尿碘水平对Graves甲亢患者甲状腺摄锝功能的影响

目的 探讨尿碘水平对Graves甲亢患者甲状腺摄锝功能的影响。 方法 选取2018年7月至11月于中国医科大学附属第一医院行甲状腺锝显像初诊为Graves甲亢的患者100例，其中男性20例、女性80例，年龄（40.33±11.85）岁。对所有患者的尿液样本进行尿碘、尿肌酐浓度的测定，依据尿碘水平标准将患者分为低、中、高尿碘水平组（≤100、101~249、≥250 μg/gCr）；根据检查前2周患者是否食用海产品情况分为海产品食用组和无海产品食用组。所有患者行SPECT/CT显像，计算甲状腺与颈部软组织的放射性计数（T/C）比值。多组间比较采用单因素方差分析，多组间两两比较采用LSD-t检验；两组间比较采用Mann-Whitney U检验和t检验；采用Pearson检验进行相关性分析。 结果 （1）低、中、高尿碘水平组患者的T/C比值分别为24.18±8.43、20.35±6.94、16.81±4.93，3组间的差异有统计学意义（F=5.40，P=0.006）。低、中尿碘水平组的T/C比值均高于高尿碘水平组，且差异均有统计学意义（t=3.05、2.38，P=0.003、0.019），低、中尿碘水平组的T/C比值差异无统计学意义。尿碘水平与T/C比值呈负相关（r=?0.24，P=0.023）。（2）海产品食用组与无海产品食用组尿碘水平的M（P25，P75）分别为229.2（163.06，400.16）、178.97（118.86，245.54） μg/gCr，差异有统计学意义（Z=2.87，P=0.004）；2组的T/C比值分别为16.65±6.41、21.03±6.73，差异有统计学意义（t=3.10，P=0.003）。 结论 Graves甲亢患者尿碘水平升高显著抑制其甲状腺摄锝功能，甲状腺锝显像前食用海产品会提高患者的尿碘水平。     

维甲酸联合曲古抑素诱导及治疗荷人甲状腺滤泡状癌裸鼠的实验研究

目的探讨全反式维甲酸（ATRA）和曲古抑素（TSA）对人甲状腺滤泡状癌细胞株（FTC-133）和荷人甲状腺滤泡状癌裸鼠（NMB—hFTC）肿瘤模型摄碘能力的影响。方法不同量ATRA、TSA诱导VFC-133细胞：ARTA 1．0×10^-6mo／L（A低组）、1．0×10^-4mol／L（A高组）、TSA1．65×10^-7mol／L（T组）、A低＋T组、A高＋T组和无水乙醇（对照组）,96h后行HE染色,测定FTC-133细胞摄碘率;制备NMB—hFTC,成瘤后分组：ATRA组（2mg／kg灌胃）、TSA组（10mg／kg腹腔注射）、联合组（ATRA＋TSA,用量同前）、对照组（生理盐水灌胃＋腹腔注射,均为10ml／kg）,剂量均按鼠体质量给予。给药22d后,腹腔注射37MBq ^131I,分别于注射后4,6,12和24h行γ显像,测定体内生物分布;显像后取肿瘤组织行HE染色观察细胞形态。实验结果采用SPSS13．0软件进行单因素方差分析。结果FTC-133细胞摄碘率A低＋T组、A高＋T组分别为（23885±616．0）和（13849±728．2）计数·min^-1·10^-6细胞,其他各组在（985±84．2）～（17600±782．7）计数·min^-1·10^-6细胞范围内,各组间比较差异有统计学意义（F=600．879,P〈0．001）。^131I注射后6,12和24h联合组裸鼠种植瘤％ID／g分别为6．17±0．46,9．34±0．61,11．19±0．98,其余各组保持在（1．97±0．34）～（5．14±0．65）之间;肿瘤质量各组间比较差异有统计学意义（F=3．723,P〈0．05）。结论ATRA联合TSA,可增强FTC-133细胞和NMB—hFTC病灶的分化、摄碘能力,达到增强^131I杀死甲状腺癌病灶的协同作用。     

