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排序方式: 共有579条查询结果,搜索用时 17 毫秒
21.
John A. Martignetti Lifeng Tian Dong Li Maria Celeste M. Ramirez Olga Camacho-Vanegas Sandra Catalina Camacho Yiran Guo Dina J. Zand Audrey M. Bernstein Sandra K. Masur Cecilia E. Kim Frederick G. Otieno Cuiping Hou Nada Abdel-Magid Ben Tweddale Denise Metry Jean-Christophe Fournet Eniko Papp Elizabeth W. McPherson Carrie Zabel Guy Vaksmann Cyril Morisot Brendan Keating Patrick M. Sleiman Jeffrey A. Cleveland David B. Everman Elaine Zackai Hakon Hakonarson 《American journal of human genetics》2013
22.
Yee?Him Cheung Tenzin Gayden Philippe?M. Campeau Charles?A. LeDuc Donna Russo Van-Hung Nguyen Jiancheng Guo Ming Qi Yanfang Guan Steffen Albrecht Brenda Moroz Karen?W. Eldin James?T. Lu Jeremy Schwartzentruber David Malkin Albert?M. Berghuis Sherif Emil Richard?A. Gibbs David?L. Burk Megan Vanstone Brendan?H. Lee David Orchard Kym?M. Boycott Wendy?K. Chung Nada Jabado 《American journal of human genetics》2013,92(6):996-1000
Infantile myofibromatosis (IM) is the most common benign fibrous tumor of soft tissues affecting young children. By using whole-exome sequencing, RNA sequencing, and targeted sequencing, we investigated germline and tumor DNA in individuals from four distinct families with the familial form of IM and in five simplex IM cases with no previous family history of this disease. We identified a germline mutation c.1681C>T (p.Arg561Cys) in platelet-derived growth factor receptor β (PDGFRB) in all 11 affected individuals with familial IM, although none of the five individuals with nonfamilial IM had mutations in this gene. We further identified a second heterozygous mutation in PDGFRB in two myofibromas from one of the affected familial cases, indicative of a potential second hit in this gene in the tumor. PDGFR-β promotes growth of mesenchymal cells, including blood vessels and smooth muscles, which are affected in IM. Our findings indicate p.Arg561Cys substitution in PDGFR-β as a cause of the dominant form of this disease. They provide a rationale for further investigations of this specific mutation and gene to assess the benefits of targeted therapies against PDGFR-β in aggressive life-threatening familial forms of the disease. 相似文献
23.
Imane Sabaouni Ahmed Moussa Brigitte Vannier Oussama Semlali Terri A Pietka Nada A Abumrad Azeddine Ibrahimi 《Bioinformation》2013,9(17):849-852
We have previously shown that CD36 is a membrane protein that facilitates long chain fatty acid (FA) transport by muscle tissues.
We also documented the significant impact of muscle CD36 expression on heart function, skeletal muscle insulin sensitivity as well
as on overall metabolism. To identify a comprehensive set of genes that are differentially regulated by CD36 expression in the
heart, we used two microarray technologies (Affymetrix and Agilent) to compare gene expression in heart tissues from CD36
KnocK-Out (KO-CD36) versus wild type (WT-CD36) mice. The obtained results using the two technologies were similar with
around 35 genes differentially expressed using both technologies. Absence of CD36 led to down-regulation of the expression of
three groups of genes involved in pathways of FA metabolism, angiogenesis/apoptosis and structure. These data are consistent
with the fact that the CD36 protein binds FA and thrombospondin 1 invoved respectively in lipid metabolism and anti-angiogenic
activities. In conclusion, our findings led to validate our data analysis workflow and identify specific pathways, possibly
underlying the phenotypic abnormalities in CD36 Knock -Out hearts. 相似文献
24.
Ying Zhu Stuart G. Dashper Yu-Yen Chen Simon Crawford Nada Slakeski Eric C. Reynolds 《PloS one》2013,8(8)
Chronic periodontitis has a polymicrobial biofilm aetiology and interactions between key bacterial species are strongly implicated as contributing to disease progression. Porphyromonas gingivalis, Treponema denticola and Tannerella forsythia have all been implicated as playing roles in disease progression. P. gingivalis cell-surface-located protease/adhesins, the gingipains, have been suggested to be involved in its interactions with several other bacterial species. The aims of this study were to determine polymicrobial biofilm formation by P. gingivalis, T. denticola and T. forsythia, as well as the role of P. gingivalis gingipains in biofilm formation by using a gingipain null triple mutant. To determine homotypic and polymicrobial biofilm formation a flow cell system was employed and the biofilms imaged and quantified by fluorescent in situ hybridization using DNA species-specific probes and confocal scanning laser microscopy imaging. Of the three species, only P. gingivalis and T. denticola formed mature, homotypic biofilms, and a strong synergy was observed between P. gingivalis and T. denticola in polymicrobial biofilm formation. This synergy was demonstrated by significant increases in biovolume, average biofilm thickness and maximum biofilm thickness of both species. In addition there was a morphological change of T. denticola in polymicrobial biofilms when compared with homotypic biofilms, suggesting reduced motility in homotypic biofilms. P. gingivalis gingipains were shown to play an essential role in synergistic polymicrobial biofilm formation with T. denticola. 相似文献
25.
