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1.
Mohammad-Panah Raha; Demolombe Sophie; Riochet David; Leblais Veronique; Loussouarn Gildas; Pollard Helene; Baro Isabelle; Escande Denis 《American journal of physiology. Cell physiology》1998,274(2):C310
We investigated whether high levels of expression of the cysticfibrosis transmembrane conductance regulator (CFTR) would alter thefunctional properties of newly synthesized recombinant proteins. COS-7,CFPAC-1, and A549 cells were intranuclearly injected with a Simianvirus 40-driven pECE-CFTR plasmid and assayed for halide permeabilityusing the6-methoxy-N-(3-sulfopropyl)quinolinium fluorescent probe. With increasing numbers of microinjected pECE-CFTR copies, the baseline permeability to halide dose dependently increased, and the response to adenosine 3',5'-cyclic monophosphate(cAMP) stimulation decreased. In cells hyperexpressing CFTR, the high level of halide permeability was reduced when a cell metabolism poisoning cocktail was applied to decrease intracellular ATP and, inversely, was increased by orthovanadate. In CFPAC-1 cellsinvestigated with the patch-clamp technique, CFTR hyperexpression ledto a time-independent nonrectifying chloride current that was notsensitive to cAMP stimulation. CFPAC-1 cells hyperexpressing CFTRexhibited no outward rectifying chloride current nor inward rectifyingpotassium current either spontaneously or under cAMP stimulation. Weconclude that hyperexpression of recombinant CFTR proteins modifiestheir properties inasmuch as 1) CFTRchannels are permanently activated and not susceptible to cAMPregulation and 2) they lose their capacity to regulate heterologous ionic channels. 相似文献
2.
Nina Bertaux-Skeirik Rui Feng Michael A. Schumacher Jing Li Maxime M. Mahe Amy C. Engevik Jose E. Javier Richard M. Peek Jr Karen Ottemann Veronique Orian-Rousseau Gregory P. Boivin Michael A. Helmrath Yana Zavros 《PLoS pathogens》2015,11(2)
The cytotoxin-associated gene (Cag) pathogenicity island is a strain-specific
constituent of Helicobacter pylori (H. pylori) that
augments cancer risk. CagA translocates into the cytoplasm where it stimulates cell
signaling through the interaction with tyrosine kinase c-Met receptor, leading
cellular proliferation. Identified as a potential gastric stem cell marker,
cluster-of-differentiation (CD) CD44 also acts as a co-receptor for c-Met, but
whether it plays a functional role in H. pylori-induced epithelial
proliferation is unknown. We tested the hypothesis that CD44 plays a functional role
in H. pylori-induced epithelial cell proliferation. To assay changes
in gastric epithelial cell proliferation in relation to the direct interaction with
H. pylori, human- and mouse-derived gastric organoids were
infected with the G27 H. pylori strain or a mutant G27 strain
bearing cagA deletion (∆CagA::cat). Epithelial proliferation
was quantified by EdU immunostaining. Phosphorylation of c-Met was analyzed by
immunoprecipitation followed by Western blot analysis for expression of CD44 and
CagA. H. pylori infection of both mouse- and human-derived gastric
organoids induced epithelial proliferation that correlated with c-Met
phosphorylation. CagA and CD44 co-immunoprecipitated with phosphorylated c-Met. The
formation of this complex did not occur in organoids infected with
∆CagA::cat. Epithelial proliferation in response to
H. pylori infection was lost in infected organoids derived from
CD44-deficient mouse stomachs. Human-derived fundic gastric organoids exhibited an
induction in proliferation when infected with H. pylorithat was not
seen in organoids pre-treated with a peptide inhibitor specific to CD44. In the
well-established Mongolian gerbil model of gastric cancer, animals treated with CD44
peptide inhibitor Pep1, resulted in the inhibition of H.
pylori-induced proliferation and associated atrophic gastritis. The current
study reports a unique approach to study H. pylori interaction with
the human gastric epithelium. Here, we show that CD44 plays a functional role in
H. pylori-induced epithelial cell proliferation. 相似文献
3.
Although diabetes has been identified as a major risk factor for atrial fibrillation, little is known about glucose metabolism in the healthy and diabetic atria. Glucose transport into the cell, the rate-limiting step of glucose utilization, is regulated by the Glucose Transporters (GLUTs). Although GLUT4 is the major isoform in the heart, GLUT8 has recently emerged as a novel cardiac isoform. We hypothesized that GLUT-4 and -8 translocation to the atrial cell surface will be regulated by insulin and impaired during insulin-dependent diabetes. GLUT protein content was measured by Western blotting in healthy cardiac myocytes and type 1 (streptozotocin-induced, T1Dx) diabetic rodents. Active cell surface GLUT content was measured using a biotinylated photolabeled assay in the perfused heart. In the healthy atria, insulin stimulation increased both GLUT-4 and -8 translocation to the cell surface (by 100% and 240%, respectively, P<0.05). Upon insulin stimulation, we reported an increase in Akt (Th308 and s473 sites) and AS160 phosphorylation, which was positively (P<0.05) correlated with GLUT4 protein content in the healthy atria. During diabetes, active cell surface GLUT-4 and -8 content was downregulated in the atria (by 70% and 90%, respectively, P<0.05). Akt and AS160 phosphorylation was not impaired in the diabetic atria, suggesting the presence of an intact insulin signaling pathway. This was confirmed by the rescued translocation of GLUT-4 and -8 to the atrial cell surface upon insulin stimulation in the atria of type 1 diabetic subjects. In conclusion, our data suggest that: 1) both GLUT-4 and -8 are insulin-sensitive in the healthy atria through an Akt/AS160 dependent pathway; 2) GLUT-4 and -8 trafficking is impaired in the diabetic atria and rescued by insulin treatment. Alterations in atrial glucose transport may induce perturbations in energy production, which may provide a metabolic substrate for atrial fibrillation during diabetes. 相似文献
4.