知母活性成分ZMR对慢性帕金森病模型小鼠多巴胺系统的调节

目的研究知母活性成分ZMR在慢性1-甲基4-苯基-1,2,3,6-四氢吡啶（MPTP）损伤拟帕金森病小鼠模型中对脑内多巴胺转运蛋白（DAT）及多巴胺（DA）代谢的影响。方法将C57BIV6小鼠分为4组：对照组、模型组、ZMR低剂量组和ZMR高剂量组。除对照组注射生理盐水外,其他3组小鼠按体质量腹腔注射丙磺舒250mg／kg,0．5h后按体质量皮下注射MPTP 15mg／kg,每周注射2次,连续5周,共计10次。低剂量组按体质量灌胃给予ZMR 10mg／kg,高剂量组给予ZMR 26mg／kg,每日1次,造模开始后1周起连续给药60d。采用DAT放射自显影、单胺氧化酶B（MAO—B）活力测定和DA及其代谢产物的高效液相色谱法测定等方法研究ZMR在慢性MPTP损伤小鼠模型中对脑内DA失活的作用。采用SAS6.12软件,多组间比较采用单因素方差分析,两组间的比较采用团体Student’s t检验。结果与模型组[（10．3±0．9）U／mg蛋白]比较,ZMR低剂量组[（10．6±0．8）U／mg蛋白]和高剂量组[（10．7±0．9）U／mg蛋白]的脑内MAO—B活力无显著改变（F=0．0717,P〉0．05）;而DAT密度分别从0．212±0．012增加到0．268±0．019和0．281±0．018,分别增加了26．42％和32．55％（t=2．5314和3．1124,P〈0．05和〈0．01）;每克纹状体内的DA质量分别从（3．00±0．25）μg/g增加到（4．21±0．32）μg／g和（4．58±0．39）μg／g,分别提高了40．04％和52．29％（t=2．9879和3．4163,P〈0．05和〈0．01）。小鼠每克纹状体内DA质量与DAT密度呈明显正相关（r=0．6833,P〈0．01）。结论ZMR能提高慢性MPTP损伤小鼠模型的纹状体DA水平,这种作用与DA降解无关,与提高DAT密度有关。     

治疗用碘[^131I]化钠胶囊在格雷夫斯病患者体内的药代动力学及疗效的前瞻性对照研究

目的 比较诊断期及治疗期碘[^131I]化钠胶囊与口服液在格雷夫斯病（GD）患者体内的血液药代动力学及患者甲状腺摄碘率的差异,评价两者治疗GD的疗效及安全性.方法 采用开放、平行、随机、对照的前瞻性临床研究.纳入44例GD患者[男14例,女30例,年龄（33.84±4.96）岁].其中试验组（A组,22例）诊断期口服碘[^131I]化钠口服液,治疗期口服碘[^131I]化钠胶囊;对照组（B组,22例）反之.测定2组诊断期及治疗期服药后0、5、10、20、40和80 min血放射性计数,以及2、4、6和24 h甲状腺摄碘率,采用梯形法计算两者时间曲线的AUC、峰浓度（cmax）及达峰时间（tmax）.观察3、6个月疗效及不良反应.采用SAS 9.3软件对试验数据进行多因素方差分析、t检验及χ^2检验.结果 每组各有1例失访,有效病例每组各21例.诊断期A组血放射性计数占给药放射性计数百分比（OD％）的时间曲线AUC0→t[（450.70±258.00）％·min]小于B组[（684.45±237.00）％·min],cmax[（8.43±4.00）％]低于B组[（13.28±4.20）％],Z=2.640 7、t=3.923 0,均P＜0.01;2组tmax分别为（37.27±23.10）和（34.55±21.30） min,Z=-0.335 9,P＞0.05.治疗期A、B组tmax分别为（46.36±24.98）和（28.64±19.35） min,Z=-2.681 8,P＜0.01;而2组AUC0→t和cmax差异均无统计学意义（t=1.707 4、1.357 4,均P＞0.05）.诊断期及治疗期2组摄碘率AUC0→t、cmax及tmax差异均没有统计学意义（t=0.420 8、1.596 8、0.797 8、1.688 0,Z=0.556 4、-0.013 8,均P＞0.05）.治疗后3个月A组甲状腺功能亢进症（简称甲亢）缓解者占66.7％（14/21）,B组相应比例为61.9％（13/21）,χ^2=0.104,P＞0.05;2组发生甲状腺功能减退症（简称甲减）比例分别为23.8％（5/21）和28.6％（6/21）,χ^2=0.123,P＞0.05.治疗后6个月2组甲亢和甲减发生比例差异也均无统计学意义（χ^2=1.118、1.714,均P＞0.05）.无一例出现不良反应.结论 诊断期和治疗期2种剂型碘[^131I]化     

