include slings, colposuspensions, bulking agents and artificial urinary sphincters. These treatments have limitations with effectiveness and bear the risk of long-term side effects. Furthermore, surgical options do not treat the underlying pathophysiological causes of SUI. Thus, there is an urgent need for alternative treatments, which are effective, minimally invasive and have only a limited risk for adverse effects. Regenerative medicine is an emerging field, focusing on the repair, replacement or regeneration of human tissues and organs using precursor cells and their components. This article critically reviews recent advances in the therapeutic strategies for the management of SUI and outlines future possibilities and challenges. 相似文献
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156.
Lei Wang Charlotte E. Pelgrim Daniël H. Swart Guido Krenning Adrianus C. van der Graaf Aletta D. Kraneveld Thea Leusink-Muis Ingrid van Ark Johan Garssen Gert Folkerts Saskia Braber 《International journal of molecular sciences》2021,22(9)
Chronic obstructive pulmonary disease (COPD) caused by cigarette smoke (CS) is featured by oxidative stress and chronic inflammation. Due to the poor efficacy of standard glucocorticoid therapy, new treatments are required. Here, we investigated whether the novel compound SUL-151 with mitoprotective properties can be used as a prophylactic and therapeutic treatment in a murine CS-induced inflammation model. SUL-151 (4 mg/kg), budesonide (500 μg/kg), or vehicle were administered via oropharyngeal instillation in this prophylactic and therapeutic treatment setting. The number of immune cells was determined in the bronchoalveolar lavage fluid (BALF). Oxidative stress response, mitochondrial adenosine triphosphate (ATP) production, and mitophagy-related proteins were measured in lung homogenates. SUL-151 significantly decreased more than 70% and 50% of CS-induced neutrophils in BALF after prophylactic and therapeutic administration, while budesonide showed no significant reduction in neutrophils. Moreover, SUL-151 prevented the CS-induced decrease in ATP and mitochondrial mtDNA and an increase in putative protein kinase 1 expression in the lung homogenates. The concentration of SUL-151 was significantly correlated with malondialdehyde level and radical scavenging activity in the lungs. SUL-151 inhibited the increased pulmonary inflammation and mitochondrial dysfunction in this CS-induced inflammation model, which implied that SUL-151 might be a promising candidate for COPD treatment. 相似文献
157.
158.
Helena Kratochvílov Milo Mrz Barbora J. Kasperov Daniel Hlav
ek Jakub Mahrík Ivana Lakov Anna Cinkajzlov Zdenk Matloch Zdeka Lacinov Jaroslava Trnovsk Peter Ivk Peter Novodvorský Ivan Netuka Martin Haluzík 《International journal of molecular sciences》2021,22(9)
The aim of our study was to analyze mitochondrial and endoplasmic reticulum (ER) gene expression profiles in subcutaneous (SAT) and epicardial (EAT) adipose tissue, skeletal muscle, and myocardium in patients with and without CAD undergoing elective cardiac surgery. Thirty-eight patients, 27 with (CAD group) and 11 without CAD (noCAD group), undergoing coronary artery bypass grafting and/or valvular surgery were included in the study. EAT, SAT, intercostal skeletal muscle, and right atrium tissue and blood samples were collected at the start and end of surgery; mRNA expression of selected mitochondrial and ER stress genes was assessed using qRT-PCR. The presence of CAD was associated with decreased mRNA expression of most of the investigated mitochondrial respiratory chain genes in EAT, while no such changes were seen in SAT or other tissues. In contrast, the expression of ER stress genes did not differ between the CAD and noCAD groups in almost any tissue. Cardiac surgery further augmented mitochondrial dysfunction in EAT. In our study, CAD was associated with decreased expression of mitochondrial, but not endoplasmic reticulum stress genes in EAT. These changes may contribute to the acceleration of coronary atherosclerosis. 相似文献
159.
Wioletta Rozpdek-Kamiska Grzegorz Galita Natalia Siwecka Steven L. Carroll John Alan Diehl Ewa Kucharska Dariusz Pytel Ireneusz Majsterek 《International journal of molecular sciences》2021,22(9)
Primary open-angle glaucoma (POAG) constitutes the most common type of glaucoma. Emerging evidence suggests that Endoplasmic Reticulum (ER) stress and the protein kinase RNA-like endoplasmic reticulum kinase (PERK)-mediated Unfolded Protein Response (UPR) signaling pathway play a key role in POAG pathogenesis. Thus, the main aim of the study was to evaluate the effectiveness of the PERK inhibitor LDN-0060609 in cellular model of glaucoma using primary human trabecular meshwork (HTM) cells. To evaluate the level of the ER stress marker proteins, Western blotting and TaqMan gene expression assay were used. The cytotoxicity was measured by XTT, LDH assays and Giemsa staining, whereas genotoxicity via comet assay. Changes in cell morphology were assessed by phase-contrast microscopy. Analysis of apoptosis was performed by caspase-3 assay and flow cytometry (FC), whereas cell cycle progression by FC. The results obtained have demonstrated that LDN-0060609 triggered a significant decrease of ER stress marker proteins within HTM cells with induced ER stress conditions. Moreover, LDN-0060609 effectively increased viability, reduced DNA damage, increased proliferation, restored normal morphology, reduced apoptosis and restored normal cell cycle distribution of HTM cells with induced ER stress conditions. Thereby, PERK inhibitors, such as LDN-0060609, may provide an innovative, ground-breaking treatment strategy against POAG. 相似文献
160.
Gaofeng Yuan Mengmeng Xu Meijuan Tan Jian Dong Xiaoe Chen 《European Journal of Lipid Science and Technology》2021,123(1):2000224
The study aims to investigate the effect of combined supplementation with docosahexaenoic acid (C22:6 n-3, DHA) and vitamin E (VE) on the oxidative stress and liver triglycerides (TG) accumulation induced by high-fat diet (HFD) in mice. C57BL/6J mice are fed either a control diet or an HFD for 8 weeks. Animals are supplemented with DHA, VE, or DHA + VE, respectively. Supplementation with DHA alone shows significant improvement in oxidative stress and hepatic steatosis in mice. Supplementation with DHA significantly reduces the liver TG and total cholesterol contents, and the alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, compared with the HFD. Supplementation with DHA also significantly decreases the mRNA expression level of sterol regulatory element-binding protein 1C. However, supplementation with VE alone does not show improvement in oxidative stress and hepatic steatosis. DHA + VE supply obtains a superior effect in alleviation of hepatic steatosis than DHA supplementation alone in mice fed by HFD. The efficacy of DHA potentiated by VE can be due to that VE enhances the effect of DHA in decrease of ALT and AST levels and increase of antioxidant enzyme activity and glutathione level in mice fed by HFD. Practical Applications: Supplementation with DHA significantly improves the oxidative stress and hepatic steatosis induced by HFD in mice. The efficacy of DHA in the alleviation of hepatic steatosis induced by HFD is potentiated by VE. These findings may provide a rational basis for the use of DHA and VE co-supplementation in patients with liver steatosis. 相似文献