全文获取类型
收费全文 | 19888篇 |
免费 | 1890篇 |
国内免费 | 2271篇 |
出版年
2024年 | 23篇 |
2023年 | 270篇 |
2022年 | 370篇 |
2021年 | 828篇 |
2020年 | 595篇 |
2019年 | 842篇 |
2018年 | 834篇 |
2017年 | 705篇 |
2016年 | 913篇 |
2015年 | 1264篇 |
2014年 | 1506篇 |
2013年 | 1617篇 |
2012年 | 1940篇 |
2011年 | 1832篇 |
2010年 | 1150篇 |
2009年 | 1049篇 |
2008年 | 1284篇 |
2007年 | 1127篇 |
2006年 | 967篇 |
2005年 | 850篇 |
2004年 | 762篇 |
2003年 | 683篇 |
2002年 | 595篇 |
2001年 | 365篇 |
2000年 | 302篇 |
1999年 | 246篇 |
1998年 | 171篇 |
1997年 | 121篇 |
1996年 | 114篇 |
1995年 | 66篇 |
1994年 | 74篇 |
1993年 | 55篇 |
1992年 | 77篇 |
1991年 | 70篇 |
1990年 | 65篇 |
1989年 | 54篇 |
1988年 | 32篇 |
1987年 | 22篇 |
1986年 | 32篇 |
1985年 | 20篇 |
1984年 | 19篇 |
1983年 | 27篇 |
1982年 | 14篇 |
1981年 | 15篇 |
1980年 | 9篇 |
1979年 | 18篇 |
1978年 | 7篇 |
1977年 | 9篇 |
1976年 | 9篇 |
1975年 | 8篇 |
排序方式: 共有10000条查询结果,搜索用时 309 毫秒
991.
2020年江苏省邳州市于3月31日发现草地贪夜蛾Spodoptera frugiperda成虫,远早于该地区2019年草地贪夜蛾的始见期6月份。为明确该地区草地贪夜蛾种群性质,利用昆虫轨迹分析方法,模拟分析了2020年江苏省邳州市早期发现的草地贪夜蛾的迁飞路径及天气背景场。结果表明:邳州市2019年12月-2020年2月温度低,草地贪夜蛾无法在此地越冬存活,2020年3月31日所诱捕的草地贪夜蛾为外地迁入,其虫源来自广西和广东西部的周年繁殖区;虽然邳州市3月份常年盛行北风和西北风,西南风发生概率低导致草地贪夜蛾迁入邳州市概率较小,但2020年3月底850 hPa的强西南气流为草地贪夜蛾从我国华南地区迁入邳州市提供了条件。本研究结果阐明了在极端条件下草地贪夜蛾从华南地区迁入江苏省的可能性,丰富了江苏省草地贪夜蛾春季早期迁入的理论依据。 相似文献
992.
993.
Runan Yang Lin Li Huilong Yuan Hui Liu Yingxin Gong Lifang Zou Shunhua Li Zilin Wang Liran Shi Tianyu Jia Shanhong Zhao Bing Wu Zhihua Yi Yun Gao Guilin Li Hong Xu Shuangmei Liu Chunping Zhang Guodong Li Shangdong Liang 《Journal of cellular physiology》2019,234(3):2756-2764
The upregulation of nociceptive ion channels expressed in dorsal root ganglia (DRG) contributes to the development and retaining of diabetic pain symptoms. The flavonoid quercetin (3,3′,4′,5,7-pentahydroxyflavone) is a component extracted from various fruits and vegetables and exerts anti-inflammatory, analgesic, anticarcinogenic, antiulcer, and antihypertensive effects. However, the exact mechanism underlying quercetin's analgesic action remains poorly understood. The aim of this study was to investigate the effects of quercetin on diabetic neuropathic pain related to the P2X4 receptor in the DRG of type 2 diabetic rat model. Our data showed that both mechanical withdrawal threshold and thermal withdrawal latency in diabetic rats treated with quercetin were higher compared with those in untreated diabetic rats. The expression levels of P2X4 messenger RNA and protein in the DRG of diabetic rats were increased compared with the control rats, while quercetin treatment significantly inhibited such enhanced P2X4 expression in diabetic rats. The satellite glial cells (SGCs) enwrap the neuronal soma in the DRG. Quercetin treatment also lowered the elevated coexpression of P2X4 and glial fibrillary acidic protein (a marker of SGCs) and decreased the upregulation of phosphorylated p38 mitogen-activated protein kinase (p38MAPK) in the DRG of diabetic rats. Quercetin significantly reduced the P2X4 agonist adenosine triphosphate-activated currents in HEK293 cells transfected with P2X4 receptors. Thus, our data demonstrate that quercetin may decrease the upregulation of the P2X4 receptor in DRG SGCs, and consequently inhibit P2X4 receptor-mediated p38MAPK activation to relieve the mechanical and thermal hyperalgesia in diabetic rats. 相似文献
994.