维甲酸对人乳腺癌细胞NIS基因表达和摄碘功能的影响

目的探讨9-顺-维甲酸（9-cis—RA）对人乳腺癌细胞钠／碘同向转运体（NIS）基因功能表达的影响。方法应用9-cis—RA和全反式维甲酸（ATRA）分别在不同浓度下对雌激素受体（ER）阳性的乳腺癌细胞（MCF-7）和ER阴性的乳腺癌细胞（MDA—MB-231）进行干预，于不同时间点提取细胞总RNA，通过半定量逆转录-聚合酶链反应（RT—PCR）检测乳腺癌细胞NIS mRNA表达水平的变化；在体外培养条件下研究RA刺激后乳腺癌细胞对放射性碘的摄取情况。结果9-cis—RA处理后，MCF-7细胞NIS mRNA表达增强，呈浓度依赖性（F=114．17，P〈0．001），在10^-6mol／L浓度下NIS mRNA的表达随时间上调，16h时达到最高，是对照组（0h）的8．2倍（q=8．32，P〈0．01），此后随时间逐渐下调；且9-cis—RA（10^-6mol／L，24h）的作用强于ATRA（t=6．572，P〈0．01）。MDA—MB-231基础状态下几乎无NIS表达，9-cis—RA刺激后可上调其表达（t=20．195，P〈0．001），但表达量（NIS／B—actin）远低于MCF-7（t=10．395，P〈0．001）。碘摄取实验表明，10^-6mol／L 9-cis—RA干预12h后，MCF-7细胞摄碘开始增加，干预24h时碘摄取达最大，是基础状态下的3．2倍，其摄碘能力可被KCl0。抑制。结论9-cis—RA能明显增强ER阳性的MCF-7细胞NIS基因的表达及摄碘功能。     

实验性甲状腺功能亢进大鼠脑多巴胺转运蛋白及多巴胺含量的变化

目的研究甲状腺激素升高时脑纹状体多巴胺转运蛋白（DAT）、多巴胺（DA）及其代谢产物3,4二羟苯乙酸（DOPAC）的含量变化。方法将24只大鼠分为2组,其中一组采用灌胃法连续每天给予大鼠左甲状腺素钠（优甲乐,用量按大鼠体质量25μg／100g,溶于生理盐水中,体积1ml）造成实验性大鼠甲状腺激素增高状态;对照组仅采用灌胃法给予生理盐水1ml;于模型建立前后按随机数字表法抽取左甲状腺素钠组及对照组大鼠各6只,分别取尾静脉血1ml,采用放射免疫法测定TT3及,TT4水平。14d后将上述对照组及左甲状腺素钠组大鼠再各自平均分为2组,一组用于99^Tc^m-2β-[N,N’-双（2-巯乙基）乙撑二胺基]甲基-3β-（4-氯苯基）托烷（TRODAT-1）大鼠脑内分布研究,另一组用于高效液相-电化学检测器（HPLC-ECD）测纹状体DA及DOPAC含量,观察上述大鼠脑纹状体区DAT的分布及DA、DOPAC含量的变化。多组比较采用ANOVA分析,2组间比较采用均数t检验。结果左甲状腺素钠组大鼠在服用左甲状腺素钠后活动明显增加,体质量增长低于正常对照组[（223．90±8．40）与（261．60±14．20）g,t=6．98,P〈0．05]。甲状腺激素水平测定示：左甲状腺素钠组给药前后TT3,分别为（1．46±0．17）和（2．72±0．29）nmol／L（t=10．51,P〈0．0001）;TT4分别为（83．52±10．06）和（187．12±36．48）nmol／L（t=7．74,P〈0．0001）;对照组生理盐水注射前后TT3分别为（1．54±0．09）和（1．71±0．20）nmol／L（t=1．68,P〉0．05）,TT4分别为（98．38±9．77）和（88．38±6．76）nmol／L（t=1．36,P〉0．05）。99^Tc^m-TRODAT-1大鼠脑内分布（每克脑组织百分注射剂量率,％ID／g）研究示：左甲状腺素钠组纹状体为（2．80±0．25）％ID／g,明显低于正常对照组[（3．13±0．14）％ID／g,t=-3．62,P〈0．05]。经检测左甲状腺     

