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Expression of an ovalbumin-specific V{beta}8.2 TCR transgene inhibits collagen arthritis in B10.Q mice 总被引:1,自引:1,他引:0
Nabozny Gerald H.; Rimm Ilonna J.; Griffiths Marie M.; Luthra Harvinder S.; David Chella S. 《International immunology》1995,7(8):1279-1286
Previous studies have illustrated the importance of T cellsbearing ß TCRs in the induction and development ofcollagen induced arthritis (CIA) in mice. However, the scopeof TCR usage in CIA has yet to be clearly defined. Given theinherent diversity of the TCR repertoire, the relative flexibilityof the arthritogenic TCR repertoire specific for type II collagen(CII) is not clear. Therefore, we chose to examine the influenceof a highly skewed TCR repertoire on CIA. Arthritis susceptibleB10.Q (H-2q) mice were mated with C57L (H-2b) animals expressingan ovalbuminspecific Vß8.2 TCR transgene (Tg) andTg+ offspring were further backcrossed to B10.Q. HomozygousH-2a/q, Vß8.2 Tg+ mice displayed a high level of Vß8.2+T cells in peripheral blood. However, expression of some endogenousVß TCR, such as Vß14, was still detected.Upon immunization with bovine CII in adjuvant, Vß8.2Tg+ mice were highly resistant to CIA when compared with Tg–littermates. Analysis of sera demonstrated a marked reductionin antibody specific for homologous mouse CII as well as heterologousbovine CII in Tg+ animals. Interestingly, Vß8.2 Tg+mice still mounted good antibody responses following immunizationwith human thyroglobulin, indicating that the skewed TCR repertoireaffected anti-CII but not antithyroglobulin responses. Thus,our findings show that constraints placed on the TCR repertoireInhibit pathogenic responses against CII and suggest that inH-2q mice the arthritogenlc TCR repertoire bears only limitedflexibility. 相似文献
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Leontiou CA Gueorguiev M van der Spuy J Quinton R Lolli F Hassan S Chahal HS Igreja SC Jordan S Rowe J Stolbrink M Christian HC Wray J Bishop-Bailey D Berney DM Wass JA Popovic V Ribeiro-Oliveira A Gadelha MR Monson JP Akker SA Davis JR Clayton RN Yoshimoto K Iwata T Matsuno A Eguchi K Musat M Flanagan D Peters G Bolger GB Chapple JP Frohman LA Grossman AB Korbonits M 《The Journal of clinical endocrinology and metabolism》2008,93(6):2390-2401
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Alexander Dimitri Miras Anna Kamocka Beln Prez-Pevida Sanjay Purkayastha Krishna Moorthy Ameet Patel Harvinder Chahal Gary Frost Paul Bassett Lidia Castagnetto-Gissey Lucy Coppin Nicola Jackson Anne Margot Umpleby Stephen Robert Bloom Tricia Tan Ahmed Rashid Ahmed Francesco Rubino 《Diabetes care》2021,44(5):1082
OBJECTIVERoux-en-Y gastric bypass (RYGB) characteristically enhances postprandial levels of glucagon-like peptide 1 (GLP-1), a mechanism that contributes to its profound glucose-lowering effects. This enhancement is thought to be triggered by bypass of food to the distal small intestine with higher densities of neuroendocrine L-cells. We hypothesized that if this is the predominant mechanism behind the enhanced secretion of GLP-1, a longer intestinal bypass would potentiate the postprandial peak in GLP-1, translating into higher insulin secretion and, thus, additional improvements in glucose tolerance. To investigate this, we conducted a mechanistic study comparing two variants of RYGB that differ in the length of intestinal bypass.RESEARCH DESIGN AND METHODSA total of 53 patients with type 2 diabetes (T2D) and obesity were randomized to either standard limb RYGB (50-cm biliopancreatic limb) or long limb RYGB (150-cm biliopancreatic limb). They underwent measurements of GLP-1 and insulin secretion following a mixed meal and insulin sensitivity using euglycemic hyperinsulinemic clamps at baseline and 2 weeks and at 20% weight loss after surgery.RESULTSBoth groups exhibited enhancement in postprandial GLP-1 secretion and improvements in glycemia compared with baseline. There were no significant differences in postprandial peak concentrations of GLP-1, time to peak, insulin secretion, and insulin sensitivity.CONCLUSIONSThe findings of this study demonstrate that lengthening of the intestinal bypass in RYGB does not affect GLP-1 secretion. Thus, the characteristic enhancement of GLP-1 response after RYGB might not depend on delivery of nutrients to more distal intestinal segments. 相似文献
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DRB1*0402 may influence arthritis by promoting naive CD4+ T‐cell differentiation in to regulatory T cells 下载免费PDF全文
