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1.
目的探讨高龄急性缺血性脑卒中(AIS)患者静脉溶栓后出血性转化(HT)的危险因素。方法收集2016年1月至2019年3月海口市第三人民医院急诊科收治的高龄AIS患者326例。根据其静脉溶栓后是否发生HT,分为HT组(51例)和无HT组(275例)。采用SPSS 20.0统计软件进行数据分析。应用单因素分析及多因素logistic回归分析,评价影响高龄AIS患者静脉溶栓后发生HT的危险因素。结果单因素分析显示,HT组的心房颤动、尿蛋白阳性、溶栓后24 h收缩压、血糖、国际标准化比值、溶栓前美国国立卫生研究院卒中量表(NIHSS)评分、溶栓后24 h NIHSS评分及发病至溶栓时间3 h明显高于无HT组,差异有统计学意义(P0.05)。多因素logistic回归分析显示,溶栓后24 h收缩压(OR=1.935,95%CI 1.226~4.162)、血糖(OR=2.240,95%CI 1.638~5.237)、溶栓前NIHSS评分(OR=2.435,95%CI 1.805~5.726)、溶栓后24 h NIHSS评分(OR=3.381,95%CI 2.216~7.250)及发病至溶栓时间3 h(OR=2.703,95%CI 1.914~6.116)是高龄AIS患者静脉溶栓后发生HT的独立危险因素(P0.05)。结论溶栓后24 h收缩压、血糖、溶栓前NIHSS评分、溶栓后24 h NIHSS评分及发病至溶栓时间3 h是高龄AIS患者静脉溶栓后发生HT的独立危险因素,可为临床溶栓治疗提供参考。  相似文献   

2.
背景出血转化是溶栓治疗的主要并发症,其会加重患者神经功能缺损程度甚至导致患者死亡,因此提前预测患者出血转化风险对临床治疗具有重要意义。目的分析经阿替普酶静脉溶栓治疗的急性缺血性脑卒中(AIS)合并心房颤动患者出血转化及预后的影响因素。方法选取2017—2019年郴州市第四人民医院神经内科收治的AIS合并心房颤动患者60例为研究对象,所有患者入院后接受阿替普酶静脉溶栓治疗。根据溶栓治疗后24 h有无出血转化将所有患者分为出血转化组27例和无出血转化组33例,根据溶栓治疗后3个月预后将所有患者分为预后良好组[改良Rankin量表(m RS)评分≤2分]39例和预后不良组(m RS评分> 2分)21例。收集所有患者出血转化和预后的可能影响因素,并采用多因素Logistic回归分析探讨经阿替普酶静脉溶栓治疗的AIS合并心房颤动患者出血转化及预后的影响因素。结果多因素Logistic回归分析结果显示,溶栓治疗后24 h收缩压> 140 mm Hg [OR=2.356,95%CI(1.337,4.151)]、基线空腹血糖> 5.6 mmol/L[OR=3.525,95%CI(2.190,5.676)]、发病至溶栓治疗时间> 3 h[OR=4.773,95%CI(1.586,14.361)]、基线美国国立卫生研究院卒中量表(NIHSS)评分> 7分[OR=4.609,95%CI(2.258,9.407)]、溶栓治疗后2 h NIHSS评分> 7分[OR=1.241,95%CI(1.047,1.472)]是经阿替普酶静脉溶栓治疗的AIS合并心房颤动患者发生出血转化的独立危险因素(P <0.05);基线空腹血糖> 5.6 mmol/L[OR=2.394,95%CI(1.666,3.440)]、溶栓治疗后2 h NIHSS评分> 7分[OR=2.620,95%CI(1.173,5.851)]是经阿替普酶静脉溶栓治疗的AIS合并心房颤动患者预后不良的独立危险因素(P <0.05)。结论溶栓治疗后24 h收缩压> 140 mm Hg、基线空腹血糖> 5.6 mmol/L、发病至溶栓治疗时间> 3 h、基线及溶栓治疗后2 h NIHSS评分> 7分是经阿替普酶静脉溶栓治疗的AIS合并心房颤动患者发生出血转化的危险因素,基线空腹血糖> 5.6 mmol/L和溶栓治疗后2 h NIHSS评分> 7分是经阿替普酶静脉溶栓治疗的AIS合并心房颤动患者预后不良的危险因素,应引起临床医生重视。  相似文献   