影响131I治疗甲状腺功能亢进疗效的因素

为探讨^131I治疗Graves′病甲亢的疗效及影响疗效的因素，将^131I治疗后1年的患者，根据随访结果分为早发甲状腺功能减低（早发甲减）组、无甲减组，各抽取46例、60例，采用SAS统计软件分析甲状腺重量、最高摄碘率、吸收剂量、甲状腺球蛋白抗体（TGA）和甲状腺微粒体抗体（TMA）与早发甲减的关系。结果发现，两组间甲状腺重量差异有显著性意义（P=0.0106），两组间的吸收剂量差异无显著性意义（P=0.4420），但最高摄碘率差异有显著性意义（t=2.1725，P=0.0321）；两组间的TGA、TMA阳性数差异无显著性意义（X^2=1.156，P=0.282）。提示早发甲减与甲状腺重量、最高摄碘率有关，与计算剂量时所给的吸收剂量、TGA和TMA是否阳性无关。     

脂多糖对大鼠肺微血管内皮细胞cAMP的影响

目的探讨脂多糖（LPS）作用后,大鼠肺微血管内皮细胞（RPMVEC）cAMP浓度变化及其与B—AR变化的关系。方法分别在100ml培养瓶内接种等量RPMVEC,细胞单层汇合后分为3组：LPS组加LPS10μg／ml;LPS＋山莨菪碱组加LPS10μg／ml和山莨菪碱10μg／ml;正常对照组加等量稀释液（各组n=4）。于作用后15、90min,采用放免法测定各组RPMVECcAMP浓度。结果正常对照组RPMVECcAMP浓度为（11．83±1．35）fmol／μl;LPS组和LPS＋山莨菪碱组15、90min两个时相点RPMVECcAMP浓度均显著高于正常对照组（P〈0．01）。10μg/mlLPS作用15min,cAMP浓度显著低于10μg／mlLPS作用90min（P〈0．01）;LPS＋山莨菪碱组作用15min,cAMP浓度也显著低于作用90min（P〈0．01）。LPS组作用15min与LPS＋山莨菪碱组作用15min比较,细胞内cAMP浓度无显著差异（P〉0．05）;两组作用90min比较,cAMP浓度也无显著差异（P〉0．05）。结论LPS作用可引起RPMVECcAMP浓度显著升高,其机制可能与LPS引起的腺苷酸环化酶活化有关,而与LPS引起的β—AR变化下调无关。     

^131I治疗甲亢后致甲减的危险因素分析

目的探讨^131I治疗甲亢患者血清甲状腺球蛋白抗体（TGAb）、甲状腺微粒抗体（TMAb）、24h最高摄碘率及甲状腺质量与治疗后甲减的联系。方法根据^131I治疗后甲减的发生情况,分为甲减和非甲减两组,比较分析两组治疗前血清TGAb、TMAb、24h最高摄碘率及甲状腺质量阳性率。结果甲减组治疗前TGAb、TMAb、24h最高摄碘率及甲状腺质量的阳性率分别是38．40％、51．45％、66．67％、68．12％,非甲减组分别是27．45％、39．71％、59．15％、57．84％,除24h最高摄碘率之外两组比较差异有统计学意义（P〈0．05）。结论^131I治疗前TGAb及TMAb滴度高、甲状腺质量较小者治疗后易发生甲减。     

