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排序方式: 共有103条查询结果,搜索用时 31 毫秒
91.
92.
Marco Antonio Montes-Cano Marta Conde-Jaldón José Raul García-Lozano Lourdes Ortiz-Fernández Norberto Ortego-Centeno María Jesús Castillo-Palma Gerard Espinosa Genaro Gra?a-Gil Miguel Angel González-Gay Ana Celia Barnosi-Marín Roser Solans Patricia Fanlo Teresa Camps Santos Casta?eda Juan Sánchez-Bursón Antonio Nú?ez-Roldán Javier Martín María Francisca González-Escribano 《Arthritis research & therapy》2013,15(5):R145
Introduction
According to genome wide association (GWA) studies as well as candidate gene approaches, Behçet’s disease (BD) is associated with human leukocyte antigen (HLA)-A and HLA-B gene regions. The HLA-B51 has been consistently associated with the disease, but the role of other HLA class I molecules remains controversial. Recently, variants in non-HLA genes have also been associated with BD. The aims of this study were to further investigate the influence of the HLA region in BD and to explore the relationship with non-HLA genes recently described to be associated in other populations.Methods
This study included 304 BD patients and 313 ethnically matched controls. HLA-A and HLA-B low resolution typing was carried out by PCR-SSOP Luminex. Eleven tag single nucleotide polymorphisms (SNPs) located outside of the HLA-region, previously described associated with the disease in GWA studies and having a minor allele frequency in Caucasians greater than 0.15 were genotyped using TaqMan assays. Phenotypic and genotypic frequencies were estimated by direct counting and distributions were compared using the χ2 test.Results
In addition to HLA-B*51, HLA-B*57 was found as a risk factor in BD, whereas, B*35 was found to be protective. Other HLA-A and B specificities were suggestive of association with the disease as risk (A*02 and A*24) or protective factors (A*03 and B*58). Regarding the non-HLA genes, the three SNPs located in IL23R and one of the SNPs in IL10 were found to be significantly associated with susceptibility to BD in our population.Conclusion
Different HLA specificities are associated with Behçet’s disease in addition to B*51. Other non-HLA genes, such as IL23R and IL-10, play a role in the susceptibility to the disease. 相似文献93.
Insect small nuclear RNA gene promoters evolve rapidly yet retain conserved features involved in determining promoter activity and RNA polymerase specificity
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In animals, most small nuclear RNAs (snRNAs) are synthesized by RNA polymerase II (Pol II), but U6 snRNA is synthesized by RNA polymerase III (Pol III). In Drosophila melanogaster, the promoters for the Pol II-transcribed snRNA genes consist of approximately 21 bp PSEA and approximately 8 bp PSEB. U6 genes utilize a PSEA but have a TATA box instead of the PSEB. The PSEAs of the two classes of genes bind the same protein complex, DmSNAPc. However, the PSEAs that recruit Pol II and Pol III differ in sequence at a few nucleotide positions that play an important role in determining RNA polymerase specificity. We have now performed a bioinformatic analysis to examine the conservation and divergence of the snRNA gene promoter elements in other species of insects. The 5' half of the PSEA is well-conserved, but the 3' half is divergent. Moreover, within each species positions exist where the PSEAs of the Pol III-transcribed genes differ from those of the Pol II-transcribed genes. Interestingly, the specific positions vary among species. Nevertheless, we speculate that these nucleotide differences within the 3' half of the PSEA act similarly to induce conformational alterations in DNA-bound SNAPc that result in RNA polymerase specificity. 相似文献
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95.
Marta Conde-Jaldón Marco Antonio Montes-Cano José Raul García-Lozano Lourdes Ortiz-Fernández Norberto Ortego-Centeno Rocío González-León Gerard Espinosa Genaro Gra?a-Gil Juan Sánchez-Bursón Miguel Angel González-Gay Ana Celia Barnosi-Marín Roser Solans Patricia Fanlo Mónica Rodríguez Carballeira Teresa Camps Santos Casta?eda Javier Martín María Francisca González-Escribano 《PloS one》2014,9(7)
Behçet''s disease (BD) is a multifactorial disorder associated with the HLA region. Recently, the ERAP1 gene has been proposed as a susceptibility locus with a recessive model and with epistatic interaction with HLA-B51. ERAP1 trims peptides in the endoplasmic reticulum to optimize their length for MHC-I binding. Polymorphisms in this gene have been related with the susceptibility to other immune-mediated diseases associated to HLA class I. Our aim was, the replication in the Spanish population of the association described in the Turkish population between ERAP1 (rs17482078) and BD. Additionally, in order to improve the understanding of this association we analyzed four additional SNPs (rs27044, rs10050860, rs30187 and rs2287987) associated with other diseases related to HLA class I and the haplotype blocks in this gene region. According to our results, frequencies of the homozygous genotypes for the minor alleles of all the SNPs were increased among patients and the OR values were higher in the subgroup of patients with the HLA-B risk factors, although differences were not statistically significant. Moreover, the presence of the same mutation in both chromosomes increased the OR values from 4.51 to 10.72 in individuals carrying the HLA-B risk factors. Therefore, although they were not statistically significant, our data were consistent with an association between ERAP1 and BD as well as with an epistatic interaction between ERAP1 and HLA-B in the Spanish population. 相似文献
96.
