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1.
目的研究微生态制剂思连康辅助治疗溃疡性结肠炎的疗效及其可能的机制。方法将溃疡性结肠炎患者79例随机分成治疗组及对照组,治疗组40例,对照组39例。对照组采用常规治疗,治疗组在常规治疗的基础上加用双歧四联活菌制剂——思连康。比较2组治疗前及治疗2个月后患者的临床症状评分、结肠黏膜炎症表现、细胞因子IL-10、IL-18的变化。结果治疗2个月后2组临床症状评分、结肠黏膜炎症评分均较治疗前有明显改善(P〈0.01),且治疗组临床症状、结肠黏膜炎症改善程度优于对照组(P〈0.01),IL-10、IL-18的含量治疗前后有明显的变化,IL-10增加,IL-18降低。结论思连康可辅助治疗溃疡性结肠炎,其机制可能是通过调节细胞因子的变化,进一步影响结肠黏膜的免疫功能。  相似文献   

2.
目的检测正常人和细菌性阴道病(BV)患者治疗前后阴道局部细胞因子的变化,探讨乳杆菌活菌制剂对女性生殖道免疫的影响,为阴道微生态平衡与阴道黏膜免疫屏障的关系的研究提供一定的依据。方法用乳杆菌活菌制剂治疗BV,通过酶联免疫吸附试验法即ELISA法来检测BV患者治疗前后及正常健康妇女阴道局部细胞因子sIgA、IL-2、IL-13的水平。结果 sIgA、IL-13水平治疗前组较对照组明显升高(P<0.01),治疗后组较治疗前组水平下降(P<0.05),治疗后组较对照组水平升高(P>0.05);IL-2水平治疗前组较对照组明显降低,治疗后组较治疗前组明显升高(P<0.05),治疗后组较对照组下降(P<0.05)。结论 BV患者阴道局部免疫功能发生了改变;乳杆菌活菌制剂对BV患者阴道局部免疫具调节作用.  相似文献   

3.
目的探讨低聚果糖对溃疡性结肠炎(UC)模型小鼠肠黏膜屏障的调节作用及可能机制。方法小鼠随机分成3组:正常对照(NC)组、模型(MD)组和低聚果糖(FOS)组,采用葡聚糖硫酸钠制作UC小鼠模型。造模7d同时给予干预治疗,停用造模药物并后续治疗7d。采用细菌定量测定法检测肠道菌群,放射免疫法检测肠黏膜sIgA,ELISA法检测小鼠肠黏膜IL-10、TNF-α和IL-6水平。结果模型组小鼠存在肠道菌群失调(t=2.088,2.036,2.203,2.109,P0.05),其TNF-α、IL-6水平高于正常对照组(t=1.734,1.801,P0.05),肠黏膜sIgA、IL-10低于正常对照组(t=1.820,1.806,P0.05);低聚果糖组肠道菌群失调状况较模型组有所改善,其TNF-α、IL-6水平低于正常对照组(t=1.980,1.816,1.936,1.920,1.969,1.893,P0.05),肠黏膜sIgA、IL-10高于正常对照组(t=1.801,1.796,P0.05)。结论低聚果糖可改善溃疡性结肠炎模型小鼠肠道菌群屏障功能,可以提高肠黏膜sIgA和抗炎细胞因子IL-10的水平并降低致炎细胞因子TNF-α和IL-6的水平,通过调节肠道过度的免疫反应,使免疫屏障功能得到一定恢复。  相似文献   

4.
目的:探讨微生态制剂思连康联合小儿康治疗儿童迁延性腹泻的疗效,并进一步探讨其机制.方法:我院共收治60例腹泻患儿,随机分为两组,均在常规治疗基础上治疗组加用思连康联合小儿康,对照组加用杜拉宝治疗儿童腹泻.观察两组的疗效,以及两组临床症状的好转情况及住院时间的比较.酶联免疫吸附双抗体夹心法(ELISA法)检测两组患者血清和粪便白介素6和8(IL-6和IL-8)的变化.结果:治疗组总有效率为90%,高于对照组(P<0.05);临床症状的好转情况及住院时间的比较优于对照组(P<0.01).治疗后血清及大便细胞因子IL-6和IL-8均有降低,并优于对照组(P<0.05).结论:思连康联合小儿康治疗儿童迁延性腹泻,疗效显著,值得广泛推广.其机制可能与下调炎性细胞因子有关.  相似文献   