3.
目的 探讨血清闭合蛋白水平与急性缺血性脑卒中(AIS)患者静脉溶栓后出血转化风险和预后的相关性。方法 选取2021年2月至2022年10月聊城市人民医院经静脉溶栓治疗的AIS患者186例作为研究对象,根据溶栓后36 h头颅CT或MRI结果分为出血组26例和未出血组160例。对比2组临床资料、血清闭合蛋白水平,采用多因素logistic回归分析和ROC曲线评价血清闭合蛋白水平对AIS患者静脉溶栓后出血转化风险预测价值。随访观察90 d,采用Kaplan-Meier曲线分析血清闭合蛋白水平与AIS溶栓后预后的相关性。结果 出血组心房颤动、基线美国国立卫生研究院卒中量表(NIHSS)评分、闭合蛋白水平显著高于未出血组,发病至溶栓时间较未出血组长(P<0.01);多因素logistic分析显示,心房颤动(OR=5.475,95%CI:1.317~22.758)、发病至溶栓时间(OR=1.040,95%CI:1.016~1.065)、基线NIHSS评分(OR=1.482,95%CI:1.196~1.838)、血清闭合蛋白(OR=3.565,95%CI:1.959~6.488)为AIS患者静...  相似文献   

4.
目的探讨老年急性缺血性脑卒中患者静脉溶栓后出血性转化的影响因素及临床预后分析。方法回顾性收集老年急性缺血性脑卒中患者102例,依据临床症状及头颅CT结果分为非出血性转化组81例和出血性转化组21例。采用改良Rankin量表评价临床预后,预后良好组46例(0~2分),预后不良组56例(3~6分)。溶栓前及溶栓后24h行美国国立卫生研究院卒中量表(NIHSS)评分,应用多变量logistic回归分析老年急性缺血性脑卒中患者出血性转化及临床预后不良的独立危险因素。结果出血性转化组溶栓前NIHSS评分及溶栓后24hNIHSS评分明显高于非出血性转化组(P0.05,P0.01)。预后不良组溶栓前NIHSS评分及溶栓后24hNIHSS评分明显高于预后良好组(P0.05,P0.01)。多变量logistic回归分析显示,溶栓前NIHSS评分(OR=1.253,95%CI:1.162~1.335,P=0.013)及溶栓后24hNIHSS评分(OR=1.427,95%CI:1.374~1.526,P=0.006)是发生出血性转化的独立危险因素。年龄(OR=0.956,95%CI:0.863~1.125,P=0.042)、溶栓前NIHSS评分(OR=1.072,95%CI:0.984~1.186,P=0.038)、溶栓后24hNIHSS评分(OR=1.516,95%CI:1.383~1.762,P=0.012)是预后不良的独立危险因素。结论溶栓前NIHSS评分及溶栓后24hNIHSS评分高是发生出血性转化的独立危险因素,高年龄、溶栓前NIHSS评分及溶栓后24hNIHSS评分高是预后不良的独立危险因素。  相似文献   

