鼻咽癌放疗前后99mTc-HL91 SPECT乏氧显像分析

目的:通过99mTc-4,9-二氮-3,3,10,10-四甲基十二烷-2,11-二酮肟(99mTc-HL91)乏氧显像研究鼻咽癌放疗前后肿瘤细胞乏氧的变化。方法:接受三维适形放疗的鼻咽癌患者35例,放疗前1～2d、放疗后(200cGy/次,5次/周)1～2d分别行99mTc-HL91SPECT显像。利用感兴趣区技术计算肿瘤/非肿瘤部位放射性计数比值(T/N),分析放疗前后肿瘤乏氧的变化。结果:放疗前、后显像的T/N(4h)分别为1.51±0.21、1.26±0.18,差异有显著性(P<0.01)。结论:99mTc-HL91SPECT乏氧显像能够为临床提供鼻咽癌放疗前后肿瘤组织乏氧的变化并再氧合提供有价值的信息。     

乳腺癌99mTc-HL91乏氧显像和HIF-1α表达相关性的实验研究

目的:研究乳腺癌99mTc-HL91乏氧显像以及与乏氧诱导因子-1α(HIF-1α)表达水平的相关性。方法:31例乳腺癌患者行SPECT 99mTc-HL91乏氧显像,利用计算机感兴趣区(ROI)技术计算乳腺癌病灶计数/对侧计数(T/TN值),免疫组化方法检测肿瘤组织HIF-1α表达水平。结果:31个病灶对99mTc-HL91的摄取均高于对侧正常乳腺组织,99mTc-HL91摄取程度与肿瘤大小无相关关系(P>0.05);注射99mTc-HL91 4小时后SPECT显像浸润性导管癌T/NT值为2.16±0.38,浸润性小叶癌T/NT值为2.10±0.32,两者无显著性差异(P>0.05);病灶的T/NT值为1.36~6.43(中位值2.95),免疫组化结果显示表达HIF-1α的细胞数为25.6%~78.5%(中位数56.3%),两者之间呈正相关(P<0.01)。结论:乳腺癌组织对乏氧显像剂99mTc-HL91有显著的摄取,摄取值与病理类型及病灶大小无相关性,但与HIF-1α的表达存在正相关。     

99mTc-HL91肿瘤阳性显像的初步临床评价

目的:研究乏氧显像剂99mTc-HL91作为肿瘤阳性显像剂的价值及最佳显像条件。方法:对25例临床确诊的恶性肿瘤患者进行99mTc-HL91平面及断层显像,通过划感兴趣区技术计算肿瘤与正常组织的放射性比值。结果:平面显像显示肿瘤的效果较差,而断层显像及延迟显像效果较好。以T/NT值为1.5为标准,99mTc-HL91显像检测病灶的灵敏度为90.6%。结论:99mTc-HL91乏氧显像是一种较灵敏和特异的肿瘤阳性显像检测方法。     