Florian Villegas Daphné Lehalle Daniela Mayer Melanie Rittirsch Michael B. Stadler Marietta Zinner Daniel Olivieri Pierre Vabres Laurence Duplomb-Jego Eveline S.J.M. De Bont Yannis Duffourd Floor Duijkers Magali Avila David Geneviève Nada Houcinat Thibaud Jouan Paul Kuentz Klaske D. Lichtenbelt Joerg Betschinger 《Cell Stem Cell》2019,24(2):257-270.e8
26.
Nachtigal P Pospisilova N Jamborova G Pospechova K Solichova D Andrys C Zdansky P Semecky V 《Canadian journal of physiology and pharmacology》2007,85(8):767-773
Endoglin (CD105) is a homodimeric transmembrane glycoprotein strongly related to transforming growth factor (TGF)-beta signaling and many pathological states. In this study, we wanted to evaluate whether endoglin is expressed in normocholesterolemic and hypercholesterolemic C57BL/6J mice as well as whether it is affected by atorvastatin treatment in these mice. C57BL/6J mice were fed with chow diet or an atherogenic diet for 12 weeks after weaning. In 2 atorvastatin-treated groups, mice were fed the same diets (chow or atherogenic) as described above except atorvastatin was added at the dosage of 10 mg x kg(-1) x day(-1) for the last 8 weeks before euthanasia. Biochemical analysis of blood samples revealed that administration of atherogenic diet significantly increased levels of total cholesterol, VLDL, LDL, and decreased levels of HDL. Atorvastatin treatment resulted in a significant decrease in total cholesterol and VLDL only in mice fed by atherogenic diet. Quantitative stereological analysis revealed that atorvastatin significantly decreased endothelial expression of endoglin in C57BL/6J mice fed the atherogenic diet. In conclusion, we demonstrated that endothelial expression of endoglin is upregulated by hypercholesterolemia and decreased by the hypolipidemic effect of atorvastatin in C57BL/6J mice, suggesting that endoglin expression could be involved in atherogenesis. 相似文献
27.
28.
Mona F. Said Riham F. George Andrea Petreni Claudiu T. Supuran Nada M. Mohamed 《Journal of enzyme inhibition and medicinal chemistry》2022,37(1):701
In continuation of our previous studies to optimise potent carbonic anhydrase inhibitors, two new series of isatin N-phenylacetamide based sulphonamides were synthesised and screened for their human (h) carbonic anhydrase (EC 4.2.1.1) inhibitory activities against four isoforms hCA I, hCA II, hCA IX and hCA XII. The indole-2,3-dione derivative 2h showed the most effective inhibition profile against hCAI and hCA II (KI = 45.10, 5.87 nM) compared to acetazolamide (AAZ) as standard inhibitor. Moreover, 2h showed appreciable inhibition activity against the tumour-associated hCA XII, similar to AAZ showing KI of 7.91 and 5.70 nM, respectively. The analogs 3c and 3d showed good cytotoxicity effects, and 3c revealed promising selectivity towards lung cell line A549. Molecular docking was carried out for 2h and 3c to predict their binding conformations and affinities towards the hCA I, II, IX and XII isoforms. 相似文献
29.
Mouse monoclonal antibodies were prepared using His-tagged Tn10-encoded metal-tetracycline/H+ antiporter [TetA(B)His] as an antigen. From them, those reacting equally with His-tagged and wild-type TetA(B) were selected and named TCL-1. Cysteine-scanning mutants were used to determine the TCL-1 binding site on the TetA(B) protein. First, 12 Cys mutants of TetA(B) in which one residue in a protruding loop region was replaced by cysteine were constructed. Western blot analysis revealed the binding of TCL-1 to all of these Cys-mutants except for R186C. Then, we constructed 13 cysteine-scanning mutants, F179C to T191C. Among them, eight mutants, F179C to T182C, N184C, and T189C to T191C, exhibited TCL-1 binding, whereas the other five, K183C, T185C, R186C, D187C, and N188C, exhibited no or lower TCL-1 binding. These results clearly indicate that the sequence recognized by TCL-1 is 183Lys-X-Thr-Arg-Asp-Asn188 in the central loop region of TetA(B). TCL-1 is the first reported antibody that binds to a region other than the C-terminus of TetA(B), and the recognized amino acid sequence was identified. 相似文献
30.