家庭肠内营养对改善晚期胃癌患者生活质量的应用价值

目的研究家庭肠内营养（HEN）对晚期胃癌患者改善生活质量的意义。方法回顾性分析浙江省人民医院胃肠外科2010年6月1日至2012年6月1日连续收治的60例无法手术切除及复发转移的晚期胃癌患者的病历资料,根据是否进行HEN分为肠内营养（EN）组（25例）和对照组（35例）。EN组营养支持方式包括经空肠造瘘管EN、经鼻胃肠管完全或部分EN;对照组中存在胃癌伴梗阻的患者进行全肠外营养（TPN）,其余患者完全经口饮食。在持续1年的随访过程中,分别于第1、3、6和12月进行Kamofsky评分和Spitzer指数测定。第6月时行EORTCQLQ—c30评分。全组患者均接受FLOFOX4方案（奥沙利铂、四氢叶酸钙、氟尿嘧啶）静脉化疗。结果两组患者在基线资料方面差异无统计学意义。1年随访期间,两组共有53例患者死亡,其中EN组21例,对照组32例。KamoHky评分结果显示,EN组在第3、6、12月的评分结果分别为平均57．4、39．6和28．2,明显优于对照组的平均45．3、29．2和20．1（分别为P=0．041、P=0．012和P=0．015）。Spitzer评分结果显示,EN组在第3、6、12月的评分结果分别为5．12、4．04和2．54,也明显优于对照组的4．32、3．21和1．97（分别为P=0．048、P=0．035和P=0．024）。EROTCQLQ-30评分结果显示,EN组在功能量表方面同样均明显优于对照组（均P〈0．05）,“呼吸费力”、“疼痛”和“疲劳”阳性症状较对照组轻（分别为P=0．025、P=0．044和P=0．016）;但“腹泻”症状较对照组明显（P=0．047）。结论HEN作为一项营养干预措施,能在有限的生存期内改善晚期胃癌患者的生活质量。     

膈下逐瘀汤对肝癌Bel-7402细胞增殖的抑制及其机制

目的:观察中药复方膈下逐瘀汤对肝癌Bel-7402细胞增殖的抑制及其相关机制。方法:实验于2005-09/2006-07在南方医科大学细胞生物实验室完成。膈下逐瘀汤(按《医林改错》方组成:五灵脂6g,当归9g,川芎6g,桃仁9g,丹皮6g,赤芍6g,乌药6g,延胡索3g,甘草9g,香附5g,红花9g,枳壳5g。均购自南方医院中药房)经研粉、煮沸、离心、过滤配成质量浓度为25,50,100,200mg/L的药液;顺铂配制成质量浓度为0.5,1.0,1.5,2.0mg/L的药液(作为阳性对照),均作用于Bel-7402细胞,并设空白对照(未加任何药物)。采用甲基噻唑基四唑(methyl thiazoly ltetrazolium,MTT)比色法检测膈下逐瘀汤各组对Bel-7402细胞生长的影响,用酶标仪测定培养细胞在600nm处吸光度值,并计算细胞抑制率,抑制率(%)=(实验组吸光度值-对照组吸光度值/对照组吸光度值)×100%。用蛋白印迹试验检测不同质量浓度药物作用48,72h时第10号染色体同源丢失性磷酸酶-张力蛋白基因蛋白的表达水平。结果:①中药复方膈下逐瘀汤对Bel-7402细胞增殖的影响:膈下逐瘀汤对肝癌Bel-7402细胞有明显的生长抑制作用,呈良好的剂量-效应关系。膈下逐瘀汤质量浓度在200mg/L时其48h细胞生长抑制率介于0.5mg/L顺铂组与1.0mg/L顺铂组之间(分别为41.27%,34.01%,47.49%);膈下逐瘀汤质量浓度在50,25mg/L时,其细胞抑制率明显低于顺铂组,72h细胞抑制率结果基本相同。②药物作用肝癌Bel-7402细胞48h后第10号染色体同源丢失性磷酸酶-张力蛋白基因蛋白的表达:第10号染色体同源丢失性磷酸酶-张力蛋白基因蛋白的表达增多,200mg/L膈下逐瘀汤组介于0.5mg/L顺铂组和1.0mg/L顺铂组之间。结论:中药复方膈下逐瘀汤抑制Bel-7402细胞的增殖机制可能是第10号染色体同源丢失性磷酸酶-张力蛋白基因表达增多的原因。     

