全文获取类型
收费全文 | 3636篇 |
免费 | 322篇 |
国内免费 | 466篇 |
专业分类
4424篇 |
出版年
2024年 | 20篇 |
2023年 | 61篇 |
2022年 | 161篇 |
2021年 | 234篇 |
2020年 | 166篇 |
2019年 | 202篇 |
2018年 | 175篇 |
2017年 | 160篇 |
2016年 | 181篇 |
2015年 | 243篇 |
2014年 | 276篇 |
2013年 | 335篇 |
2012年 | 340篇 |
2011年 | 291篇 |
2010年 | 189篇 |
2009年 | 195篇 |
2008年 | 188篇 |
2007年 | 149篇 |
2006年 | 150篇 |
2005年 | 113篇 |
2004年 | 74篇 |
2003年 | 72篇 |
2002年 | 51篇 |
2001年 | 39篇 |
2000年 | 36篇 |
1999年 | 49篇 |
1998年 | 29篇 |
1997年 | 25篇 |
1996年 | 22篇 |
1995年 | 36篇 |
1994年 | 25篇 |
1993年 | 23篇 |
1992年 | 21篇 |
1991年 | 11篇 |
1990年 | 9篇 |
1989年 | 9篇 |
1988年 | 11篇 |
1987年 | 10篇 |
1986年 | 6篇 |
1985年 | 14篇 |
1984年 | 5篇 |
1983年 | 5篇 |
1982年 | 4篇 |
1981年 | 2篇 |
1980年 | 2篇 |
1979年 | 1篇 |
1978年 | 1篇 |
1974年 | 1篇 |
1971年 | 1篇 |
1970年 | 1篇 |
排序方式: 共有4424条查询结果,搜索用时 15 毫秒
121.
122.
123.
124.
Yizhi Jiang Dongping Huang Yuji Kondo Miao Jiang Zhenni Ma Lu Zhou Jian Su Xia Bai Changgeng Ruan Zhaoyue Wang Lijun Xia 《Journal of cellular and molecular medicine》2020,24(7):4356-4361
Hereditary thrombotic thrombocytopenic purpura (TTP) is an autosomal recessive thrombosis disorder, caused by loss-of-function mutations in ADAMTS13. Mutations in the CUB domains of ADAMTS13 are rare, and the exact mechanisms through which these mutations result in the development of TTP have not yet been fully elucidated. In this study, we identified two novel mutations in the CUB domains in a TTP family with an acceptor splice-site mutation (c.3569−1, G>A, intron 25) and a point missense mutation (c.3923, G>A, exon 28), resulting in a glycine to aspartic acid substitution (p.G1308D). In vitro splicing analysis revealed that the intronic mutation resulted in abnormal pre-mRNA splicing, and an in vitro expression assay revealed that the missense mutation significantly impaired ADAMTS13 secretion. Although both the patient and her brother displayed significantly reduced ADAMTS13 activity and increased levels of ultra-large VWF (ULVWF) multimers in plasma, only the female developed acute episodes of TTP. Our findings indicate the importance of the CUB domains for the protein stability and extracellular secretion of ADAMTS13. 相似文献
125.
Wu‐Xia Qiu Xiao‐Li Ma Xiao Lin Fan Zhao Di‐Jie Li Zhi‐Hao Chen Ke‐Wen Zhang Ru Zhang Pai Wang Yun‐Yun Xiao Zhi‐Ping Miao Kai Dang Xiao‐Yang Wu Ai‐Rong Qian 《Journal of cellular and molecular medicine》2020,24(1):317-327
Microtubule actin cross‐linking factor 1 (Macf1) is a spectraplakin family member known to regulate cytoskeletal dynamics, cell migration, neuronal growth and cell signal transduction. We previously demonstrated that knockdown of Macf1 inhibited the differentiation of MC3T3‐E1 cell line. However, whether Macf1 could regulate bone formation in vivo is unclear. To study the function and mechanism of Macf1 in bone formation and osteogenic differentiation, we established osteoblast‐specific Osterix (Osx) promoter‐driven Macf1 conditional knockout mice (Macf1f/fOsx‐Cre). The Macf1f/fOsx‐Cre mice displayed delayed ossification and decreased bone mass. Morphological and mechanical studies showed deteriorated trabecular microarchitecture and impaired biomechanical strength of femur in Macf1f/fOsx‐Cre mice. In addition, the differentiation of primary osteoblasts isolated from calvaria was inhibited in Macf1f/fOsx‐Cre mice. Deficiency of Macf1 in primary osteoblasts inhibited the expression of osteogenic marker genes (Col1, Runx2 and Alp) and the number of mineralized nodules. Furthermore, deficiency of Macf1 attenuated Bmp2/Smad/Runx2 signalling in primary osteoblasts of Macf1f/fOsx‐Cre mice. Together, these results indicated that Macf1 plays a significant role in bone formation and osteoblast differentiation by regulating Bmp2/Smad/Runx2 pathway, suggesting that Macf1 might be a therapeutic target for bone disease. 相似文献
126.
