急性脑梗死患者外周血CD34+细胞水平的变化及临床意义

目的 测定急性脑梗死患者外周血CD34 +细胞水平,并探讨其临床意义. 方法 采用流式细胞仪测定发病72 h以内的急性期脑梗死患者(梗死组,45例)、有脑血管危险因素但无脑梗死发生的患者(高危组,27例)和健康体检者(对照组,20例)外周血CD34+细胞水平,分别记录梗死组患者神经功能缺损评分、梗死病灶体积以及颈动脉内中膜厚度. 结果 梗死组(0.034±0.012)％与高危组(0.047±0.009)％患者外周血CD34+细胞百分比均低于对照组(0.063±0.009)％,且梗死组低于高危组(均P＜0.05);梗死组轻度(0.047±0.009)％、中度(0.036±0.009)％、重度(0.022±0.007)％神经功能缺损评分患者外周血CD34+细胞百分比均较对照组降低(P＜0.05),重度组低于中度组,中度组低于轻度组(均P＜0.05);梗死组外周血CD34+细胞百分比均明显低于对照组(P＜0.05),其中大灶组低于中灶组,中灶组低于小灶组(均P＜0.05);(4)颈动脉内膜增厚组(0.043±0.010)％、颈动脉斑块组(0.036±0.010)％及颈动脉狭窄组(0.023±0.009)％,3组患者外周血CD34+细胞百分比均较对照组显著降低.其中颈动脉斑块及颈动脉狭窄组低于颈动脉斑块组,颈动脉斑块组低于颈动脉内膜增厚组(均P＜0.05). 结论 外周血CD34+细胞水平在脑缺血急性期明显降低,与脑梗死后神经功能缺损程度、梗死灶体积、颈动脉粥样硬化程度有关.     

分泌型与包涵体型粒细胞集落刺激因子对骨髓干细胞动员效率的比较

目的观察两种不同粒细胞集落刺激因子(G CSF)动员剂(分泌型与包涵体型)对急性心肌梗死(AMI)患者骨髓血干细胞动员效率。方法一组予以包涵体型G CSF(商品名惠尔血)300μg(包涵体型G CSF组),每日2次,皮下注射,连续5天;另一组予以分泌型G CSF(商品名金磊赛强)300μg(分泌型G CSF组),每日2次,皮下注射,连续5天。第6日经美国Baxter公司生产的CS3000PLUS血细胞分离机,分离外周血干细胞,采集外周血干细胞悬液经流式细胞仪测定CD34+的细胞数量。结果给G CSF前及给G CSF后第3、4、5、6天两组间外周血中细胞表面标记蛋白CD34+细胞数量和白细胞计数无明显统计学差异;在应用两组不同的动员剂后,外周血中白细胞计数与动员时间变化曲线显示曲线高峰在动员后第5天;在包涵体型G CSF组,CD34+细胞数量与时间变化曲线高峰为第5天,但在分泌型G CSF组,CD34+细胞数量与时间变化曲线显示CD34+细胞数量在3～4天内呈急剧升高趋势,但在第5天后升幅明显减缓;显示分泌型G CSF组动员后外周血中干细胞下降较慢;患者外周血中CD34+细胞数量与白细胞计数变化呈正相关(r=0.835),与性别、体重、年龄及AMI发生时间无显著性相关。结论在AMI患者中应用两种不同G CSF动员剂,两组在外周血干细胞动员效率方面无明显统计学差异。     