绞股蓝总皂甙对小鼠四氯化碳肝损伤肝组织一氧化氮和谷胱甘肽的影响

目的观察绞股蓝总皂甙（Gypenosides,GPs）对肝损伤小鼠肝组织一氧化氮（NO）和谷胱甘肽（Glu-tathione,GSH）含量的影响。方法给四氯化碳（CCl4）诱导的三组慢性肝损害小鼠灌喂不同剂量的GPs（0、75、150mg／kg）,观察和比较各组小鼠肝功能（血清ALT活性和白蛋白含量）的变化,并测定肝组织NO和GSH的含量。结果肝损伤对照组（即0mg／kgGPs组）NO（80．0±19．0μg／g湿肝）明显高于正常对照组（43．1±18．9μg／g湿肝）（P＜0．05）;GSH（0．48±0.25mg／g湿肝）较正常对照组（0．79±0.19mg／g湿肝）明显降低（P＜0．05）。用GPs75mg／kg和150mg／kg灌胃治疗肝损伤小鼠3周,均能降低肝组织NO含量和增加GSH含量,其中75mg／kg组肝组织NO为68．4±23．7μg湿肝,GSH为0．54±0.34μg／g湿肝;150mg／kg组肝组织NO为52．3±12.7μg／g湿肝,GSH为0．62±0.30mg／g湿肝。150mg／kg组与肝损伤对照组比较,肝组织NO和GSH均有显著性差异（P＜0．05）。同时,小鼠血清白蛋白含量及A／G比值均较肝损伤对照组升高,ALT活性降性,并与GPs剂量的增加相关。结论GPs在保护小鼠CCl4肝损伤的同时能降低肝组织NO含量和升高肝组织GSH水平。     

99TcmO4-与99Tcm-HL91联合显像对甲状腺结节的诊断价值

目的用99Tcm-高锝酸钠（99TcmO4-）与99Tcm-4,9-二氮一3,3,10,10-四甲基十二烷-2,11-二酮（99Tcm-HL91）联合显像鉴别甲状腺结节的性质,评价其临床价值。方法对65例甲状腺结节患者行99TcmO4-动、静态双时相显像,48h后再对其进行99TcmO4-静态显像,显像结果示为冷结节的46例患者再行99Tcm-HL91乏氧显像,最后将两种显像结果与病理活检结果进行对比分析。结果99TcmO4-显像对甲状腺结节诊断的灵敏度、特异度和准确度分别为78．6％、71．9％、73．9％;99Tcm-HL91显像为88．7％、92．3％、91．4％,两者联合显像对甲状腺结节的诊断灵敏度为92．9％、特异度为93．8％、准确度为93．5％。结论99TcmO4-与99Tcm-HL91两种显像方法相结合有助于提高诊断符合率。     

99Tcm-MIBI甲状腺显像对甲状腺癌诊断价值的再评价

目的 评价99Tcm-甲氧基异丁基异腈(MIBI)甲状腺显像对甲状腺癌的诊断价值.方法 167例甲状腺"冷(凉)"结节患者进行了甲状腺99Tcm-MIBI显像.所有患者均依据病理或穿刺活组织检查诊断.99Tcm-MIBI显像早期相甲状腺结节完全或部分放射性填充视为阳性,轻度或不填充视为阴性;早期相放射性浓聚区与正常组织边界分明者视为分界清楚,否则为模糊;延迟相99Tcm-MIBI从浓聚区清除慢于正常组织者视为清除慢,快于或相同者视为清除快.计算99Tcm-MIBI显像的阳性和阴性预测率,以显像阳性病灶边界模糊和放射性清除慢为标准预测甲状腺癌的发生率.结果 99Tcm-MIBI显像对甲状腺癌的阳性预测率为23.5%(19/81),对甲状腺良性病变的阴性预测率为97.7%(84/86).显像阳性者单独用边界模糊预测甲状腺痛的发生率为36.2%(17/47),单独用清除速度慢预测甲状腺癌的发生率为43.9%(18/41).若放射性浓聚区边界模糊和清除速度慢二者都有时,其预测甲状腺癌的发生率为73.9%(17/23).结论 99Tcm-MIBI甲状腺显像阴性对甲状腺良性结节具有较大的诊断价值;阳性对甲状腺癌的诊断价值不大,但如果同时结合放射性浓聚区边界模糊和清除速度慢,则可提高其诊断价值.     

