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排序方式: 共有109条查询结果,搜索用时 15 毫秒
31.
32.
Jake K Nikota Fernando M Botelho Carla MT Bauer Manel Jordana Anthony J Coyle Alison A Humbles Martin R Stampfli 《Respiratory research》2011,12(1):39
Background
While the presence of the chitinase-like molecule YKL40 has been reported in COPD and asthma, its relevance to inflammatory processes elicited by cigarette smoke and common environmental allergens, such as house dust mite (HDM), is not well understood. The objective of the current study was to assess expression and function of BRP-39, the murine equivalent of YKL40 in a murine model of cigarette smoke-induced inflammation and contrast expression and function to a model of HDM-induced allergic airway inflammation.Methods
CD1, C57BL/6, and BALB/c mice were room air- or cigarette smoke-exposed for 4 days in a whole-body exposure system. In separate experiments, BALB/c mice were challenged with HDM extract once a day for 10 days. BRP-39 was assessed by ELISA and immunohistochemistry. IL-13, IL-1R1, IL-18, and BRP-39 knock out (KO) mice were utilized to assess the mechanism and relevance of BRP-39 in cigarette smoke- and HDM-induced airway inflammation.Results
Cigarette smoke exposure elicited a robust induction of BRP-39 but not the catalytically active chitinase, AMCase, in lung epithelial cells and alveolar macrophages of all mouse strains tested. Both BRP-39 and AMCase were increased in lung tissue after HDM exposure. Examining smoke-exposed IL-1R1, IL-18, and IL-13 deficient mice, BRP-39 induction was found to be IL-1 and not IL-18 or IL-13 dependent, while induction of BRP-39 by HDM was independent of IL-1 and IL-13. Despite the importance of BRP-39 in cellular inflammation in HDM-induced airway inflammation, BRP-39 was found to be redundant for cigarette smoke-induced airway inflammation and the adjuvant properties of cigarette smoke.Conclusions
These data highlight the contrast between the importance of BRP-39 in HDM- and cigarette smoke-induced inflammation. While functionally important in HDM-induced inflammation, BRP-39 is a biomarker of cigarette smoke induced inflammation which is the byproduct of an IL-1 inflammatory pathway. 相似文献33.
Nadia Felli Federica Felicetti Anna Maria Lustri M. Cristina Errico Lisabianca Bottero Alessio Cannistraci Alessandra De Feo Marina Petrini Francesca Pedini Mauro Biffoni Ester Alvino Massimo Negrini Manuela Ferracin Gianfranco Mattia Alessandra Carè 《PloS one》2013,8(2)
The abnormal expression of several microRNAs has a causal role in tumorigenesis with either antineoplastic or oncogenic functions. Here we demonstrated that miR-126 and miR-126* play a tumor suppressor role in human melanoma through the direct or indirect repression of several key oncogenic molecules. The expression levels of miR-126&126* were elevated in normal melanocytes and primary melanoma cell lines, whereas they markedly declined in metastatic cells. Indeed, the restored expression of miR-126&126* in two advanced melanoma cell lines was accompanied by a significant reduction of proliferation, invasion and chemotaxis in vitro as well as of growth and dissemination in vivo. In accordance, the reverse functional effects were obtained by knocking down miR-126&126* by transfecting antisense LNA oligonucleotides in melanoma cells. Looking for the effectors of these antineoplastic functions, we identified ADAM9 and MMP7, two metalloproteases playing a pivotal role in melanoma progression, as direct targets of miR-126&126*. In addition, as ADAM9 and MMP7 share a role in the proteolytic cleavage of the HB-EGF precursor, we looked for the effectiveness of this regulatory pathway in melanoma, confirming the decrease of HB-EGF activation as a consequence of miR-126&126*-dependent downmodulation of ADAM9 and MMP7. Finally, gene profile analyses showed that miR-126&126* reexpression was sufficient to inactivate other key signaling pathways involved in the oncogenic transformation, as PI3K/AKT and MAPK, and to restore melanogenesis, as indicated by KIT/MITF/TYR induction. In view of this miR-126&126* wide-ranging action, we believe that the replacement of these microRNAs might be considered a promising therapeutic approach. 相似文献
34.
Lombardo C Bottero S d'Alessandro F Giacomini M Guderzo A Moretti F Marincola M Pesce G Pierotti MA Spagnoli LG Belardelli F 《The International journal of biological markers》2011,26(2):136-138
Training through Research Application Italian iNitiative (TRAIN) is a mobility program financed under the EU action called "Cofinancing of regional, national and international programs" (COFUND) of the European Commission Seventh Framework Program (FP7) - People, and has been designed to encourage the promotion and development of international programs of research through mobility at various stages of research careers. The aim of TRAIN is to improve translational skills in the field of cancer by promoting a three-year international mobility program assigning a total of 51 fellowships subdivided into incoming, outgoing and reintegration fellowships.?The TRAIN proposal has been submitted in February 2009 to the European Commission in reply to the 2008 FP7-PEOPLE-COFUND call and has been successfully evaluated. TRAIN is addressed to postdoctoral scientists or scientists who have at least four years' full-time equivalent research experience and who wish to improve their careers spending one year abroad. The mobility program is open also to non-Italian experienced scientists wishing to spend one year in an Italian research center or private company. Part of the scheme is targeted to experienced Italian scientists who have completed at least three years of research in a foreign country and are interested in returning to Italy.?TRAIN is part of an overall Italian strategy outlined by the International Program of the Italian Cancer Network "Alleanza Contro il Cancro" to promote Italian participation in the building of the European Area for translational cancer research and to enhance the interaction between academy and industry. 相似文献
35.
