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231.
The variation of the translocation time with respect to the solvent quality was also studied. It showed that there is a transition, as the solvent quality improves from \poor to \good: when ABc, τ increases with increasing AB. When the chain length was changed, it was found that when the absorbed energy u0 was greater than uc, τ was proportional to N1:602; for u0相似文献
232.
先采用均匀沉淀法制备出CuO—ZnO催化剂,然后以CuO—ZnO催化剂作为晶核采用水热合成法制备出CuO—ZnO/HZSM-5(氢型ZSM-5分子筛)复合催化剂.利用X射线衍射和氨程序升温脱附手段对复合催化剂进行表征,并应用于CO2催化加氢合成二甲醚的反应.研究结果表明,在相同的反应条件下,这种CuO—ZnO/HZSM-5复合催化剂与采用物理混合法制备出的复合催化剂相比具有更好的催化效果,不但提高了CO2的转化率、二甲醚的选择性以及二甲醚和甲醇的总选择性,同时还改善了催化剂的稳定性. 相似文献
233.
234.
近年来,作为第三代有机发光二极管(organic light-emitting diodes, OLED)发光材料的热活化延迟荧光(thermally activated delayed fluorescence, TADF)材料受到了学术界和产业界的广泛关注. TADF分子由于其单线态与三线态之间的能级差较小,三线态激子可以被环境热活化而通过反系间窜越上转换至单线态,理论上可实现100%的激子利用率,从而使得OLED器件外量子效率显著提高.TADF材料被认为是突破高效稳定有机电致蓝光发射瓶颈的潜在解决方案.一般, TADF分子为含有电子给体(donor, D)和电子受体(acceptor, A)的纯有机推拉电子体系.通过改变给体单元和受体单元的结构、数量和取代基及其位置可以有效调节TADF分子的单线态-三线态能级差、前线轨道分布、聚集态结构、电致发光颜色及其性能.同时取代基在调控给、受体单元的推拉电子能力及TADF材料的分子构型、聚集态结构和稳定性等物化特性方面扮演着非常重要的角色.本综述分别对D-A型和多重共振型TADF蓝光分子的取代基效应进行了综述,以期为高效稳定的蓝光TADF分... 相似文献
235.
我们利用具有不同对称性的同分异构体,通过改变分子间氢键网络,操控单链磁体行为,成功合成了2例化合物:[NiⅡ(L1)][FeⅢ(Tp)(CN)3]2·3.5H2O (1)和[NiⅡ(L2)][FeⅢ(Tp)(CN)3]2·3H2O (2),其中Tp=hydrotris (pyrazolyl) borate,L1=3,4-bis (1H-imid-azol-1-yl) thiophen,L2=1,2-bis (1H-imidazol-1-yl) thiophen)。磁性研究表明,1和2表现为具有不同矫顽场的单链磁体行为。1的矫顽场为8.41 kOe,而2的矫顽场为3.84 kOe。 相似文献
236.
为理解绕水翼云空化流动的发展机理和探究水翼吸力面开孔射流的影响,采用密度修正的RNG k-ε湍流模型和Schnerr-Sauer空化模型对原始NACA66(mod)水翼和采用射流后的水翼的云空化非定常过程进行模拟和对比分析;采用在水翼吸力面近壁区设立监测线的方法对近壁区的流场进行监测,得到近壁区汽相体积分数、回射流速度、压力及压力梯度的时空分布云图;开展了云空化流场特性的涡动力学分析,进而分析水翼云空化的发生机理和射流抑制空化的抑制机理.结果表明:游离型空泡在下游溃灭时产生强烈的局部高压,其向上游传播导致前缘空穴的一次回缩,而空穴的二次回缩受回射流的影响.回射流的发展区域受限于较高的压力梯度,高的压力梯度一直存在,但回射流在一个周期内的首次出现需要时间的积累.在水翼吸力面射流使得射流孔附近压力升高,弥补了由于空化和绕流造成的压降,压力梯度增大,抗逆压能力增强,对回射流起到阻挡作用;另一方面,射流使得回射流区域面积和回射流的强度也有所减小,从而对云空化的发展起到抑制的效果.Q准则的涡结构云图相比于汽相体积分数云图能显示复杂的流动结构,前缘附着型空穴和尾缘游离型空穴内存在旋涡,回射流对空穴... 相似文献
237.
Over recent decades, studies in porous media have focused on many fields, typically in the development of oil and gas reservoirs. The imbibition phenomenon, a common mechanism affecting multi-phase flows in porous media, has shown more significant impacts on unconventional reservoir development, where the effect of the pore space increases with decreased pore sizes. In this paper, a comprehensive SPH method is applied, considering the binary interactions among the particles to study the imbibition phenomenon in porous media. The model is validated with physically meaningful results showing the effects of surface tension, contact angle, and pore structures. A heterogeneous porous medium is also constructed to study the effect of heterogeneity on the imbibition phenomenon; it can be referred from the results that the smaller pore throats and wetting surfaces are more preferred for the imbibition. The results show that the SPH method can be applied to solve the imbibition problems, but the unstable problem is still a sore point for the SPH method. 相似文献
238.
