全文获取类型
收费全文 | 3716篇 |
免费 | 290篇 |
国内免费 | 215篇 |
出版年
2024年 | 10篇 |
2023年 | 77篇 |
2022年 | 76篇 |
2021年 | 180篇 |
2020年 | 186篇 |
2019年 | 210篇 |
2018年 | 190篇 |
2017年 | 164篇 |
2016年 | 171篇 |
2015年 | 252篇 |
2014年 | 342篇 |
2013年 | 478篇 |
2012年 | 188篇 |
2011年 | 170篇 |
2010年 | 138篇 |
2009年 | 146篇 |
2008年 | 143篇 |
2007年 | 125篇 |
2006年 | 127篇 |
2005年 | 108篇 |
2004年 | 109篇 |
2003年 | 80篇 |
2002年 | 64篇 |
2001年 | 41篇 |
2000年 | 27篇 |
1999年 | 36篇 |
1998年 | 39篇 |
1997年 | 27篇 |
1996年 | 23篇 |
1995年 | 33篇 |
1994年 | 29篇 |
1993年 | 24篇 |
1992年 | 19篇 |
1991年 | 21篇 |
1990年 | 24篇 |
1989年 | 15篇 |
1988年 | 11篇 |
1987年 | 16篇 |
1986年 | 8篇 |
1985年 | 13篇 |
1984年 | 22篇 |
1983年 | 15篇 |
1982年 | 22篇 |
1981年 | 5篇 |
1980年 | 10篇 |
1978年 | 2篇 |
1977年 | 1篇 |
1974年 | 1篇 |
1973年 | 1篇 |
1972年 | 1篇 |
排序方式: 共有4221条查询结果,搜索用时 15 毫秒
1.
Sebastián Moran Miguel Vizoso Anna Martinez-Cardús Antonio Gomez Xavier Matías-Guiu Sebastián M Chiavenna Andrés G Fernandez Manel Esteller 《Epigenetics》2014,9(6):829-833
A formalin-fixed paraffin-embedded (FFPE) sample usually yields highly degraded DNA, which limits the use of techniques requiring high-quality DNA, such as Infinium Methylation microarrays. To overcome this restriction, we have applied an FFPE restoration procedure consisting of DNA repair and ligation processes in a set of paired fresh-frozen (FF) and FFPE samples. We validated the FFPE results in comparison with matched FF samples, enabling us to use FFPE samples on the Infinium HumanMethylation450 Methylation array. 相似文献
2.
《Developmental cell》2021,56(21):2995-3005.e4
- Download : Download high-res image (168KB)
- Download : Download full-size image
3.
4.
《Developmental cell》2021,56(16):2329-2347.e6
- Download : Download high-res image (154KB)
- Download : Download full-size image
5.
6.
Pancreatic cancer is a lethal disease with limited treatment options for cure. A high degree of intrinsic and acquired therapeutic resistance may result from cellular alterations in genes and proteins involved in drug transportation and metabolism, or from the influences of cancer microenvironment. Mechanistic basis for therapeutic resistance remains unclear and should profoundly impact our ability to understand pancreatic cancer pathogenesis and its effective clinical management. Recent evidences have indicated the importance of epigenetic changes in pancreatic cancer, including posttranslational modifications of proteins. We will review new knowledge on protein arginine methylation and its consequential contribution to therapeutic resistance of pancreatic cancer, underlying molecular mechanism, and clinical application of potential strategies of its reversal. 相似文献
7.
《Molecular cell》2020,77(6):1265-1278.e7
- Download : Download high-res image (317KB)
- Download : Download full-size image
8.
9.
Mengnan Wang Dongjie Li Mingyue Zhang Wenzhi Yang Yali Cui Shijie Li 《Animal genetics》2015,46(4):354-360
The CDKN1C gene encodes a cyclin‐dependent kinase inhibitor and is one of the key genes involved in the development of Beckwith–Wiedemann syndrome and cancer. In this study, using a direct sequencing approach based on a single nucleotide polymorphism (SNP) at genomic DNA and cDNA levels, we show that CDKN1C exhibits monoallelic expression in all seven studied organs (heart, liver, spleen, lung, kidney, muscle and subcutaneous fat) in cattle. To investigate how methylation regulates imprinting of CDKN1C in cattle, allele‐specific methylation patterns in two putative differential methylation regions (DMRs), the CDKN1C DMR and KvDMR1, were analyzed in three tissues (liver, spleen and lung) using bisulfite sequencing PCR. Our results show that in the CDKN1C DMR both parental alleles were unmethylated in all three analyzed tissues. In contrast, KvDMR1 was differentially methylated between the two parental alleles in the same tissues. Statistical analysis showed that there is a significant difference in the methylation level between the two parental alleles (P < 0.01), confirming that this region is the DMR of KvDMR1 and that it may be correlated with CDKN1C imprinting. 相似文献
10.
The degree of methylation at the c-myc proto-oncogene was found to change in human lymphoproliferative diseases, when examined using a methylation-sensitive restriction enzyme. In peripheral blood mononuclear cells (PBMC) c-myc DNA showed hypomethylation in human lymphoproliferative diseases, in comparison to normal subjects matched in age and sex. In cases of chronic lymphocytic leukemia (CLL), the change was amplified in the crisis. When the DNA was examined at the actin gene, no significant change was observed. The results suggest that the change in c-myc proto-oncogene methylation might become an important clue in understanding the relationship between levels of gene expression and methylation in human lymphoproliferative diseases. 相似文献