全文获取类型
收费全文 | 144篇 |
免费 | 4篇 |
国内免费 | 1篇 |
出版年
2021年 | 1篇 |
2018年 | 1篇 |
2017年 | 2篇 |
2015年 | 1篇 |
2014年 | 1篇 |
2013年 | 5篇 |
2012年 | 3篇 |
2011年 | 6篇 |
2010年 | 4篇 |
2009年 | 2篇 |
2008年 | 10篇 |
2007年 | 9篇 |
2006年 | 2篇 |
2005年 | 8篇 |
2004年 | 6篇 |
2003年 | 11篇 |
2002年 | 11篇 |
2001年 | 4篇 |
2000年 | 3篇 |
1999年 | 3篇 |
1998年 | 4篇 |
1997年 | 5篇 |
1996年 | 3篇 |
1994年 | 1篇 |
1993年 | 1篇 |
1992年 | 2篇 |
1991年 | 1篇 |
1990年 | 5篇 |
1989年 | 5篇 |
1988年 | 4篇 |
1987年 | 2篇 |
1986年 | 2篇 |
1985年 | 1篇 |
1983年 | 1篇 |
1982年 | 2篇 |
1975年 | 4篇 |
1974年 | 4篇 |
1971年 | 1篇 |
1970年 | 3篇 |
1968年 | 3篇 |
1967年 | 1篇 |
1965年 | 1篇 |
排序方式: 共有149条查询结果,搜索用时 906 毫秒
51.
Ito Y Kanai T Totsuka T Okamoto R Tsuchiya K Nemoto Y Yoshioka A Tomita T Nagaishi T Sakamoto N Sakanishi T Okumura K Yagita H Watanabe M 《American journal of physiology. Gastrointestinal and liver physiology》2008,294(1):G199-G207
It has been recently demonstrated that NKG2D is an activating costimulatory receptor on natural killer (NK) cells, natural killer T (NKT) cells, activated CD8(+) T cells, and gammadelta T cells, which respond to cellular stress, such as inflammation, transformation, and infection. Here we show that intestinal inflammation in colitic SCID mice induced by adoptive transfer of CD4(+)CD45RB(high) T cells is characterized by significant increase of CD4(+)NKG2D(+) T cells and constitutive expression of NKG2D ligands, such as H60, Mult-1, and Rae-1, by lamina propria CD11c(+) dendritic cells. Furthermore, treatment with nondepleting and neutralizing anti-NKG2D MAb after transfer of CD4(+)CD45RB(high) T cells into SCID mice significantly suppressed wasting disease with colitis, abrogated leukocyte infiltration, and reduced production of IFN-gamma by lamina propria CD4(+) T cells. These findings demonstrate that NKG2D signaling pathway is critically involved in CD4(+) T cell-mediated disease progression and suggest a new therapeutic target for inflammatory bowel diseases. 相似文献
52.
Yoshikazu Totsuka Yasumitsu Nagao Takuro Horii Hiromichi Yonekawa Hiroshi Imai Hideo Hatta Yoshiaki Izaike Tomoyuki Tokunaga Yoriko Atomi 《Journal of applied physiology》2003,95(2):720-727
We compared four inbred mouse strains in their physical performance, measured as a maximal treadmill running time, characteristics of soleus muscle, anatomic character, and growth. The strains used were Mus musculus domesticus [C57BL/6 (B6) and BALB/c], Mus musculus molossinus (MSM/Ms), and Mus spretus. Maximal running time was significantly different among these four mouse strains. Running time until exhaustion was highest in MSM/Ms and lowest in M. spretus. Maximal times for the laboratory mouse strains were nearly identical. Soleus muscle fiber type and cross-sectional area also differed significantly among the species. In particular, M. spretus was significantly different from the other inbred mouse strains. Growth in the wild-derived inbred mice appeared to be complete earlier than in the laboratory mice, and the body size of the wild strains was about half that of the laboratory strains. From these results, we propose that wild-derived inbred mouse strains are useful models for enhancing phenotypic variation in physical performance and adaptability. 相似文献
53.
