全文获取类型
收费全文 | 545篇 |
免费 | 38篇 |
出版年
2023年 | 4篇 |
2022年 | 9篇 |
2021年 | 7篇 |
2020年 | 8篇 |
2019年 | 4篇 |
2018年 | 9篇 |
2017年 | 10篇 |
2016年 | 17篇 |
2015年 | 10篇 |
2014年 | 15篇 |
2013年 | 23篇 |
2012年 | 38篇 |
2011年 | 43篇 |
2010年 | 28篇 |
2009年 | 14篇 |
2008年 | 36篇 |
2007年 | 33篇 |
2006年 | 28篇 |
2005年 | 24篇 |
2004年 | 24篇 |
2003年 | 25篇 |
2002年 | 22篇 |
2001年 | 8篇 |
2000年 | 14篇 |
1999年 | 5篇 |
1998年 | 5篇 |
1997年 | 4篇 |
1996年 | 3篇 |
1993年 | 2篇 |
1992年 | 6篇 |
1991年 | 9篇 |
1990年 | 7篇 |
1989年 | 9篇 |
1988年 | 5篇 |
1987年 | 4篇 |
1986年 | 5篇 |
1985年 | 7篇 |
1984年 | 4篇 |
1983年 | 5篇 |
1982年 | 2篇 |
1981年 | 4篇 |
1980年 | 3篇 |
1979年 | 5篇 |
1978年 | 2篇 |
1976年 | 2篇 |
1974年 | 5篇 |
1973年 | 4篇 |
1972年 | 7篇 |
1965年 | 2篇 |
1964年 | 2篇 |
排序方式: 共有583条查询结果,搜索用时 390 毫秒
81.
An efficient orange–red‐emitting LiNa3P2O7:Sm3+ pyrophosphate: Structural and optical analysis for solid‐state lighting 下载免费PDF全文
G.R. Dillip K. Munirathnam B. Deva Prasad Raju N. John Sushma S.W. Joo 《Luminescence》2017,32(5):772-778
A trivalent rare‐earth ion (Sm3+)‐doped LiNa3P2O7 (LNPO) phosphor was synthesized using a conventional high‐temperature solid‐state reaction route. A predominant orthorhombic phase of LNPO was observed in all X‐ray diffraction patterns. The surface states of the LNPO:Sm phosphor were confirmed by X‐ray photoelectron spectroscopy. Under 401 nm excitation, the Sm‐doped LNPO phosphors showed sharp emission peaks at 563, 600 and 647 nm that are related to the f–f transition of Sm3+ ions. The optimum concentration of Sm3+ (9 mol%) produced Commission Internationale de l'Eclairage chromaticity coordinates, color rendering index and correlated color temperature of (0.564, 0.434), 42 and 1843 K, respectively. 相似文献
82.
Sushma Boppana Kai Qin Jacob K. Files Ronnie M. Russell Regina Stoltz Frederic Bibollet-Ruche Anju Bansal Nathan Erdmann Beatrice H. Hahn Paul A. Goepfert 《PLoS pathogens》2021,17(7)
T-cell immunity is likely to play a role in protection against SARS-CoV-2 by helping generate neutralizing antibodies. We longitudinally studied CD4 T-cell responses to the M, N, and S structural proteins of SARS-CoV-2 in 26 convalescent individuals. Within the first two months following symptom onset, a majority of individuals (81%) mounted at least one CD4 T-cell response, and 48% of individuals mounted detectable SARS-CoV-2-specific circulating T follicular helper cells (cTfh, defined as CXCR5+PD1+ CD4 T cells). SARS-CoV-2-specific cTfh responses across all three protein specificities correlated with antibody neutralization with the strongest correlation observed for S protein-specific responses. When examined over time, cTfh responses, particularly to the M protein, increased in convalescence, and robust cTfh responses with magnitudes greater than 5% were detected at the second convalescent visit, a median of 38 days post-symptom onset. CD4 T-cell responses declined but persisted at low magnitudes three months and six months after symptom onset. These data deepen our understanding of antigen-specific cTfh responses in SARS-CoV-2 infection, suggesting that in addition to S protein, M and N protein-specific cTfh may also assist in the development of neutralizing antibodies and that cTfh response formation may be delayed in SARS-CoV-2 infection. 相似文献
83.
Paras Sehgal Samatha Mathew Ambily Sivadas Arjun Ray Jyoti Tanwar Sushma Vishwakarma Gyan Ranjan K V Shamsudheen Rahul C Bhoyar Abhishek Pateria Elvin Leonard Mukesh Lalwani Archana Vats Rajeev R Pappuru Mudit Tyagi Saumya Jakati Shantanu Sengupta Binukumar B K Subhabrata Chakrabarti Inderjeet Kaur Rajender K Motiani Vinod Scaria Sridhar Sivasubbu 《The EMBO journal》2021,40(15)
Long non‐coding RNAs (lncRNAs) are emerging as key regulators of endothelial cell function. Here, we investigated the role of a novel vascular endothelial‐associated lncRNA (VEAL2) in regulating endothelial permeability. Precise editing of veal2 loci in zebrafish (veal2 gib005Δ8/+) induced cranial hemorrhage. In vitro and in vivo studies revealed that veal2 competes with diacylglycerol for interaction with protein kinase C beta‐b (Prkcbb) and regulates its kinase activity. Using PRKCB2 as bait, we identified functional ortholog of veal2 in humans from HUVECs and named it as VEAL2. Overexpression and knockdown of VEAL2 affected tubulogenesis and permeability in HUVECs. VEAL2 was differentially expressed in choroid tissue in eye and blood from patients with diabetic retinopathy, a disease where PRKCB2 is known to be hyperactivated. Further, VEAL2 could rescue the effects of PRKCB2‐mediated turnover of endothelial junctional proteins thus reducing hyperpermeability in hyperglycemic HUVEC model of diabetic retinopathy. Based on evidence from zebrafish and hyperglycemic HUVEC models and diabetic retinopathy patients, we report a hitherto unknown VEAL2 lncRNA‐mediated regulation of PRKCB2, for modulating junctional dynamics and maintenance of endothelial permeability. 相似文献
84.