5.
目的探讨动态动脉僵硬指数(ambulatoryarterialstiffnessindex,AASI)与老年急性缺血性脑卒中(acuteischemicstroke,AIS)患者静脉溶栓后出血转化的相关性。方法选择2016年1月~2019年12月于葫芦岛市中心医院接受静脉溶栓治疗的老年(年龄65岁)AIS患者224例,根据欧洲急性卒中协作组分类标准分为出血转化组48例和非出血转化组176例。比较2组人口学资料、脑血管病危险因素、实验室检查等指标。采用logistic回归分析和ROC曲线分析。结果本研究出血转化率为21.4%。与非出血转化组比较,出血转化组年龄、高血压、心房颤动、心源性栓塞型比例、入院时NIHSS评分、空腹血糖及AASI明显升高,小动脉闭塞型比例明显降低,差异有统计学意义(P0.05,P0.01)。多因素logistic分析模型显示,年龄、心房颤动、入院时NIHSS评分及AASI是老年AIS患者溶栓后出血转化的独立危险因素(OR=1.095,95%CI:1.031~1.163,P=0.003;OR=2.931,95%CI:1.292~6.653,P=0.010;OR=1.085,95%CI:1.018~1.156,P=0.012;OR=1.723,95%CI:1.166~2.544,P=0.006)。AASI预测出血转化发生的潜在最佳临界值为0.619,ROC曲线下面积为0.631(95%CI:0.564~0.694,P=0.004),敏感性为77.08%,特异性为47.16%。结论 AASI是老年AIS患者接受静脉溶栓治疗后发生出血转化的一个独立危险因素。  相似文献   

6.
目的 探讨合并非瓣膜性心房颤动(non-valvular atrial fibrillation,NVAF)的急性缺血性卒中患者出血性转化(hemorrhagic transformation,HT)风险以及溶栓治疗后3个月时的转归及其影响因素.方法 回顾性纳入连续的合并NVAF的急性缺血性卒中患者,收集其人口统计学、血管危险因素以及其他临床资料.采用改良Rankin量表(modified Rankin Scale,mRS)评价发病3个月时的转归,mRS评分≤2分定义为转归良好,>2分定义为转归不良.结果 共纳入合并NVAF的急性缺血性卒中患者119例,其中男性63例(52.9%),女性56例(47.1%);平均年龄(72.1±10.0)岁;45例(37.81%)接受重组组织型纤溶酶原激活剂(recombinant tissue plasminogen activator,rtPA)溶栓治疗,55例(46.2%)转归良好,27例(22.7%)合并HT.与转归不良组相比,转归良好组平均年龄较小(P =0.028),合并缺血性心脏病以及发病至治疗时间>4.5h的患者构成比较低(P均<0.05),基线收缩压和舒张压以及美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分较低(P均<0.05),而接受rtPA静脉溶栓的患者比例较高(P=0.019).多变量logistic回归分析显示,合并缺血性心脏病[优势比(odds ratio,OR)4.572,95%可信区间(confidence interval,CI)1.392~15.014;P=0.012]、治疗前收缩压(OR 1.028,95% CI1.007 ~1.049;P=0.009)、基线NIHSS评分(OR 1.058,95% CI1.002~1.117;P=0.042)是转归不良的独立危险因素,而rtPA静脉溶栓治疗(OR 0.264,95% CI0.102 ~0.683;P=0.006)是转归不良的独立保护因素.HT组基线收缩压、空腹血糖和NIHSS评分以及既往卒中或短暂性脑缺血发作(transient ischemic attack,TIA)史患者构成比均显著性高于非HT组(P均<0.05).多变量logistic回归分析显示,基线NIHSS评分(OR 1.147,95% CI1.068 ~1.231;P<0.001)、基线收缩压(OR 1.951,95% CI1.921~1.982;P=0.002)和血糖水平(OR 1.191,95% CI1.095 ~ 1.294;P<0.001)为HT的独立危险因素.与非溶栓组相比,溶栓组平均年龄较低(P=0.021),基线收缩压、空腹血糖和NIHSS评分以及合并高脂血症、既往卒中或TIA史以及入院前使用抗高血压药的患者比例较高(P均< 0.05),合并缺血性心脏病的患者比例较低(P=0.035),但转归良好的患者比例更高(P=0.019).结论 合并缺血性心脏病、治疗前收缩压和基线NIHSS评分高是转归不良的独立危险因素,而rtPA静脉溶栓治疗是转归不良的独立保护因素;基线NIHSS评分、基线收缩压和血糖水平高为HT的独立危险因素.对于合并NVAF的急性缺血性卒中患者,如无明显溶栓禁忌证,则能从静脉溶栓治疗中获益,且不会增高HT风险,但应适当控制患者的血压和血糖水平.  相似文献   