粒细胞集落刺激因子对老年急性心肌梗死患者骨髓干细胞动员效率的临床观察

目的观察粒细胞集落刺激因子(G-CSF)对老年急性心肌梗死(AMI)患者外周血干细胞的动员效率。方法AMI患者20例按年龄分为≥70岁组和<70岁组,两组均给予包涵体型G-CSF 300~600μg/d皮下注射,连用5 d,检查动员前及动员后第3、4、5、67、d患者外周血白细胞计数,流式细胞仪测定CD34+细胞数量,观察动员过程中不良反应发生的情况。结果≥70岁组在动员前及动员后第3、4、5、6、7 d外周血中白细胞(×109/L)分别为6.75、28.16、34.93、34.40、38.93、21.85,CD34+细胞(×106/L)分别为6.25、51.10、92.60、109.65、134.69、45.09;<70岁组白细胞(×109/L)分别为8.73、28.21、33.67、33.95、32.93、18.71,CD34+分别细胞(×106/L)为9.01、71.79、128.54、268.17、249.51、72.25,两组外周血白细胞比较,差异无统计学意义(均为P>0.05),仅动员后第3 d<70岁组外周血中CD34+较≥70岁组有显著增加(P<0.05);≥70岁组在动员前及动员后第3、4、5、6、7 d外周血中白细胞、CD34+显示,在动员后第6 d出现高峰。患者外周血中CD34+细胞数量与白细胞数量变化呈正相关(r=0.94)。两组不良反应发生情况比较,差异无统计学意义(P>0.05)。结论老年AMI患者行G-CSF动员安全、可行,外周血中CD34+细胞数量与白细胞变化峰值均出现在第6 d,且白细胞与CD34+细胞数量呈正相关。     

特发性膜性肾病患者调节性T细胞和B淋巴细胞的变化及其临床意义

目的:观察特发性膜性肾病(IMN)患者外周血调节性T细胞、B淋巴细胞亚群以及肾组织中B淋巴细胞浸润分布的变化,探讨与膜性肾病(MN)发病机制及临床表现的关系. 方法:66例(男性45例,女性21例,年龄15～71岁)经肾活检确诊为MN,排除各种继发因素,近期未使用大剂量免疫抑制剂的IMN患者,流式细胞仪测定外周血调节性T细胞(CD4+CD25+Foxp3+Treg细胞)、B淋巴细胞(CD20+细胞)和T淋巴细胞亚群(CD3+、CD4+、CD8+细胞)的计数;另采用免疫组织化学方法检测患者肾组织中B淋巴细胞数量及分布.40例年龄、性别匹配的健康志愿者作为对照.根据患者尿蛋白水平,将其分为大量蛋白尿组(尿蛋白定量≥3.5 g/d)及非大量蛋白尿组(尿蛋白定量＜3.5g/d).比较IMN患者外周血调节性T细胞,B淋巴细胞及T淋巴细胞亚群与正常对照的差别,以及IMN患者中大量蛋白尿者和非大量蛋白尿者之间上述淋巴细胞亚群水平的差异及其可能的临床意义. 结果:(1)IMN患者外周血调节性T细胞计数较正常对照组显著降低[(23.2±10.7) cells/μl vs (31.4±7.29) cells/μl,P<0.01].(2)与正常对照组比较,IMN患者外周血B淋巴细胞计数显著升高[(208±111) cells/μl vs (137±64) cells/μl,P<0.01].(3)IMN患者和正常对照组相比,其CD4+细胞计数有升高趋势[(715±267) cells/μl vs (657±214) cells/μl,P>0.05],CD8+细胞计数有降低趋势[(393±178) cells/μl vs (464±200) cells/μl,P>0.05],而CD4+/CD8+比值较正常对照显著升高(2.04±0.92 vs 1.52±0.48,P<0.01).(4)大量蛋白尿组B淋巴细胞计数明显高于非大量蛋白尿组[(246±117) cells/μl vs (186±108) cells/μl,P<0.05],但两组之间调节性T细胞、CD4+细胞、CD8+细胞计数及CD4+/CD8+比值均无统计学差异(P>0.05).(5)IMN患者肾组织中B淋巴细胞浸润数量较正常对照升高,伴肾组织B淋巴细胞灶性聚集者其尿NAG酶水平升高. 结论:IMN患者表现出调节性T细胞水平降低,B淋巴细胞水平上调和CD4+/CD8+细胞比值的偏移.外周血B淋巴细胞水平升高与IMN患者大量蛋白尿关系密切,肾组织中B淋巴细胞浸润数目较正常对照升高,存在局灶B淋巴细胞聚集的患者小管间质急性损伤加重.对IMN患者B淋巴细胞的数目和组织分布进行观察,有可能为监测病情、指导治疗提供帮助.     