Adenovirus E4orf6 targets pp32/LANP to control the fate of ARE-containing mRNAs by perturbing the CRM1-dependent mechanism
下载免费PDF全文
![点击此处可从《The Journal of cell biology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Higashino F Aoyagi M Takahashi A Ishino M Taoka M Isobe T Kobayashi M Totsuka Y Kohgo T Shindoh M 《The Journal of cell biology》2005,170(1):15-20
E4orf6 plays an important role in the transportation of cellular and viral mRNAs and is known as an oncogene product of adenovirus. Here, we show that E4orf6 interacts with pp32/leucine-rich acidic nuclear protein (LANP). E4orf6 exports pp32/LANP from the nucleus to the cytoplasm with its binding partner, HuR, which binds to an AU-rich element (ARE) present within many protooncogene and cytokine mRNAs. We found that ARE-mRNAs, such as c-fos, c-myc, and cyclooxygenase-2, were also exported to and stabilized in the cytoplasm of E4orf6-expressing cells. The oncodomain of E4orf6 was necessary for both binding to pp32/LANP and effect for ARE-mRNA. C-fos mRNA was exported together with E4orf6, E1B-55kD, pp32/LANP, and HuR proteins. Moreover, inhibition of the CRM1-dependent export pathway failed to block the export of ARE-mRNAs mediated by E4orf6. Thus, E4orf6 interacts with pp32/LANP to modulate the fate of ARE-mRNAs by altering the CRM1-dependent export pathway. 相似文献
54.
Veillonellophage N2 adsorbed to polysaccharides (PSs) on Veillonella rodentium ATCC 17743 cell wall, and the bacteriophage receptor contained only glucosamine. D(+)-glucosamine hydrochloride (Sigma) also adsorbed the veillonellophage N2. These results therefore indicate that the receptor to the veillonellophage N2 is cell wall PSs. The PSs of the host cells as receptor have been characterized. Glucosamine accounted for approximately 100% of the weight of the PSs. The PSs which were partially resolved by Sephadex G-75 chromatography comprised approximately four glucosamine units. Their primary structure was determined by 400 MHz n.m.r. spectroscopy. One- and two-dimensional 1H-nmr experiments showed the PS to be a branched polymer. Glucosamine linkage was detected in one of the branches. 相似文献
55.
Y Totsuka M Tabuchi I Kojima Y Eto H Shibai E Ogata 《Biochemical and biophysical research communications》1989,158(3):1060-1065
Effects of transforming growth factor-beta (TGF-beta) on insulin secretion were studied in rat pancreatic islets. When islets were incubated in a batch incubation system with various concentrations of TGF-beta in the presence of 2.8 mM glucose, TGF- beta increased insulin release in a concentration-dependent manner. Both TGF- beta 1 and TGF- beta 2 were equally effective. The stimulatory action of TGF- beta was greater in the presence of stimulatory concentration of glucose. In perifusion system, TGF- beta induced an immediate monotonic increase in insulin secretion. These results indicate that TGF- beta is a stimulator of insulin secretion. 相似文献
56.
57.
Takashi Saiki Teruji Suzuki Yoshimasa Takagi Teiiti Narasaki Gakuzo Tamura Kei Arima 《Bioscience, biotechnology, and biochemistry》2013,77(7):1101-1103
Respiratory inhibition by piericidin A was overcome by addition of vitamin K3 to the inhibited respiratory chain in mammalian mitochondria but not in insect mitochondria.Antagonistic effect of vitamin K3 on the inhibition of piericidin A was apparently found in respiration, blood pressure and heart rate in rat in vivo. Furthermore, toxicity of piericidin A to mouse and rat decreased when piericidin A was administered as the mixture of vitamin K3 in intraperitoneal route.No antagonistic effect of vitamin K3 was observed on the inhibition of piericidin A in TTC reaction of american cockroach nerve cord, femorals and digestive organs. Toxicity of piericidin A to some insects were not affected by vitamin K3. 相似文献
58.
In order to understand the pathogenesis of mouse muscular dystrophy, we investigated the levels of the thiobarbituric acid-reactive substances (TBARS), H2O2 and NADPH oxidase activity, which were relative to the acceleration of oxidative conditions, in tongue and hindleg skeletal muscles from C57BL/6J-dy mice. The TBARS content (702 nmol/g protein) in skeletal muscles from 2-months-old dystrophic mice was increased significantly over that (384 nmol/g protein) in muscles from age-matched normal mice. The H2O2 concentration in dystrophic skeletal muscles was 30% higher than that in normal ones. Microsomal NADPH oxidase activity which was related to the production of superoxide anions, was similar between dystrophic muscles (4.66 nmol/10 min/mg protein) and normal muscles (4.11 nmol/ 10 min/mg protein). These results indicate that oxidation is accelerated in the dystrophic muscles. However, the TBARS content in the tongues of dystrophic mice was identical to that of normal mice. This finding supports our bone-muscle growth imbalance hypothesis for the pathogenesis of mouse muscular dystrophy. 相似文献
59.
60.