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Objective To investigate the pathogenesis mechanism of radiation esophagitis from the perspective of mucosal regeneration and to determine whether it is associated with TGF-β1/p38MAPKs/FN signaling pathway. Methods The pathological analysis of esophageal specimens was performed by HE staining method. The expression of FN and TGF-β1 genes were observed by real time-PCR method, and the expression of tissue proteins TGF-β1, p38 and FN were detected by Western blot. Results The weights, food intakes and water intakes at the first week after the occurrence of radiation esophagitis were significantly decreased (P<0.05) and recovered at the fourth week. The esophageal mucosa was destructed at the first and second weeks, and the regeneration occurred in the fourth weeks; TGF-β1 and p38MAPK protein expression increased first and then decreased, while FN protein expression decreased first and then increased. Conclusion The TGF-β1/p38MAPK/FN signaling pathway may be involved in the process of mucosal repair. © 2020, CHINA RESEARCH ON PREVENTION AND TREATMENT. All rights reserved. 相似文献
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目的观察消瘤方加减对化疗后正虚痰凝型弥漫大B细胞淋巴瘤(DLBCL)患者生活质量、肿瘤负荷情况及机体免疫的影响。方法收集化疗4~6个疗程结束临床评估为完全缓解或不确定的完全缓解的DLBCL患者60例,随机分为对照组与治疗组各30例。两组患者均遵医嘱随访观察定期复查,入组后每个月进行1次随访。治疗组在此基础上予消瘤方加减口服,2周为1个疗程,共治疗6个疗程。对比两组患者治疗前后中医症状积分、生活质量(EORTC-QLQ-C30)评分、KPS评分、肿瘤负荷指标[包括乳酸脱氢酶(LDH)、β2-微球蛋白(β2-MG)]、免疫球蛋白[包括免疫球蛋白M(IgM)、免疫球蛋白G(IgG)、免疫球蛋白A(IgA)]水平,并判定中医证候疗效、生活质量疗效,计算复发率。结果治疗组中医证候疗效总有效率为96.67%,明显优于对照组的33.3%,差异有统计学意义(P<0.05)。治疗组无复发,对照组复发率为16.67%,差异有统计学意义(P<0.05)。治疗组生活质量疗效中好转率(80.00%)高于对照组(13.33%),治疗组恶化率(0)低于对照组(6.67%,P<0.01)。与本组治疗前比较,治疗后治疗组疲倦、恶心呕吐、气促、失眠、食欲不振、便秘评分,中医症状积分,LDH、β2-MG水平均明显降低,社会功能、情绪功能、躯体功能、角色功能、总体健康状况评分,IgA、IgG、IgM水平均明显升高(P<0.05);对照组中医症状积分明显降低(P<0.05),其余指标差异均无统计学意义(P>0.05),两组各指标差值比较差异均有统计学意义(P<0.05)。结论消瘤方加减可以有效改善化疗后正虚痰凝型DLBCL患者中医证候,提高生活质量及机体免疫力,有效降低肿瘤负荷指标,并可减少复发。 相似文献
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再生障碍性贫血是血液系统常见难治病,周永明教授采用治病求本求属、调理脾胃健运、师古不泥求新、掌握标本缓急、结合药理研究、辨证辨病结合的用药经验等,治疗再障取得了良好的临床疗效。 相似文献
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目的:研究细胞外信号调节激酶(extracellular signal-regulated protein kinase,ERK)对脂多糖(LPS)诱导内皮细胞β-1,4-半乳糖基转移酶-Ⅰ(β-1,4-galactosyltransferase-Ⅰ,β-1,4-GalT-Ⅰ)表达的调节作用。方法:应用ERK通路抑制剂U0126预处理人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)2 h,再用LPS刺激HUVECs 4 h,分别用RT-PCR和Western-blot方法检测β-1,4-GalT-ⅠmRNA及蛋白水平表达变化,并通过内皮-单核细胞黏附试验观察HUVECs黏附能力的改变。结果:U0126显著抑制LPS引起的HUVECsβ-1,4-GalT-Ⅰ表达的上调及其黏附能力的上词。结论:ERK信号转导通路可能参与调节LPS诱导的内皮细胞β-1,4-GalT-Ⅰ的表达,并影响内皮细胞的黏附能力。 相似文献