美沙拉秦治疗溃疡性结肠炎的疗效观察

目的研究美沙拉秦（惠迪）治疗溃疡性结肠炎（uc）的治疗疗效。方法收集2007年3月-2008年6月在我院治疗的活动性UC病人112例,随机分为治疗组62人和对照组50人。治疗组患者服用惠迪每次1．0g,4次／d,疗程4周,缓解后改为2g,继续服用4周;对照组服用柳氮磺胺吡啶（SASP）每次1．0g,4次／d,疗程4周,缓解后改为2g,继续服用4周。比较治疗组和对照组患者的临床症状、生化和免疫学指标,以及肠镜下的改变。结果治疗8周后,发现惠迪和柳氮磺胺吡啶（SASP）都可有效控制UC患者的临床症状（总有效率为88．7％和80．O％）,治疗2周后,惠迪比SAsP能更迅速缓解患者的临床症状。惠迪对患者的肝、肾功能无影响,治疗后血细胞沉降率和C反应蛋白的水平显著降低（P〈0．05）,而且不良反应发生率明显低于SASP（P〈0．01）。结论惠迪是一种能有效控制活动性UC的药物,不良反应少。     

重症溃疡性结肠炎的内科治疗

参照1973年全国慢性非感染肠道疾病学术研讨会制定的溃疡性结肠炎的诊断标准,对北京协和医院1974年1月至1995年1月的溃疡性结肠炎住院病人共148例进行了分析,着重探讨了我院对重症溃疡性结肠炎的药物治疗经验。结果显示:21年间溃疡性结肠炎在内科消化病的年住院率呈上升趋势,重症患者占 72.3 ％。其临床治疗仍以激素,水杨酸偶氮磺胺吡啶和免疫抑制剂为主要治疗药物。本病在我院内科治疗的临床缓解率达95.9 ％,其中重症的临床缓解率达95,3 ％,死亡率为6.08 ％。我们提出对溃疡性结肠炎的内科治疗应遵循尽早控制症状、维持缓解、预防复发、防治并发症和掌握手术时机的原则;并根据病变的范围、疾病的活动性和严重程度、病程、病人的全身情况、以前用药情况和有无并发症等进行综合治疗。     

重症溃疡性结肠炎的药物治疗

本文参照1993年全国慢性非感染性肠道疾病学术研讨会制定的溃疡性结肠炎的诊断标准,对北京协和医院1974年1月至1995年1月的溃疡性结肠炎住院病人共148例进行了分析,着重探讨了我院对重症溃疡性结肠炎的药物治疗经验。结果显示,21年间溃疡性结肠炎在内科消化病的年住院率呈上升趋势,重症患者占72.3％。其临床治疗方法仍以激素、水杨酸偶氮磺胺吡啶和免疫抑制剂为主要治疗药物。本病在我院内科治疗的临床缓解率达95.9％,其中重症的临床缓解率达95.3％。死亡率为6.08％。我们提出对溃疡性结肠炎的内科治疗应遵循尽早控制症状、维持缓解、预防复发、防治并发症和掌握手术时机的原则:并根据病变的范围、疾病的活动性和严重程度、病程、病人的全身情况,以前用药情况和有无并发症等进行综合治疗。     

Targets of Immune Regeneration in Rheumatoid Arthritis

Many of the aging-related morbidities, including cancer, cardiovascular disease, neurodegenerative disease, and infectious susceptibility, are linked to a decline in immune competence with a concomitant rise in proinflammatory immunity, placing the process of immune aging at the center of aging biology. Immune aging affects individuals older than 50 years and is accelerated in patients with the autoimmune disease rheumatoid arthritis. Immune aging results in a marked decline in protective immune responses and a parallel increase in tissue inflammatory responses. By studying immune cells in patients with rheumatoid arthritis, several of the molecular underpinnings of the immune aging process have been delineated, such as the loss of telomeres and inefficiencies in the repair of damaged DNA. Aging T cells display a series of abnormalities, including the unopposed up-regulation of cytoplasmic phosphatases and the loss of glycolytic competence, that alter their response to stimulating signals and undermine their longevity. Understanding the connection between accelerated immune aging and autoimmunity remains an area of active research. With increasing knowledge of the molecular pathways that cause immunosenescence, therapeutic interventions can be designed to slow or halt the seemingly inevitable deterioration of protective immunity with aging.     

红藤灌肠液灌肠联合SASP治疗溃疡性结肠炎40例

目的:观察红藤灌肠液灌肠联合SASP治疗溃疡性结肠炎的疗效。方法:将40例溃疡性结肠炎患者随机分为两组,每组20例,治疗组予以红藤灌肠液灌肠qd联合SASP1.0gqid,对照组予以SASP1.0gqid,治疗3周后观察疗效。结果:治疗组总有效率95.0%,对照组总有效率80.0%,两组比较有显著差异。结论:红藤灌肠液灌肠联合SASP疗效明显优于SASP治疗。     