Qiong Wu Min Shi Wenying Meng Yugang Wang Pingping Hui Jiali Ma 《Journal of cellular physiology》2019,234(12):21889-21902
More and more documents have proved that the abnormal expression of long noncoding RNAs (lncRNAs) are correlated with the initiation and progression of colorectal cancer (CRC). lncRNA FOXD3-AS1 has been reported in glioma for its oncogenic property. According to the survival analysis of The Cancer Genome Atlas database, FOXD3-AS1 upregulation implied lower survival rate of patients with CRC. Quantitative real-time polymerase chain reaction showed the overexpression of FOXD3-AS1 in both CRC tissues and cells. The Kaplan–Meier method demonstrated the prognostic value of FOXD3-AS1 for patients with CRC. To explore the effect of FOXD3-AS1 on CRC progression, loss-of-function experiments were carried out, whose results indicated that knockdown of FOXD3-AS1 suppressed cell proliferation, migration, and invasion, inhibited cell cycle and promoted cell apoptosis in vitro. In vivo experiments affirmed that FOXD3-AS1 affected tumor growth. FOXD3-AS1 expression was enriched in the cytoplasm of CRC cells. Mechanism experiments revealed that FOXD3-AS1 served as a competing endogenous RNA to upregulate SIRT1 by sponging miR-135a-5p. In addition, SIRT1 silencing also restrained cell proliferation and motility. Rescue assays revealed the biological function of FOXD3-AS1/miR-135a-5p/SIRT1 axis in CRC progression. In conclusion, FOXD3-AS1 promotes CRC progression by regulating miR-135a-5p/SIRT1 axis, shedding lights on the way to CRC treatments. 相似文献
995.
996.
Ailin Liu Wanli Zhang Tao Zhao Ming Xiao Qijian Mei Hui Zhu 《Journal of cellular physiology》2019,234(12):23437-23447
As an indicator for the malignancy of thyroid nodules (TN), the doubling time of TN was studied in this study to evaluate the effect of rs712 polymorphism on the progression of TN. In addition, we aimed to study the potential molecular mechanisms underlying the pathological effect of rs712 polymorphism upon TN. A Taqman method was used to genotype the patients according to their rs712 polymorphism. Real-time polymerase chain reaction, western blot, Terminal deoxynucleotidyl transferase dUTP nick end labeling assay and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assay was conducted to study the correlation between KRAS expression and the pathological effect of rs712 polymorphism. In-silicon analysis and luciferase assay were utilized to establish the regulatory relationship between let-7g and KRAS. KRAS messenger RNA (mRNA)/protein levels in the GG group were upregulated with a decreased apoptosis index. KRAS mRNA was validated to be a virtual target of let-7g. In addition, the mRNA/protein level of KRAS as well as cell proliferation index was decreased in primary thyroid cancer cells genotyped as TT/TG and transfected with KRAS small interfering RNA (siRNA)/let-7g precursors. The cell apoptosis index was evidently elevated in the KRAS siRNA/let-7g precursors group compared with that in the scramble controls. Moreover, KRAS mRNA/protein only showed slight reduction when GG-genotyped primary thyroid cancer cells were transfected by let-7g precursors. Additionally, let-7g precursors exhibited no significant effect on cell proliferation index or cell apoptosis in GG cells. Rs712 polymorphism T>G in the 3′-untranslated region of KRAS interrupts the interactions between let-7g and KRAS mRNA, leading to a higher cell proliferation index and reduced doubling time of TN. 相似文献
997.
998.
Chengchuang Song Zhaoxin Yang Dong Dong Jiawei Xu Jian Wang Hui Li Yongzhen Huang Xianyong Lan Chuzhao Lei Yun Ma Hong Chen 《Journal of cellular physiology》2019,234(6):9839-9848
MicroRNAs (miRNAs) have been established to regulate skeletal muscle development in mammals. However, few studies have been conducted on the regulation of proliferation and differentiation of bovine myoblast cells by miRNAs. The aim of our study was to explore the function of miR-483 in cell proliferation and differentiation of bovine myoblast. Here, we found that miR-483 declined in both proliferation and differentiation stages of bovine myoblast cells. During the proliferation phase, the overexpression of miR-483 downregulated the cell cycle–associated genes cyclin-dependent kinase 2 (CDK2), proliferating cell nuclear antigen (PCNA) messenger RNA (mRNA), and the protein levels. At the cellular level, cell cycle, cell counting kit-8, and 5-ethynyl-2´-deoxyuridine results indicated that the overexpression of miR-483 block cell proliferation. During differentiation, the overexpression of miR-483 led to a decrease in the levels of the myogenic marker genes MyoD1 and MyoG mRNA and protein. Furthermore, the immunofluorescence analysis results showed that the number of MyHC-positive myotubes was reduced. In contrast, the opposite experimental results were obtained concerning both proliferation and differentiation after the inhibition of miR-483. Mechanistically, we demonstrated that miR-483 target insulin-like growth factor 1 (IGF1) and downregulated the expression of key proteins in the PI3K/AKT signaling pathway. Altogether, our findings indicate that miR-483 acts as a negative regulator of bovine myoblast cell proliferation and differentiation. 相似文献
999.
