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21.
Andersen DC Kortesidis A Zannettino AC Kratchmarova I Chen L Jensen ON Teisner B Gronthos S Jensen CH Kassem M 《Molecules and cells》2011,32(2):133-142
Human mesenchymal stem cells (hMSC) are currently being introduced for cell therapy, yet, antibodies specific for native and
differentiated MSCs are required for their identification prior to clinical use. Herein, high quality antibodies against MSC
surface proteins were developed by immunizing mice with hMSC, and by using a panel of subsequent screening methods. Flow cytometry
analysis revealed that 83.5, 1.1, and 8.5% of primary cultures of hMSC were double positive for STRO-1 and either of DJ 3,
9, and 18, respectively. However, none of the three DJ antibodies allowed enrichment of clonogenic hMSC from BMMNCs as single
reagents. Using mass-spectrometric analysis, we identified the antigen recognised by DJ3 as CD44, whereas DJ9 and DJ18 recognized
HLA-DRB1 and Collagen VI, respectively. The identified proteins were highly expressed throughout in vitro osteogenic- and adipogenic differentiation. Interestingly, undifferentiated cells revealed a sole cytoplasmic distribution
pattern of Collagen VI, which however changed to an extracellular matrix appearance upon osteogenic- and adipogenic differentiation.
In relation to this, we found that STRO-1+/−/Collagen VI− sorted hMSC contained fewer differentiated alkaline phosphatase+ cells compared to STRO-1+/−/Collagen VI+ hMSC, suggesting that Collagen VI on the cell membrane exclusively defines differentiated MSCs. In conclusion, we have generated
a panel of high quality antibodies to be used for characterization of MSCs, and in addition our results may suggest that the
DJ18 generated antibody against Collagen VI can be used for negative selection of cultured undifferentiated MSCs. 相似文献
22.
Bone regeneration and stem cells 总被引:1,自引:0,他引:1
Arvidson K Abdallah BM Applegate LA Baldini N Cenni E Gomez-Barrena E Granchi D Kassem M Konttinen YT Mustafa K Pioletti DP Sillat T Finne-Wistrand A 《Journal of cellular and molecular medicine》2011,15(4):718-746
This invited review covers research areas of central importance for orthopaedic and maxillofacial bone tissue repair, including normal fracture healing and healing problems, biomaterial scaffolds for tissue engineering, mesenchymal and foetal stem cells, effects of sex steroids on mesenchymal stem cells, use of platelet-rich plasma for tissue repair, osteogenesis and its molecular markers. A variety of cells in addition to stem cells, as well as advances in materials science to meet specific requirements for bone and soft tissue regeneration by addition of bioactive molecules, are discussed. 相似文献
23.
24.
Cladière L Hamze K Madec E Levdikov VM Wilkinson AJ Holland IB Séror SJ 《Molecular genetics and genomics : MGG》2006,275(4):409-420
YloQ, from Bacillus subtilis, was identified previously as an essential nucleotide-binding protein of unknown function. YloQ was successfully over-expressed
in Escherichia coli in soluble form. The purified protein displayed a low GTPase activity similar to that of other small bacterial GTPases such
as Bex/Era. Based on the demonstrated GTPase activity and the unusual order of the yloQ G motifs, we now designate this protein as CpgA (circularly permuted GTPase). An unexpected property of this low abundance
GTPase was the demonstration, using gel filtration and ultracentrifugation analysis, that the protein formed stable dimers,
dependent upon the concentration of YloQ(CpgA), but independent of GTP. In order to investigate function, cpgA was placed under the control of the pspac promotor in the B. subtilis chromosome. When grown in E or Spizizen medium in the absence of IPTG, the rate of growth was significantly reduced. A large
proportion of the cells exhibited a markedly perturbed morphology, with the formation of swollen, bent or ‘curly’ shapes.
To confirm that this was specifically due to depleted CpgA a plasmid-borne cpgA under pxyl control was introduced. This restored normal cell shape and growth rate, even in the absence of IPTG, provided xylose was
present. The crystal structure of CpgA(YloQ) suggests a role as a translation initiation factor and we discuss the possibility
that CpgA is involved in the translation of a subset of proteins, including some required for shape maintenance.
Electronic Supplementary Material Supplementary material is available for this article at and is accessible for authorized users. 相似文献
25.
M. J. Iqbal K. Meksem V. N. Njiti My. A. Kassem D. A. Lightfoot 《TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik》2001,102(2-3):187-192
Resistance to the sudden-death syndrome (SDS) of soybean (Glycine max L. Merr.), caused by Fusarium solani f. sp. glycines, is controlled by a number of quantitatively inherited loci (QTLs). Forrest showed a strong field resistance to SDS while
Essex is susceptible to SDS. A population of 100 recombinant inbred lines (RILs) derived from a cross of Essex × Forrest was
used to map the loci effecting resistance to SDS using phenotypic data obtained from six environments. Six loci involved in
resistance to SDS were identified in this population. Four of the QTLs identified by BARC-Satt214 (P = 0.0001, R2= 24.1%), BARC-Satt309 (P = 0.0001, R2 = 16.3), BARC-Satt570 (P = 0.0001, R2 = 19.2%) and a random amplified polymorphic DNA (RAPD) marker OEO21000 (P = 0.0031, R2=12.6) were located on linkage group (LG) G (Satt309 and OEO21000 were previously reported). Jointly the four QTLs on LG G explained 50% of the variation in SDS disease incidence (DI). All
the QTLs on LG G derived the beneficial allele from Forrest. Two QTLs, BARC-Satt371 (P = 0.0019, R2 = 12%) on LG C2 (previously reported) and BARC-Satt354 (P = 0.0015, R2 = 11.5%) on LG I, derived their beneficial allele from Essex and jointly explained about 40% of the variation in SDS DI.