脑脉通对骨髓干细胞动员保护大鼠脑缺血损伤的影响

目的 研究脑脉通对脑缺血大鼠骨髓干细胞动员 (BMSCs) 在血液和脑组织的变化及脑保护作用的影响.方法 大鼠随机分为假手术组、模型组、脑脉通组、动员组、脑脉通+动员组,线栓法制备MCAO动物模型.皮下注射人重组粒细胞集落刺激因子(rG-CSF);脑脉通灌胃用药.检测大鼠外周血WBC及CD34+、脑组织CD34+变化;观察神经功能和脑组织病理改变;测定脑组织含水量和脑梗死面积.结果 模型组大鼠外周血WBC(8.07±1.27)×109/L和CD34+细胞(3.17±0.75)个/μl增加,3 d达到峰值,各治疗组增加更为明显;联合组2和3 d外周血WBC、各时间点CD34+细胞均较动员组增加.各模型组大鼠脑组织CD34+表达增强,7 d达到峰值(33.04±2.62)个/μl;各联合组较动员组增强明显.各模型组大鼠神经评分降低、脑含水量增加、脑梗死面积增大、脑组织病理损伤明显,以7 d显著;动员组大鼠7和14 d的上述指标改善;各联合组较动员组的改善明显.结论 血液WBC数CD34+计数,脑组织、CD34+表达均显著显示,脑缺血可引起BMSCs进入外周血并向脑组织归巢,峰值时间存在差异;G-CSF可使BMSCs分布增加;脑脉通使动员后血液和脑组织BMSCs增多、脑组织峰值时间延长,且使其脑保护作用增强.     

心肌梗死患者CD4~+CD25~+Foxp3~+ T细胞检测及意义

目的探讨心肌梗死患者外周血CD4+CD25+Foxp3+T细胞的水平及意义。方法采用流式细胞分析法,检测20例急性心肌梗死患者(AMI组)、21例陈旧性心肌梗死患者(OMI组)和36例健康体检者(对照组)外周血CD4+CD25+Foxp3+T细胞水平。结果 AMI组、OMI组的CD4+CD25+T细胞/CD4+T细胞比例分别为(7.20±1.96)%和(7.55±1.77)%均低于对照组的(8.81±1.50)%(P0.05);CD4+CD25+Foxp3+T细胞/CD4+T细胞比例AMI组为(1.42±0.38)%和OMI组为(1.46±0.55)%均比对照组(1.75±0.58)%低(P0.05)。结论 CD4+CD25+调节性T细胞比例降低可能打破了外周免疫耐受,参与了心肌梗死患者动脉粥样硬化的发生发展。     