Identification of novel susceptibility loci for non‐syndromic cleft lip with or without cleft palate
Lan Ma Shu Lou Ziyue Miao Siyue Yao Xin Yu Shiyi Kan Guirong Zhu Fan Yang Chi Zhang Weibing Zhang Meilin Wang Lin Wang Yongchu Pan 《Journal of cellular and molecular medicine》2020,24(23):13669
Although several genome‐wide association studies (GWAS) of non‐syndromic cleft lip with or without cleft palate (NSCL/P) have been reported, more novel association signals are remained to be exploited. Here, we performed an in‐depth analysis of our previously published Chinese GWAS cohort study with replication in an extra dbGaP case‐parent trios and another in‐house Nanjing cohort, and finally identified five novel significant association signals (rs11119445: 3’ of SERTAD4, P = 6.44 × 10−14; rs227227 and rs12561877: intron of SYT14, P = 5.02 × 10−13 and 2.80 × 10−11, respectively; rs643118: intron of TRAF3IP3, P = 4.45 × 10−6; rs2095293: intron of NR6A1, P = 2.98 × 10−5). The mean (standard deviation) of the weighted genetic risk score (wGRS) from these SNPs was 1.83 (0.65) for NSCL/P cases and 1.58 (0.68) for controls, respectively (P = 2.67 × 10−16). Rs643118 was identified as a shared susceptible factor of NSCL/P among Asians and Europeans, while rs227227 may contribute to the risk of NSCL/P as well as NSCPO. In addition, sertad4 knockdown zebrafish models resulted in down‐regulation of sox2 and caused oedema around the heart and mandibular deficiency, compared with control embryos. Taken together, this study has improved our understanding of the genetic susceptibility to NSCL/P and provided further clues to its aetiology in the Chinese population. 相似文献
127.
Dafeng Yang Zhousheng Yang Lei Chen Dabin Kuang Yang Zou Jie Li Xu Deng Songyuan Luo Jianfang Luo Jun He Miao Yan Guixia He Yang Deng Rong Li Qiong Yuan Yangzhao Zhou Pei Jiang Shenglan Tan 《Journal of cellular and molecular medicine》2020,24(10):5911-5925
Natural products were extracted from traditional Chinese herbal emerging as potential therapeutic drugs for treating cardiovascular diseases. This study examines the role and underlying mechanism of dihydromyricetin (DMY), a natural compound extracted from Ampelopsis grossedentata, in atherosclerosis. DMY treatment significantly inhibits atherosclerotic lesion formation, proinflammatory gene expression and the influx of lesional macrophages and CD4-positive T cells in the vessel wall and hepatic inflammation, whereas increases nitric oxide (NO) production and improves lipid metabolism in apolipoprotein E-deficient (Apoe−/−) mice. Yet, those protective effects are abrogated by using NOS inhibitor L-NAME in Apoe−/− mice received DMY. Mechanistically, DMY decreases microRNA-21 (miR-21) and increases its target gene dimethylarginine dimethylaminohydrolase-1 (DDAH1) expression, an effect that reduces asymmetric aimethlarginine (ADMA) levels, and increases endothelial NO synthase (eNOS) phosphorylation and NO production in cultured HUVECs, vascular endothelium of atherosclerotic lesions and liver. In contrast, systemic delivery of miR-21 in Apoe−/− mice or miR-21 overexpression in cultured HUVECs abrogates those DMY-mediated protective effects. These data demonstrate that endothelial miR-21-inhibited DDAH1-ADMA-eNOS-NO pathway promotes the pathogenesis of atherosclerosis which can be rescued by DMY. Thus, DMY may represent a potential therapeutic adjuvant in atherosclerosis management. 相似文献
128.
