Cyclin alterations in giant cell tumor of bone.

Cyclins play an important role in regulating the passage of dividing cells through critical checkpoints in the cell cycle. Because alterations of several cyclins, especially cyclin D1, have been implicated in the development of many human neoplasms, we examined 32 cases of giant cell tumor of long bones for cyclin D1 gene amplification and protein overexpression using differential polymerase chain reaction and immunohistochemistry, respectively. In addition, the expression of cyclin D3, cyclin B1, and the proliferation-associated antigen Ki-67 (MIB-1) was assessed immunohistochemically. Low-level cyclin D1 gene amplification was detected in 61% of giant cell tumor cases. All tumors showed cyclin D1, cyclin D3, cyclin B1, and Ki-67 (MIB-1) staining; however, the distribution was very characteristic. Cyclin D1 protein expression was seen predominantly in the nuclei of the giant cells, with occasional mononuclear cells staining. There was no correlation between cyclin D1 gene amplification and protein overexpression. Cyclin D3 staining showed a similar distribution, with 88% of cases showing protein overexpression. Cyclin D1 and/or D3 staining in the giant cells was never associated with staining for either cyclin B1 or Ki-67 (MIB-1), as the expression of the latter two proteins was restricted to the mononuclear cells. Cyclin B1 overexpression was seen in 44% of cases. Ki-67 (MIB-1) staining was present in all cases, and between 10 to 50% of the mononuclear cells were positive. These results suggest that alterations in cyclin D1 and/or D3 might play a role in the pathogenesis of giant cell tumor of bone.     

原位检测新基因SNC66在胃癌组织与正常胃粘膜中的表达

目的: 观察新基因SNC66在胃癌组织中的表达水平,分析SNC66表达水平与胃癌发生的相关性。 方法:以β-actin为对照,对20例胃癌组织及其配对正常胃粘膜的石蜡切片,进行原位cRNA/mRNA分子杂交和原位RT-PCR扩增。 结果:两种检测方法表明,SNC66在正常胃粘膜组织中都呈强阳性表达。而在胃癌组织中,原位分子杂交检测表明,20例标本SNC66不表达和弱阳性表达各8例,强阳性表达4例。原位RT-PCR检测表明,当循环数为10时,此20例胃癌标本中不表达、弱阳性和呈强阳性表达数分别为6,9和5;而当循环数为25时,则4例不表达,16例呈强阳性表达。 结论:SNC66基因在胃癌组织中存在明显的表达降低和表达缺陷。SNC66可以作为一个胃癌负相关基因加以进一步研究。     

Changes in ultrastructure and Ca2+ distribution in the isolated working rabbit heart after ischemia. A time-related study.

Ultrastructural changes in cardiac muscle of isolated working rabbit hearts after various periods of ischemia are described and compared with distributional changes in calcium. The effects of reperfusion on these structural parameters were also investigated. The purposes of this study were to relate the role of calcium in the degeneration of cardiac muscle; to determine whether Ca2+ localizations could serve as additional criteria to determine more closely the point of no return; and to investigate the contributory role of reoxygenation to the development of myocardial damage. This study shows the existence of topographic differences in the tolerance to ischemia in the mid area, subendocardium, and subepicardium; that the sequestration of Ca2+ by mitochondria is an energy-requiring (active) process that occurs only during reperfusion; the loss of the sarcolemma's ability to bind Ca2+ during ischemia to coincide with increased Ca2+ entry during postischemic reperfusion (this Ca2+ is scavenged by mitochondria as long as sufficient energy remains available; these changes are interpreted as being at the edge of irreversibility); and the lack of additional damage and and lack of Ca2+ accumulation in mitochondria during reperfusion in cells that are damaged to such an extent that mitochondria possess flocculent densities already at the end of the ischemic insult.     

Somatic mitochondrial mutation in gastric cancer.

Likely hot spots for mutations are mitochondrial sequences as there is less repair and more damage by carcinogens compared with nuclear sequences. A somatic 50-bp mitochondrial D-loop deletion was detected in four gastric adenocarcinomas. The deletion included the CSB2 region and was flanked by 9-bp direct repeats. The deletion was more frequent in adenocarcinomas arising from the gastroesophageal junction (4/32, 12.5%) compared with more distal tumors (0/45). Topographical analysis revealed the absence of the deletion from normal tissues except in focal portions of smooth muscle in one case. In two cases, apparent mutant homoplasmy was present throughout two tumors, including their metastases. In the two other cases, the mutation was present in only minor focal portions ( < 5%) of their primary tumors. These findings document the presence of somatic mitochondrial alterations in gastric cancer, which may reflect the environmental and genetic influences operative during tumor progression.     

