冠心病患者治疗前后血清SOD、ET及T淋巴细胞亚群水平

目的:探讨了冠心病患者治疗前后血清SOD、ET及T淋巴细胞亚群水平。方法:分别应用放免法和单克隆抗体法对42例冠心病患者进行了血清SOD、ET及T淋巴细胞亚群水平检测,并与35名正常健康人作比较。结果:冠心病患者在治疗前血清ET水平显著地高于正常人组(P<0.01),而SOD和CD4/CD8比值明显地低于正常人组(P<0.01),经治疗后一个月则与正常人组比较差异无显著性(P>0.05)。结论:检测冠心病患者血清SOD、ET及T淋巴细胞亚群水平对判断病情及其预后均具有一定的临床实用价值。     

Upregulation of vascular endothelial growth factor by cobalt chloride-simulated hypoxia is mediated by persistent induction of cyclooxygenase-2 in a metastatic human prostate cancer cell line

Upregulation of vascular endothelial growth factor (VEGF) expression induced by hypoxia is crucial event leading to neovascularization. Cyclooxygenase-2, an inducible enzyme that catalyzes the formation of prostaglandins (PGs) from arachidonic acid, has been demonstrated to be induced by hypoxia and play role in angiogenesis and metastasis. To investigate the potential effect of COX-2 on hypoxia-induced VEGF expression in prostate cancer. We examined the relationship between COX-2 expression and VEGF induction in response to cobalt chloride (CoCl₂)-simulated hypoxia in three human prostate cancer cell lines with differing biological phenotypes. Northern blotting and ELISA revealed that all three tested cell lines constitutively expressed VEGF mRNA, and secreted VEGF protein to different degrees (LNCaP > PC-3 > PC3ML). However, these cell lines differed in the ability to produce VEGF in the presence of CoCl₂-simulated hypoxia. CoCl₂ treatment resulted in 40% and 75% increases in VEGF mRNA, and 50% and 95% in protein secretion by LNCaP and PC-3 cell lines, respectively. In contrast, PC-3ML cell line, a PC-3 subline with highly invasive, metastatic phenotype, exhibits a dramatic upregulation of VEGF, 5.6-fold in mRNA and 6.3-fold in protein secretion after treatment with CoCl₂. The upregulation of VEGF in PC-3ML cells is accompanied by a persistent induction of COX-2 mRNA (6.5-fold) and protein (5-fold). Whereas COX-2 expression is only transiently induced in PC-3 cells and not affected by CoCl₂ in LNCaP cells. Moreover, the increases in VEGF mRNA and protein secretion induced by CoCl₂ in PC-3ML cells were significantly suppressed following exposure to NS398, a selective COX-2 inhibitor. Finally, the effect of COX-2 inhibition on CoCl₂-induced VEGF production was reversed by the treatment with exogenous PGE₂. Our data demonstrate that VEGF induction by cobalt chloride-simulated hypoxia is maintained by a concomitant, persistent induction of COX-2 expression and sustained elevation of PGE₂ synthesis in a human metastatic prostate cancer cell line, and suggest that COX-2 activity, reflected by PGE₂ production, is involved in hypoxia-induced VEGF expression, and thus, modulates prostatic tumor angiogenesis. This revised version was published online in July 2006 with corrections to the Cover Date.     

肱骨髁上骨折合并肱动脉损伤的诊治

目的：为探讨肱骨髁上骨折合并不同类型肱动脉损伤的诊断与治疗。方法：采用交区克氏针固定骨折，应用机械扩张、血管探查、修补、吻合等措施修复肱动脉。结果：16例于术中探查肱动脉，有断裂伤、刺破伤及顽固性痉挛，均采用手术治疗，使前臂血运得到恢复，骨折得到固定。本组除1例因伤后24小时入院出现前臂缺血性肌挛维、1例因严重粉碎性骨折术后肘关节活动中度受限外，14例均恢复良好，结论：肱骨髁上骨折台井脏动脉损伤的后果严重，但通过及时诊断和有效手术治疗、预后良好。     

多发性骨髓瘤患者血清IL-6活性与急性相蛋白浓度的相关性研究

运用敏感的B_9细胞增殖试验检测了81例多发性骨髓瘤(MM)患者血清IL-6活性,同时分析了标本的几种急性相蛋白含量,结果表明,68％MM患者血清中IL-6活性大于5μ/ml(正常对照为5μ/ml以下),几种急性相蛋白中C-反应性蛋白(CRP)在MM时升高(P<0.01),平均达正常对照组的17倍以上,MM患者补体C_4与正常对照组无差异(p>0.05),C_3、白蛋白及转铁蛋白在MM时分别比正常下降24.42％、38.83％和32.80％,且与疾病分期有关,在血清IL-6大于5μ/ml的55例中,IL-6活性与CRP、C_3、白蛋白的相关系数分别为0.46,-0.34和-0.29,IL-6与转铁蛋白浓度相关不明显。本文结果提示:CRP、C_3及白蛋白等含量的变化可作为反映MM病情的简易而敏感的指标。     