5.
目的:通过检测白细胞介素23受体(IL-23R)及白细胞介素17A(IL-17A)在炎症性肠病(IBD)患者肠黏膜及血清中的表达水平,探讨其在IBD发病过程中的作用及意义。方法:收集32例克罗恩病(CD)患者、29例溃疡性结肠炎(UC)患者及27例对照者的内镜肠黏膜活检标本,采用荧光定量PCR技术检测肠黏膜内IL-23R、IL-17AmRNA的表达情况,免疫组化技术分析IL-23R、IL-17A在肠黏膜中的原位表达。结果:与健康对照组相比,CD及UC患者肠黏膜组织内IL-23R mRNA表达显著增高(P<0.05),CD及UC组间的表达量差异无统计学意义(P>0.05)。CD及UC患者肠黏膜组织内IL-17A mRNA表达显著增高(P<0.05),CD组肠黏膜组织内IL-17AmRNA表达显著高于UC组(P<0.05)。免疫组化分析显示IL-23R阳性细胞在CD与UC肠黏膜固有层内有较多表达,较正常黏膜内的肠上皮细胞相比,CD及UC患者肠黏膜IL-23R蛋白表达量最著增高(P<0.05),UC及CD组间的表达量差异无统计学意义(P>0.05)。IL-17A阳性细胞在CD与UC肠黏膜固有层内有较多表达,较正常黏膜内的肠上皮细胞相比,CD及UC患者肠黏膜IL-17A蛋白表达量最著增高(P<0.05)。结论:IL-23R及IL-17A在IBD患者肠黏膜中表达显著增高,提示IL-23R及IL-17A表达异常与IBD的发生发展密切相关,有可能成为IBD治疗的新靶点。  相似文献   

6.
目的观察马齿苋多糖对溃疡性结肠炎小鼠肠黏膜细胞因子及肠道菌群的影响。方法应用硫酸葡聚糖钠(DSS)制备溃疡性结肠炎小鼠模型,随机分成2组:正常对照组、模型组,造模成功后模型组再分为自然恢复组、马齿苋多糖治疗组。分别于造模后、给药7 d后处死小鼠,进行肠黏膜细胞因子测定、肠道菌群检测。结果 DSS造模后模型组小鼠肠黏膜细胞因子TNF-а、IL-6升高,IL-10减少;小鼠肠道菌群失调。马齿苋多糖治疗7 d后治疗组小鼠与模型组小鼠比TNF-α、IL-6下降,IL-10增加;肠道双歧杆菌和乳杆菌数量上升。结论马齿苋多糖可以提高抗炎细胞因子IL-10的水平并降低致炎细胞因子TNF-α、IL-6的水平;可以提高双歧杆菌和乳杆菌数量。马齿苋多糖通过抗炎和降低肠道过度的免疫反应以及调节肠道微生态失调,对溃疡性结肠炎发挥治疗作用。  相似文献   

7.
目的 旨在研究复合微生态制剂对小鼠肠道黏膜免疫功能的影响方法 选取28日龄BALB/C小鼠80只,通过灌胃低、中、高不同剂量(2.5、5、10 g/kg体重)的复合微生态制剂,第14天和第28天采取血液样本和空肠组织,并取材免疫器官进行免疫器官指数测定。用比浊法检测血液中溶菌酶含量,用ELISA法检测小鼠空肠黏膜免疫细胞因子(IL-4、IL-10、IFN-γ)和SIgA含量;用荧光定量PCR检测小鼠空肠黏膜免疫细胞因子mRNA表达水平。结果 (1)不同剂量复合微生态制剂均可提高小鼠肠道黏膜免疫细胞因子及SIgA的含量和免疫细胞因子mRNA的表达水平。第14天,中剂量组小鼠空肠黏膜免疫细胞因子IL-4、IL-10、IFN-γ及SIgA含量和mRNA表达水平极显著高于对照组(P<0.01)。第28天,低剂量组和中剂量组空肠黏膜IL-4含量极显著提高(P<0.01);中剂量组IL-10、IFN-γ及SIgA含量和mRNA表达水平极显著高于对照组(P<0.01);中、高剂量组IL-4、IL-10及IFN-γ的mRNA表达水平均不同程度高于对照组(P<0.05或P<...  相似文献   

