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排序方式: 共有329条查询结果,搜索用时 218 毫秒
1.
Soumen Devidutta Chennapragada Sridevi Calambur Narasimhan 《Indian pacing and electrophysiology journal》2016,16(1):40-45
Cardiac resynchronization therapy device (CRT-P and CRT-D) implantation has increased tremendously with increasing operator experience, eligible patients and expansion of indications. Refinements in devices and algorithms now aid physicians to improve biventricular pacing and optimize CRT. We report a case in which an interesting device program was used to achieve biventricular pacing after repeated dislodgement of the atrial lead in a patient implanted with CRT-D. 相似文献
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Nripendra Vikram Singh Shilpa Parashuram Jyotsana Sharma Roopa Sowjanya Potlannagari Dhinesh Babu Karuppannan Ram Krishna Pal Prakash Patil Dhananjay M. Mundewadikar Vipul R. Sangnure P.V. Parvati Sai Arun Naresh V.R. Mutha Bipin Kumar Abhishek Tripathi Sathish Kumar Peddamma Harish Kothandaraman Sailu Yellaboina Dushyant Singh Baghel Umesh K. Reddy 《Saudi Journal of Biological Sciences》2020,27(12):3514-3528
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Leberg Samuel S Barriga Ramiro Bart Henry Olivo Alfredo Narasimhan Kaushik Karubian Jordan 《Environmental Biology of Fishes》2021,104(3):239-251
Environmental Biology of Fishes - Environmental conditions influence ecological processes that shape stream community diversity and abundance. Deforestation has the potential to limit available... 相似文献
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J.Ronald Munro Saroja Narasimhan Steve Wetmore J.R. Riordan Harry Schachter 《Archives of biochemistry and biophysics》1975,169(1):269-277
A GDP-l-fucose:glycoprotein fucosyltransferase which transfers l-fucose to terminal β-N-acetyl-d-glucosaminyl residues of sialidase-, β-galactosidase-treated α1-acid glycoprotein and a CMP-sialic acid:glycoprotein sialyltransferase acting on sialidase-treated apolipoprotein-Ala1 from human very low density lipoprotein have been shown to be concentrated in rat liver Golgi apparatus preparations at enrichments of 40- and 45-fold, respectively, and in pork liver Golgi-rich fractions at enrichments of 35- and 20-fold, respectively. A second fucosyltransferase acting on sialidase-treated α1-acid glycopretein was absent from rat liver and was enriched only 13-fold in a pork liver Golgi-rich fraction. The smooth-surfaced microsome fraction was the only other rat liver subcellular fraction with appreciable levels of the GDP-l-fucose: β-N-acetyl-d-glucosaminide fucosyltransferase and the lipoprotein sialyltransferase (enrichments of 2.6- and 5.2-fold, respectivley). This enrichment could not be attributed to the plasma membrane content of the smooth microsome fraction since plasma membrane fractions from rat liver were shown to have relatively low concentrations of these two transferases (enrichments of 0.3 or less). Rat liver plasma membrane was also shown to have similarly low relative specific activities for three other glycosyltransferases (sialyl-, galactosyl-, and N-acetylglucosaminyl-). The accurate determination of the glycosyltransferase activities of the plasma membrane fraction required the use of relatively low concentrations of plasma membrane and relatively high concentrations of nucleotide-sugars in order to avoid interference by the high nucleotide-sugar pyrophosphatase and hydrolase activities of this fraction. 相似文献
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Jordan Woodrick Suhani Gupta Pooja Khatkar Sanchita Sarangi Ganga Narasimhan Akriti Trehan Sanjay Adhikari Rabindra Roy 《Nucleic acids research》2014,42(14):9033-9046
Repair of oxidative stress- and inflammation-induced DNA lesions by the base excision repair (BER) pathway prevents mutation, a form of genomic instability which is often observed in cancer as ‘mutation hotspots’. This suggests that some sequences have inherent mutability, possibly due to sequence-related differences in repair. This study has explored intrinsic mutability as a consequence of sequence-specific repair of lipid peroxidation-induced DNA adduct, 1, N6-ethenoadenine (εA). For the first time, we observed significant delay in repair of ϵA at mutation hotspots in the tumor suppressor gene p53 compared to non-hotspots in live human hepatocytes and endothelial cells using an in-cell real time PCR-based method. In-cell and in vitro mechanism studies revealed that this delay in repair was due to inefficient turnover of N-methylpurine-DNA glycosylase (MPG), which initiates BER of εA. We determined that the product dissociation rate of MPG at the hotspot codons was ≈5–12-fold lower than the non-hotspots, suggesting a previously unknown mechanism for slower repair at mutation hotspots and implicating sequence-related variability of DNA repair efficiency to be responsible for mutation hotspot signatures. 相似文献