The effect of protein or energy restriction on the biodistribution of Na99TcmO4 in Wistar rats

The effect of malnutrition on the biodistribution of radiopharmaceuticals is not known. We studied the biodistribution of 99Tcm-labelled sodium pertechnetate (Na99TcmO4) in two rat models of malnutrition. Three groups of 2-month-old rats were separated according to their diets: (1) control diet, 23% protein (C); (2) protein-restricted, receiving 8% protein (PR), both ad libitum; and (3) energy-restricted, receiving 60% of control diet (ER). After 21 days of the diet, 99Tcm was injected and the animals were killed after 30 min. The organs were isolated, their weight determined and the absolute per cent (%ID) and the per cent per gram injected dose (%ID x g(-1)) calculated. The %ID and %ID x g(-1) had a similar pattern, increasing in stomach and brain and decreasing in the thyroid, but did not change significantly in kidney, lung, liver, bone or testis in PR rats, except in the heart where the increase was only observed in the %ID x g(-1). In the ER group the %ID x g(-1) was decreased in the bone only, and did not change in the other organs. It is suggested that when using Na99TcmO4 scintigraphy in malnourished patients, the different patterns of distribution must be kept in mind.     

99Tcm-p-aminohippuric acid as a new renal agent

99Tcm-p-aminohippuric acid (99Tcm-PAH) is a new renal radiopharmaceutical prepared from a lyophilized kit by the addition of sodium pertechnetate (Na99TcmO4). Each vial contains PAH, the calcium trisodium salt of diethylenetriamine pentaacetic acid (CaNa3DTPA) and stannous chloride (SnCl2.2H2O) in an inert atmosphere. It is a stable radiopharmaceutical with high radiochemical purity (> 95%). Its protein binding is very similar to that of 131I-OIH, but it is hydrophilic in character. Animal studies using 99Tcm-PAH have indicated that it provides renal images of satisfactory quality with no external background. Despite its almost identical radiochemical purity and HPLC analysis results to 99Tcm-DTPA, 99Tcm-PAH is rapidly secreted by the kidneys in a manner consistent with tubular secretion, as confirmed by rat probenecid studies, whereas 99Tcm-DTPA is excreted by glomerular filtration. The pharmacokinetic parameters of 99Tcm-PAH (t1/2(alpha)) = 2.5 min, t1/2(beta) = 41.7 min, Cl = 5.22 ml.min-1, Kel = 5.1 x 10(-4) min-1) differ from those of 99Tcm-DTPA. Evaluation of 99Tcm-PAH in two human volunteers confirmed its good renal characteristics: rapid disappearance from the vascular system, high uptake in kidneys followed by its very fast elimination, and low residual activity 20 min after its intravenous administration.     