7.
目的探讨急性缺血性脑卒中患者阿替普酶静脉溶栓后早期神经功能恶化的危险因素。方法选择接受阿替普酶静脉溶栓的急性缺血性脑卒中患者136例,根据早期神经功能恶化发生情况分为恶化组24例,非恶化组112例。收集患者临床资料、美国国立卫生研究院卒中量表(NIHSS)评分,多因素logistic回归分析急性缺血性脑卒中患者早期神经功能恶化的危险因素。结果恶化组年龄、糖尿病、既往脑梗死、近端血管狭窄/闭塞、溶栓前NIHSS评分、白细胞计数、中性粒细胞、溶栓后4h纤维蛋白原、随机血糖及空腹血糖水平较非恶化组明显升高,抗血小板治疗比例较非恶化组明显降低(P0.05,P0.01)。多因素logistic回归分析显示,近端血管狭窄/闭塞、溶栓前随机血糖、白细胞计数是阿替普酶溶栓后发生早期神经功能恶化的独立危险因素(OR=6.986,95%CI:1.331~36.678,P=0.022;OR=2.186,95%CI:1.481~3.227,P=0.000;OR=1.500,95%CI:1.158~1.942,P=0.002),而发病前抗血小板治疗是早期神经功能恶化的保护因素(P=0.020)。结论急性缺血性脑卒中患者阿替普酶静脉溶栓治疗后,有诸多相关危险因素的存在,其有助于识别早期神经功能恶化的高危患者。  相似文献   

8.
目的探讨缺血性脑卒中患者静脉溶栓后出血性转化(HT)的危险因素。方法分析156例经尿激酶静脉溶栓治疗的缺血性脑卒中患者的临床资料,根据溶栓后复查头颅CT有无HT分为HT组及无HT组,采用单因素和Logistic回归分析溶栓后HT危险因素。结果单因素分析发现,与无HT组比较,HT组继发心房纤颤患者较多(P=0.028),大面积脑梗死患者较多(P=0.009),溶栓前NIHSS评分较高(P=0.001)。经Logistic回归分析发现溶栓前NIHSS评分高(OR=1.108,95%CI:1.027~1.195,P=0.008)是继发HT的危险因素。结论溶栓前NIHSS评分高是急性脑梗死患者静脉溶栓后发生HT的危险因素。  相似文献   

9.
目的探讨老年急性脑梗死患者静脉溶栓治疗临床预后的影响因素。方法回顾性分析我院所有接受静脉溶栓治疗的急性老年脑梗死患者151例,预后终点为发病3个月后改良的Rankin量表评分,其中0~2分(预后良好组)77例,≥3分(预后不良组)74例。比较2组患者的基线临床资料、溶栓时间窗、溶栓前美国国立卫生研究院卒中量表(NIHSS)评分、溶栓前脑卒中分型、早期症状改善、溶栓后脑出血等因素。结果预后不良组患者溶栓前血糖、C反应蛋白、溶栓前NIHSS评分≥9分、心房颤动、溶栓后脑出血等显著高于预后良好组(P0.05,P0.01)。多因素logistic回归分析显示:溶栓前NIHSS评分(OR=1.262,95%CI:1.075~1.482,P=0.005)、OCSP(牛津郡社区卒中项目)分型(OR=0.203,95%CI:0.066~0.628,P=0.006)、溶栓前血糖(OR=1.264,95%CI:1.042~1.532,P=0.017)、溶栓后24h症状改善(OR=25.764,95%CI:5.131~129.361,P=0.000)是患者预后的独立影响因素。结论老年急性脑梗死患者行静脉溶栓治疗的预后受多种因素影响,溶栓前NIHSS评分、OCSP分型、溶栓前血糖及溶栓后24h症状改善等因素是患者临床预后的独立影响因素。  相似文献   