8.
目的探讨双歧杆菌四联活菌片联合美沙拉嗪对溃疡性结肠炎(UC)患者肠黏膜氧化应激损伤的修复作用。方法选取2016年10月至2018年12月我院内科门诊就诊的活动期轻、中度UC患者92例,随机分为观察组和对照组各46例。两组患者均给予美沙拉嗪肠溶片1.0 g/次,4次/d,口服。观察组在此基础上加用双歧杆菌四联活菌片1.5 g/次,3次/d,口服。两组均连用8周。观察两组患者治疗前后血清氧化应激指标[氧化低密度脂蛋白(ox-LDL)和过氧化脂质(LPO)]、肠黏膜屏障受损情况指标[血清降钙素原(PCT)和二胺氧化酶(DAO)]及肠镜下肠黏膜评分变化,并比较临床效果。结果治疗8周后,两组患者血清ox-LDL、LPO、PCT和DAO水平及肠黏膜评分均较治疗前显著下降(均P<0.05),且治疗后观察组患者上述指标水平下降幅度大于对照组(均P<0.05)。观察组患者临床总有效率(95.65%)高于对照组(82.61%),差异有统计学意义(χ^2=4.04,P<0.05)。结论双歧杆菌四联活菌片联合美沙拉嗪对轻中度活动性UC患者的疗效显著,能降低患者血清ox-LDL、LPO、PCT和DAO水平,对肠黏膜氧化应激损伤具有良好的修复作用。  相似文献   

9.
目的探讨围术期给予微生态制剂酪酸梭菌活菌片对电切肠息肉患者肠黏膜再生修复的影响。方法选择我院2017年1月至2019年6月期间收治的104例择期电切手术的肠息肉患者为研究对象,随机分为对照组和研究组,各52例。两组患者均给予围术期常规治疗,研究组在此基础上于术前2 d至术后4周给予酪酸梭菌活菌片。采用乳果糖/甘露醇(LAC/MAN)吸收试验评价患者肠黏膜功能,复查电子结肠镜评价肠黏膜修复率和肠黏膜评分。结果研究组患者术后肠黏膜修复情况优于对照组,肠黏膜评分低于对照组,组间差异具有统计学意义(P0.05)。术前两组患者LAC、MAN和LAC/MAN比较差异无统计学意义(P0.05),术后研究组患者LAC和LAC/MAN显著低于对照组(P0.05)。术前两组患者D-乳酸、DAO、ET和PCT水平比较,差异无统计学意义(P0.05),术后研究组患者D-乳酸、DAO、ET和PCT水平低于对照组,差异有统计学意义(P0.05)。结论围术期给予电切肠息肉患者微生态制剂酪酸梭菌活菌片可降低肠黏膜通透性,促进肠黏膜的再生和修复。  相似文献   

10.
摘要:目的 研究纳米山药多糖合生元结肠靶向微生态调节剂对抗生素脱污染菌群失调白兔的免疫学效应和机制。方法 用盐酸林可霉素建立菌群失调白兔模型,不同时间点取样,检测各组实验动物胸腺、脾脏指数,采用ELISA法,对各组实验动物肠黏膜sIgA、血清IL-2、IL-6进行检测。结果 各组指标检测结果,制剂组优于阳性对照组,差异有统计学意义(P<0.01)。结论 纳米山药多糖合生元结肠靶向微生态调节剂对抗生素脱污染菌群失调白兔免疫学指标有显著影响。  相似文献   

11.
目的:比较美沙拉秦+安慰剂与美沙拉秦+益生菌诱导轻至中度活动期溃疡性结肠炎(UC)缓解的疗效。方法:32例轻、中度活动期溃疡性结肠炎患者随机分为2组,试验组用美沙拉秦联用益生菌治疗,对照组用美沙拉秦及安慰剂治疗。治疗8周后评估患者UC-DAI评分及肠镜。结果:经统计学处理,两组治疗前后UC-DAI指数评分比较,均有效,P<0.05,两组间UC-DAI治疗前后有差异,P<0.05,但两组间缓解率无明显差异,表明美沙拉秦加用益生菌对诱导轻中度活动溃结促进缓解作用。结论:对于轻中度活动性溃疡性结肠炎,加用益生菌有改善病情作用,但可能无益于诱导缓解。  相似文献   