非小细胞肺癌放疗前后~(18)F-FDG符合线路正电子显像与~(99)Tc~m-HL91乏氧显像临床研究

目的观察非小细胞肺癌(non-small cell lung cancer,NSCLC)患者放疗前、后~(99)Tc~m-HL91乏氧显像与~(18)F-FDG符合线路正电子显像变化,探讨2种方法评价NSCLC放疗疗效的价值。方法 NSCLC患者20例,均行三维适形放疗,分别于放疗前1周、放疗结束后8周行18F-FDG符合线路正电子显像、静脉注射~(99)Tc~m-HL91后4h平面及SPECT/CT断层显像,采用半定量法测量肿瘤病灶和对侧正常肺组织摄取~(18)F-FDG及~(99)Tc~m-HL91比值(T/N);依据放疗疗效将20例患者分为放疗有效组和无效组,观察2组放疗前、后T/N比值变化,分析其与放疗疗效的关系。结果放疗后病灶和对侧正常肺组织摄取18F-FDG T/N比值(5.47±1.69)较放疗前(7.51±1.53)降低(P0.05);放疗后病灶和对侧正常肺组织摄取~(99)Tc~m-HL91的4h平面及SPECT/CT断层显像T/N比值(1.20±0.11、1.61±0.27)较放疗前(1.44±0.08、1.98±0.21)降低(P0.05);放疗前后摄取~(99)Tc~m-HL91的4h平面及SPECT/CT断层显像T/N比值明显低于摄取~(18)F-FDG T/N比值(P0.05);放疗结束后8周评价放疗疗效,有效13例,无效6例,死亡1例;放疗有效组、无效组放疗后病灶与对侧正常肺组织摄取~(99)Tc~m-HL91的4h断层显像T/N比值(1.34±0.13、1.82±0.35)低于放疗前(1.69±0.21、2.04±0.32)(P0.05),且2组放疗前后T/N比值比较差异有统计学意义(P0.05);有效组治疗前~(18)F-FDG显像T/N比值(7.34±1.25)与无效组(7.58±1.62)比较差异无统计学意义(P0.05),放疗后有效组T/N比值(4.61±1.32)较放疗前降低,且低于无效组放疗后(7.23±1.34)(P0.05);病灶摄取~(18)F-FDG和~(99)Tc~m-HL91 4h断层显像的T/N比值呈直线相关(r=0.641,P=0.034)。结论放疗可有效降低肿瘤的乏氧水平和肿瘤的葡萄糖代谢活性;~(99)Tc~m-HL91显像可反映病灶的乏氧状态及放疗前后乏氧水平改善程度,初步评价放疗疗效。     

99Tcm-HL91乏氧显像在非小细胞肺癌放疗中的初步临床应用研究

目的 通过研究非小细胞肺癌三维适形放疗前后乏氧显像结果与放疗疗效的关系,探讨利用99Tcm-HL91乏氧显像来检测肿瘤乏氧及预测和评价放疗疗效的临床价值.方法 拟接受三维适形放疗的10例非小细胞肺癌患者,在放疗前1～2 天和结束后1～2天各进行一次99Tcm-HL91显像.应用感兴趣区(ROI)技术测定肿瘤/对侧相应部位放射性计数比值(T/N),分析放疗前T/N比值和放疗前后T/N比值的变化与疗效的关系.结果 放疗有效组(CR+PR)与无效组(NC+PD)的放疗前3 h断层显像T/N比值分别为1.90±0.16和2.20±0.21(P=0.040),两组3 h断层显像T/N比值下降率分别为(21.63±5.83)%和(11.40±5.16)%(P=0.031).结论 可利用放疗前99Tcm-HL91断层显像和放疗前后乏氧显像的改变来预测和评价非小细胞肺癌三维适形放疗疗效.     

99mTc-HL91乏氧显像、CT及纤维支气管镜检查在肺癌诊断中的对比研究

目的探讨^99mTc-HL91乏氧显像、CT及纤维支气管镜检查在诊断肺癌的价值。方法82例经病理确诊的肺肿瘤患者行SPECT ^99mTc-HL91乏氧显像、CT及纤支镜检查，比较分析诊断效能。结果^99mTc-HL91乏氧显像诊断肺癌的灵敏度、特异性和准确率分别为92．7％、100％、95．1％，CT和纤支镜分别为94．5％、66.6％、85.4％和63．6％、100%和75．6％，^99mTc-HL91乏氧显像诊断的灵敏度和准确率高于纤支镜检查，特异性明显高于CT检查，差异均有显著性。^99mTc-HL91乏氧显像和CT联合诊断肺癌的灵敏度、特异性和准确率为96．4％、100％和97．6％。结论^99mTc-HL91乏氧显像诊断肺癌有较高的临床价值，联合CT检查可进一步提高诊断的准确性。     

