全文获取类型
收费全文 | 1099篇 |
免费 | 60篇 |
出版年
2022年 | 4篇 |
2021年 | 6篇 |
2020年 | 8篇 |
2019年 | 9篇 |
2018年 | 13篇 |
2017年 | 10篇 |
2016年 | 15篇 |
2015年 | 35篇 |
2014年 | 43篇 |
2013年 | 45篇 |
2012年 | 61篇 |
2011年 | 45篇 |
2010年 | 39篇 |
2009年 | 31篇 |
2008年 | 61篇 |
2007年 | 56篇 |
2006年 | 50篇 |
2005年 | 55篇 |
2004年 | 61篇 |
2003年 | 55篇 |
2002年 | 60篇 |
2001年 | 49篇 |
2000年 | 45篇 |
1999年 | 27篇 |
1998年 | 18篇 |
1997年 | 20篇 |
1996年 | 5篇 |
1995年 | 11篇 |
1994年 | 15篇 |
1993年 | 7篇 |
1992年 | 14篇 |
1991年 | 18篇 |
1990年 | 6篇 |
1989年 | 14篇 |
1988年 | 10篇 |
1987年 | 17篇 |
1986年 | 12篇 |
1985年 | 12篇 |
1984年 | 9篇 |
1983年 | 11篇 |
1982年 | 11篇 |
1981年 | 7篇 |
1980年 | 10篇 |
1979年 | 8篇 |
1978年 | 7篇 |
1977年 | 7篇 |
1976年 | 7篇 |
1973年 | 4篇 |
1970年 | 4篇 |
1969年 | 4篇 |
排序方式: 共有1159条查询结果,搜索用时 15 毫秒
1.
A Nicotiana tabacum cell line, KS-1, which is tolerant to morethan 1% NaCl, was treated with buthiobate. The cells accumulated14a-methylsterols such as obtusifoliol, instead of campesteroland sitosterol. The buthiobate-treated cells lost their salttolerance. These results suggest that the buthiobate-inducedsalt sensitivity is closely associated with changes in the molecularspecies of sterols in the cell membranes. (Received October 16, 1986; Accepted April 13, 1987) 相似文献
2.
3.
Morphology and function of the nervous system is maintained via well-coordinated processes both in central and peripheral nervous tissues, which govern the homeostasis of organs/tissues. Impairments of the nervous system induce neuronal disorders such as peripheral neuropathy or cardiac arrhythmia. Although further investigation is warranted to reveal the molecular mechanisms of progression in such diseases, appropriate model systems mimicking the patient-specific communication between neurons and organs are not established yet. In this study, we reconstructed the neuronal network in vitro either between neurons of the human induced pluripotent stem (iPS) cell derived peripheral nervous system (PNS) and central nervous system (CNS), or between PNS neurons and cardiac cells in a morphologically and functionally compartmentalized manner. Networks were constructed in photolithographically microfabricated devices with two culture compartments connected by 20 microtunnels. We confirmed that PNS and CNS neurons connected via synapses and formed a network. Additionally, calcium-imaging experiments showed that the bundles originating from the PNS neurons were functionally active and responded reproducibly to external stimuli. Next, we confirmed that CNS neurons showed an increase in calcium activity during electrical stimulation of networked bundles from PNS neurons in order to demonstrate the formation of functional cell-cell interactions. We also confirmed the formation of synapses between PNS neurons and mature cardiac cells. These results indicate that compartmentalized culture devices are promising tools for reconstructing network-wide connections between PNS neurons and various organs, and might help to understand patient-specific molecular and functional mechanisms under normal and pathological conditions. 相似文献
4.
5.
Kaori Ishikawa Kazuto Nakada 《Biochimica et Biophysica Acta (BBA)/General Subjects》2021,1865(3):129835
BackgroundMitochondrial disease is a general term for a disease caused by a decline in mitochondrial function. The pathology of this disease is extremely diverse and complex, and the mechanism of its pathogenesis is still unknown. Using mouse models that develop the disease via the same processes as in humans is the easiest path to understanding the underlying mechanism. However, creating a mouse model is extremely difficult due to the lack of technologies that enable editing of mitochondrial DNA (mtDNA).Scope of reviewThis paper outlines the complex pathogenesis of mitochondrial disease, and the difficulties in producing relevant mouse models. Then, the paper provides a detailed discussion on several mice created with mutations in mtDNA. The paper also introduces the pathology of mouse models with mutations including knockouts of nuclear genes that directly affect mitochondrial function.Major conclusionsSeveral mice with mtDNA mutations and those with nuclear DNA mutations have been established. Although these models help elucidate the pathological mechanism of mitochondrial disease, they lack sufficient diversity to enable a complete understanding. Considering the variety of factors that affect the cause and mechanism of mitochondrial disease, it is necessary to account for this background diversity in mouse models as well.General significanceMouse models are indispensable for understanding the pathological mechanism of mitochondrial disease, as well as for searching new treatments. There is a need for the creation and examination of mouse models with more diverse mutations and altered nuclear backgrounds and breeding environments. 相似文献
6.
7.
A mouse macrophage clone (line nH-1) transformed by simian virus 40 (SV40) was examined by electron microscopy. In the growing phase of the cultures, NH-1 cells were non-phagocytic and SV40 T antigen-positive, and contained a large number of filament sheaths within their pseudopodia. In the late stationary phase, they became phagocytic, SV40 T antigen-negative and contained a filamentous network within their psudopodia. In addition, NH-1 cells in the late stationary phase were very similar to normal macrophages in other morphological properties. 相似文献
8.
9.
Ryutaro Kakinuma Noriyuki Moriyama Yukio Muramatsu Shiho Gomi Masahiro Suzuki Hirobumi Nagasawa Masahiko Kusumoto Tomohiko Aso Yoshihisa Muramatsu Takaaki Tsuchida Koji Tsuta Akiko Miyagi Maeshima Naobumi Tochigi Shun-ichi Watanabe Naoki Sugihara Shinsuke Tsukagoshi Yasuo Saito Masahiro Kazama Kazuto Ashizawa Kazuo Awai Osamu Honda Hiroyuki Ishikawa Naoya Koizumi Daisuke Komoto Hiroshi Moriya Seitaro Oda Yasuji Oshiro Masahiro Yanagawa Noriyuki Tomiyama Hisao Asamura 《PloS one》2015,10(12)
10.
Tsutomu Murakami Tsutomu Yoshikawa Yuichiro Maekawa Tetsuro Ueda Toshiaki Isogai Konomi Sakata Ken Nagao Takeshi Yamamoto Morimasa Takayama 《PloS one》2015,10(8)