冠心病外周血IL-7表达变化对机体免疫应答的影响及可能机制

目的探讨冠状动脉粥样硬化性心脏病(冠心病)外周血白细胞介素(IL)-7表达变化对机体免疫应答的影响及可能机制。方法选取稳定型心绞痛患者44例、不稳定型心绞痛患者78例、急性心肌梗死患者42例;另取体检的健康人群40例为正常对照组。流式细胞术检测T细胞表面黏蛋白结构域的分子(Tim)3水平,酶联免疫吸附试验检测血清IL-7水平。体外培养外周血单核细胞,重组IL-7刺激12 h后检测T细胞表面Tim3水平;通过Western印迹法检测IL-7信号通路相关分子的表达水平。结果稳定型心绞痛组、不稳定型心绞痛组、急性心肌梗死组外周血Tim3阳性细胞占CD4^+T细胞的比例明显高于正常对照组,急性心肌梗死组外周血Tim3阳性细胞占CD4^+T细胞的比例明显高于稳定型心绞痛组、不稳定型心绞痛组(P<0.05)。不稳定型心绞痛组、急性心肌梗死组外周血Tim3阳性细胞占CD8+T细胞的比例明显高于正常对照组,急性心肌梗死组外周血Tim3阳性细胞占CD8+T细胞的比例明显高于稳定型心绞痛组、不稳定型心绞痛组(P<0.05)。急性心肌梗死组血清IL-7水平明显高于正常对照组(P<0.01);稳定型心绞痛组和不稳定型心绞痛组血清IL-7水平与正常对照组之间差异无统计学意义(P>0.05);血清IL-7浓度与Tim3+CD4^+T、CD8+T细胞比例均无相关性。急性心肌梗死组重组IL-7刺激12 h的CD4^+T细胞表面Tim3表达水平较未刺激者明显升高(P<0.05)。正常对照组、急性心肌梗死组重组IL-7刺激12 h的CD8^+T细胞表面Tim3表达水平较未刺激者明显升高(P<0.05)。重组IL-7刺激后p-STAT-5蛋白相对表达量明显高于未刺激的细胞(P<0.01);重组IL-7刺激后SOCS3蛋白相对表达量明显高于未刺激的细胞(P<0.05)。结论IL-7可上调Tim3表达,在冠心病发生、发展中发挥抑制炎症应答的作用。     

冠心病患者冠状动脉病变与免疫细胞的相关研究

目的冠状动脉粥样硬化性心脏病(冠心病)患者冠状动脉粥样硬化病变与免疫细胞的关系。方法选取2014年1月~2016年1月于济宁医学院附属医院治疗的冠心病患者100例,其中急性心肌梗死(AMI)组患者35例、不稳定型心绞痛(UAP)组患者40例、稳定型心绞痛组(SAP)患者25例。同时选取30例健康者作为对照组。采用流式细胞仪检测各组外周血CD4+CD25+调节性T细胞(Treg)和单核细胞CD36比例,同时检测高敏C反应蛋白(hs-CRP)、白细胞介素-17(IL-17)和肿瘤坏死因子-α(TNF-α)水平。结果 AMI组和UAP组外周血CD4+CD25+Treg比例分别为(8.60±1.55)%和(8.17±1.43)%,低于对照组的(10.40±1.43)%和SAP组的(10.72±1.66)%,差异有统计学意义(P均0.05)。与对照组比较,SAP组、AMI组和UAP组单核细胞CD36比例均升高;AMI组和UAP组高于SAP组,差异有统计学意义(P均0.05)。对照组、SAP组、UAP组以及AMI组hs-CRP、IL-17和TNF-α水平均呈升高趋势,差异有统计学意义(P均0.05)。相关性分析结果显示,冠心病患者CD4+CD25+Treg和单核细胞CD36比例与hs-CRP、IL-17、TNF-α等炎症因子水平无明显相关(P均0.05)。结论冠心病患者冠状动脉粥样斑块的不稳定与炎症和免疫反应有关,外周血单核细胞CD36比例明显增加,CD4+CD25+Treg比例明显减低,炎症因子水平升高。     

高密度脂蛋白胆固醇和甘油三酯与心血管病剩余风险的关系

目的分析高密度脂蛋白胆固醇(HDL-C)和甘油三酯(TG)与心血管病剩余风险的关系,探讨HDL-C、TG对心血管病剩余风险的预测价值。方法选择60例低密度脂蛋白胆固醇(LDL-C)2.60 mmol/L的冠状动脉粥样硬化性心脏病(CHD)患者,分为急性心肌梗死组(n=22)、稳定性心绞痛组(n=38),测定血脂和血糖指标,详细记录临床特征并进行分析。结果急性心肌梗死组HDL-C水平低于稳定性心绞痛组(P0.05),急性心肌梗死组TG/HDL-C的比值显著高于稳定性心绞痛组(P0.01)。急性心肌梗死的危险性与TG/HDL-C的比值呈正相关(回归系数β值=0.033 2,P0.001),与HDL-C呈负相关(回归系数β值=-0.095 5,P=0.022),而与总胆固醇(TC)、TG和LDL-C无显著相关。结论 HDLC水平低和TG/HDL-C的比值高是CHD患者发生心血管事件的危险因素,TG/HDL-C的比值能更强地预测CHD患者的心血管病剩余风险。     

