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141.
Interaction of translation initiation factor eIF4B with the poliovirus internal ribosome entry site
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Poliovirus translation is initiated at the internal ribosome entry site (IRES). Most likely involving the action of standard initiation factors, this highly structured cis element in the 5" noncoding region of the viral RNA guides the ribosome to an internal silent AUG. The actual start codon for viral protein synthesis further downstream is then reached by ribosomal scanning. In this study we show that two of the secondary structure elements of the poliovirus IRES, domain V and, to a minor extent, domain VI, are the determinants for binding of the eukaryotic initiation factor eIF4B. Several mutations in domain V which are known to greatly affect poliovirus growth also seriously impair the binding of eIF4B. The interaction of eIF4B with the IRES is not dependent on the presence of the polypyrimidine tract-binding protein, which also binds to the poliovirus IRES. In contrast to its weak interaction with cellular mRNAs, eIF4B remains tightly associated with the poliovirus IRES during the formation of complete 80S ribosomes. Binding of eIF4B to the IRES is energy dependent, and binding of the small ribosomal subunit to the IRES requires the previous energy-dependent association of initiation factors with the IRES. These results indicate that the interaction of eIF4B with the 3" region of the poliovirus IRES may be directly involved in translation initiation. 相似文献
142.
Sustained norepinephrine contraction in the rat portal vein is lost when Ca(2+) is replaced with Sr(2+) 总被引:2,自引:0,他引:2
Bonnevier J Malmqvist U Sonntag D Schroeter M Nilsson H Pfitzer G Arner A 《American journal of physiology. Cell physiology》2002,282(4):C845-C852
Agonist-induced activation of smoothmuscle involves a rise in intracellular Ca2+ concentrationand sensitization of myosin light chain phosphorylation toCa2+. Sr2+ can enter through Ca2+channels, be sequestered and released from sarcoplasmic reticulum, andreplace Ca2+ in activation of myosin light chainphosphorylation. Sr2+ cannot replace Ca2+ infacilitation of agonist-activated Ca2+-dependentnonselective cation channels. It is not known whether Sr2+can replace Ca2+ in small G protein-mediated sensitizationof phosphorylation. To explore mechanisms involved in-receptor-activated contractions in smooth muscle, effects ofreplacing Ca2+ with Sr2+ were examined in ratportal vein. Norepinephrine (NE) at >3.0 × 107 Min the presence of Ca2+ resulted in a strong sustainedcontraction, whereas this sustained component was absent in thepresence of Sr2+; only the amplitude of phasic contractionsincreased. Pretreatment with low (~0.05 mM) free Ca2+followed by 2.5 mM Sr2+ resulted in a sustained componentof the NE response. In -escin-permeabilized preparations,phenylephrine in the presence of GTP or guanosine 5'-O-(3-thiotriphosphate) alone induced sensitization toSr2+. In conclusion, a Ca2+-regulatedmembrane/channel process is required for the sustained component of NEresponses in rat portal vein. Sensitization alone is not responsiblefor the sustained phase of the NE contraction. 相似文献
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144.
Yonathan Freund Benjamin Bloom Jerome Bokobza Nacera Baarir Said Laribi Tim Harris Vincent Navarro Maguy Bernard Rupert Pearse Bruno Riou Pierre Hausfater the BISTRO investigators 《PloS one》2015,10(4)
Objective
To evaluate the performance of S100-B protein and copeptin, in addition to clinical variables, in predicting outcomes of patients attending the emergency department (ED) following a seizure.Methods
We prospectively included adult patients presented with an acute seizure, in four EDs in France and the United Kingdom. Participants were followed up for 28 days. The primary endpoint was a composite of seizure recurrence, all-cause mortality, hospitalization or rehospitalisation, or return visit in the ED within seven days.Results
Among the 389 participants included in the analysis, 156 (40%) experienced the primary endpoint within seven days and 195 (54%) at 28 days. Mean levels of both S100-B (0.11 μg/l [95% CI 0.07–0.20] vs 0.09 μg/l [0.07–0.14]) and copeptin (23 pmol/l [9–104] vs 17 pmol/l [8–43]) were higher in participants meeting the primary endpoint. However, both biomarkers were poorly predictive of the primary outcome with a respective area under the receiving operator characteristic curve of 0.57 [0.51–0.64] and 0.59 [0.54–0.64]. Multivariable logistic regression analysis identified higher age (odds ratio [OR] 1.3 per decade [1.1–1.5]), provoked seizure (OR 4.93 [2.5–9.8]), complex partial seizure (OR 4.09 [1.8–9.1]) and first seizure (OR 1.83 [1.1–3.0]) as independent predictors of the primary outcome. A second regression analysis including the biomarkers showed no additional predictive benefit (S100-B OR 3.89 [0.80–18.9] copeptin OR 1 [1.00–1.00]).Conclusion
The plasma biomarkers S100-B and copeptin did not improve prediction of poor outcome following seizure. Higher age, a first seizure, a provoked seizure and a partial complex seizure are independently associated with adverse outcomes. 相似文献145.