Sadagopan S Valiya Veettil M Paudel N Bottero V Chandran B 《Journal of virology》2011,85(6):2666-2685
36.
37.
Ewa Przybytkowski Elizabeth Lenkiewicz Michael T Barrett Kathleen Klein Sheida Nabavi Celia MT Greenwood Mark Basik 《BMC genomics》2014,15(1)
Background
Chromosomal breakage followed by faulty DNA repair leads to gene amplifications and deletions in cancers. However, the mere assessment of the extent of genomic changes, amplifications and deletions may reduce the complexity of genomic data observed by array comparative genomic hybridization (array CGH). We present here a novel approach to array CGH data analysis, which focuses on putative breakpoints responsible for rearrangements within the genome.Results
We performed array comparative genomic hybridization in 29 primary tumors from high risk patients with breast cancer. The specimens were flow sorted according to ploidy to increase tumor cell purity prior to array CGH. We describe the number of chromosomal breaks as well as the patterns of breaks on individual chromosomes in each tumor. There were differences in chromosomal breakage patterns between the 3 clinical subtypes of breast cancers, although the highest density of breaks occurred at chromosome 17 in all subtypes, suggesting a particular proclivity of this chromosome for breaks. We also observed chromothripsis affecting various chromosomes in 41% of high risk breast cancers.Conclusions
Our results provide a new insight into the genomic complexity of breast cancer. Genomic instability dependent on chromosomal breakage events is not stochastic, targeting some chromosomes clearly more than others. We report a much higher percentage of chromothripsis than described previously in other cancers and this suggests that massive genomic rearrangements occurring in a single catastrophic event may shape many breast cancer genomes.Electronic supplementary material
The online version of this article (doi:10.1186/1471-2164-15-579) contains supplementary material, which is available to authorized users. 相似文献38.
39.
Development and characterization of highly polymorphic long TC repeat microsatellite markers for genetic analysis of peanut 总被引:4,自引:0,他引:4
Selma E Macedo Márcio C Moretzsohn Soraya C M Leal-Bertioli Dione MT Alves Ediene G Gouvea Vania CR Azevedo David J Bertioli 《BMC research notes》2012,5(1):1-10
Background
The immune system has paradoxical roles during cancer development and the prognostic significance of immune modulating factors is controversial. The aim of this study was to determine the expression of cyclooxygenase 2 (COX-2), transforming growth factor-beta (TGF- beta), interleukin-10 (IL-10) and their prognostic significance in breast cancers. Ki67 was included as a measure of growth fraction of tumor cells.Methods
On immunohistochemical stained slides from 38 breast cancer patients, we performed digital video analysis of tumor cell areas and adjacent tumor stromal areas from the primary tumors and their corresponding lymph node metastases. COX-2 was recorded as graded staining intensity.Results
The expression of TGF-beta, IL-10 and Ki67 were recorded in tumor cell areas and adjacent tumor stromal areas. In both primary tumors and metastases, the expression of COX-2 was higher in the tumor stromal areas than in the tumor cell areas (both P < 0.001). High stromal staining intensity in the primary tumors was associated with a 3.9 (95% CI 1.1-14.2) times higher risk of death compared to the low staining group (P = 0.036). The expression of TGF-beta was highest in the tumor cell areas of both primary tumors and metastases (both P < 0.001). High stromal expression of TGF-beta was associated with increased mortality. For IL-10, the stromal expression was highest in the primary tumors (P < 0.001), whereas in the metastases the expression was highest in tumor cell areas (P < 0.001). High IL-10 expression in tumor- and stromal cell areas of primary tumors predicted mortality. Ki67 was higher expressed in tumor stromal areas of the metastases, and in tumor cell areas of the primary tumors (P < 0.001). Ki67 expression in tumor cell areas and stromal areas of the metastases was independently associated with breast cancer mortality.Conclusions
Stromal expression of COX-2, TGF-beta and Ki67 may facilitate tumor progression in breast cancer. 相似文献40.
Ribosomal RNA secondary structure: compensatory mutations and implications for phylogenetic analysis 总被引:6,自引:0,他引:6
Using sequence data from the 28S ribosomal RNA (rRNA) genes of selected
vertebrates, we investigated the effects that constraints imposed by
secondary structure have on the phylogenetic analysis of rRNA sequence
data. Our analysis indicates that characters from both base-pairing regions
(stems) and non-base-pairing regions (loops) contain phylogenetic
information, as judged by the level of support of the phylogenetic results
compared with a well-established tree based on both morphological and
molecular data. The best results (the greatest level of support of
well-accepted nodes) were obtained when the complete data set was used.
However, some previously supported nodes were resolved using either the
stem or loop bases alone. Stem bases sustain a greater number of
compensatory mutations than would be expected at random, but the number is
< 40% of that expected under a hypothesis of perfect compensation to
maintain secondary structure. Therefore, we suggest that in phylogenetic
analyses, the weighting of stem characters be reduced by no more than 20%,
relative to that of loop characters. In contrast to previous suggestions,
we do not recommend weighting of stem positions by one-half, compared with
that of loop positions, because this overcompensates for the constraints
that selection imposes on the secondary structure of rRNA.
相似文献