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排序方式: 共有102条查询结果,搜索用时 203 毫秒
1.
Koda Ryosuke Agetsuma Naoki Agetsuma-Yanagihara Yoshimi Tsujino Riyou Fujita Noboru 《Ecological Research》2011,26(1):227-231
The accuracy of estimating deer density using the fecal pellet count method is greatly limited by variability of the fecal
decomposition rate. The fecal accumulation rate technique can avoid the issue of decomposition rate. However, the precision
of this technique is not clear when the decomposition rate is relatively high, such as in Japanese forests. We estimated deer
population densities on Yakushima Island by the fecal accumulation rate technique and compared them between seasons. The estimated
densities were similar to reported estimates, and did not differ seasonally, in accord with reports that deer on Yakushima
do not migrate seasonally. Thus, we conclude that the fecal accumulation rate technique is applicable in Japanese forests. 相似文献
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Yoshiyuki Sato Yu Onozaki Tetsuya Sugimoto Hideki Kurihara Kaori Kamijo Chie Kadowaki Toshiaki Tsujino Akiko Watanabe Sachie Otsuki Morihiro Mitsuya Masato Iida Kyosuke Haze Takumitsu Machida Yoko Nakatsuru Hideya Komatani Hidehito Kotani Yoshikazu Iwasawa 《Bioorganic & medicinal chemistry letters》2009,19(16):4673-4678
A novel class of imidazopyridine derivatives was designed as PLK1 inhibitors. Extensive SAR studies supported by molecular modeling afforded a highly potent and selective compound 36. Compound 36 demonstrated good antitumor efficacy in xenograft nude rat model. 相似文献
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Natsuko Tsujino Tomomi Tsunematsu Motokazu Uchigashima Kohtarou Konno Akihiro Yamanaka Kazuto Kobayashi Masahiko Watanabe Yoshimasa Koyama Takeshi Sakurai 《PloS one》2013,8(7)
Narcolepsy patients often suffer from insomnia in addition to excessive daytime sleepiness. Narcoleptic animals also show behavioral instability characterized by frequent transitions between all vigilance states, exhibiting very short bouts of NREM sleep as well as wakefulness. The instability of wakefulness states in narcolepsy is thought to be due to deficiency of orexins, neuropeptides produced in the lateral hypothalamic neurons, which play a highly important role in maintaining wakefulness. However, the mechanism responsible for sleep instability in this disorder remains to be elucidated. Because firing of orexin neurons ceases during sleep in healthy animals, deficiency of orexins does not explain the abnormality of sleep. We hypothesized that chronic compensatory changes in the neurophysiologica activity of the locus coeruleus (LC) and dorsal raphe (DR) nucleus in response to the progressive loss of endogenous orexin tone underlie the pathological regulation of sleep/wake states. To evaluate this hypothesis, we examined firing patterns of serotonergic (5-HT) neurons and noradrenergic (NA) neurons in the brain stem, two important neuronal populations in the regulation of sleep/wakefulness states. We recorded single-unit activities of 5-HT neurons and NA neurons in the DR nucleus and LC of orexin neuron-ablated narcoleptic mice. We found that while the firing pattern of 5-HT neurons in narcoleptic mice was similar to that in wildtype mice, that of NA neurons was significantly different from that in wildtype mice. In narcoleptic mice, NA neurons showed a higher firing frequency during both wakefulness and NREM sleep as compared with wildtype mice. In vitro patch-clamp study of NA neurons of narcoleptic mice suggested a functional decrease of GABAergic input to these neurons. These alterations might play roles in the sleep abnormality in narcolepsy. 相似文献
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Yoshiro Naito Hisashi Sawada Makiko Oboshi Aya Fujii Shinichi Hirotani Toshihiro Iwasaku Yoshitaka Okuhara Akiyo Eguchi Daisuke Morisawa Mitsumasa Ohyanagi Takeshi Tsujino Tohru Masuyama 《PloS one》2013,8(10)
Although iron is reported to be associated with the pathogenesis of chronic kidney disease, it is unknown whether iron participates in the pathophysiology of nephrosclerosis. Here, we investigate whether iron is involved in the development of hypertensive nephropathy and the effects of iron restriction on nephrosclerosis in salt- loaded stroke-prone spontaneously hypertensive rats (SHRSP). SHRSP were given either a normal or high-salt diet for 8 weeks. Another subset of SHRSP were fed a high-salt with iron-restricted diet. SHRSP given a high-salt diet developed severe hypertension and nephrosclerosis. As a result, survival rate was decreased after 8 weeks diet. Importantly, massive iron accumulation and increased iron content were observed in the kidneys of salt-loaded SHRSP, along with increased superoxide production, urinary 8-Hydroxy-2′-deoxyguanosine excretion, and urinary iron excretion; however, these changes were markedly attenuated by iron restriction. Of interest, expression of cellular iron transport proteins, transferrin receptor 1 and divalent metal transporter 1, was increased in the tubules of salt-loaded SHRSP. Notably, iron restriction attenuated the development of severe hypertension and nephrosclerosis, thereby improving survival rate in salt-loaded SHRSP. Taken together, these results suggest a novel mechanism by which iron plays a role in the development of hypertensive nephropathy and establish the effects of iron restriction on salt-induced nephrosclerosis. 相似文献