Shupeng Shi Mimi Tang Honglei Li Hui Ding Yangfan Lu Lijuan Gao Qian Wu Luo Zhou Yujiao Fu Bo Xiao Mengqi Zhang 《Journal of cellular physiology》2019,234(6):9316-9327
Angiogenesis is positively correlated with the survival rate of stroke patients. Therefore, studying factors that initiate and promote angiogenesis after ischemic stroke is crucial for finding novel and effective treatment targets that improve the prognosis of stroke. X-box binding protein l splicing (XBP1s) plays a positive regulatory role in cell proliferation and angiogenesis. However, the role and mechanism of XBP1s on the proliferation of brain microvascular endothelial cells (BMECs) and angiogenesis after cerebral ischemia remains unclear. In the current study, we investigated the role XBP1s plays in BMEC proliferation and angiogenesis following cerebral ischemia. In this study, the roles of XBP1s on cell survival, apoptosis, cycle migration, and angiogenesis were determined in oxygen-glucose deprivation (OGD) treated BMECs. The expression of XBP1s in BMECs, which were exposed to OGD at 0, 2, 4, and 6 hr, increased in a time-dependent manner. The overexpression of XBP1s promoted cell survival, cell cycle, migration, and angiogenesis of BMECs, and inhibited the apoptosis in OGD-treated BMECs. In addition, the overexpression of XBP1s promoted the expression of cyclin D1, matrix metalloproteinase (MMP-2), and MMP-9, but inhibited cleaved Caspase-3 and cleaved Caspase-9 expression in OGD-treated BMECs. The overexpression of XBP1s also promoted the expression of hypoxia-inducible factor 1-alpha, vascular endothelial growth factor, phosphatidylinositol-4,5-bisphosphate 3-kinase, p-AKT, p-mTOR, p-GSK3β, and p-extracellular signal-regulated kinase1/2 in OGD-treated BMECs. The effect of XBP1s silencing was opposite to that of XBP1s overexpression. In conclusion, using an in vitro OGD model, we demonstrated that XBP1s may be a promising target for ischemic stroke therapy to maintain BMECs survival and induce angiogenesis. 相似文献
1000.
Guang-Cai Li Xu-Ling Qin Huai-Hua Song Ying-Ni Li Yu-Yan Qiu Shi-Chang Cui Yong-Sheng Wang Hui Wang Jun-Ling Gong 《Journal of cellular physiology》2019,234(12):22331-22342
Ovarian cancer characterizes as the fourth leading consequence of death associated with cancer for women. Accumulating evidence underscores the vital roles of microRNAs (miRNAs) in preventing ovarian cancer development. Besides, induction of the phosphatidylinositol-3 kinase/serine/threonine kinase (PI3K/Akt) pathway associated with the ovarian cancer cell migration and invasion. The study aims to examine the effects of miR-15b on the proliferation, apoptosis, and senescence of human ovarian cancer cells by binding to lysophosphatidic acid receptor 3 (LPAR3) with the involvement of the PI3K/Akt pathway. The positive expression of LPAR3 protein was detected by immunohistochemistry. Then the interaction between miR-15b and LPAR3 was examined. The possible role of miR-15b in ovarian cancer was explored using gain- and loss-of-function experiments. Subsequently, the functions of miR-15b on PI3K/Akt pathway, proliferation, migration, invasion, senescence and apoptosis of ovarian cancer cells were assessed. Furthermore, in vivo tumorigenicity assay in nude mice was performed. LPAR3 was overexpressed, whereas miR-15b was poorly expressed in ovarian cancer tissues. LPAR3 is a direct target of miR-15b. Restored miR-15b promoted Bax expression, apoptosis, and senescence, inhibited expression of LPAR3 and Bcl-2, the extent of PI3K and Akt phosphorylation, as well as ovarian cancer cell proliferation, migration, and invasion. Further, tumor growth was observed to be prevented by miR-15b overexpression. Collectively, our study demonstrates that miR-15b represses the proliferation and drives the senescence and apoptosis of ovarian cancer cells through the suppression of LPAR3 and the PI3K/Akt pathway, highlighting an antitumorigenic role of miR-15b. 相似文献