Quantitative analysis of the tomographic technetium-99m MIBI (99mTc-MIBI) myocardial bullseye display: Application to diagnosis of coronary artery disease

Summary In this study, the^99mTc-MIBI myocardial bullseye display of 31 healthy persons and 34 patients with myocardial ischemia and 17 patients with myocardial infarction were analyzed quantitatively, and compared with the results of myocardial tomography analysis and qualitative bullseye analysis. The sensitivities of the three methods were 88.2%, 91.2% and 94.1% respectively (P>0.05), and the specificities were 93.5%, 83, 9% and 83.9% respectively (P<0.05). On the other hand, the quantitative analysis obviously outperformed the other two methods in the detection of ischemic segments of myocardhum near infarction zone (P<0.01). The quantitative analysis of^99mTc-MLBI myocardial bullseye (quantitative bullseye) was an objective, specific and sensitive method for diagnosis of coronary artery disease.     

电位滴定法测定胰激肽释放酶活力测试条件探讨

本文用ＦＩＰ推荐的方法，以具有国际单位的参照品为标样，滴定液为０．０１ｍｏｌ／ＬＮａＯＨ标准溶液，考查了以ＢＡＥＥ为底物的电位滴定法测定胰激肽释放酶活力的实验条件，通过正交试验得出直观和方差分析的结果，依据酶活力单位高、ＳＤ和ＲＳＤ％较小的原则，求出酶活力测定的最适条件是：酶反应温度为２５℃；缓冲液为０．００１５ｍｏｌ／ＬＮａ２Ｂ４Ｏ７－０．２５ｍｏｌ／ＬＮａＣＬ－２×１０（－４）ｍｏｌ／ＬＥＤＴＡ，ｐＨ为８．００；反应液中酶浓度为０．４８ＩＵ／ｍｌ；底物浓度为５×１０（－３）ｍｏｌ／Ｌ；胰蛋白酶抑制剂浓度为１２５μｇ／ｍｌ。胰激肽释放酶活力测定的实验数据的相对标准偏差小于５％。     

兔心肌挫伤心功能障碍与心肌细胞内Ca2+和线粒体ATP酶的变化

目的：探讨心肌细胞内游离钙([Ca^2 ]i)和心肌ATP酶变化在心肌挫伤（MC）后心功能障碍发生机制中的意义。方法：随机选取兔36只，分为6组：正常对照、伤后2、4、8、12、24h，每组6只。经右颈总动脉插管至左心室测左室压力。采用BIM-II型生物撞击机致成MC模型。在上述时相点测定左室压力，并测定心肌细胞内[Ca^2 ]i和心肌匀浆组织及线粒体ATP酶活力。结果：心脏收缩/舒张功能受到损害，心肌细胞内[Ca^2 ]i升高，心肌匀浆组织及线粒体ATP酶下降，相关分析表明心功能障碍与心肌细胞内[Ca^2 ]i含量升高呈明显负相关，与ATP酶活性降低呈明显正相关。结论：MC后心脏功能下降，心肌细胞内[Ca^2 ]i含量升高和ATP酶活性下降可能是其原因之一。     

白血病抑制因子反义寡核苷酸对髓母细胞体外生长的抑制作用

为进一步认识白血病抑制因子（LIF）对人髓母细胞瘤生长的生物学作用，我们使用LIF反义寡核苷酸，在髓母细胞内特异性阻断LIF基因表达并观察它对靶细胞的生物学效应。结果发现，被处理细胞的LIF表达降低至RT／PCR检出的阈值之下，抗LIF的免疫组织化学染色亦呈阴性，同时，这些细胞的生长速度明显减缓。相反，用与反义寡核苷酸互补的正义序列处理的细胞无论在基因表达／产生，还是在生长速度方面，均和正常培养细胞的细胞相似，本研究从而提示了一条以LIF为对象的髓母细胞瘤以及其它LIF生长依赖性肿瘤的基因和免疫治疗途径。     

Clinicopathologic analysis of eight cases of pancreatic carcinoid tumors

Carcinoids of the pancreas are exceedingly rare tumors that orieinate from the enterochromaffin cells of the gastroenteropancreatic neuroendocrine system. According to a recent report,1 pancreatic carcinoids are found in only 0.58% (79/13 715 cases) of the entire carcinoid group. Todate, very limited information regarding the detection and diagnosis of this entity has been reported in the available literature. Although pancreatic carcinoid tumors grow.     