骨髓干细胞动员对高龄大鼠缺血心脏功能的保护作用

目的:了解从老年大鼠中动员出的骨髓干细胞归巢于梗死心肌和分化的能力,以及对缺血心脏功能的影响,并探讨其可能机制。方法:W istar大鼠分为3组:高龄心肌梗死+动员组、高龄心肌梗死组和青年心肌梗死+动员组。结扎大鼠左冠状动脉制作急性心肌梗死（AM I）模型,动员组大鼠用骨髓干细胞动员剂干细胞因子动员自体骨髓干细胞释放并归巢于心肌梗死灶,于建模后24 h、48 h和4周杀死各组大鼠,取出心脏,通过免疫组化、HE染色方法观察老年大鼠心肌梗死灶、边缘区和正常心肌组织CD34阳性细胞浸润及心肌再生的情况,应用流式细胞仪比较动员前后外周血中CD34阳性细胞数量的变化,并应用BL-420E生物机能实验系统检测老年大鼠心功能指标。结果:使用干细胞因子后,高龄动员组及青年动员组大鼠外周血中CD34细胞数量显著升高,两组大鼠心肌梗死灶均可见大量CD34细胞浸润;高龄动员组大鼠在制模4周时心功能指标显著比高龄心肌梗死组改善,而高龄动员组和青年动员组的心功能指标无显著差异,均显著改善。制模后24 h,高龄动员组大鼠和青年动员组大鼠心肌梗死程度轻,可见CD34阳性的幼稚心肌细胞样细胞,4周后瘢痕组织少,缺血心肌的基本结构得到保护。结论:在骨髓干细胞动员剂作用下,从老年大鼠个体中动员出的骨髓干细胞归巢梗死心肌能力仍得到增强,有较多干细胞向梗死灶迁移,并向心肌细胞等分化,保护缺血心肌基本结构,改善心功能。     

胰岛素瘤的解剖分布特点分析

目的胰岛素瘤是最常见的胰腺神经内分泌肿瘤，因其临床表现多样，导致诊断困难。影像学诊断尤其是超声内镜(EUS)在胰岛素瘤的诊断中起着重要作用，拥有较高的敏感性和特异性。本研究拟通过明确胰岛素瘤的解剖分布特点，以期有助于提高影像学的诊断准确率和降低漏诊率，尤其是在教育和培训实践中对于EUS的学习者更具有指导价值。 方法回顾性分析解放军总医院第一医学中心病案资料数据库1993年1月至2019年11月经外科手术、病理确诊为胰岛素瘤的患者的临床资料，检索方法采取搜索术后病理诊断为"胰岛素瘤"的病例，通过查阅病例的方法，提取出胰岛素瘤的大小和解剖分布等数据，进一步分析其特点。 结果共检索到确诊为胰岛素瘤的患者116例，其中，男45例、女71例，年龄13～76岁，平均年龄(44.4±14.85)岁。胰岛素瘤单发110例(94.8%)、多发6例(5.2%)。位置分布：头颈部46例(39.7%)，单发45例、多发1例；体尾部68例(58.6%)，单发65例、多发3例；全胰腺多发2例(1.7%)。病变大小特点：最大径0.4～3.4 cm，平均大小(1.53±0.58)cm。≤1 cm 29例、>1 cm而≤1.5 cm41例、>1.5 cm而≤2.0 cm28例，≤3 cm 15例，>3 cm 3例。年龄与肿瘤的大小相关，≤44岁患者肿瘤平均大小为(1.36±0.51)cm、>44岁患者肿瘤平均大小为(1.70±0.60)cm，P<0.05。头颈部的肿瘤大于体尾部的肿瘤，头颈部肿瘤平均大小(1.66±0.63)cm，体尾部(1.42±0.52)cm，P<0.05。 结论胰岛素瘤在胰腺体尾部较头颈部更好发；绝大多数单发，但可以全胰腺多发；多数小于1.5 cm，肿瘤的大小与患者年龄和肿瘤的解剖分布相关。     