Elena Marinova Sandy P. Harrison Fran Bragg Simon Connor Veronique de Laet Suzanne A.G. Leroy Petra Mudie Juliana Atanassova Elissaveta Bozilova Hülya Caner Carlos Cordova Morteza Djamali Mariana Filipova‐Marinova Natalia Gerasimenko Susanne Jahns Katerina Kouli Ulrich Kotthoff Eliso Kvavadze Maria Lazarova Elena Novenko Elias Ramezani Astrid Röpke Lyudmila Shumilovskikh Ioan Tanţǎu Spassimir Tonkov 《Journal of Biogeography》2018,45(2):484-499
5.
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7.
Braden Kuo Manoj Bhasin Jolene Jacquart Matthew A. Scult Lauren Slipp Eric Isaac Kagan Riklin Veronique Lepoutre Nicole Comosa Beth-Ann Norton Allison Dassatti Jessica Rosenblum Andrea H. Thurler Brian C. Surjanhata Nicole N. Hasheminejad Leslee Kagan Ellen Slawsby Sowmya R. Rao Eric A. Macklin Gregory L. Fricchione Herbert Benson Towia A. Libermann Joshua Korzenik John W. Denninger 《PloS one》2015,10(4)
8.
The red death meets the abdominal bristle: Polygenic mutation for susceptibility to a bacterial pathogen in Caenorhabditis elegans 下载免费PDF全文
Veronique Etienne Erik C. Andersen José Miguel Ponciano Dustin Blanton Analucia Cadavid Joanna Joyner‐Matos Chikako Matsuba Brandon Tabman Charles F. Baer 《Evolution; international journal of organic evolution》2015,69(2):508-519
Understanding the genetic basis of susceptibility to pathogens is an important goal of medicine and of evolutionary biology. A key first step toward understanding the genetics and evolution of any phenotypic trait is characterizing the role of mutation. However, the rate at which mutation introduces genetic variance for pathogen susceptibility in any organism is essentially unknown. Here, we quantify the per‐generation input of genetic variance by mutation (VM) for susceptibility of Caenorhabditis elegans to the pathogenic bacterium Pseudomonas aeruginosa (defined as the median time of death, LT50). VM for LT50 is slightly less than VM for a variety of life‐history and morphological traits in this strain of C. elegans, but is well within the range of reported values in a variety of organisms. Mean LT50 did not change significantly over 250 generations of mutation accumulation. Comparison of VM to the standing genetic variance (VG) implies a strength of selection against new mutations of a few tenths of a percent. These results suggest that the substantial standing genetic variation for susceptibility of C. elegans to P. aeruginosa can be explained by polygenic mutation coupled with purifying selection. 相似文献
9.
Blood and cloacal swab sampling for avian influenza monitoring has no effect on survival rates of free‐ranging ducks 下载免费PDF全文
Matthieu Guillemain Jocelyn Champagnon Marie‐Lucile Gourlay‐Larour Francois Cavallo Anne‐Laure Brochet Jean Hars Gregoire Massez Thierry George Pierre‐Yves Perroi Veronique Jestin Alain Caizergues 《Ibis》2015,157(4):743-753
Concerns about the spread of avian influenza viruses (AIVs) have led to cloacal swab sampling of hundreds of thousands of birds worldwide as part of AIV surveillance schemes, but the effects of cloacal swabbing have not been adequately evaluated. We tested for differences between swabbed, swabbed and bled, and non‐sampled wild ducks in terms of live re‐encounter and dead recoveries for Common Pochard Aythya ferina and Tufted Duck Aythya fuligula, and also determined re‐encounter and recovery rates for Mallard Anas platyrhynchos and Common Teal Anas crecca. No effects of sampling methods were detected, except in Teal. Re‐encounter rates were lower in sampled Teal than in controls, with annual re‐encounter probabilities being 25% and 35% lower in males and females, respectively. Teal possibly left or avoided sampling sites, or sought sites where they were less detectable after sampling. In general, no deleterious effects were found, suggesting that cloacal swabbing and blood sampling are suitable methods for conducting AIV surveillance in ducks. 相似文献
10.