12.
目的探讨肠道菌群和粪便炎性标志物在炎症性肠病(IBD)活动度评估中的临床价值。方法共纳入120例IBD患者为研究组,其中溃疡性结肠炎(UC)患者68例,克罗恩病(CD)患者52例。选择30例经结肠镜检查正常的健康体检者为对照组。采集全部研究对象的新鲜粪便标本进行粪便细菌培养及炎性标志物检测,比较不同疾病活动度IBD患者的肠道菌群及粪便钙卫蛋白(FC)、乳铁蛋白(LF)、基质金属蛋白酶-9(MMP-9)、髓过氧化酶(MPO)水平的变化。结果与对照组比,UC和CD患者肠道中肠杆菌、肠球菌、拟杆菌、消化球菌及酵母菌数量均明显增加(P0.05),双歧杆菌、乳杆菌及真杆菌数量明显减少(P0.05)。UC患者梭菌数量较对照组增加(P0.05),CD患者梭菌数量较对照组减少(P0.05)。UC、CD活动期患者肠杆菌、肠球菌、拟杆菌、消化球菌及酵母菌数量明显多于缓解期患者(P0.05),双歧杆菌、乳杆菌及真杆菌数量明显少于缓解期患者(P0.05),且重度活动期患者肠道菌群改变较轻、中度活动期改变更明显(P0.05)。UC活动期患者梭菌数量明显多于缓解期(P0.05),CD活动期患者梭菌数量明显少于缓解期(P0.05)。UC和CD患者粪便中FC、LF、MMP-9及MPO水平均显著高于对照组(P0.05)。UC、CD活动期患者FC、LF、MMP-9及MPO水平显著高于缓解期患者(P0.05),且重度活动期患者高于轻、中度活动期患者(P0.05)。结论肠道菌群变化和粪便中FC、LF、MMP-9及MPO水平可作为IBD患者疾病活动性评估的辅助指标。  相似文献   

13.
摘要 目的:探讨血清免疫炎症相关蛋白复合物(IIRPCs)、25-羟维生素D[25(OH)D]、脂肪细胞因子(Chemerin)与炎症性肠病(IBD)患者疾病活动性和肠道菌群的相关性。方法:选取2020年12月~2021年12月我院收治的150例IBD患者,其中溃疡性结肠炎(UC)组65例、克罗恩病(CD)组85例,另取同期健康体检者70例作为对照组,检测并比较三组血清IIRPCs、25(OH)D、Chemerin水平。此外,UC组和CD组患者分别根据克罗恩病活动指数(CDAI)和溃疡性结肠炎的改良梅奥(Mayo)评分分为活动期组、缓解期组,分别比较UC组和CD组患者活动期组与缓解期组间的血清IIRPCs、25(OH)D、Chemerin水平、肠道菌群差异,并作相关性分析。结果:IBD患者的血清IIRPCs、Chemerin水平高于对照组,而25(OH)D水平低于对照组(P<0.05);UC组血清IIRPCs、Chemerin水平高于CD组,25(OH)D水平低于CD组(P<0.05)。活动期UC、CD患者的血清IIRPCs、Chemerin水平以及肠球菌、肠杆菌、酵母菌、拟杆菌数量均高于缓解期UC、CD患者,而血清25(OH)D水平以及双歧杆菌、乳酸杆菌数量均低于缓解期UC、CD患者(P<0.05)。Pearsonn相关性分析结果显示,UC、CD患者的血清IIRPCs、Chemerin水平与肠球菌、肠杆菌、酵母菌、拟杆菌数量呈正相关,与双歧杆菌、乳酸杆菌数量呈负相关(P<0.05);UC、CD患者的血清25(OH)D水平与肠球菌、肠杆菌、酵母菌、拟杆菌数量呈负相关,与双歧杆菌、乳酸杆菌数量呈正相关(P<0.05)。结论:血清IIRPCs、25(OH)D、Chemerin与IBD患者的疾病活动性、肠道菌群有关,检测上述指标对评估IBD患者病情程度有一定价值。  相似文献   

