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121.
【目的】明确马铃薯Y病毒(potato virus Y,PVY)侵染后诱导的烟草营养成分的变化及其对烟蚜Myzus persicae生命特性的影响,旨在进一步解析PVY-烟草-烟蚜三者间的互作机制。【方法】通过蒽酮比色法和氨基酸自动分析仪测定了PVY不同侵染时期烟株体内的可溶性糖和游离氨基酸含量的变化;测定和比较了感病与健康烟草植株上烟蚜种群生长发育、成虫寿命、繁殖力和有翅蚜产生量的差异性。【结果】PVY侵染前、中、后期(分别为侵染后5,12和20 d)的烟草叶片中游离氨基酸的总量均显著高于健康烟草叶片。相较于健康烟草叶片,在PVY侵染前期的烟草叶片中,谷氨酸、脯氨酸、天冬氨酸、色氨酸、缬氨酸、赖氨酸和组氨酸的含量显著增加;PVY侵染中期,感病叶片中丝氨酸含量显著下降,谷氨酸、天冬氨酸、色氨酸、缬氨酸、亮氨酸、苯丙氨酸、精氨酸和组氨酸含量显著提高;PVY侵染后期,感病叶片中甘氨酸含量显著下降,谷氨酸、脯氨酸、天冬氨酸、苏氨酸、缬氨酸、亮氨酸、丙氨酸、苯丙氨酸、组氨酸、酪氨酸和精氨酸含量显著提高。在PVY侵染的前期和中期,感病叶片中的可溶性糖含量显著高于健康烟叶,而在侵染后期感病叶片中可溶性糖含量显著低于健康烟草叶片的。PVY侵染前期和中期的烟草叶片中总糖和总游离氨基酸的含量比值显著高于健康烟草叶片中的。在PVY侵染的烟草植株和健康烟草植株上取食的烟蚜其发育历期、若蚜历期、成蚜繁殖期、繁殖后期、寿命、烟蚜种群的内禀增长率、周限增长率和平均世代周期均无显著差异,但在感病烟草植株上取食的烟蚜成蚜繁殖前期显著缩短,其繁殖力和净生殖率显著提高。相较于健康烟草植株,在PVY侵染烟草植株上定殖的烟蚜种群有翅蚜发生的高峰期提前。【结论】PVY侵染前期和中期提高了寄主烟草的营养品质,从而提高了烟蚜的繁殖力。侵染后期烟草营养品质的下降,促使烟蚜种群有翅蚜的产生和扩散,从而有利于PVY自身的传播。 相似文献
122.
Qian Wang Xiao-Ping Li Xi Zhou Chun-Fen Yang Zhu Zhu 《Journal of cellular biochemistry》2020,121(10):4108-4119
This study aimed to identify the association between lnc-LAMC2-1:1 polymorphism rs2147578 and the recurrence of ovary cancer, as well as to study the underlying mechanism of rs2147578 in ovary cancer. Real-time polymerase chain reaction, Western blot analysis, immunohistochemistry, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, Logrank test, and Kaplan-Meier analysis were carried out to explore the role of rs2147578 in ovary cancer. No obvious difference was observed concerning all clinical characteristics among 90 patients genotyped as CC (N = 28), CG (N = 38), and GG (N = 24) in their rs2147578 polymorphism. In addition, the subjects carrying the CC genotype had longer recurrence-free survival time and showed a lower level of malignancy compared with those carrying CG and GG genotypes. Lnc-LAMC2-1:1 and miR-128 were lowly expressed in the CC group, while deleted in colorectal cancer (DCC) was highly expressed in the CC group. Furthermore, DCC was identified as a target gene of miR-128, and miR-128 mimics decreased the luciferase activity of cells cotransfected with wild-type DCC 3′-untranslated region. Lnc-LAMC2:1-1 directly targeted and affected miR-128 expression, and the G allele in lnc-LAMC2-1:1 rs2147578 upregulated miR-128 expression. Transfection with a miR-128 precursor evidently downregulated the expression of lnc-LAMC2-1:1, miR-128, and DCC expression, but did not affect the expression of ABCC5 and body mass index. Finally, miR-128 precursor promoted cell proliferation and inhibited cell apoptosis. Compared with lnc-LAMC2-1:1 rs2147578C allele, the G allele increases the risk of ovarian cancer by reducing the binding between lnc-LAMC2-1:1 and miR-128-3p, which in turn further decreases the expression of DCC and inhibits cell apoptosis. 相似文献
123.