99mTc-HL91乏氧显像监测放疗后荷H22肝癌KM小鼠肿瘤再氧合状态

目的 探讨99mTc-HL91乏氧显像监测肿瘤再氧合状态情况,同时检测肿瘤乏氧诱导因子-1a(HIF-1a)表达,分析两种检查方法的相关性.方法 荷H22肝癌KM小鼠随机分为对照组和实验组,实验组又根据放疗后时间1 d、3 d、5 d进行实验.对照组不进行60Co放疗,实验组接受单次15 Gy的60Co放疗.各组小鼠注射99mTc-HL91显像剂2 h后进行SPECT平面显像.各组小鼠图像通过ROI技术,计算T/NT比值.图像采集结束后立即处死小鼠,完整剥离肿瘤,称重并计算放射性计数,计算肿瘤微分摄取率(DUR).之后迅速将肿瘤组织常规制成蜡块,用免疫组化技术测定HIF-1a的表达.最后将DUR、T/NT数值分别与HIF-1a的表达进行等级相关性分析.结果 与对照组相比,随着放疗时间的延长,DUR及T/NT比值呈现先减少后增加的趋势,HIF-1a阳性细胞数量也呈现先减少后增加的表达.结果显示DUR及T/NT比值分别与HIF-1a的表达呈正相关(r值分别为0.75和0.86,P<0.05,双侧).结论 99mTc-HL91乏氧显像与HIF-1a的表达可用于监测肿瘤放疗后的再氧合状态,二者呈正相关.     

201TI和99mTc-HL91联合显像在诊断急性心肌梗死患者存活心肌中的初步应用

目的研究201Tl与99mTc-HL91双核素心肌显像方法学,评价其在诊断急性心肌梗死(AMI)患者存活心肌中的临床应用价值.方法18例AMI患者及10例对照者行静息和24 h延迟201Tl与99mTc-HL91双核素心肌显像,核素显像行5分法评价图像质量,用17节段法来分析201Tl显像缺损与乏氧显影心肌节段.结果双核素显像图像质量良好,99mTc-HL91图像质量不如201Tl(t=6.007,P＜0.01);201Tl静息显像诊断AMI灵敏度为100.0%,特异度为90.0%,准确度为96.4%,24 h延迟显像22.2%AMI患者多节段存活心肌显影;83.3%的AMI患者201Tl灌注缺损心肌节段在99mTc-HL91显像中显影,对照者也有部分心肌节段显影.结论201Tl与99mTc-HL91双核素心肌显像能明确AMI患者心肌梗死部位并初步判断是否有存活心肌,具有临床应用前景.     

99Tcm-HL91与99Tcm-MIBI比较显像对甲状腺冷结节的诊断价值

目的：比较99Tcm-HL91和99Tcm-MIBI显像定性及半定量分析对甲状腺冷结节的诊断价值。方法：对103例99TcmO4-甲状腺扫描提示为冷结节的患者手术前行SPECT亲肿瘤显像,其中99Tcm-HL91显像组35例,99Tcm-MIBI显像组68例;并对两组患者早期和延迟图像的定性和半定量分析结果进行比较。结果：99Tcm-HL91乏氧显像对甲状腺冷结节诊断的准确度和特异度均高于99Tcm-MIBI亲肿瘤显像,差异有显著性（P<0.001）;两种显像方法的敏感度无显著差异。结论：99Tcm-HL91乏氧显像对甲状腺冷结节良恶性的鉴别诊断更具有优越性。     