肝癌病人血浆和癌组织中血栓调节蛋白的检测

目的　检测肝癌病人血浆和肝癌组织中血栓调节蛋白 (TM )的表达 ,探讨TM与肝癌临床病理特征的关系。方法　用酶联免疫吸附夹心法检测 45例肝癌和 6例肝良性占位病人手术前后的血浆TM水平 ;用免疫组织化学法检测肝癌及肝良性占位组织中的TM蛋白表达水平。结果　术前肝癌组血浆TM水平 ( 10 .2± 5 .7)ng/mL明显高于肝良性占位组 ( 6.1± 2 .2 )ng/mL和正常人对照组 ( 5 .7± 1.0 )ng/mL ,P <0 .0 5 ;术前TM血浆水平肝癌伴门静脉癌栓组 ( 6.9± 4.5 )ng/mL和多发肝癌结节组 ( 8.1± 4.6)ng/mL明显低于无门静脉癌栓组( 11.4± 5 .6)ng/mL和单发肝癌结节组 ( 11.5± 5 .9)ng/mL ,P <0 .0 5 ;40例肝癌病人肝癌切除术前TM水平( 10 .8± 5 .3 )ng/mL与肝癌切除术后 ( 7.6± 4.2 )ng/mL相比差异显著 ,P <0 .0 5。肝良性占位组术前与术后相比差异无显著性 ,P >0 .0 5。肝癌组织中TM蛋白表达阳性的病人术前血浆TM水平明显高于TM表达阴性者 ,P <0 .0 5 ;而术后血浆TM水平两者则无显著性差异 ,P >0 .0 5。结论　肝癌病人血浆中TM水平升高 ,TM水平的高低与门静脉癌栓的形成有关     

三七总甙对人增生性瘢痕成纤维细胞TGF-β1和细胞周期的作用

目的 观察三七总甙对人增生性瘢痕成纤维细胞TGF-β1和细胞周期的作用。方法体外培养人增生性瘢痕成纤维细胞，并应用三七总甙进行干预，用免疫细胞化学染色法结合图像分析观察TGF-β1的表达变化，用流式细胞仪测定细胞周期的变化。结果与对照组相比，三七总甙能够显著抑制细胞TGF-β1的表达，并使细胞停滞于S期，而G0-G1期、G2-M期细胞明显减少（P〈0．01）。结论三七总甙改变细胞周期和抑制增生性瘢痕成纤维细胞TGF-β1的表达，可能成为防治增生性瘢痕的药物。     

安氏Ⅱ类错(牙合)畸形对青春期面部骨轮廓发育的影响

目的:研究安氏II类错畸形对青春期面部骨轮廓发育的影响。方法:收集安氏II类错畸形的成人患者和青少年患者共362例。摄取头颅定位侧位片及头颅定位正位片。对面高、面宽等19项测量项目做比较分析及t检验。结果:①安氏II类青少年患者与正常青少年相比,下颌基骨长度、下颌长度较小,但无统计学差异。②安氏II类成年患者与正常成年人相比,下颌基骨长度、下颌长度有显著性差异。③安氏II类患者下颌骨在青春发育期有向前、向上旋转的趋势。结论:安氏II类错畸形患者经过青春期发育,使面部畸形程度更加严重。本研究得出安氏II类错畸形对青春期面部骨轮廓发育的影响,对正颌外科和正畸治疗具有参考意义。     

(足母)甲瓣切取术后供区创面覆盖的方法选择

目的探讨[足母]甲瓣切取术后供区修复的方法，减少供区并发症的发生。方法对[足母]甲瓣切取术后25例[足母]趾创面，采用三种不同的方法处理，其中采用游离皮瓣移植修复9例，采用足背或足底局部带蒂皮瓣修复12例，采用第二足趾皮甲瓣修复4例。结果移植皮瓣全部成活，术后平均随访10个月，其中2例游离皮瓣在术后6个月进行二期削薄，外观和功能满意。第二趾皮甲瓣修复后的功能在3种方法中效果最好。结论根据[足母]甲瓣供区的缺损情况，采用不同的手术方法进行即时修复，能最大限度减少供区并发症的发生。     

Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats.

Cerebral ischemic preconditioning protects against stroke, but is clinically feasible only when the occurrence of stroke is predictable. Reperfusion plays a critical role in cerebral injury after stroke; we tested the hypothesis that interrupting reperfusion lessens ischemic injury. We found for the first time that such postconditioning with a series of mechanical interruptions of reperfusion significantly reduces ischemic damage. Focal ischemia was generated by permanent distal middle cerebral artery (MCA) occlusion plus transient bilateral common carotid artery (CCA) occlusion. After 30 secs of CCA reperfusion, ischemic postconditioning was performed by occluding CCAs for 10 secs, and then allowing for another two cycles of 30 secs of reperfusion and 10 secs of CCA occlusion. Infarct size was measured 2 days later. Cerebral blood flow (CBF) was measured in animals subjected to permanent MCA occlusion plus 15 mins of bilateral CCA occlusion, which demonstrates that postconditioning disturbed the early hyperemia immediately after reperfusion. Postconditioning dose dependently reduced infarct size in animals subjected to permanent MCA occlusion combined with 15, 30, and 60 mins of bilateral CCA occlusion, by reducing infarct size approximately 80%, 51%, and 17%, respectively. In addition, postconditioning blocked terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling-positive staining, a marker of apoptosis, in the penumbra 2 days after stroke. Furthermore, in situ superoxide detection using hydroethidine suggested that postconditioning attenuated superoxide products during early reperfusion after stroke. In conclusion, postconditioning reduced infarct size, most plausibly by blocking apoptosis and free radical generation. With further study it may eventually be clinically applicable for stroke treatment.