85.
KAP1 protein: an enigmatic master regulator of the genome 总被引:1,自引:0,他引:1
86.
Diclofenac sodium is known to interfere with renal physiology by inhibiting prostaglandins. Previous studies indicate that various nephrotoxins damage proximal renal tubules by altering alkaline phosphatase (APase) activity. APase has been reported to be a function related marker in renal proximal tubular epithelia where it is highly expressed. Present investigation deals with toxicity caused in mice kidney at histological and biochemical levels after diclofenac administration. Diclofenac toxicity was assessed by localizing APase in kidney histochemically and biochemically. Intramuscular diclofenac administration (10 mg/kg/body wt) for 30 days exhibited substantial degeneration in kidney. A marked change in APase activity was observed in histochemical and biochemical studies. A change was noticed in specific activity of APase at different periods of diclofenac treatment. Decrease in specific activity of APase after 10 days (18.41 %) and 30 days (55.3 %) of diclofenac exposure was observed. However, an insignificant hike in APase was observed after 20 days of drug therapy. Similar trends in APase activity were evidenced by the electrophoretic analysis. Histological and ultrastructural observations also corroborated above mentioned findings. Present investigation gives an insight into probable mechanism of renal pathology caused by diclofenac administration in mice. 相似文献
87.
88.
89.
Sandrine Ragu Michèle Dardalhon Sushma Sharma Ismail Iraqui Géraldine Buhagiar-Labarchède Virginie Grondin Guy Kienda Laurence Vernis Roland Chanet Richard D. Kolodner Meng-Er Huang Gérard Faye 《PloS one》2014,9(9)
The absence of Tsa1, a key peroxiredoxin that scavenges H2O2 in Saccharomyces cerevisiae, causes the accumulation of a broad spectrum of mutations. Deletion of TSA1 also causes synthetic lethality in combination with mutations in RAD51 or several key genes involved in DNA double-strand break repair. In the present study, we propose that the accumulation of reactive oxygen species (ROS) is the primary cause of genome instability of tsa1Δ cells. In searching for spontaneous suppressors of synthetic lethality of tsa1Δ rad51Δ double mutants, we identified that the loss of thioredoxin reductase Trr1 rescues their viability. The trr1Δ mutant displayed a CanR mutation rate 5-fold lower than wild-type cells. Additional deletion of TRR1 in tsa1Δ mutant reduced substantially the CanR mutation rate of tsa1Δ strain (33-fold), and to a lesser extent, of rad51Δ strain (4-fold). Loss of Trr1 induced Yap1 nuclear accumulation and over-expression of a set of Yap1-regulated oxido-reductases with antioxidant properties that ultimately re-equilibrate intracellular redox environment, reducing substantially ROS-associated DNA damages. This trr1Δ -induced effect was largely thioredoxin-dependent, probably mediated by oxidized forms of thioredoxins, the primary substrates of Trr1. Thioredoxin Trx1 and Trx2 were constitutively and strongly oxidized in the absence of Trr1. In trx1Δ trx2Δ cells, Yap1 was only moderately activated; consistently, the trx1Δ trx2Δ double deletion failed to efficiently rescue the viability of tsa1Δ rad51Δ. Finally, we showed that modulation of the dNTP pool size also influences the formation of spontaneous mutation in trr1Δ and trx1Δ trx2Δ strains. We present a tentative model that helps to estimate the respective impact of ROS level and dNTP concentration in the generation of spontaneous mutations. 相似文献
90.
Arrestin‐Domain Containing Protein 1 (Arrdc1) Regulates the Protein Cargo and Release of Extracellular Vesicles 下载免费PDF全文
Sushma Anand Natalie Foot Ching‐Seng Ang Kelly M. Gembus Shivakumar Keerthikumar Christopher G. Adda Suresh Mathivanan Sharad Kumar 《Proteomics》2018,18(17)
Extracellular vesicles (EVs) are lipid‐bilayered vesicles that are released by multiple cell types and contain nucleic acids and proteins. Very little is known about how the cargo is packaged into EVs. Ubiquitination of proteins is a key posttranslational modification that regulates protein stability and trafficking to subcellular compartments including EVs. Recently, arrestin‐domain containing protein 1 (Arrdc1), an adaptor for the Nedd4 family of ubiquitin ligases, has been implicated in the release of ectosomes, a subtype of EV that buds from the plasma membrane. However, it is currently unknown whether Arrdc1 can regulate the release of exosomes, a class of EVs that are derived endocytically. Furthermore, it is unclear whether Arrdc1 can regulate the sorting of protein cargo into the EVs. Exosomes and ectosomes are isolated from mouse embryonic fibroblasts isolated from wild type and Arrdc1‐deficient (Arrdc1?/?) mice. Nanoparticle tracking analysis–based EV quantitation shows that Arrdc1 regulates the release of both exosomes and ectosomes. Proteomic analysis highlights the change in protein cargo in EVs upon deletion of Arrdc1. Functional enrichment analysis reveals the enrichment of mitochondrial proteins in ectosomes, while proteins implicated in apoptotic cleavage of cell adhesion proteins and formation of cornified envelope are significantly depleted in exosomes upon knockout of Arrdc1. 相似文献