阻断入肝血流施行肝部分切除手术中肝细胞呼吸功能的研究

目的：探讨在肝脏部分切除手术前增加肝细胞糖原含量能否减轻因阻断肝血流所引发的肝细胞呼吸功能损伤。方法:将本院近9年收治的32例原发性肝癌病人分为实验组及对照组。实验组于术前24 h内静脉滴注高浓度的葡萄糖; 对照组不做特殊处理。2组病人均采用阻断第1肝门方法行病变肝脏切除术。术中测定肝组织ATP含量、肝脏酶学改变及肝细胞线粒体呼吸控制率(RCR) 及磷氧比率(P/O ratio)。结果:糖原含量高的实验组肝脏，组织ATP含量、肝细胞线粒体RCR 及P/O值越高，而肝功能损伤越轻。结论:临床上在阻断肝脏血流施行复杂的肝脏手术之前，增加肝细胞内糖原含量可有效地改进肝细胞的呼吸功能，降低手术风险。     

帕金森病大鼠模型额叶皮质的代谢及形态改变

目的：探讨帕金森病中大脑额叶皮质的形态及代谢改变。方法：大鼠实验组于6-OHDA毁损后用BIOSPEC47／30磁共振波谱仪(4．7T)，采用点分辨波谱法对双侧额叶皮质行H-MRS检测，分析该区N-乙酰天门冬氨酸／肌酸(NAA／Cr)和胆碱／肌酸(Cho／Cr)比值的变化，并用电镜观察该区神经元及突触的形态变化。结果：实验组大鼠损毁侧额叶皮质．NA．A／Cr比值显著低于对侧，对照组两侧无显著差别；Cho／Cr比值在两组的两侧相比均无显著差别。电镜观察显示：损毁侧额叶皮质的突触数量较对侧减少，突触前、后膜和突触小泡结构异常，典型突触结构消失，树突棘出现大片低电子密度区，细胞器消失。结论：帕金森病大鼠模型损毁侧额叶皮质内存在神经元缺失或突触数量的减少，突触结构异常及功能异常。     

Effects of mutation and growth rates on patterns of microsatellite instability.

The detection of somatic microsatellite (MS) alterations in tumors is often interpreted as a sign of underlying genomic instability. However, it is unclear why the proportions of altered MS loci vary between different mutator phenotype tumors. We present a simple mathematical analysis that can account for some of these differences, recognizing that the mutations accumulated in a tumor reflect both its mutation rate and number of cell divisions. Only a small proportion of mutated MS loci are expected in tumors with normal or low mutation rates. In contrast, tumors with high mutation rates may or may not acquire mutations depending on the numbers of divisions that proceed the onset of the mutator phenotype. The majority of MS loci should accumulate mutations if high mutation rates are acquired early in tumor progression. Somatic MS mutations provide clues to both the mode and tempo of tumori-genesis.     

肝脏血管瘤的手术指征和手术方法选择（附46例报告）

目的 探讨肝脏血管瘤的手术指征和手术方法。方法 回顾性分析采用手术治疗46例肝脏血管瘤病人资料，判断其手术指征，评价不同手术方法的治疗效果厦其手术并发症发生情况。结果 46例病人中，19例采用肝叶或肝段切除术，17例出现并发症，以胸腔积液和膈下积液多见，采用血管瘤摘除术的27例病人无并发症。结论 对肝脏血管瘤直径大于5cm并有明显临床症状，或不能除外恶性肿瘤的病人可以采用手术治疗。血管瘤摘除术是安全有效、并发症少的手术方法。     

CVB3-VP1基因免疫诱导特异性抗病毒免疫应答及保护作用

目的 :构建表达柯萨奇病毒B3(CVB3)主要包膜蛋白VP1的基因疫苗 ,并研究该疫苗诱导CVB3特异性免疫应答及免疫保护的作用。方法 :抽提CVB3RNA ,以RT PCR扩增VP1基因 ,克隆于真核表达载体 pcDNA3中 ,构建质粒pcDNA3 VP1。将该质粒转染Hela细胞 ,观察其表达情况 ;以 5 0 μgpcDNA3 VP1质粒DNA肌注免疫BALB/c小鼠 3次 ,检测CVB3特异性体液和细胞免疫应答。间隔 4wk以 5×LD50 的CVB3攻击小鼠 ,观察攻击后小鼠的存活情况。结果 :构建了重组质粒 pcDNA3 VP1,并在体外获得有效表达。以该质粒肌肉免疫BALB/c小鼠 ,可诱生高水平的IgM和IgG ,VP1多肽特异性淋巴细胞增殖反应及CTL活性均显著高于 pcDNA3免疫的对照组。病毒攻击试验表明 ,pcDNA3 VP1免疫组33.3%小鼠可长期存活 ,其心肌组织未见明显的病理学改变 ;而对照小鼠平均仅存活 6 .7d ,心肌显示大量的局灶性坏死和炎性细胞浸润。结论 :pcDNA3 VP1免疫可诱生CVB3特异性体液及细胞免疫应答 ,保护免疫小鼠抵抗CVB3的致死性攻击