Hui-Hui Yang Hui-Ling Jiang Jia-Hao Tao Chen-Yu Zhang Jian-Bing Xiong Jin-Tong Yang Yu-Biao Liu Wen-Jing Zhong Xin-Xin Guan Jia-Xi Duan Yan-Feng Zhang Shao-Kun Liu Jian-Xin Jiang Yong Zhou Cha-Xiang Guan 《Experimental & molecular medicine》2022,54(11):2077
Necroptosis is the major cause of death in alveolar epithelial cells (AECs) during acute lung injury (ALI). Here, we report a previously unrecognized mechanism for necroptosis. We found an accumulation of mitochondrial citrate (citratemt) in lipopolysaccharide (LPS)-treated AECs because of the downregulation of Idh3α and citrate carrier (CIC, also known as Slc25a1). shRNA- or inhibitor–mediated inhibition of Idh3α and Slc25a1 induced citratemt accumulation and necroptosis in vitro. Mice with AEC-specific Idh3α and Slc25a1 deficiency exhibited exacerbated lung injury and AEC necroptosis. Interestingly, the overexpression of Idh3α and Slc25a1 decreased citratemt levels and rescued AECs from necroptosis. Mechanistically, citratemt accumulation induced mitochondrial fission and excessive mitophagy in AECs. Furthermore, citratemt directly interacted with FUN14 domain-containing protein 1 (FUNDC1) and promoted the interaction of FUNDC1 with dynamin-related protein 1 (DRP1), leading to excessive mitophagy-mediated necroptosis and thereby initiating and promoting ALI. Importantly, necroptosis induced by citratemt accumulation was inhibited in FUNDC1-knockout AECs. We show that citratemt accumulation is a novel target for protection against ALI involving necroptosis.Subject terms: Infection, Respiratory tract diseases 相似文献
239.
Jing Zhou Ji Feng Yong Wu Hui-Qi Dai Guang-Zhi Zhu Pan-Hong Chen Li-Ming Wang Guang Lu Xi-Wen Liao Pei-Zhi Lu Wen-Jing Su Shing Chuan Hooi Xin-Pin Ye Han-Ming Shen Tao Peng Guo-Dong Lu 《Experimental & molecular medicine》2022,54(11):2007
Transarterial chemoembolization (TACE) is the first-line treatment for unresectable intermediate-stage hepatocellular carcinoma (HCC). It is of high clinical significance to explore the synergistic effect of TACE with antiangiogenic inhibitors and the molecular mechanisms involved. This study determined that glucose, but not other analyzed nutrients, offered significant protection against cell death induced by sorafenib, as indicated by glucose deprivation sensitizing cells to sorafenib-induced cell death. Next, this synergistic effect was found to be specific to sorafenib, not to lenvatinib or the chemotherapeutic drugs cisplatin and doxorubicin. Mechanistically, sorafenib-induced mitophagy, as indicated by PINK1 accumulation, increased the phospho-poly-ubiquitination modification, accelerated mitochondrial membrane protein and mitochondrial DNA degradation, and increased the amount of mitochondrion-localized mKeima-Red engulfed by lysosomes. Among several E3 ubiquitin ligases tested, SIAH1 was found to be essential for inducing mitophagy; that is, SIAH1 silencing markedly repressed mitophagy and sensitized cells to sorafenib-induced death. Notably, the combined treatment of glucose restriction and sorafenib abolished ATP generation and mitophagy, which led to a high cell death rate. Oligomycin and antimycin, inhibitors of electron transport chain complexes, mimicked the synergistic effect of sorafenib with glucose restriction to promote cell death mediated via mitophagy inhibition. Finally, inhibition of the glucose transporter by canagliflozin (a clinically available drug used for type-II diabetes) effectively synergized with sorafenib to induce HCC cell death in vitro and to inhibit xenograft tumor growth in vivo. This study demonstrates that simultaneous treatment with sorafenib and glucose restriction is an effective approach to treat HCC, suggesting a promising combination strategy such as transarterial sorafenib-embolization (TASE) for the treatment of unresectable HCC.Subject terms: Liver cancer, Mitophagy, Apoptosis 相似文献
240.
Eight new 11-methoxymethylgermacranolides (1–8) were isolated from the ethanol extract of the whole plant of Carpesium divaricatum. The planar structures and relative configurations of the new compounds were determined by detailed spectroscopic analysis. The absolute configuration of 1 was established by electronic circular dichroism (ECD) spectrum and X-ray crystallographic analysis, and the stereochemistry of the new compounds 2–8 were determined by similar ECD data with 1. The absolute configurations of 5 and 7 were further confirmed by using quantum chemical electronic circular dichroism (ECD) calculations. Compound 4 exhibited weak cytotoxicity against MCF-7 cells. Compound 8 could potently decrease PGE2 productions in LPS-induced RAW 264.7 cells. 相似文献