全文获取类型
收费全文 | 149篇 |
免费 | 0篇 |
专业分类
系统科学 | 1篇 |
现状及发展 | 52篇 |
研究方法 | 25篇 |
综合类 | 70篇 |
自然研究 | 1篇 |
出版年
2016年 | 1篇 |
2015年 | 1篇 |
2013年 | 1篇 |
2012年 | 8篇 |
2011年 | 7篇 |
2009年 | 1篇 |
2008年 | 6篇 |
2007年 | 9篇 |
2006年 | 16篇 |
2005年 | 3篇 |
2004年 | 5篇 |
2003年 | 9篇 |
2002年 | 3篇 |
2001年 | 6篇 |
2000年 | 6篇 |
1999年 | 4篇 |
1998年 | 2篇 |
1997年 | 1篇 |
1995年 | 3篇 |
1994年 | 1篇 |
1992年 | 1篇 |
1991年 | 2篇 |
1990年 | 8篇 |
1989年 | 2篇 |
1988年 | 1篇 |
1987年 | 1篇 |
1985年 | 3篇 |
1984年 | 1篇 |
1983年 | 1篇 |
1982年 | 1篇 |
1979年 | 2篇 |
1978年 | 5篇 |
1977年 | 2篇 |
1976年 | 3篇 |
1974年 | 2篇 |
1973年 | 1篇 |
1971年 | 4篇 |
1970年 | 1篇 |
1969年 | 2篇 |
1968年 | 6篇 |
1967年 | 2篇 |
1965年 | 1篇 |
1964年 | 1篇 |
1963年 | 1篇 |
1958年 | 1篇 |
1955年 | 1篇 |
排序方式: 共有149条查询结果,搜索用时 15 毫秒
111.
Synthesis and some characteristics of [13C]-specially enriched tetragastrin and the related compound
S. Yamada M. Sakagami N. Yanaihara H. Nishikawa H. Watari 《Cellular and molecular life sciences : CMLS》1977,33(12):1566-1567
Summary [13C]-enriched tetragastrin and the related compound were synthesized in solution. Conversion of S-[13C]-methylated tetragastrin to the enriched tetragastrin gave 10.5 ppm upfield chemical shift of C resonance. The potency of the synthetic tetragastrin to stimulate gastric acid secretion was virtually identical with that of pentagastrin (ICI).Acknowledgment. A part of this research was supported by scientific research funds (No. 944059, 048253) from the Japanese Ministry of Education. 相似文献
112.
C Masutani R Kusumoto A Yamada N Dohmae M Yokoi M Yuasa M Araki S Iwai K Takio F Hanaoka 《Nature》1999,399(6737):700-704
Xeroderma pigmentosum variant (XP-V) is an inherited disorder which is associated with increased incidence of sunlight-induced skin cancers. Unlike other xeroderma pigmentosum cells (belonging to groups XP-A to XP-G), XP-V cells carry out normal nucleotide-excision repair processes but are defective in their replication of ultraviolet-damaged DNA. It has been suspected for some time that the XPV gene encodes a protein that is involved in trans-lesion DNA synthesis, but the gene product has never been isolated. Using an improved cell-free assay for trans-lesion DNA synthesis, we have recently isolated a DNA polymerase from HeLa cells that continues replication on damaged DNA by bypassing ultraviolet-induced thymine dimers in XP-V cell extracts. Here we show that this polymerase is a human homologue of the yeast Rad30 protein, recently identified as DNA polymerase eta. This polymerase and yeast Rad30 are members of a family of damage-bypass replication proteins which comprises the Escherichia coli proteins UmuC and DinB and the yeast Rev1 protein. We found that all XP-V cells examined carry mutations in their DNA polymerase eta gene. Recombinant human DNA polymerase eta corrects the inability of XP-V cell extracts to carry out DNA replication by bypassing thymine dimers on damaged DNA. Together, these results indicate that DNA polymerase eta could be the XPV gene product. 相似文献
113.
Resistance to viomycin conferred by RNA of either ribosomal subunit. 总被引:15,自引:0,他引:15
114.
E-cadherin plays an essential role in collective directional migration of large epithelial sheets 总被引:1,自引:1,他引:0
Li L Hartley R Reiss B Sun Y Pu J Wu D Lin F Hoang T Yamada S Jiang J Zhao M 《Cellular and molecular life sciences : CMLS》2012,69(16):2779-2789
In wound healing and development, large epithelial sheets migrate collectively, in defined directions, and maintain tight cell-cell adhesion. This type of movement ensures an essential function of epithelia, a barrier, which is lost when cells lose connection and move in isolation. Unless wounded, epithelial sheets in cultures normally do not have overall directional migration. Cell migration is mostly studied when cells are in isolation and in the absence of mature cell-cell adhesion; the mechanisms of the migration of epithelial sheets are less well understood. We used small electric fields (EFs) as a directional cue to instigate and guide migration of epithelial sheets. Significantly, cells in monolayer migrated far more efficiently and directionally than cells in isolation or smaller cell clusters. We demonstrated for the first time the group size-dependent directional migratory response in several types of epithelial cells. Gap junctions made a minimal contribution to the directional collective migration. Breaking down calcium-dependent cell-cell adhesion significantly reduced directional sheet migration. Furthermore, E-cadherin blocking antibodies abolished migration of cell sheets. Traction force analysis revealed an important role of forces that cells in the leading rows exert on the substratum. With EF, the traction forces of the leading edge cells coordinated in directional re-orientation. Our study thus identifies a novel mechanism--E-cadherin dependence and coordinated traction forces of leading cells in collective directional migration of large epithelial sheets. 相似文献
115.
