全文获取类型
收费全文 | 1945篇 |
免费 | 92篇 |
专业分类
2037篇 |
出版年
2023年 | 3篇 |
2022年 | 11篇 |
2021年 | 21篇 |
2020年 | 11篇 |
2019年 | 21篇 |
2018年 | 24篇 |
2017年 | 23篇 |
2016年 | 47篇 |
2015年 | 68篇 |
2014年 | 80篇 |
2013年 | 108篇 |
2012年 | 149篇 |
2011年 | 146篇 |
2010年 | 84篇 |
2009年 | 81篇 |
2008年 | 129篇 |
2007年 | 166篇 |
2006年 | 128篇 |
2005年 | 145篇 |
2004年 | 133篇 |
2003年 | 125篇 |
2002年 | 127篇 |
2001年 | 13篇 |
2000年 | 17篇 |
1999年 | 21篇 |
1998年 | 19篇 |
1997年 | 14篇 |
1996年 | 8篇 |
1995年 | 14篇 |
1994年 | 14篇 |
1993年 | 11篇 |
1992年 | 15篇 |
1991年 | 10篇 |
1990年 | 6篇 |
1989年 | 10篇 |
1988年 | 4篇 |
1987年 | 8篇 |
1986年 | 1篇 |
1985年 | 3篇 |
1984年 | 2篇 |
1983年 | 2篇 |
1982年 | 3篇 |
1981年 | 3篇 |
1980年 | 1篇 |
1979年 | 1篇 |
1978年 | 3篇 |
1976年 | 1篇 |
1971年 | 1篇 |
1966年 | 1篇 |
1958年 | 1篇 |
排序方式: 共有2037条查询结果,搜索用时 15 毫秒
151.
Nanami Senoo Noriyuki Miyoshi Naoko Goto-Inoue Kimiko Minami Ryoji Yoshimura Akihito Morita Naoki Sawada Junichiro Matsuda Yoshihiro Ogawa Mitsutoshi Setou Yasutomi Kamei Shinji Miura 《Journal of lipid research》2015,56(12):2286-2296
Exercise training influences phospholipid fatty acid composition in skeletal muscle and these changes are associated with physiological phenotypes; however, the molecular mechanism of this influence on compositional changes is poorly understood. Peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), a nuclear receptor coactivator, promotes mitochondrial biogenesis, the fiber-type switch to oxidative fibers, and angiogenesis in skeletal muscle. Because exercise training induces these adaptations, together with increased PGC-1α, PGC-1α may contribute to the exercise-mediated change in phospholipid fatty acid composition. To determine the role of PGC-1α, we performed lipidomic analyses of skeletal muscle from genetically modified mice that overexpress PGC-1α in skeletal muscle or that carry KO alleles of PGC-1α. We found that PGC-1α affected lipid profiles in skeletal muscle and increased several phospholipid species in glycolytic muscle, namely phosphatidylcholine (PC) (18:0/22:6) and phosphatidylethanolamine (PE) (18:0/22:6). We also found that exercise training increased PC (18:0/22:6) and PE (18:0/22:6) in glycolytic muscle and that PGC-1α was required for these alterations. Because phospholipid fatty acid composition influences cell permeability and receptor stability at the cell membrane, these phospholipids may contribute to exercise training-mediated functional changes in the skeletal muscle. 相似文献
152.
153.
154.
Miyata Seiko Noda Akiko Iwamoto Kunihiro Kawano Naoko Banno Masahiro Tsuruta Yoshiyuki Noda Yukihiro Ozaki Norio 《Sleep and biological rhythms》2015,13(4):387-394
Sleep and Biological Rhythms - Chronic sleep restriction adversely effects cognitive performance and mood, resulting in accidents and economic loss. We examined the effects of three nights of sleep... 相似文献
155.
156.
Emerging evidence indicates that R4/B subfamily RGS (regulator of G protein signaling) proteins play roles in functional regulation in the cardiovascular system. In this study, we compared effects of three R4/B subfamily proteins, RGS2, RGS4 and RGS5 on angiotensin AT1 receptor signaling, and investigated roles of the N-terminus of RGS2. In HEK293T cells expressing AT1 receptor stably, intracellular Ca2+ responses induced by angiotensin II were much more strongly attenuated by RGS2 than by RGS4 and RGS5. N-terminally deleted RGS2 proteins lost this potent inhibitory effect. Replacement of the N-terminal residues 1-71 of RGS2 with the corresponding residues (1-51) of RGS5 decreased significantly the inhibitory effect. On the other hand, replacement of the residues 1-51 of RGS5 with the residues 1-71 of RGS2 increased the inhibitory effect dramatically. Furthermore, we investigated functional contribution of N-terminal subdomains of RGS2, namely, an N-terminal region (residues 16-55) with an amphipathic α helix domain (the subdomain N1), a probable non-specific membrane-targeting subdomain, and another region (residues 56-71) between the α helix and the RGS box (the subdomain N2), a probable GPCR-recognizing subdomain. RGS2 chimera proteins with the residues 1-33 or 34-52 of RGS5 showed weak inhibitory activity, and either of RGS5 chimera proteins with residues 1-55 or 56-71 of RGS2 showed strong inhibitory effects on AT1 receptor signaling. The present study indicates the essential roles of both N-terminal subdomains for the potent inhibitory activity of RGS2 on AT1 receptor signaling. 相似文献
157.