Pathogenesis of carcinoma of the papilla of Vater

Most adenomas and carcinomas of the small intestine and extrahepatic bile ducts arise in the region of the papilla of Vater. In familial adenomatous polyposis (FAP) it is the main location for carcinomas after proctocolectomy. In many cases symptoms due to stenosis lead to diagnosis at an early tumor stage. In about 80%, curative intended resection is possible. Operability is the most relevant prognostic factor. Most ampullary carcinomas resp. carcinomas of the papilla of Vater develop from adenomatous or flat dysplastic precursor lesions. They can be sited in the ampulloduodenal part of the papilla of Vater, which is lined by intestinal mucosa. They also can develop in deeper parts of the ampulla, which are lined by pancreaticobiliary duct mucosa. Intestinal-type adenocarcinoma and pancreaticobiliary-type adenocarcinoma represent the main histological types of ampullary carcinoma. Furthermore, there exist unusual types and undifferentiated carcinomas. Many carcinomas of intestinal type express the immunohistochemical marker profile of intestinal mucosa (keratin 7?, keratin 20+, MUC2+). Carcinomas of pancreaticobiliary type usually show the immunohistochemical profile of pancreaticobiliary duct mucosa (keratin 7+, keratin 20?, MUC2?). Even poorly differentiated carcinomas, as well as unusual histological types, may conserve the marker profile of the mucosa they developed from. These findings underline the concept of histogenetically different carcinomas of the papilla of Vater which develop either from intestinal- or from pancreaticobiliary-type mucosa of the papilla of Vater. Molecular alterations in ampullary carcinomas are similar to those of colorectal as well as pancreatic carcinomas, although they appear at different frequencies. In future studies, molecular alterations in ampullary carcinomas should be correlated closely with the different histologic tumor types. Consequently, the histologic classification should reflect the histogenesis of ampullary tumors from the two different types of papillary mucosa.     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.     

Demonstration of the mechanism of action of biguanides

Summary Palmitic acid oxidation in rat diaphragm homogenate is depressed by biguanide concentrations that are still incapable of inhibiting oxidative phosphorylation. Glucose oxidation is not directly effected by the same biguanide concentrations: however, the inhibitory effect of palmitic acid on glucose oxidation is partly removed by biguanides. Inhibition of fatty acid oxidation, which accounts for most of the metabolic effects caused by these drugs, can be regarded as the fundamental mechanism of action of biguanides. There is some evidence suggesting that these drugs might interact with carnitine, thus preventing long-chain fatty acids from being transported across the mitochondrial membrane to the site of oxidation. Traduzione a cura degli AA.     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

124例耐多药结核分枝杆菌基因突变特征分析

目的对临床分离的耐多药结核分枝杆菌相关基因的突变特征进行分析。方法对124例耐多药结核分枝杆菌以及50株敏感株的耐药相关基因(包括异烟肼inh A、kat G、oxyR-ahp C间隔区以及利福平rpo B)进行序列测定,分析其基因突变情况。结果异烟肼耐药inh A基因突变率为14.5%;kat G基因突变率为70.2%(87/124),主要位于315位;oxyR-ahp C间隔区突变率为15.3%;inh A、kat G两种基因同时突变率75.0%,三种基因同时突变率为89.5%。利福平rpo B基因突变的检出率高达95.2%,突变主要发生在531、526、516位点。结论我省耐多药菌异烟肼耐药相关基因最常见突变为kat G 315、inh A C-T(-15)、axyR-ahp C间隔区(-10)C-T,利福平为rpo B531、526、516。结合MDR-TB耐药相关基因的特征分析,可以建立一种快速、准确、特异的适合于我省的检测结核菌耐多药性的新方法。     

Assessment of quality of life of parents of children with juvenile chronic arthritis