Obesity is a multifactorial and heterogeneous condition that results from alterations of various genes, each having a partial
and additive effect. The inheritance pattern of obesity is thus complex, and environmental factors play an important role
in promoting or delaying its development. The identification of susceptibility genes and genetic variants for obesity requires
various methodological approaches. Obesity is classified into three main categories on the basis of genetic etiology: monogenic,
syndromic, and polygenic obesity. Here we review monogenic and syndromic obesity. We also review the linkage analysis studies
followed by the candidate gene approaches and genome-wide association studies. Identification of the underlying genetic causes
of obesity will likely provide a basis both for the development of new therapeutic agents and for the personalized prevention
of this condition.
Received 2 October 2007; received after revision 15 November 2007; accepted 19 November 2007 相似文献
116.
Yasuda K Miyake K Horikawa Y Hara K Osawa H Furuta H Hirota Y Mori H Jonsson A Sato Y Yamagata K Hinokio Y Wang HY Tanahashi T Nakamura N Oka Y Iwasaki N Iwamoto Y Yamada Y Seino Y Maegawa H Kashiwagi A Takeda J Maeda E Shin HD Cho YM Park KS Lee HK Ng MC Ma RC So WY Chan JC Lyssenko V Tuomi T Nilsson P Groop L Kamatani N Sekine A Nakamura Y Yamamoto K Yoshida T Tokunaga K Itakura M Makino H Nanjo K Kadowaki T Kasuga M 《Nature genetics》2008,40(9):1092-1097
We carried out a multistage genome-wide association study of type 2 diabetes mellitus in Japanese individuals, with a total of 1,612 cases and 1,424 controls and 100,000 SNPs. The most significant association was obtained with SNPs in KCNQ1, and dense mapping within the gene revealed that rs2237892 in intron 15 showed the lowest Pvalue (6.7 x 10(-13), odds ratio (OR) = 1.49). The association of KCNQ1 with type 2 diabetes was replicated in populations of Korean, Chinese and European ancestry as well as in two independent Japanese populations, and meta-analysis with a total of 19,930 individuals (9,569 cases and 10,361 controls) yielded a P value of 1.7 x 10(-42) (OR = 1.40; 95% CI = 1.34-1.47) for rs2237892. Among control subjects, the risk allele of this polymorphism was associated with impairment of insulin secretion according to the homeostasis model assessment of beta-cell function or the corrected insulin response. Our data thus implicate KCNQ1 as a diabetes susceptibility gene in groups of different ancestries. 相似文献
117.
118.
Na?Li Marcus?Parrish Tze?Khee?Chan Lu?Yin Prashant?Rai Yamada?Yoshiyuki Nona?Abolhassani Kong?Bing?Tan Orsolya?Kiraly Vincent?T.?K.?Chow Bevin?P.?EngelwardEmail author 《Cellular and molecular life sciences : CMLS》2015,72(15):2973-2988
Influenza viruses account for significant morbidity worldwide. Inflammatory responses, including excessive generation of reactive oxygen and nitrogen species (RONS), mediate lung injury in severe influenza infections. However, the molecular basis of inflammation-induced lung damage is not fully understood. Here, we studied influenza H1N1 infected cells in vitro, as well as H1N1 infected mice, and we monitored molecular and cellular responses over the course of 2 weeks in vivo. We show that influenza induces DNA damage to both, when cells are directly exposed to virus in vitro (measured using the comet assay) and also when cells are exposed to virus in vivo (estimated via γH2AX foci). We show that DNA damage, as well as responses to DNA damage persist in vivo until long after virus has been cleared, at times when there are inflammation associated RONS (measured by xanthine oxidase activity and oxidative products). The frequency of lung epithelial and immune cells with increased γH2AX foci is elevated in vivo, especially for dividing cells (Ki-67-positive) exposed to oxidative stress during tissue regeneration. Additionally, we observed a significant increase in apoptotic cells as well as increased levels of DNA double strand break (DSB) repair proteins Ku70, Ku86 and Rad51 during the regenerative phase. In conclusion, results show that influenza induces DNA damage both in vitro and in vivo, and that DNA damage responses are activated, raising the possibility that DNA repair capacity may be a determining factor for tissue recovery and disease outcome. 相似文献
119.
Fibronectins--adhesive glycoproteins of cell surface and blood. 总被引:79,自引:0,他引:79
A recently characterised class of adhesive, high molecular weight glycoproteins is present on the surfaces of cells, in connective tissue matrices, and in extracellular fluids. These proteins may have important roles in cellular adhesion, malignant transformation, reticuloendothelial system function, and embryonic differentiation. 相似文献
120.
Padiath QS Saigoh K Schiffmann R Asahara H Yamada T Koeppen A Hogan K Ptácek LJ Fu YH 《Nature genetics》2006,38(10):1114-1123
Adult-onset autosomal dominant leukodystrophy (ADLD) is a slowly progressive neurological disorder characterized by symmetrical widespread myelin loss in the central nervous system, with a phenotype similar to chronic progressive multiple sclerosis. In this study, we identify a genomic duplication that causes ADLD. Affected individuals carry an extra copy of the gene for the nuclear laminar protein lamin B1, resulting in increased gene dosage in brain tissue from individuals with ADLD. Increased expression of lamin B1 in Drosophila melanogaster resulted in a degenerative phenotype. In addition, an abnormal nuclear morphology was apparent when cultured cells overexpressed this protein. This is the first human disease attributable to mutations in the gene encoding lamin B1. Antibodies to lamin B are found in individuals with autoimmune diseases, and it is also an antigen recognized by a monoclonal antibody raised against plaques from brains of individuals with multiple sclerosis. This raises the possibility that lamin B may be a link to the autoimmune attack that occurs in multiple sclerosis. 相似文献