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221.
Wong TK Lam TW Yang W Yiu SM 《Journal of bioinformatics and computational biology》2008,6(5):1021-1033
We consider the problem of predicting alternative splicing patterns from a set of expressed sequences (cDNAs and ESTs). Some of these expressed sequences may be errorous, thus forming incorrect exons/introns. These incorrect exons/introns may cause a lot of false positives. For example, we examined a popular alternative splicing database, ECgene, which predicts alternate splicing patterns from expressed sequences. The result shows that about 81.3%-81.6% (sensitivity) of known patterns are found, but the specificity can be as low as 5.9%. Based on the idea that errorous sequences are usually not consistent with other sequences, in this paper we provide an alternative approach for finding alternative splicing patterns which ensures that individual exons/introns of the reported patterns have enough support from the expressed sequences. On the same dataset, our approach can achieve a much higher specificity and a slight increase in sensitivity (38.9% and 84.9%, respectively). Our approach also gives better results compared with popular alternative splicing databases (ASD, ECgene, SpliceNest) and the software ClusterMerge. 相似文献
222.
Aim of study: To examine the resting motor threshold of the tongue in healthy adults and stroke survivors.Methods: Thirty-five healthy adults were classified into three groups: Group 1 (19–38?years; n?=?11), Group 2 (50–64?years; n?=?12) and Group 3 (66–78?years; n?=?12). Six chronic stroke survivors (mean age =59?years, SD?=?9.1?years) were recruited (Group 4). The resting motor thresholds (RMTs) of the tongue were measured and compared (i) among the four groups and (ii) between stroke survivors and age-matched healthy adults.Results: Group 3 showed significantly higher RMTs than Group 1 (p?=?.001) and 2 (p =?0.007). Group 4 showed significantly higher RMTs than Group 1 (p =?.003) and 2 (p?=?.001). The RMTs of Group 3 and 4 were not significantly different (p =?.385). The RMT was positively correlated with age (r?=?0.534; p =?.001). Group 4 showed significantly higher RMTs than the age-matched controls (U?= 2.5, p?=?.009, r?=?0.77).Conclusions: The resting motor threshold of the tongue is significantly increased in adults aged above 65 and in stroke survivors when compared with healthy adults. The findings suggested that the cortical excitability of the tongue deteriorates in the elderly and the stroke population. 相似文献
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Estrogen-induced abnormally high cystic fibrosis transmembrane conductance regulator expression results in ovarian hyperstimulation syndrome 总被引:2,自引:0,他引:2
Ajonuma LC Tsang LL Zhang GH Wong CH Lau MC Ho LS Rowlands DK Zhou CX Ng CP Chen J Xu PH Zhu JX Chung YW Chan HC 《Molecular endocrinology (Baltimore, Md.)》2005,19(12):3038-3044
Ovarian hyperstimulation syndrome (OHSS) remains one of the most life-threatening and potentially fatal complications of assisted reproduction treatments, arising from excessive stimulation of the ovaries by exogenous gonadotropins administrated during in vitro fertilization procedures, which is characterized by massive fluid shift and accumulation in the peritoneal cavity and other organs, including the lungs and the reproductive tract. The pathogenesis of OHSS remains obscure, and no definitive treatments are currently available. Using RT-PCR, Western blot, and electrophysiological techniques we show that cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated chloride channel expressed in many epithelia, is involved in the pathogenesis of OHSS. Upon ovarian hyperstimulation, rats develop OHSS symptoms, with up-regulated CFTR expression and enhanced CFTR channel activity, which can also be mimicked by administration of estrogen, but not progesterone, alone in ovariectomized rats. Administration of progesterone that suppresses CFTR expression or antiserum against CFTR to OHSS animals results in alleviation of the symptoms. Furthermore, ovarian hyperstimulation does not induce detectable OHSS symptoms in CFTR mutant mice. These findings confirm a critical role of CFTR in the pathogenesis of OHSS and may provide grounds for better assisted reproduction treatment strategy to reduce the risk of OHSS and improve in vitro fertilization outcome. 相似文献
225.