Ernesto J. V. Crescenti Vanina A. Medina Lorena A. Sambuco Graciela A. Cremaschi Ana M. Genaro Graciela P. Cricco Gabriela A. Martín Eduardo Valli Diego J. Martinel Lamas Juan C. Perazzo Elena S. Rivera Rosa M. Bergoc 《Biological trace element research》2014,157(2):138-146
Scleroderma, sclerosis of the skin, is a severe autoimmune disease refractant to all kind of treatments. To study the in vivo effects of a combination of three oligoelements selenium (Se), zinc (Zn), and manganese (Mn) plus Lachesis muta venom (O-LM) on the bleomycin (BLM)-induced scleroderma mouse experimental model. C3H mice were randomly divided into four groups: control (phosphate-buffered saline (PBS)), O-LM, BLM, and BLM?+?O-LM. All administrations were performed subcutaneously into the back of mice. BLM was injected 5 days per week for three consecutive weeks and O-LM was administered simultaneously with BLM from the beginning of the experiments and lasted for 3 weeks after the final BLM or PBS injection (for O-LM and BLM?+?O-LM groups), when animals were sacrificed and histopathological, immunohistochemical, thiobarbituric acid reactive species (TBARS) evaluation, and autoantibodies detection were determined. O-LM significantly reduced BLM-induced enhanced dermal thickness (605?±?47 vs. 956?±?59 μm, P?<?0.01), collagen deposition, and mast cells infiltration (43.1?±?1.0 vs. 102?±?14.1 mast cells, P?<?0.05). O-LM administration significantly blocked BLM-induced oxidative damage and the enhanced immunoreactive fibroblasts for α-smooth muscle actin while reduced BLM-induced autoantibodies that strongly react mainly with skin and spleen. O-LM significantly reduced BLM-induced scleroderma through the modulation of antioxidant and immunological pathways. 相似文献
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98.
99.
The induction of intracellular signals coupled to alpha1-adrenoceptor by haloperidol, were studied in rat cerebral frontal cortex. The neuroleptic exerts a biphasic effect on nitric oxide synthase (NOS), inhibiting the enzymatic activity at low concentrations (10(-9) M), while higher concentrations (10(-5) M) increased it. Protein kinase C (PKC) and phosphoinositol turnover (PIs) were involved in these actions, as haloperidol induced PKC translocation at low concentrations, and increased PIs turnover at high concentrations. All the effects of haloperidol were blocked by the alpha-adrenoceptor antagonist prazosin and the phospholipase C (PLC) inhibitor NCDC. The possibility that a cross-talk between both enzymatic pathways depending on the neuroleptic concentration used in rat cerebral frontal cortex, is also discussed. 相似文献
100.
María Silvia Di Genaro María Esther Escudero Lidia Del Carmen Velzquez Estela Muoz Claudia Aguilera Amrico Jurez Luis Scardapane Ana María Stefanini de Guzmn 《Microbiology and immunology》1997,41(8):615-620
Yersinia enterocolitica can cause extraintestinal sequelae such as reactive arthritis. The immunopathogenic mechanisms of this disease have not been completely clarified. Autoimmunity and persistent immune responses against bacterial antigens have been related to Yersinia-induced arthritis. The arthritogenic capacity of Y. enterocolitica O:5 and the kinetics of the development of autoantibodies and Yersinia antigen-specific antibodies were studied in hamsters. The results indicated that Y. enterocolitica O:5 was arthritogenic in the animal model studied. The animals developed septic arthritis on day 2 post-infection (p.i.) and reactive arthritis on day 65 p.i. An important IgG response to types I and II collagen and the persistence of antibodies against lipopolysaccharide and bacterial cellular extract were observed. By immunoblotting, it was obtained that IgG reacted against a large number of bacterial antigens, the strongest being the responses against 88, 76, 63 and 36-33 kDa peptides. From the results obtained, it can be concluded that serovar O:5 was experimentally arthritogenic, and that both autoimmune mechanisms and Yersinia-specific antibodies participated in the development of Yersinia-induced reactive arthritis in the animal model studied. 相似文献