The aim of the study was to assess the quality of life (QOL) and the psychological status of parents of children with juvenile chronic arthritis (JCA). The QOL, anxiety and depression of the parents of 28 children with JCA were evaluated and compared to those of the parents of 28 healthy children. Mothers of JCA children and mothers of healthy children reported similar QOL. The reported anxiety and depression levels were similar for mothers and fathers in both groups. The parents of children with pauciarticular-type JCA reported lower QOL and higher levels of anxiety and depression than the parents of children with other types, namely polyarticular and systemic JCA. These findings may be explained by the fact that the pauciarticular patients had shorter disease duration and were less frequently seen in the outpatient clinic. The QOL of mothers of children with JCA was found to be slightly impaired in the group of children with pauciarticular JCA. Future larger studies are needed to confirm these results, as the number of subjects in the three groups was rather low. Received: 26 September 2001 / Accepted: 8 February 2002     

氯硝柳胺悬浮剂的毒性评价

目的评价氯硝柳胺悬浮剂的毒性，为现场大规模应用灭螺提供依据。方法按照中华人民共和国国家标准GB 15670-1995《农药登记毒理学试验方法》和鱼类毒性试验方法进行。结果经口、经皮肤的LDso雌、雄性大鼠均>5 000 mg/kg，经呼吸道的LCso雌、雄性大鼠均>5 000mg/m3，该药经口、经皮肤、经呼吸道毒性均属微毒类药物；兔眼用药后，观察期内无不良反应，对眼无刺激性；皮肤用药后对皮肤无刺激性。与氯硝柳胺原药、氯硝柳胺乙醇胺盐原药和氯硝柳胺乙醇胺盐可湿性粉剂相比，氯硝柳胺悬浮剂对鱼急性毒性最低。结论氯硝柳胺悬浮剂属微毒类药物，对鱼的毒性低于其乙醇胺盐可湿性粉剂，适合于现场应用。     

Numerical Simulation of the Effect of Rate of Change of Glucose on Measurement Error of Continuous Glucose Monitors

Background

A 5-day in-patient study designed to assess the accuracy of the FreeStyle Navigator® Continuous Glucose Monitoring System revealed that the level of accuracy of the continuous sensor measurements was dependent on the rate of glucose change. When the absolute rate of change was less than 1 mg•dl⁻¹•min⁻¹ (75% of the time), the median absolute relative difference (ARD) was 8.5%, with 85% of all points falling within the A zone of the Clarke error grid. When the absolute rate of change was greater than 2 mg•dl⁻¹•min⁻¹ (8% of the time), the median ARD was 17.5%, with 59% of all points falling within the Clarke A zone.

Method

Numerical simulations were performed to investigate effects of the rate of change of glucose on sensor measurement error. This approach enabled physiologically relevant distributions of glucose values to be reordered to explore the effect of different glucose rate-of-change distributions on apparent sensor accuracy.

Results

The physiological lag between blood and interstitial fluid glucose levels is sufficient to account for the observed difference in sensor accuracy between periods of stable glucose and periods of rapidly changing glucose.

Conclusions

The role of physiological lag on the apparent decrease in sensor accuracy at high glucose rates of change has implications for clinical study design, regulatory review of continuous glucose sensors, and development of performance standards for this new technology. This work demonstrates the difficulty in comparing accuracy measures between different clinical studies and highlights the need for studies to include both relevant glucose distributions and relevant glucose rate-of-change distributions.     

治疗高血压药物的经济学评价

重视高血压治疗中的经济学评价,对利用我国有限的卫生资源来遏制高血压对人民群众的危害有着重要的现实意义。药物经济学对于药物治疗的成本和治疗的结果给予同样的关注。因为治疗高血压的费用,不仅涉及药物价格,还包括患者的危险水平,降压疗效和对临床终点事件的影响,以及治疗的依从性和安全性。因此药物经济学更强调整体成本和价-效比。低危病人,若非药价低廉,治疗的价-效比不够理想。而在高危的患者,价-效比越小越经济而不是药费越便宜越好。