乳腺单纯癌细胞连接变化的形态定量研究

通过光镜和电镜对21例乳腺单纯癌和10例小叶增生病的观察,将其中9例单纯癌和7例小叶增生病的细胞连接变化,用Weibel氏形态定量法进行形态定量对比分析。结果表明:癌细胞的缝隙、桥粒、相嵌、并列和紧密等连接量的减少,与小叶增生病相比,两者差异有显著性。癌细胞连接量的减少与细胞分化程度有关。缝隙连接的减少,显示细胞恶变的开始;桥粒、相嵌和并列连接的减少,显示癌细胞分化程度的变化。减少程度愈高,分化程度愈低;恶性度愈高,侵袭性愈强。     

急性脑血管病之脑电地形图与脑CT对比研究

本文报告了急性脑血管病的脑电地形图与脑CT的对比研究。介绍了急性脑血管病的脑电地形图改变,对脑电地形图与脑CT在急性脑血管病诊断上的优劣进行了对比,进一步讨论了脑电地形图在急性脑血管病中的临床应用价值。     

镁对在体兔缺血—再灌心脏的电生理效应

本实验通过结扎兔冠状动脉左室支复制动脉缺血－再灌注模型，应用心外膜接触电极记录单相动作电位，观察后除极电位在再灌注性心律失常中及镁离子的拮抗作用。结果表明，再灌性心律失常的５２．６％与早期后去极化有关。硫酸镁可终止及预防ＲＡ，对再灌中出现触发活动有抑制作用。     

Comparison of different PCR approaches for characterization of Burkholderia (Pseudomonas) cepacia isolates.

In this study, we evaluated three PCR methods for epidemiological typing of Burkholderia (Pseudomonas) cepacia--PCR-ribotyping, arbitrarily primed PCR (AP-PCR) and enterobacterial repetitive intergenic consensus sequence PCR (ERIC-PCR)--and compared them with pulsed-field gel electrophoresis. The analysis was performed with 31 isolates of B. cepacia, comprising 23 epidemiologically unrelated isolates and 8 isolates collected from the same patient during two episodes of bacteremia. Pulsed-field gel electrophoresis, ERIC-PCR, and AP-PCR identified 23 distinct types among the 23 unrelated isolates, while PCR-ribotyping only identified 12 strain types, even after AluI digestion of the amplification products. Among the eight isolates collected from the same patient, all typing techniques revealed two clones of strains. The day-to-day reproducibilities of PCR-ribotyping and ERIC-PCR were good, while greater day-to-day variations were noted in the fingerprints obtained by AP-PCR. We conclude that all three PCR techniques are useful for rapid epidemiological typing of B. cepacia, but ERIC-PCR seems to be more reproducible and discriminative.     

Effects of tetraphenylboron-induced increase in inner surface charge on Ca2+ release from sarcoplasmic reticulum

We studied the relationship between surface charge and release of Ca2+ in the heavy sarcoplasmic reticulum (SR) of skeletal muscle. The inner and outer surface potentials and charge densities of the membrane treated with a lipophilic anion, tetraphenylboron (TPB-), were measured using 1-anilino-8-naphthalene-sulfonate fluorescence. Ca2+ was loaded passively or actively by the SR. Ca2+ release was estimated by the fluorescence of chlortetracycline, and protein conformational change was monitored by use of the sulfhydryl group fluorescent probe, N-(7-dimethylamino-4-methyl-3-coumarinyl) maleimide (DACM). Treatment of Ca2(+)-loaded SR vesicles with micromolar TPB- dose-dependently increased the local fixed negative charge on the inner surface, and changed the DACM fluorescence intensity in parallel with the Ca2+ release. The changes in surface charge and in DACM fluorescence intensity did not originate from the Ca2+ flux. A lipophilic cation, tetraphenylarsonium (TPA+), screened the negative inner surface charge which was increased by TPB-, and inhibited both TPB(-)-induced change in DACM fluorescence intensity and Ca2+ release. Millimolar Mg2+ reduced degrees of TPB(-)-induced Ca2+ release from the SR and of TPB(-)-induced contraction in mechanically skinned fibers. Mg2+ did not inhibit the increase in the negative inner surface charge and DACM fluorescence intensity produced by TPB-. Thus, the local increase in negative charge on the SR inner membrane leaflet seems to be causally related to the Ca2+ release. Mg2+ and TPA+ are suggested to inhibit TPB(-)-induced Ca2+ release by different mechanisms.     

Ras mediates translation initiation factor 4E-induced malignant transformation.

Translation initiation factor eIF-4E binds to the eukaryotic mRNA 5' cap structure (m7 GpppN, where N is any nucleotide). eIF-4E is a limiting factor in translation and plays a key role in regulation of translation. We have shown previously that overexpression of eIF-4E in rodent fibroblasts results in tumorigenic transformation. eIF-4E also exhibits mitogenic activity when microinjected into serum-starved NIH-3T3 cells. To understand the mechanisms by which eIF-4E exerts its mitogenic property, we examined the involvement of the Ras signaling pathway in this activity. Here, we report that Ras is activated in eIF-4E-overexpressing cells, as the proportion of GTP-bound Ras is increased. Overexpression of the negative effector of cellular Ras, GTPase activating protein, causes reversion of the transformed phenotype. Furthermore, we show that neutralizing antibodies to Ras, or a dominant-negative mutant of Ras, inhibit the mitogenic activity of eIF-4E. We conclude that eIF-4E exerts its mitogenic and oncogenic activities by the activation of Ras.