129.
Miao Zeng Xiaojing Wang Ruijie Ma Weiya Zhu Yuan Li Zhongxin Chen Jiawen Zhou Wenqiang Li Tao Liu Zhicai He He Yan Fei Huang Yong Cao 《Liver Transplantation》2020,10(25)
Poly(3,4‐ethylenedioxythiophene):poly(styrenesulfonate) (PEDOT:PSS) has been is applied as hole transport material in organic electronic devices for more than 20 years. However, the redundant sulfonic acid group of PEDOT:PSS has often been overlooked. Herein, PEDOT:PSS‐DA is prepared via a facile doping of PEDOT:PSS with dopamine hydrochloride (DA·HCl) which reacts with the redundant sulfonic acid of PSS. The PEDOT:PSS‐DA film exhibits enhanced work function and conductivity compared to those of PEDOT:PSS. PEDOT:PSS‐DA‐based devices show a power conversion efficiency of 16.55% which is the highest in organic solar cells (OSCs) with (poly[(2,6‐(4,8‐bis(5‐(2‐ethylhexyl)‐4‐fluorothiophen‐2‐yl)benzo[1,2‐b:4,5‐b′]dithio‐phene))‐co‐(1,3‐di(5‐thiophene‐2‐yl)‐5,7‐bis(2‐ethylhexyl)‐benzo[1,2‐c:4,5‐c′]dithiophene‐4,8‐dione))] (PM6):(2,2′‐((2Z,2′Z)‐((12,13‐bis(2‐ethylhexyl)‐3,9‐diundecyl‐12,13‐dihydro‐[1,2,5]thiadiazolo[3,4‐e]thieno[2′′,3′:4′,5′]thieno[2′,3′:4,5]pyrrolo[3,2‐g]thieno[2′,3′:4,5]thieno[3,2‐b]indole‐2,10‐diyl)bis(methanylylidene))bis(5,6‐difluoro‐3‐oxo‐2,3‐dihydro‐1H‐indene‐2,1‐diylidene))dimalononitrile) (Y6) as the active layer. Furthermore, PEDOT:PSS‐DA also exhibits enhanced performance in three other donor/acceptor systems, exhibiting high compatibility in OSCs. This work demonstrates that doping PEDOT:PSS with various amino derivatives is a potentially efficient strategy to enhance the performance of PEDOT:PSS in organic electronic devices. 相似文献
130.
摘要 目的:探讨不同浓度罗哌卡因腰硬联合麻醉用于人工髋关节置换手术对患者麻醉效果和术后运动功能的影响。方法:2017年2月至2019年12月选择在本院进行人工髋关节置换手术的患者84例,根据随机数字表法把患者分为观察组与对照组各42例。两组都给予腰硬联合麻醉,对照组采用常规浓度0.5 %罗哌卡因麻醉观察组采用低浓度0.375 %罗哌卡因麻醉,记录患者麻醉效果和术后运动功能变化情况。结果:观察组的麻醉持续时间、运动恢复时间和感觉运动时间都显著短于对照组(P<0.05)。观察组麻醉后10 min、30 min、60 min的Bromage评分都低于对照组(P<0.05)。观察组术后7 d的低血压、恶心呕吐、头晕头痛、尿潴留等不良反应发生率为7.1 %,显著低于对照组的19.0 %(P<0.05)。两组所有患者在术后2 h、术后4 h、术后24 h的呼吸、心率均在正常范围内波动,组间与组内对比都无统计学意义(P>0.05)。结论:低浓度罗哌卡因腰硬联合麻醉用于人工髋关节置换手术能改善患者的麻醉效果和运动功能,提高麻醉效果,并不影响患者的生命体征,且能减少术后不良反应的发生。 相似文献