99Tcm-HL91乏氧显像预测非小细胞肺癌放疗敏感性的临床价值

目的 对非小细胞肺癌患者放疗前行99Tcm-HL91显像,与放疗疗效进行比较,探讨99Tcm-HL91显像在预测放疗敏感性方面的应用价值.方法 对35例经CT引导下穿刺或支气管镜检查病理确诊的非小细胞肺癌患者,放疗前一周内静脉注射99Tcm-HL91 740 MBq(20 mCi),4 h后进行99Tcm-HL91平面及断层显像.半定量分析利用感兴趣区(ROI)技术,勾画圆形感兴趣区,计算肿瘤与对侧正常肺组织(T/N)的放射性比值.随访患者放疗疗效,完全缓解(CR)和部分缓解(PR)为治疗有效组,无变化(NC)和增大(PD)为无效组.结果 99Tcm-HL91平面显像35例非小细胞肺癌患者中的30例显像阳性;断层显像33例显像阳性.半定量分析断层像4 h的T/N比值显著高于平面像的T/N比值.放疗后完全缓解(CR)5例,部分缓解(PR)14例,无变化(NC)7例,增大(PD)4例,死亡或失访共5例,放疗有效组(CR+PR)与放疗无效组(NC+PD)断层显像的T/N比值分别为1.747±0.301,2.087±0.478,差异具有显著性(t=2.363,P=0.026).结论 放疗前99Tcm-HL91肺显像可预测非小细胞肺癌的放疗敏感性.     

脑缺血缺氧预处理

○AgingBluntsIschemic-Preconditioning-InducedNeuroprotectionFollowingTransientGlobalIschemiainRats.CurrentNeurovascularResearch2005;2(5):365-74衰老减弱缺血预处理对短暂全脑缺血大鼠的神经保护作用○Effectofinvivohypoxicpreconditioningonchangesinintracellularcalciumcontentinducedbylong-termanoxiainratbrainslices.BulletinofExperimentalBiologyandMedicine2004;138(4):338-40体内缺氧预处理对长期缺氧大鼠脑细胞钙含量变化的影响○TheExpressionPatternofPro-andAntiapoptoticProteinsBaxandBcl-2inRatBr…     

Chronic hypoxic pulmonary hypertension]

Hypoxic pulmonary vasoconstriction is a self-modulatory mechanism matching local blood flow to local alveolar ventilation. In pathological conditions, it may occur as an acute episode or as a sustained response with vascular remodeling and pulmonary hypertension. Chronic generalized alveolar hypoxia occurs in populations living at high altitude, in human disease states associated with decreased ventilation, or progressive lung destruction. Persistent hypoxic vasoconstriction and the associated vascular structural remodeling are the main mechanisms of the sustained pulmonary hypertension, although other factors, including secondary polycythemia, hypercapnia and increased airways resistance may be involved. Understanding of these mechanisms has increased rapidly and may result in the near future in specific treatment aimed at reversing the structural remodeling and matrix deposition in pulmonary arteries.     

Vanadate potentiates hypoxic pulmonary vasoconstriction

Vanadate, an essential trace element and an inhibitor or stimulator of many enzymes, potentiates the hypoxic vasoconstriction in isolated lung preparations. However, the mechanism of action of vanadate in the lung circulation is unclear. We compared, in isolated rat lungs, the effect of vanadate (3 x 10(-5) M) on hypoxia-induced vasoconstriction with the vasoconstriction caused by angiotensin II, KCl or NaCN, and found that vanadate preferentially enhanced the hypoxia- and NaCN-induced pressor responses. Vanadate also shifted the stimulus-response curve for oxygen such that vasoconstriction occurred at a higher PO2 than in control lungs, indicating that vanadate had affected the oxygen sensing mechanism in the lungs. We postulated that vanadate might potentiate hypoxic vasoconstriction, in part, by activating a protein kinase C (PKC), and compared the effect of phorbol myristate acetate (PMA; 5 x 10(-8) M) on hypoxic vasoconstriction with that of vanadate. Both agents, PMA and vanadate, potentiated hypoxic vasoconstriction transiently and to a similar degree and the potentiation by both agents was blocked by staurosporine (1 microgram/ml), a PKC inhibitor, and 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate, a phospholipase C inhibitor, and partially reduced by the Ca++ entry inhibitor nifedipine. We conclude that the similarities between the action of PMA and vanadate in isolated lungs point toward an involvement of the PKC in the mechanism of vanadate-induced potentiation of hypoxic vasoconstriction. In addition, our data indicate that potentiation of hypoxic vasoconstriction by PMA or vanadate may occur, in part, independent of voltage-dependent Ca++ entry.