hNIS基因转染介导Hela细胞移植瘤放射性核素显像和治疗的实验研究

目的 利用131I对转染hNIS基因的宫颈癌Hela-NIS（＋）细胞移植瘤进行显像及治疗实验研究,评价hNIS基因转染介导131I治疗宫颈癌的可行性.方法 （1）利用Hela-NIS（＋）细胞和未转染hNIS的Hela细胞分别建立荷宫颈癌裸鼠模型,进行131I及99TcmO4-显像,观察移植瘤的显影情况,并计算移植瘤部位与对侧相同部位的T/B比值.（2）通过腹腔注射法观察比较74,111和148 MBq131I对荷Hela-NIS（＋）宫颈癌裸鼠移植瘤的抑制作用,另设不行任何治疗的对照组.用SPSS 13.0软件,样本均数间差异行t检验.结果 （1）成功构建荷Hela-NIS（＋）裸鼠移植瘤与荷Hela裸鼠移植瘤模型.131I显像示荷Hela-NIS（＋）裸鼠移植瘤部位明显放射性浓聚,注射后8 h T/B比值最高达17.34,而未转染hNIS基因的荷Hela裸鼠移植瘤部位始终未见明显的放射性浓聚.99TcmO4-显像示荷Hela-NIS（＋）裸鼠移植瘤部位在注射后25 h内持续放射性浓聚.（2）经不同剂量的131I治疗后2～3周起,各治疗组荷Hela-NIS（＋）裸鼠移植瘤生长开始受到抑制,移植瘤体积有不同程度缩小.111MBq组和148 MBq组的移植瘤抑制率差异无统计学意义（t=0.13～2.17,P＞0.05）,但二者均明显高于74 MBq组的移植瘤抑制率（t=2.74～5.75,P＜0.05）.对照组荷Hela-NIS（＋）裸鼠移植瘤持续生长.结论 荷Hela-NIS（＋）宫颈癌裸鼠移植瘤可明显聚集131I及99TcmO4-,且在较长时间内持续清晰显影;131I体内治疗效果显著.     

Failure of perchlorate to inhibit Tc-99m isonitrile binding by the thyroid during myocardial perfusion studies.

The thyroid gland receives an average radiation dose of 3 rads during two Tc-99m isonitrile (MIBI) myocardial perfusion studies, if 20 mCi is administered both at rest and at peak exercise. In patients with coronary artery disease, multiple myocardial perfusion studies may be required, resulting in a high level of thyroid radiation. We attempted to reduce this radiation exposure by blocking thyroidal Tc-99m MIBI uptake with oral potassium perchlorate (KCIO4). Fourteen normal subjects received 0.6g to 0.8g KCIO4 20-25 minutes before tracer injection. Subjects who received KCIO4 at rest (n = 11) did not receive KCIO4 at their stress study, and vice versa (n = 3). Thyroid uptake values were obtained with a thyroid probe 20 minutes after injection for both rest and stress studies and were corrected for saturation effects. There was no difference between fractional thyroid uptake values with and without preceding perchlorate administration: 1.9 +/- 0.5% and 1.8 +/- 0.3% (mean +/- SD), respectively. Failure to block Tc-99m MIBI uptake after intravenous (IV) injection is probably due to high thyroidal blood flow and nonspecific tracer accumulation. The concentration of this radioisotope in adjacent muscles also contributes to the high thyroid radiation dose. In summary, administration of KCIO4 before Tc-99m MIBI studies does not reduce the thyroidal radiation dose or uptake of this tracer, suggesting that thyroidal uptake of this tracer is not mediated by the iodine trapping mechanism.     

Simple, rapid thyroid function testing with 99mTc-pertechnetate thyroid uptake ratio and neck/thigh ratio.

To avoid the technical difficulties and errors inherent in the measurement of early thyroid uptake of 99mTcO4-,techniques which are independent of absolute uptake, neck extrathyroidal background and dose standards were evaluated in a series of 108 patients. After intravenous injection of 2 mCi 99mTcO4-, radioactivity was recorded over the neck and thigh. Thyroid uptake ratios were calculated as the ratios of activity over the neck at two times. A neck/thigh ratio was calculated from the recorded activities at 15 min after injection. Examination of these parameters showed that a combination of the 15 min neck/thigh ratio and the 10'/2' thyroid uptake ratio best served to discriminate thyroid function: 92% of hyperthyroid cases were correctly identified by a neck/thigh ratio above 4.7 and 95% of hypothyroid cases were identified by the combination of a neck/thigh ratio below 3 and a 10'/2' thyroid uptake ratio below 1. Correct classification of euthyroidism was 84% but with the exclusion of patients previously treated with 131I, this rose to 91%. The accuracy of the 99mTc procedure is comparable to that of the standard 24 hr 131I uptake run concurrently in this series and duplicates the accuracy of computer assisted determinations of absolute thyroid 99mTcO4- uptakes. The procedure provides a convenient method for the evaluation of thyroid function as an accompaniment to 99mTcO4- thyroid imaging.     