Involvement of CFTR in uterine bicarbonate secretion and the fertilizing capacity of sperm 总被引:1,自引:0,他引:1
Wang XF Zhou CX Shi QX Yuan YY Yu MK Ajonuma LC Ho LS Lo PS Tsang LL Liu Y Lam SY Chan LN Zhao WC Chung YW Chan HC 《Nature cell biology》2003,5(10):902-906
Cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-activated chloride channel expressed in a wide variety of epithelial cells, mutations of which are responsible for the hallmark defective chloride secretion observed in cystic fibrosis (CF). Although CFTR has been implicated in bicarbonate secretion, its ability to directly mediate bicarbonate secretion of any physiological significance has not been shown. We demonstrate here that endometrial epithelial cells possess a CFTR-mediated bicarbonate transport mechanism. Co-culture of sperm with endometrial cells treated with antisense oligonucleotide against CFTR, or with bicarbonate secretion-defective CF epithelial cells, resulted in lower sperm capacitation and egg-fertilizing ability. These results are consistent with a critical role of CFTR in controlling uterine bicarbonate secretion and the fertilizing capacity of sperm, providing a link between defective CFTR and lower female fertility in CF. 相似文献
226.
Wise H Chow KB Wing KY Kobayashi T Tse DL Cheng CH 《Journal of receptor and signal transduction research》2003,23(1):83-97
Mouse prostacyclin (mIP) receptors transiently expressed in Chinese hamster ovary (CHO) cells activated both adenylyl cyclase and phospholipase C, with a 33-fold preference for signaling through Gs. The prostacyclin (IP) receptor agonists cicaprost, iloprost, carbacyclin, and prostaglandin E1 showed a similar order of potency for activation of both signaling pathways in cells transiently transfected with the mIP and the chimeric prostacyclin/prostaglandin D2 (IPN-VII/DPC and IPN-V/DPVI-C) receptors. Substitution of the carboxyl-terminal tail of the prostacyclin receptor with the corresponding region of the mDP receptor (IPN-VII/DPC) produced a receptor with increased coupling to both Gs and Gq. However, this increased G-protein coupling was lost in the IPN-V/DPVI-C receptor. The observation that both these chimeric receptors can activate phospholipase C indicates that the carboxyl-terminal tail of the IP receptor is not entirely responsible for its ability to couple to Gq. Site-directed mutagenesis studies suggest that isoleucine at position 323 in the IPN-VII/DPC receptor plays an important role in mediating the increased potency of this chimeric receptor. 相似文献
227.
Elucidation of the c-Jun N-terminal kinase pathway mediated by Estein-Barr virus-encoded latent membrane protein 1 总被引:8,自引:0,他引:8 下载免费PDF全文
Wan J Sun L Mendoza JW Chui YL Huang DP Chen ZJ Suzuki N Suzuki S Yeh WC Akira S Matsumoto K Liu ZG Wu Z 《Molecular and cellular biology》2004,24(1):192-199
Epstein-Barr virus (EBV) is associated with several human diseases including infectious mononucleosis and nasopharyngeal carcinoma. EBV-encoded latent membrane protein 1 (LMP1) is oncogenic and indispensable for cellular transformation caused by EBV. Expression of LMP1 in host cells constitutively activates both the c-Jun N-terminal kinase (JNK) and NF-kappaB pathways, which contributes to the oncogenic effect of LMP1. However, the underlying signaling mechanisms are not very well understood. Based mainly on overexpression studies with various dominant-negative constructs, LMP1 was generally thought to functionally mimic members of the tumor necrosis factor (TNF) receptor superfamily in signaling. In contrast to the prevailing paradigm, using embryonic fibroblasts from different knockout mice and the small interfering RNA technique, we find that the LMP1-mediated JNK pathway is distinct from those mediated by either TNF-alpha or interleukin-1. Moreover, we have further elucidated the LMP1-mediated JNK pathway by demonstrating that LMP1 selectively utilizes TNF receptor-associated factor 6, TAK1/TAB1, and c-Jun N-terminal kinase kinases 1 and 2 to activate JNK. 相似文献
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