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Toshio Naka Takashi Doi Takeshi Tsujino Tohru Masuyama Seinosuke Kawashima 《Preparative biochemistry & biotechnology》2013,43(2):87-99
Abstract Viral vector systems are efficient for transfection of foreign genes into many tissues. Especially, retrovirus based vectors integrate the transgene into the genome of the target cells, which can sustain long term expression. However, it has been demonstrated that the transduction efficiency using retrovirus is relatively lower than those of other viruses. Ultrasound was recently reported to increase gene expression using plasmid DNA, with or without, a delivery vehicle. However, there are no reports, which show an ultrasound effect to retrovirus‐mediated gene transfer efficiency. Retrovirus‐mediated gene transfer systems were used for transfection of 293T cells, bovine aortic endothelial cells (BAECs), rat aortic smooth muscle cells (RASMCs), and rat skeletal muscle myoblasts (L6 cells) with β‐galactosidase (β‐Gal) genes. Transduction efficiency and cell viability assay were performed on 293T cells that were exposed to varying durations (5 to 30 seconds) and power levels (1.0 watts/cm2 to 4.0 watts/cm2) of ultrasound after being transduced by a retrovirus. Effects of ultrasound to the retrovirus itself was evaluated by transduction efficiency of 293T cells. After exposure to varying power levels of ultrasound to a retrovirus for 5 seconds, 293T cells were transduced by a retrovirus, and transduction efficiency was evaluated. Below 1.0 watts/cm2 and 5 seconds exposure, ultrasound showed increased transduction efficiency and no cytotoxicity to 293T cells transduced by a retrovirus. Also, ultrasound showed no toxicity to the virus itself at the same condition. Exposure of 5 seconds at the power of 1.0 watts/cm2 of an ultrasound resulted in significant increases in retrovirus‐mediated gene expression in all four cell types tested in this experiment. Transduction efficiencies by ultrasound were enhanced 6.6‐fold, 4.8‐fold, 2.3‐fold, and 3.2‐fold in 293T cells, BAECs, RASMCs, and L6 cells, respectively. Furthermore, β‐Gal activities were also increased by the retrovirus with ultrasound exposure in these cells. Adjunctive ultrasound exposure was associated with enhanced retrovirus‐mediated transgene expression in vitro. Ultrasound associated local gene therapy has potential for not only plasmid‐DNA‐, but also retrovirus‐mediated gene transfer. 相似文献
7.
Rapsyn Mutations in Humans Cause Endplate Acetylcholine-Receptor Deficiency and Myasthenic Syndrome 总被引:11,自引:0,他引:11 下载免费PDF全文
Kinji Ohno Andrew G. Engel Xin-Ming Shen Duygu Selcen Joan Brengman C. Michel Harper Akira Tsujino Margherita Milone 《American journal of human genetics》2002,70(4):875-885
Congenital myasthenic syndromes (CMSs) stem from genetic defects in endplate (EP)-specific presynaptic, synaptic, and postsynaptic proteins. The postsynaptic CMSs identified to date stem from a deficiency or kinetic abnormality of the acetylcholine receptor (AChR). All CMSs with a kinetic abnormality of AChR, as well as many CMSs with a deficiency of AChR, have been traced to mutations in AChR-subunit genes. However, in a subset of patients with EP AChR deficiency, the genetic defect has remained elusive. Rapsyn, a 43-kDa postsynaptic protein, plays an essential role in the clustering of AChR at the EP. Seven tetratricopeptide repeats (TPRs) of rapsyn subserve self-association, a coiled-coil domain binds to AChR, and a RING-H2 domain associates with beta-dystroglycan and links rapsyn to the subsynaptic cytoskeleton. Rapsyn self-association precedes recruitment of AChR to rapsyn clusters. In four patients with EP AChR deficiency but with no mutations in AChR subunits, we identify three recessive rapsyn mutations: one patient carries L14P in TPR1 and N88K in TPR3; two are homozygous for N88K; and one carries N88K and 553ins5, which frameshifts in TPR5. EP studies in each case show decreased staining for rapsyn and AChR, as well as impaired postsynaptic morphological development. Expression studies in HEK cells indicate that none of the mutations hinders rapsyn self-association but that all three diminish coclustering of AChR with rapsyn. 相似文献
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Taku Watanabe Ichizo Tsujino Satoshi Konno Yoichi M. Ito Chisa Takashina Takahiro Sato Akira Isada Hiroshi Ohira Yoshinori Ohtsuka Yuma Fukutomi Hiroyuki Nakamura Yukio Kawagishi Chiharu Okada Nobuyuki Hizawa Masami Taniguchi Akira Akasawa Masaharu Nishimura 《PloS one》2016,11(3)