Ueno R Hamada-Sato N Ishida M Urano N 《Bioscience, biotechnology, and biochemistry》2011,75(9):1654-1661
Apart from Xanthophyllomyces dendrorhous, pink colony-forming yeasts have not been examined as a pigmentation source in captive animals. In this study, aquatic yeasts were screened with a view to abundances of carotenoids. Phylogenetic analyses of these caroetnoid-rich yeasts based on large subunit ribosomal RNA gene (LSU rDNA) partial sequences showed that all belonged to the order Sporidiobolales. Both the qualitative and the quantitative differences in carotenoids between the yeasts appeared to be consistent with their phylogenetic affiliations. This information might be useful in the selection of pigment-rich yeasts containing specific carotenoids from a large number of strains. We also found, for the first time, the potential of a pigment-rich Rhodotorula strain as a colorant for aquaculture. The integuments of tilapia and carp fed the alkali-treated cells of strain Rhodotorula dairenensis Sag 17 were pigmented after 3 months of cultivation. The fish integuments retained the yeast carotenes shortly after the start of feeding, and were converted to the fish-specific xanthophylls in vivo. 相似文献
158.
Mizuhara N Kuroda M Ogita A Tanaka T Usuki Y Fujita K 《Bioorganic & medicinal chemistry》2011,19(18):5300-5310
Cyclothiazomycin B1 (CTB1) is an antifungal cyclic thiopeptide isolated from the culture broth of Streptomyces sp. HA 125-40. CTB1 inhibited the growth of several filamentous fungi including plant pathogens along with swelling of hyphae and spores. The antifungal activity of CTB1 was weakened by hyperosmotic conditions, and hyphae treated with CTB1 burst under hypoosmotic conditions, indicating increased cell wall fragility. CTB1-sensitive fungal species contain high levels of cell wall chitin and/or chitosan. Unlike nikkomycin Z, a competitive inhibitor of chitin synthase (CHS), CTB1 did not inhibit CHS activity. Although CTB1 inhibited CHS biosynthesis, the same result was also obtained with a non-specific proteins inhibitor, cycloheximide, which did not reduce cell wall rigidity. These results indicate that the primary target of CTB1 is not CHS, and we concluded that CTB1 antifungal activity was independent of this sole inhibition. We found that CTB1 bound to chitin but did not bind to β-glucan and chitosan. The results of the present study suggest that CTB1 induces cell wall fragility by binding to chitin, which forms the fungal cell wall. The antifungal activity of CTB1 could be explained by this chitin-binding ability. 相似文献
159.
160.
A Uto-Konomi K Miyauchi N Ozaki Y Motomura Y Suzuki A Yoshimura S Suzuki D Cua M Kubo 《PloS one》2012,7(7):e40343
Homeostatic regulation of epidermal keratinocytes is controlled by the local cytokine milieu. However, a role for suppressor of cytokine signaling (SOCS), a negative feedback regulator of cytokine networks, in skin homeostasis remains unclear. Keratinocyte specific deletion of Socs3 (Socs3 cKO) caused severe skin inflammation with hyper-production of IgE, epidermal hyperplasia, and S100A8/9 expression, although Socs1 deletion caused no inflammation. The inflamed skin showed constitutive STAT3 activation and up-regulation of IL-6 and IL-20 receptor (IL-20R) related cytokines, IL-19, IL-20 and IL-24. Disease development was rescued by deletion of the Il6 gene, but not by the deletion of Il23, Il4r, or Rag1 genes. The expression of IL-6 in Socs3 cKO keratinocytes increased expression of IL-20R-related cytokines that further facilitated STAT3 hyperactivation, epidermal hyperplasia and neutrophilia. These results demonstrate that skin homeostasis is strictly regulated by the IL-6-STAT3-SOCS3 axis. Moreover, the SOCS3-mediated negative feedback loop in keratinocytes has a critical mechanistic role in the prevention of skin inflammation caused by hyperactivation of STAT3. 相似文献