红外线对萎缩性胃炎大鼠胃黏膜细胞修复后体质量及热休克蛋白表达的影响

目的:利用红外线对实验性萎缩性胃炎大鼠进行照射的体质量变化情况,分析比较各组大鼠胃黏膜的病理形态及热休克蛋白(heatshockpro-teins,HSP)70表达状况与意义。方法:实验在河北北方学院实验中心完成。35只大鼠作为正常对照组,27只进行造模,采用水杨酸钠、乙醇灌胃,刺激大鼠胃黏膜,并结合劳累、饥饱失常等多因素方法连续造模8周,建立萎缩性胃炎大鼠模型。随机取5只进行预实验,确认模型成功后,将22只造模大鼠随机分为非治疗组(11只)和红外线治疗组(11只)。红外线治疗采用220V,200W的红外线灯,垂直照射大鼠胃部投影区,1次/d,10min/次,连续照射20d。光镜下观察胃黏膜厚度、炎症程度及壁细胞的形态、结构等变化,免疫组化法检测HSP70的表达状况。结果:造模大鼠体质量明显减轻(P<0.01),胃黏膜变薄(P<0.01)。光镜下可见胃黏膜层腺体细胞明显萎缩,炎细胞浸润,部分标本粘液腺化生。经红外线照射后,HSP70100%表达;病理形态学观察可见大鼠胃黏膜增厚,与非治疗组比较差异有显著性意义(P<0.01),炎细胞明显减少,胃上皮细胞的形态、结构、体积均恢复或接近正常。结论:红外线是治疗大鼠萎缩性胃炎的一种有效途径。萎缩性胃炎大鼠在红外线刺激下,胃黏膜细胞增生。HSP70在防御功能中发挥一定作用。     

Tonsillitis exacerbates renal injury in IgA nephropathy through promoting Th22 cells chemotaxis

Background

Tonsillitis can promote the progression of IgA nephropathy (IgAN) by aggravating immunopathologic response. Th22 cell disorder is involved in the pathogenesis of IgAN with tonsillitis. This study was determined to explore the possible mechanism of IgAN with tonsillitis underlying Th22 cell chemotaxis response to the effect of CCL20, CCL22, and CCL27.

Methods

This research was conducted on 65 subjects including 16 healthy controls (HC group), 5 patients with  renal carcinoma (HTC group) and 44 patients with IgAN between 2015 and 2016. According to clinical symptoms and results of throat swab culture, patients with IgAN were divided into two groups: IgAN with tonsillitis (IgAN + tonsillitis, n = 14) and IgAN patients without tonsillitis (IgAN, n = 30). Distribution of Th22 cells in IgAN patients was determined. The expression of CCL20, CCL22, and CCL27 in both peripheral blood and kidneys of IgAN patients was investigated. Severity of pathological lesions in IgAN patients was analyzed. Coculture assay and transwell assay were performed to explore the impacts of human mesangial cells (HMC) on Th22 cell chemotaxis and Th22 cell local accumulation under hemolytic streptococcus (HS) infection.

Results

Th22 cell percentages in IgAN patients increased compared with healthy controls. This increased Th22 cell percentage was positively correlated with the renal lesions of IgAN patients. Correspondingly, the expression of CCL20, CCL22, and CCL27 in renal tissue increased in IgAN patients. Tonsillitis exacerbated these overrepresentations of Th22 cells and chemokines. It was found that HMC could produce CCL20, CCL22, and CCL27. The supernatant of HMC was chemotactic for Th22 cells. This activity of HMC was stimulated by HS infection, whereas treatment of anti-CCL20, anti-CCL22, and anti-CCL27 antibodies partly blocked this chemoattractant effect of HMC.

Conclusions

Tonsil infection may aggravate the renal pathological lesions of IgAN by exacerbating Th22 cell accumulation. Our data suggested a collaboration between HMC and Th22 cells in IgAN with tonsillitis underlying the effects of CCL20, CCL22, and CCL27.