David Luckey Marshall Behrens Michele Smart Harvinder Luthra Chella S. David Veena Taneja 《European journal of immunology》2014,44(11):3429-3438
HLA‐DRB1*0401 expression in humans has been associated with a predisposition to developing rheumatoid arthritis (RA) and collagen‐induced arthritis (CIA), while HLA‐DRB1*0402 is not associated with susceptibility. Here, we determined if mice transgenic (Tg) for human *0401 have a CD4+ T‐cell repertoire that predetermines proinflammatory cytokine production. The data show that both *0401 and *0402 Tg mice can produce TH1/TH17 cytokines, although the kinetics of response may be different. However, in the context of antigen‐specific responses in a CIA model, *0402 Tg mice generate a TH2 response that may explain their resistance to developing arthritis. In addition, a significant subset of naïve CD4+ T cells from *0402 Tg mice can be activated in polarizing conditions to differentiate into Treg cells that produce IFN‐γ. *0401 Tg mice harbor memory CD4+ T cells that differentiate into IL‐17+ cells in various polarizing conditions. Our data suggest that *0401 Tg mice generate a strong immune response to lipopolysaccharide and may be efficient in clearing infection, and may *0401 have been evolutionarily selected for this ability. Autoimmunity, such as RA, could likely be a bystander effect of the cytokine storm that, along with the presence of low Treg‐cell numbers in *0401 Tg mice, causes immune dysregulation. 相似文献
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Josh E. Schroeder Fredrico P. Girardi Harvinder Sandhu Joseph Weinstein Frank P. Cammisa Andrew Sama 《European spine journal》2016,25(4):1029-1033
Purpose
Wound infection after spine surgery is a debilitating complication. Local placement of vancomycin powder into the surgical wounds prior to closing of the fascia has been introduced as a method to reduce deep infection rates.Methods
The infection rates of all the patients who were treated with intra-operative local vancomycin between June 2012 and June 2013 were compared to all cases that were not treated with vancomycin between January 2009 and December 2010. Patients for both groups were operated by four senior, fellowship-trained spine surgeons with a combined experience of 55 years of practice at a referral orthopedic center. Patients’ charts and microbiology reports were reviewed.Results
1224 cases were performed with the use of vancomycin. The average age was 56.3 years (SD ?13.2; NS). The male to female ratio was 1:1.12 (NS). 2253 cases were performed without the use of vancomycin. The average patient age was 57.1 years (SD 14.5). The male to female ratio was 1:1.14. There were 30 cases of deep infections needing a surgical irrigation and debridement without vancomycin versus 5 when vancomycin was used (P = 0.04). Infections in patients treated with vancomycin were not vancomycin-resistant bacteria.Conclusion
In conclusion, the use of vancomycin reduces the rate of deep wound infections and irrigation and debridement procedures after spine surgery in a referral center among surgeons with a high surgical volume.10.
Taneja V Krco CJ Behrens MD Luthra HS Griffiths MM David CS 《Molecular immunology》2007,44(11):2988-2996
Rheumatoid arthritis and its animal model, collagen-induced arthritis, are known as a T and B cell dependent disease. To analyze the role of B cells in arthritis, we generated B cell deficient (microMT) mice carrying HLA-DQ8 as transgene, Abetao.DQ8.micromt mice. HLA-DQ8 transgenic mice (Abetao.DQ8) are susceptible to collagen induced arthritis, an animal model for inflammatory arthritis. Deletion of IgM gene led to the absence of B cells while T cells were comparable to Abetao.DQ8 mice. Arthritis and autoantibodies was completely abrogated in B cell deficient DQ8 mice. T cell response and proinflammatory cytokine production in response to type II collagen and its derived peptides in vitro was significantly decreased despite an increased number of Mac-1 positive cells in DQ8.micromt mice compared to DQ8 mice suggesting B cells could be important for antigen presentation as well. In vitro substitution of B cells from wild type mice restored the response in DQ8.micromt mice. B cells could also present CII-derived peptides to antigen-specific DQ8-restricted hybridomas reinforcing the role of B cells in presentation of antigens to T cells. The data suggest that B cells can be involved in pathogenesis of arthritis by producing autoantibodies and antigen presentation. 相似文献