14.
The aim of this study was to evaluate the effect of active ulcerative colitis (UC) treatment on transforming growth factor beta(1) (TGF-beta(1)) concentration in plasma and rectal mucosa measured in 28 patients. The highest plasma values were observed in patients with the severe course of the disease (74.2+/-14.0 ng/ml), and they were significantly higher than in the group with mild one (43.7+/-5.6 ng/ml). Mean TGF-beta(1) measured in mucosal samples from patients with severe UC (563+/-146 pg/mg protein) doubled values from patients with mild UC (286+/-65 pg/mg protein). Plasma and mucosal TGF-beta(1) correlated significantly with disease activity index (DAI) and clinical activity index (CAI). Plasma TGF-beta(1) correlated additionally with scored endoscopic degree of mucosal injury. Treatment caused significant decrease of plasma and mucosal TGF-beta(1) concentrations. Patients who responded completely had higher baseline plasma and mucosal TGF-beta(1) that decreased significantly after the treatment. These results show that plasma and mucosal concentrations of transforming growth factor beta(1) are strongly associated with ulcerative colitis activity, and successful treatment of the disease results with decrease of their levels. More effective response to the treatment can be achieved in patients with higher baseline concentrations of TGF-beta(1).  相似文献   

15.
Abrogating tolerance against unidentified antigens is a critical step in the pathogenesis of ulcerative colitis (UC). T cell anergy, one of the main mechanisms of tolerance, has been shown to be induced by E3 ubiquitin ligases, such as gene related to anergy in lymphocytes (GRAIL), Itch, and c-Cbl in mice. However, it is not well known whether these E3 ligases play roles in human diseases. The pathophysiological role of the E3 ligases in patients with UC was investigated. At first, the expression of GRAIL, Itch, and c-Cbl in human anergic T cells was analyzed by quantitative RT-PCR and Western immunoblotting. Next, the mRNA expression of the E3 ligases was analyzed in peripheral CD4+ T cells of 20 patients with UC and 10 healthy volunteers (HV). mRNA expression was analyzed in patients with active UC before and after treatment with prednisolone and leukocytapheresis. Anergic human CD4+ T cells expressed significantly higher levels of GRAIL, Itch, and c-Cbl than nonanergic cells. GRAIL expression was significantly higher in patients with UC in remission than in patients with active disease and in HV (P < 0.01). The level of GRAIL expression was also significantly increased in patients with active disease whose clinical activity index scores improved after treatment (P < 0.05). There were no significant differences in Itch and c-Cbl expression among patients with active UC, patients with UC in remission, and HV. These data suggest that GRAIL plays an important role in maintaining remission in patients with UC.  相似文献   

16.
目的:探讨美沙拉嗪联合双歧三联活菌治疗溃疡性结肠炎(UC)的临床疗效及对患者TNF-琢、IL-8 及IL-10 水平的影响。方 法:选择2013 年1 月~2014 年1 月我院收治的UC 患者60 例,随机分为研究组与对照组,每组30 例。对照组患者应用美沙拉嗪 治疗,研究组在此基础上联合双歧三联活菌治疗。观察两组临床疗效、血清TNF-alpha、IL-8及IL-10 水平变化及药物不良反应。结果: 研究组治疗的总有效率为86.67%,显著高于对照组的63.33%(P <0.05);治疗后,两组TNF-alpha、IL-8 水平显著降低,IL-10 水平显著 升高(均P<0.01),研究组TNF-alpha、IL-8 显著低于对照组,IL-10 水平显著高于对照组(均P<0.05);研究组不良反应发生率为 6.67%,明显低于对照组的33.33%(P<0.05)。结论:美沙拉嗪联合双歧三联活菌对UC 患者黏膜的保护作用显著,且有效抑制UC 相关的炎性反应,安全可靠,适于临床推广与应用。  相似文献   