Two-way and multi-way interactions indicated that gene action was additive among the loci underlying resistance to SDS. These
results suggest that cultivars with durable resistance to SDS can be developed via gene pyramiding.
Received: 19 January 2000 / Accepted: 30 April 2000 相似文献
26.
Kassem Ghaddar Ahmad Merhi Elie Saliba Eva-Maria Krammer Martine Prévost Bruno André 《Molecular and cellular biology》2014,34(24):4447-4463
Many plasma membrane transporters are downregulated by ubiquitylation, endocytosis, and delivery to the lysosome in response to various stimuli. We report here that two amino acid transporters of Saccharomyces cerevisiae, the general amino acid permease (Gap1) and the arginine-specific permease (Can1), undergo ubiquitin-dependent downregulation in response to their substrates and that this downregulation is not due to intracellular accumulation of the transported amino acids but to transport catalysis itself. Following an approach based on permease structural modeling, mutagenesis, and kinetic parameter analysis, we obtained evidence that substrate-induced endocytosis requires transition of the permease to a conformational state preceding substrate release into the cell. Furthermore, this transient conformation must be stable enough, and thus sufficiently populated, for the permease to undergo efficient downregulation. Additional observations, including the constitutive downregulation of two active Gap1 mutants altered in cytosolic regions, support the model that the substrate-induced conformational transition inducing endocytosis involves remodeling of cytosolic regions of the permeases, thereby promoting their recognition by arrestin-like adaptors of the Rsp5 ubiquitin ligase. Similar mechanisms might control many other plasma membrane transporters according to the external concentrations of their substrates. 相似文献
27.
Lynn Meurs Moustapha Mbow Kim Vereecken Joris Menten Souleymane Mboup Katja Polman 《PLoS neglected tropical diseases》2012,6(9)
Background
The global distribution map of schistosomiasis shows a large overlap of Schistosoma haematobium- and S. mansoni-endemic areas in Africa. Yet, little is known about the consequences of mixed Schistosoma infections for the human host. A recent study in two neighboring co-endemic communities in Senegal indicated that infection intensities of both species were higher in mixed than in single infections. Here, we investigated the relationship between mixed Schistosoma infections and morbidity in the same population. So far, this has only been studied in children.Methods
Schistosoma infection was assessed by microscopy. Schistosoma-specific morbidity was assessed by ultrasound according to WHO guidelines. Multivariable logistic regression models were used to identify independent risk factors for morbidity.Principal Findings
Complete parasitological and morbidity data were obtained from 403 individuals. Schistosoma haematobium-specific bladder morbidity was observed in 83% and S. mansoni-specific hepatic fibrosis in 27% of the participants. Bladder morbidity was positively associated with S. haematobium infection intensity (OR = 1.9 (95% CI 1.3–2.9) for a 10-fold increase in intensity). Moreover, people with mixed infections tended to have less bladder morbidity than those with single S. haematobium infections (OR = 0.3 (95% CI 0.1–1.1)). This effect appeared to be related to ectopic S. mansoni egg elimination in urine. Hepatic fibrosis on the other hand was not related to S. mansoni infection intensity (OR = 0.9 (95% CI 0.6–1.3)), nor to mixed infections (OR = 1.0 (95% CI 0.7–1.7)).Conclusions/Significance
This is the first population-wide study on the relationship between mixed Schistosoma infections and morbidity. Mixed infections did not increase the risk of S. mansoni-associated morbidity. They even tended to reduce the risk of S. haematobium-associated morbidity, suggesting a protective effect of S. mansoni infection on bladder morbidity. These unexpected results may have important consequences for schistosomiasis control in co-endemic areas and warrant further investigation. 相似文献28.
29.
30.
Bahare Shokoohian Babak Negahdari Hamidreza Aboulkheyr Es Manuchehr Abedi-Valugerdi Kaveh Baghaei Tarun Agarwal Tapas Kumar Maiti Moustapha Hassan Mustapha Najimi Massoud Vosough 《Journal of cellular and molecular medicine》2021,25(18):8602-8614
Hepatocellular carcinoma (HCC), the most common type of liver cancer, is usually a latent and asymptomatic malignancy caused by different aetiologies, which is a result of various aberrant molecular heterogeneity and often diagnosed at advanced stages. The incidence and prevalence have significantly increased because of sedentary lifestyle, diabetes, chronic infection with hepatotropic viruses and exposure to aflatoxins. Due to advanced intra- or extrahepatic metastasis, recurrence is very common even after radical resection. In this paper, we highlighted novel therapeutic modalities, such as molecular-targeted therapies, targeted radionuclide therapies and epigenetic modification-based therapies. These topics are trending headlines and their combination with cell-based immunotherapies, and gene therapy has provided promising prospects for the future of HCC treatment. Moreover, a comprehensive overview of current and advanced therapeutic approaches is discussed and the advantages and limitations of each strategy are described. Finally, very recent and approved novel combined therapies and their promising results in HCC treatment have been introduced. 相似文献