Wen-Jing Li Xin-Hui Chen Jia-Cheng Zeng Li-Li Duan 《Journal of biomolecular structure & dynamics》2020,38(14):4336-4343
Communicated by Ramaswamy H. Sarma 相似文献
124.
Xi Long Qian Li Li-Jun Zhi Jin-Mao Li Zheng-Yu Wang 《Journal of cellular physiology》2020,235(3):3013-3021
Several studies have shown that low expression of epoxide hydrolase 1 (EPHX1) is closely associated with varying human cancers, including hepatocellular carcinoma (HCC). This study aims to explore the potential mechanism of EPHX1 silencing and revealed a novel regulatory pathway in the pathogenesis of HCC. In this study, micro ribonucleic acid (miR)-184 was predicted and validated to be a regulator of EPHX1 through experiments, and its expression was negatively correlated with the messenger RNA (mRNA) levels of EPHX1 in primary tumors. Elevation of EPHX1 suppressed cell proliferation and migration as well as cell cycle progression, and induced apoptosis, while downregulation of miR-184 exhibited the opposite effect on cellular processes. Moreover, LINC00205 interacted with miR-184 and was markedly downregulated in tumors. The effects of the miR-184 inhibitor on cell proliferation, apoptosis, and migration were reversed in part by the transfection with LINC00205 small interfering RNAs. In addition, LINC00205 acted as a molecular sponge to positively regulate the mRNA and protein levels of EPHX1 via regulating miR-184. The tumorigenicity of HCC cells was enhanced by LINC00205 shRNA but diminished by overexpression of EPHX1 in vivo. Clinically, the EPHX1 expression in patients with HCC was markedly downregulated. Taken together, the results of this study suggest that as a competing endogenous RNA, LINC00205 may regulate EPHX1 by inhibiting miR-184 in the progression of HCC and that targeting the LINC00205/miR-184/EPHX1 axis may provide a treatment protocol for patients. 相似文献
125.
circRNA-14723 promotes hepatocytes proliferation in rat liver regeneration by sponging rno-miR-16-5p
Xueqiang Guo Lingling Xi Lifei Li Jianlin Guo Wei Jin Cuifang Chang Jingbo Zhang Cunshuan Xu Guangwen Chen 《Journal of cellular physiology》2020,235(11):8176-8186
Circular RNA (circRNA) is a subclass of noncoding RNA (ncRNA) detected within mammalian tissues and cells. However, its regulatory role during the proliferation phase of rat liver regeneration (LR) remains unreported. This study was designed to explore their regulatory mechanisms in cell proliferation of LR. The circRNA expression profile was detected by high-throughput sequencing. It was indicated that 260 circRNAs were differentially expressed during the proliferation phase of rat LR. Among them, circ-14723 displayed a significantly differential expression. We further explored its regulatory mechanism in rat hepatocytes (BRL-3A cells). First, EdU, flow cytometry and western blot (WB) indicated that knocking down circ-14723 inhibited BRL-3A cells proliferation. Second, RNA-Pulldown and dual-luciferase report assay showed that circ-14723 could sponge rno-miR-16-5p. At last, WB showed that the reported target genes of rno-miR-16-5p, CCND1, and CCNE1 were downregulated after knocking down circ-14723. In conclusion, we found that circ-14723 exerted a critical role in G1/S arrest to promote cell proliferation via rno-miR-16-5p/CCND1 and CCNE1 axis in rat LR. This finding further revealed the regulatory mechanisms of circRNA on cell proliferation of LR, and might provide a potential target for clinical problems. 相似文献
126.