培菲康胶囊对轻中度溃疡性结肠炎患者血清中IL-18和IL-4的影响

目的观察柳氮磺胺吡啶联合培菲康胶囊治疗轻、中度溃疡性结肠炎的临床疗效并探讨其作用机制。方法选择66例轻中度溃疡性结肠炎患者,随机分为联合治疗组（A组）34例,单药治疗组（B组）32例,健康对照组（C组）30例,A组口服柳氮磺胺吡啶同时加服培菲康胶囊,B组口服柳氮磺胺吡啶,疗程4周。2组患者治疗前后的临床症状、结肠镜检查情况进行比较。采用酶联免疫吸附试验（ELISA）检测2组患者治疗前后和30名健康志愿者（C组）血清中白细胞介素-18（IL-18）和白细胞介素-4（IL-4）的水平。结果A组显效率明显高于B组（P〈0.05）;A和B组治疗前IL-18水平明显高于C组,A组治疗后IL-18的水平与C组无显著差异,而B组仍高与C组;2组患者治疗前IL-4水平与C组差异无统计学意义（P〉0.05）,治疗后A组与C组比较IL-4水平明显升高（P〈0.05）;B组与C组差异无统计学意义（P〉0.05）。结论柳氮磺胺吡啶联合培菲康胶囊比单独使用柳氮磺胺吡啶治疗轻中度溃疡性结炎具有更好的临床疗效,其可能机制是通过下调IL-18,上调IL-4水平,发挥其治疗作用。     

兴城矿泉浴治疗强直性脊柱炎临床疗效评价

比较在改变病情药（DMARDs）基础上用矿泉和淡水浴治疗强直性脊柱炎（AS）的疗效。方法48例AS患者随机分为矿泉浴治疗试验组和淡水浴对照组，二组水温同为38～40℃，每次30分钟，每日1次，共60次；同时均口服柳磺毗陡（SASP）第1周0．5，每日3次，第2周起1．0，每日3次及甲氨喋呤（MTX）第1周5．0mg，第2周7．5mg，第3周10mg,第4周15mg，每周1次。治疗前后对腰背痛指数、晨僵时间、夜间痛计分、外周关节痛指数、胸廓扩张度、Schober试验、血沉（ESR）、C反应蛋白（CRP）、指地距、枕墙距及骰骼关节X线改变等指标进行评价并对比分析。结果试验组总有效率（87．50％）明显高于对照组（56．25％，P＜0．05），尤其在改善夜间痛、外周关节痛、枕墙距、指地距、腰背痛、CRP及缩短晨但时间方面优于对照组（P＜0．05）。结论兴城矿泉浴在治疗AS时可对DMARDs产生协同作用。疗效优于对照组。     

Inhibition of ASCT2 induces hepatic stellate cell senescence with modified proinflammatory secretome through an IL-1α/NF-κB feedback pathway to inhibit liver fibrosis

Senescence of activated hepatic stellate cells (aHSCs) is a stable growth arrest that is implicated in liver fibrosis regression. Senescent cells often accompanied by a multi-faceted senescence-associated secretory phenotype (SASP). But little is known about how alanine-serine-cysteine transporter type-2 (ASCT2), a high affinity glutamine transporter, affects HSC senescence and SASP during liver fibrosis. Here, we identified ASCT2 is mainly elevated in aHSCs and positively correlated with liver fibrosis in human and mouse fibrotic livers. We first discovered ASCT2 inhibition induced HSCs to senescence in vitro and in vivo. The proinflammatory SASP were restricted by ASCT2 inhibition at senescence initiation to prevent paracrine migration. Mechanically, ASCT2 was a direct target of glutaminolysis-dependent proinflammatory SASP, interfering IL-1α/NF-κB feedback loop via interacting with precursor IL-1α at Lys82. From a translational perspective, atractylenolide III is identified as ASCT2 inhibitor through directly bound to Asn230 of ASCT2. The presence of –OH group in atractylenolide III is suggested to be favorable for the inhibition of ASCT2. Importantly, atractylenolide III could be utilized to treat liver fibrosis mice. Taken together, ASCT2 controlled HSC senescence while modifying the proinflammatory SASP. Targeting ASCT2 by atractylenolide III could be a therapeutic candidate for liver fibrosis.     

Autophagy in cancer: having your cake and eating it

Autophagy, one of two major intracellular degradation pathways, plays a critical role in energy homeostasis and the quality control of macromolecules and intracellular organelles. Previous work has demonstrated the importance of autophagy in maintaining cellular fitness, both in healthy and stressful conditions, revealing the complex interplay between autophagy and other stress-responsive phenotypes. The complex outcomes of stress-responsive autophagy confer on it both pro- and anti-tumourigenic roles, depending on the cellular and environmental context. Furthermore, recent findings that functionally link autophagy to the tumour suppressor mechanism, cellular senescence, have revealed a new role of autophagy in cancer biology. In this review we summarise the current evidence on the relationship between autophagy and cancer, with a focus on its role in senescence.     

氨基水杨酸药理作用研究进展

水杨酸偶氮磺胺吡啶（SASP）、5-氨基水杨酸（5-ASA）、对氨基水杨酸（4-ASA）是治疗溃疡性结肠炎卓有成效的药物。它们具有共同的氨基水杨酸结构,但三者作用机制不甚相同,确切作用机制不清。SASP、5-ASA抑制炎性介质,而4-ASA对PG、LT无影响。5-ASA清除反应性氧代谢产物作用明显,4-ASA作用较弱。氨基水杨酸影响多种细胞因子（如IL-1,IL-2,IL-6,INF-γ、TNF-α、GM-CSF等）的功能,可能是通过抑制细胞因子与受体结合,或减少一些细胞因子的合成与释放。SASP抑制中性粒细胞脱颗粒、释放溶酶体及一些酶,改变淋巴细胞活性。氨基水杨酸类药物对一氧化氮合成酶、粘附分子及肠道通透性等亦有影响。