17.
摘要 目的:观察肠内营养对活动期溃疡性结肠炎(UC)伴营养不良患者营养状况、肠黏膜屏障功能和肠道菌群的影响。方法:选取2019年8月~2021年9月期间上海长征医院收治的120例活动期UC伴营养不良患者,根据随机数字表法分为对照组(60例,接受全肠外营养治疗)和研究组(60例,接受肠内营养治疗)。观察两组治疗3周后的临床总有效率,对比两组治疗前、治疗3周后的营养状况、肠黏膜屏障功能指标和肠道菌群数量,记录两组治疗期间不良反应发生率。结果:研究组(90.00%)临床总有效率高于对照组(68.33%)(P<0.05)。研究组治疗3周后D-乳酸(D-LA)、二胺氧化酶(DAO)、内毒素(ET)水平低于对照组同期(P<0.05)。研究组治疗3周后血清白蛋白、血红蛋白水平高于对照组同期(P<0.05)。研究组治疗3周后乳酸杆菌、双歧杆菌数量高于对照组同期,大肠杆菌数量则低于对照组同期(P<0.05)。两组不良反应发生率对比无差异(P>0.05)。结论:活动期UC伴营养不良患者选用肠内营养进行治疗,可促进营养状况和肠黏膜屏障功能改善,调节肠道菌群结构,安全有效。  相似文献   

18.
Studies in animal models and humans suggest anti-inflammatory roles on the N-acylethanolamide (NAE)-peroxisome proliferators activated receptor alpha (PPARα) system in inflammatory bowel diseases. However, the presence and function of NAE-PPARα signaling system in the ulcerative colitis (UC) of humans remain unknown as well as its response to active anti-inflammatory therapies such as 5-aminosalicylic acid (5-ASA) and glucocorticoids. Expression of PPARα receptor and PPARα ligands-biosynthetic (NAPE-PLD) and -degrading (FAAH and NAAA) enzymes were analyzed in untreated active and 5-ASA/glucocorticoids/immunomodulators-treated quiescent UC patients compared to healthy human colonic tissue by RT-PCR and immunohistochemical analyses. PPARα, NAAA, NAPE-PLD and FAAH showed differential distributions in the colonic epithelium, lamina propria, smooth muscle and enteric plexus. Gene expression analysis indicated a decrease of PPARα, PPARγ and NAAA, and an increase of FAAH and iNOS in the active colitis mucosa. Immunohistochemical expression in active colitis epithelium confirmed a PPARα decrease, but showed a sharp NAAA increase and a NAPE-PLD decrease, which were partially restored to control levels after treatment. We also characterized the immune cells of the UC mucosa infiltrate. We detected a decreased number of NAAA-positive and an increased number of FAAH-positive immune cells in active UC, which were partially restored to control levels after treatment. NAE-PPARα signaling system is impaired during active UC and 5-ASA/glucocorticoids treatment restored its normal expression. Since 5-ASA actions may work through PPARα and glucocorticoids through NAE-producing/degrading enzymes, the use of PPARα agonists or FAAH/NAAA blockers that increases endogenous PPARα ligands may yield similar therapeutics advantages.  相似文献   

19.

Background

Ulcerative colitis (UC) impairs the health-related quality of life (HRQOL). The difference in HRQOL between patients with mild and moderately active UC is not well-defined. Few studies have been conducted to explore the factors that influence HRQOL in Chinese patients. Our study aims were to (1) compare HRQOL of mildly active UC patients with moderate patients; (2) explore the factors that influence HRQOL in Chinese patients with UC; and (3) analyze demographic and disease characteristics of UC in China.

Methods

A total of 110 mild and 114 moderate patients with UC were enrolled. The demographic and disease characteristics were recorded. HRQOL was measured by the Chinese version of the inflammatory bowel disease questionnaire (IBDQ) between mild and moderate patients, male and female patients, and different disease distributions. Stepwise regression analysis was used to assess factors influencing the IBDQ score.

Results

Patients with moderate UC had significantly lower IBDQ total scores compared to patients with mild UC (P=0.001). The IBDQ total score had a negative correlation with the Mayo score (r=–0.263, P<0.001). Stepwise regression analysis showed that the disease activity index and gender had an influence on the IBDQ total score (P<0.05). The female patients had a lower score than the male patients (P<0.05), especially in the emotional function domain (P=0.002). Different disease distributions were not statistically significant in the IBDQ total score (P=0.183).

Conclusions

UC has a negative influence on HRQOL. HRQOL in patients with moderate UC was lower than HRQOL in patients with mild UC, as measured by the IBDQ. UC disease activity has a negative correlation with HRQOL. Gender and the disease activity index are important factors involved in the impairment of HRQOL in Chinese patients with UC. Chinese females may benefit from increased psychological care as part of UC therapy.  相似文献   

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