Xi Chen Jun-Gen Hu Yi-Zhou Huang Shun Li Sheng-Fu Li Min Wang Hong-Wei Xia Jesse Li-Ling Hui-Qi Xie 《Journal of cellular physiology》2020,235(1):221-231
The motility of mesenchymal stem cells (MSCs) is highly related to their homing in vivo, a critical issue in regenerative medicine. Our previous study indicated copper (Cu) might promote the recruitment of endogenous MSCs in canine esophagus defect model. In this study, we investigated the effect of Cu on the motility of bone marrow mesenchymal stem cells (BMSCs) and the underlying mechanism in vitro. Cu supplementation could enhance the motility of BMSCs, and upregulate the expression of hypoxia-inducible factor 1α (Hif1α) at the protein level, and upregulate the expression of rho family GTPase 3 (Rnd3) at messenger RNA and protein level. When Hif1α was silenced by small interfering RNA (siRNA), Cu-induced Rnd3 upregulation was blocked. When Rnd3 was silenced by siRNA, the motility of BMSCs was decreased with or without Cu supplementation, and Cu-induced cytoskeleton remodeling was neutralized. Furthermore, overexpression of Rnd3 also increased the motility of BMSCs and induced cytoskeleton remodeling. Overall, our results demonstrated that Cu enhanced BMSCs migration through, at least in part, cytoskeleton remodeling via Hif1α-dependent upregulation of Rnd3. This study provided an insight into the mechanism of the effect of Cu on the motility of BMSCs, and a theoretical foundation of applying Cu to improve the recruitment of BMSCs in tissue engineering and cytotherapy. 相似文献
127.
Jian-Guo Hu Xing-Jun Wu Yi-Fan Feng Gang-ming Xi Ling-Xiao Deng Zhen-Huan Wang Rui Wang Lin Shen Jian-Sheng Zhou He-Zuo Lü 《Neurochemical research》2013,38(3):601-609
The conditioned medium from B104 neuroblastoma cells (B104CM) induces proliferation of oligodendrocyte progenitor cells (OPCs) in vitro. However, the molecular events that occur during B104CM-induced proliferation of OPCs has not been well clarified. In the present study, using OPCs immunopanned from embryonic day 14 Sprague–Dawley rat spinal cords, we explored the activation of several signaling pathways and the expression of several important immediate early genes (IEGs) and cyclins in OPCs in response to B104CM. We found that B104CM can induce OPC proliferation through the activation of the extracellular signal-regulated kinases 1 and 2 (Erk1/2), but not PI3K or p38 MAPK signaling pathways in vitro. The IEGs involved in B104CM-induced OPC proliferation include c-fos, c-jun and Id2, but not c-myc, fyn, or p21. The cyclins D1, D2 and E are also involved in B104CM-stimulated proliferation of OPCs. The activation of Erk results in subsequent expression of IEGs (such as c-fos, c-jun and Id-2) and cyclins (including cyclin D1, D2 and E), which play key roles in cell cycle initiation and OPC proliferation. Collectively, these results suggest that the phosphorylation of Erk1/2 is an important molecular event during OPC proliferation induced by B104CM. 相似文献
128.
Yi Huang Jianqing Zhou Huadan Ye Limin Xu Yanping Le Xi Yang Weifeng Xu Xiaoyan Huang Jiangfang Lian Shiwei Duan 《Gene》2013
The goal of our study is to evaluate the contribution of CXCL12 rs1746048 (hg19, chr10:44775574) to the risk of CHD in Han Chinese, and to summarize its role in CHD through meta-analysis of existing studies among various ethnic groups. Significant association is observed between rs1746048-C and an increased risk of CHD in Han Chinese (χ2 = 5.41, df = 1, P = 0.02). Post hoc analysis reveals an even stronger association of rs1746048 with the risk of CHD for subjects aged 65 years or older (genotype: χ2 = 8.39, df = 2, P = 0.015; allele: χ2 = 9.13, df = 1, P = 0.003, odd ratio (OR) = 1.91, 95% confidential interval (CI) = 1.25–2.91). A break down analysis by gender shows that rs1746048 is likely a CHD risk factor under the recessive model in males (CC + CT versus TT: P = 0.05, χ2 = 3.59, df = 1, OR = 1.72, 95% CI = 1.00–3.04). In addition, a meta-analysis of ten studies among over 107,000 individuals confirms that rs1746048 is a risk factor of CHD (P < 0.0001, OR = 1.12, 95% CI = 1.09–1.15) and this agrees with the findings of our case–control study in Han Chinese. 相似文献
129.