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排序方式: 共有1730条查询结果,搜索用时 15 毫秒
41.
Martin RJ Szefler SJ King TS Kraft M Boushey HA Chinchilli VM Craig TJ Dimango EA Deykin A Fahy JV Israel E Lazarus SC Lemanske RF Leone FT Pesola GR Peters SP Sorkness CA Szwejbka LA Wechsler ME;National Heart Lung Blood Institute's Asthma Clinical Research Center 《The Journal of allergy and clinical immunology》2007,119(1):73-80
BACKGROUND: Although guidelines recommend anti-inflammatory therapy for persistent asthma, recent studies suggest that 25% to 35% of patients with asthma may not improve lung function with inhaled corticosteroids. OBJECTIVE: To evaluate potential biomarkers of predicting short-term (6-week) response to inhaled corticosteroid with subsequent evaluation of responders and nonresponders to asthma control over a longer interval (16 additional weeks). METHODS: Eighty-three subjects with asthma off steroid were enrolled in this multicenter study. Biomarkers and asthma characteristics were evaluated as predictors of inhaled corticosteroid response over a 6-week trial for changes in FEV(1) and methacholine PC(20). After this, an additional 4-month trial evaluated asthma control. RESULTS: Although multiple baseline predictors had significant correlations with improvements for short-term inhaled steroid success, the only strong correlations (r >or= +/- 0.6) were albuterol reversibility (r = 0.83; P < .001), FEV(1)/forced vital capacity (r = -0.75; P < .001), and FEV(1) % predicted (r = -0.71; P < .001). Dividing the subjects in the short-term inhaled steroid trial into responders (>5% FEV(1) improvement) and nonresponders (相似文献
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Alterations of the arginine metabolome in asthma 总被引:1,自引:0,他引:1
Lara A Khatri SB Wang Z Comhair SA Xu W Dweik RA Bodine M Levison BS Hammel J Bleecker E Busse W Calhoun WJ Castro M Chung KF Curran-Everett D Gaston B Israel E Jarjour N Moore W Peters SP Teague WG Wenzel S Hazen SL Erzurum SC;National Heart Lung Blood Institute's Severe Asthma Research Program 《American journal of respiratory and critical care medicine》2008,178(7):673-681
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Influence of T-cell depletion on chronic graft-versus-host disease: results of a multicenter randomized trial in unrelated marrow donor transplantation 下载免费PDF全文
Pavletic SZ Carter SL Kernan NA Henslee-Downey J Mendizabal AM Papadopoulos E Gingrich R Casper J Yanovich S Weisdorf D;National Heart Lung Blood Institute Unrelated Donor Marrow Transplantation Trial 《Blood》2005,106(9):3308-3313
Donor-derived T cells have been proposed to play a role in pathogenesis of chronic graft-versus-host disease (cGVHD). The impact of ex vivo T-cell depletion (TCD) on cGVHD was analyzed in a randomized multicenter trial involving unrelated donor marrow transplants. A total of 404 patients diagnosed with hematologic malignancies received a total body irradiation-based myeloablative conditioning regimen. GVHD prophylaxis included TCD plus cyclosporine (CSA) or unmodified grafts with CSA plus methotrexate (M/C). Median recipient age was 31.2 years (range, 0.5-55.6 years); median follow-up time since randomization was 4.2 years. The mean number of T cells infused was 1 log lower on the TCD arm. The incidence of cGVHD at 2 years was similar between the TCD and M/C arms, 29% versus 34% (P = .27), respectively. Survival at 3 years from diagnosis of cGVHD was also similar, (TCD 51% versus M/C 58%; P = .29). The proportion of patients with cGVHD who discontinued immunosuppression at 5 years was not different (TCD 72% versus M/C 63%; P = .27), and incidence of serious infections and leukemia relapse were similar on both treatment arms. In spite of a significant reduction of acute GVHD, TCD did not reduce the incidence of cGVHD or improve survival in patients who developed cGVHD. 相似文献
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Ji-Youn Youn Kin Lung Siu Heinrich E. Lob Hana Itani David G. Harrison Hua Cai 《Diabetes》2014,63(7):2344-2355
Obesity is associated with vascular diseases that are often attributed to vascular oxidative stress. We tested the hypothesis that vascular oxidative stress could induce obesity. We previously developed mice that overexpress p22phox in vascular smooth muscle, tgsm/p22phox, which have increased vascular ROS production. At baseline, tgsm/p22phox mice have a modest increase in body weight. With high-fat feeding, tgsm/p22phox mice developed exaggerated obesity and increased fat mass. Body weight increased from 32.16 ± 2.34 g to 43.03 ± 1.44 g in tgsm/p22phox mice (vs. 30.81 ± 0.71 g to 37.89 ± 1.16 g in the WT mice). This was associated with development of glucose intolerance, reduced HDL cholesterol, and increased levels of leptin and MCP-1. Tgsm/p22phox mice displayed impaired spontaneous activity and increased mitochondrial ROS production and mitochondrial dysfunction in skeletal muscle. In mice with vascular smooth muscle–targeted deletion of p22phox (p22phoxloxp/loxp/tgsmmhc/cre mice), high-fat feeding did not induce weight gain or leptin resistance. These mice also had reduced T-cell infiltration of perivascular fat. In conclusion, these data indicate that vascular oxidative stress induces obesity and metabolic syndrome, accompanied by and likely due to exercise intolerance, vascular inflammation, and augmented adipogenesis. These data indicate that vascular ROS may play a causal role in the development of obesity and metabolic syndrome. 相似文献
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