10.
目的探究急性脑梗死(ACI)患者静脉溶栓治疗后出血性转化的影响因素。方法选择2012—2014年南京市中西医结合医院收治的ACI患者100例,均行静脉溶栓治疗,根据静脉溶栓治疗后出血性转化发生情况分为未出血组69例和出血组31例。采用统一的资料收集表收集患者临床资料,包括性别、年龄、既往史(冠心病、高血压、糖尿病、心房颤动、高脂血症、吸烟)、既往服用阿司匹林情况、发病至静脉溶栓治疗时间、溶栓前斯堪的那维亚卒中量表(SSS)评分、溶栓前美国国立卫生研究院卒中量表(NIHSS)评分、舒张压、收缩压、血小板计数、血钠、血糖、CT低密度病灶情况、心源性脑栓塞及大动脉粥样硬化发生情况,采用多因素logistic回归分析筛选ACI患者静脉溶栓治疗后出血性转化的影响因素。结果本组患者出血性转化发生率为31.0%。单因素分析结果显示,两组患者性别、年龄、既往史(冠心病、高血压、心房颤动、高脂血症、吸烟)阳性率、既往阿司匹林服用率、舒张压、收缩压、血小板计数、心源性脑栓塞发生率及大动脉粥样硬化发生率比较,差异无统计学意义(P>0.05);出血组患者糖尿病病史阳性率、溶栓前NIHSS评分、血钠、血糖及CT低密度病灶检出率高于未出血组,发病至静脉溶栓治疗时间长于未出血组,溶栓前SSS评分低于未出血组(P<0.05)。多因素logistic回归分析结果显示,发病至静脉溶栓治疗时间〔OR=2.425,95%CI(1.313,4.479)〕、溶栓前SSS评分〔OR=2.670,95%CI(1.358,5.250)〕及溶栓前NIHSS评分〔OR=2.257,95%CI(1.317,3.869)〕是ACI患者静脉溶栓治疗后出血性转化的独立危险因素(P<0.05)。结论溶栓前SSS评分低、NIHSS评分高及延迟静脉溶栓治疗是ACI患者静脉溶栓治疗后出血性转化的独立危险因素。  相似文献   

11.
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。  相似文献   

12.
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.  相似文献   

13.
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.  相似文献   

14.
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.  相似文献   

15.
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。  相似文献   

16.
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。  相似文献   

17.
氯硝柳胺悬浮剂的毒性评价   总被引:2,自引:2,他引:2  
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。  相似文献   

18.
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  相似文献   

19.

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.  相似文献   

20.
The constancy of the hydrogen consuming flora of the human colon was studied in 15 healthy subjects via two measurements obtained 18 to 36 months apart. Hydrogen disappearance rate and the major products of H2-consuming bacteria, methane and sulfide, were measured during incubation of fecal homogenates with excess hydrogen and sulfate. In 11/15, the hydrogen consumption rate and the predominant hydrogen-consuming pathway (methanogenesis, sulfate reduction, or neither) remained constant. However, major shifts in these pathways were observed in four subjects, with two losing and two gaining the ability to produce methane. Methanogenesis was associated with the highest hydrogen consumption rate. This study demonstrates that clinically unrecognizable, major alterations of the colonic flora occur in healthy subjects. Understanding of the factors responsible for these alterations might allow for therapeutic manipulation of the colonic flora.Supported in part by the Department of Veterans Affairs and NIDDKD RO1 DK 13309-25.  相似文献   

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