IGF‐1 deficiency impairs neurovascular coupling in mice: implications for cerebromicrovascular aging
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Peter Toth Stefano Tarantini Nicole M. Ashpole Zsuzsanna Tucsek Ginger L. Milne Noa M. Valcarcel‐Ares Akos Menyhart Eszter Farkas William E. Sonntag Anna Csiszar Zoltan Ungvari 《Aging cell》2015,14(6):1034-1044
Aging is associated with marked deficiency in circulating IGF‐1, which has been shown to contribute to age‐related cognitive decline. Impairment of moment‐to‐moment adjustment of cerebral blood flow (CBF) via neurovascular coupling is thought to play a critical role in the genesis of age‐related cognitive impairment. To establish the link between IGF‐1 deficiency and cerebromicrovascular impairment, neurovascular coupling mechanisms were studied in a novel mouse model of IGF‐1 deficiency (Igf1f/f‐TBG‐Cre‐AAV8) and accelerated vascular aging. We found that IGF‐1‐deficient mice exhibit neurovascular uncoupling and show a deficit in hippocampal‐dependent spatial memory test, mimicking the aging phenotype. IGF‐1 deficiency significantly impaired cerebromicrovascular endothelial function decreasing NO mediation of neurovascular coupling. IGF‐1 deficiency also impaired glutamate‐mediated CBF responses, likely due to dysregulation of astrocytic expression of metabotropic glutamate receptors and impairing mediation of CBF responses by eicosanoid gliotransmitters. Collectively, we demonstrate that IGF‐1 deficiency promotes cerebromicrovascular dysfunction and neurovascular uncoupling mimicking the aging phenotype, which are likely to contribute to cognitive impairment. 相似文献
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148.
William H. Gmeiner Parag Sahasrabudhe Richard T. Pon Jacque Sonntag Shashikumar Srinivasan Patrick L. Iversen 《Nucleosides, nucleotides & nucleic acids》2013,32(1-2):243-253
Abstract A recursive protection scheme for FdUMP is employed by synthesizing oligonucleotides consisting of only FdU. 3′-O-exonuclease action releases FdUMP and a shortened oligonucleotide from which further exonuclease action releases more FdUMP. Such oligonucleotides are more cytotoxic to H4IIe, mouse fibroblast, and metastatic mouse rumor cells than are equivalent concentrations of FdU monomer. 相似文献
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150.
J?rn Reinders Robert Sonntag Leo Vot Christian Gibney Moritz Nowack Jan Philippe Kretzer 《PloS one》2015,10(3)
Resumption of daily living activities is a basic expectation for patients provided with total knee replacements. However, there is a lack of knowledge regarding the impact of different activities on the wear performance. In this study the wear performance under application of different daily activities has been analyzed. In vivo load data for walking, walking downstairs/upstairs, sitting down/standing up, and cycling (50 W & 120 W) has been standardized for wear testing. Wear testing of each activity was carried out on a knee wear simulator. Additionally, ISO walking was tested for reasons of comparison. Wear was assessed gravimetrically and wear particles were analyzed. In vivo walking produced the highest overall wear rates, which were determined to be three times higher than ISO walking. Moderate wear rates were determined for walking upstairs and downstairs. Low wear rates were determined for standing up/sitting down and cycling at power levels of 50 W and 120 W. The largest wear particles were observed for cycling. Walking based on in vivo data has been shown to be the most wear-relevant activity. Highly demanding activities (stair climbing) produced considerably less wear. Taking into account the expected number of loads, low-impact activities like cycling may have a greater impact on articular wear than highly demanding activities. 相似文献