Use of technetium-99m HMPAO scintigraphy for the detection of amiodarone lung toxicity in a rabbit model

Amiodarone (AD) is a very effective anti-arrhythmic drug, but its use is often associated with serious pulmonary complications such as pneumonitis and interstitial pulmonary disease. The aim of this study was to investigate the relationship between the amount of amiodarone intake (and the related development of lung toxicity) and the lung uptake of technetium-99m labelled D,L-hexamethylpropylene amine oxime (HMPAO). Eighteen white female New Zealand rabbits were divided into three groups and fed AD by gavage at doses of 10 (group A), 50 (group B) or 150 (group C) mg/kg daily. 99mTc-HMPAO scintigraphy was performed at baseline and after 1, 2, 3 and 4 weeks of drug intake. Anterior images of 1 min duration were acquired at 30 min after the injection of 37 MBq 99mTc-HMPAO. Regions of interest (ROIs) were drawn on the lungs (L) and the upper limb (B) as the background. L/B ratios were calculated using the mean counts. In groups A and B histopathological evaluation of the lungs of all rabbits was performed at the end of the 4 weeks of AD intake, while in group C it was performed at 2 weeks because of increased mortality. At baseline, mean L/B ratios for groups A, B and C were 2.8 +/- 0.3, 2.8 +/- 0.3 and 2.8 +/- 0.4, respectively. After 3 weeks of AD intake, L/B ratios increased to 4.1 +/- 0.6 and 4.8 +/- 0.6 in groups A and B, respectively. The L/B ratio was 3.6 +/- 0.2 after 1 week of AD intake in group C. The correlation coefficients between the lung uptake of 99mTc-HMPAO and AD doses for groups A, B and C were r = 0.51 (P = 0.037), r = 0.74 (P = 0.0002) and r = 0.96 (P = 0.0001), respectively. Histopathological findings related to AD lung toxicity, such as interstitial pneumonitis and foamy alveolar macrophages, were observed more frequently in groups B and C than in group A. According to our findings, 99mTc-HMPAO lung uptake is correlated with AD dose. 99mTc-HMPAO lung imaging can demonstrate AD-induced lung injury.     

17-AAG对转染NIS基因的未分化甲状腺癌摄碘动力学的影响

目的 探讨17-丙烯胺基-17-去甲氧基格尔德霉素(17-AAG)对已转染NIS基因的未分化甲状腺癌(ATC)细胞摄碘动力学的影响.方法 采用脂质体转染法,将携带NIS基因的重组质粒pcDNA3.1-NIS转染入ATC细胞株FRO细胞中,G418抗性筛选获得稳定表达细胞系NIS-FRO.在NIS-FRO细胞的培养基中引入125I,进行125I内流及外流的系列实验,绘制时间-放射性曲线.进一步分析经1μmol/L的17-AAG作用24 h后NIS-FRO细胞125I内流及外流的变化,并与未经转染的细胞进行对比,2组间各个时间点的放射性计数采用两样本t检验进行统计学分析.结果 NIS-FRO细胞的摄125I能力明显提高,约为FRO细胞的10.68倍(t=45.329,P＜0.001),但去除孵育环境中的125I后30 min,细胞内的125I滞留率仅为初始的10.5％.1μmol/L的17-AAG作用于NIS-FRO细胞后24h,细胞摄125I能力进一步提高,在含125I的培养基中孵育20～60 min,其放射性计数为31771.8～54815.5 min-1,摄125I能力较对照组( 24020.3～41293.8)提高了24.8％～ 35.5％(t值依次为3.096、4.275、3.055、4.292和5.496,P均＜0.05);撤掉孵育环境中的131I后5～30 min,细胞内的125I滞留率为32.7％ ～85.2％,较对照组(10.5％～56.8％)明显增加(t值依次为22.801、13.096、19.631、38.205、43.519和29.322,P均＜0.01),125I的外流减少,30 min后17-AAG作用组的细胞内125I滞留率为32.7％,为对照组的3.1倍.结论 把NIS转染入ATC细胞后获得的稳定表达细胞株在经一定浓度的17-AAG作用后,可进一步提高肿瘤细胞的摄碘率,并可明显延迟碘的外流,提高细胞内碘的滞留率.