Distinguishment of A 42 Capsomere Structure of Icosohedral Virion from A 32 One by Electron Microsco

ＤｉｓｔｉｎｇｕｉｓｈｍｅｎｔｏｆＡ４２ＣａｐｓｏｍｅｒｅＳｔｒｕｃｔｕｒｅｏｆＩｃｏｓｏｈｅｄｒａｌＶｉｒｉｏｎｆｒｏｍＡ３２ＯｎｅｂｙＥｌｅｃｔｒｏｎＭｉｃｒｏｓｃｏｐｅＣｎｅｎＢｉｎｇｙｉｎｇ（陈丙莺）；ＺｈｏｕＴｏｎｇ（周）（Ｄｅｐａｒｔｍｅ...     

局部亚低温治疗急性脑出血的临床研究

目的观察冰帽加双侧颈动脉区冰敷治疗急性脑出血的临床疗效和探讨最佳治疗时机。方法 174例急性脑出血患者随机分为治疗组和对照组 ,每组 87例。对照组给予常规治疗 ,治疗组在常规治疗的基础上同时给予亚低温治疗 ;治疗组中 46例在发病 3小时内治疗 ,41例在发病 3小时后治疗。观察治疗组与对照组以及治疗组中发病 3小时内与发病 3小时后两组的临床疗效和预后情况。结果亚低温治疗组与对照组比较 ,神经功能改善 (P <0 0 5 ) ,生存率及恢复良好率提高 (P <0 0 5 )。发病 3小时内开始治疗者优于 3小时后开始者 (P <0 0 5 )。结论亚低温治疗能有效减轻急性脑出血后的神经功能缺损 ,降低病死率和致残率 ;最佳治疗时机在发病 3小时以内。     

褪黑素对急性胰腺炎相关性肺损伤中趋化因子MIP-2表达的影响

目的观察褪黑素(MT)对ANP大鼠肺组织趋化因子巨噬细胞炎性蛋白-2(MIP-2)表达的影响,探讨MIP-2在ANP相关肺损伤发病机制中的作用。方法35只SD大鼠随机分为假手术组(SO组),ANP 3h、6h、12h组和MT 3h、6h、12h组,每组5只。采用4%牛磺胆酸钠胰胆管逆行注射制备ANP动物模型,MT组在ANP诱导前30min腹腔注射MT 20mg/kg体重。检测血淀粉酶,观察肺组织病理学改变,采用实时定量RT-PCR法和免疫组化检测肺组织中MIP-2 mRNA和蛋白的表达。结果与SO组相比,ANP 3h、6h和12h组肺组织MIP-2 mRNA表达分别增加48%,137%和230%。ANP组MIP-2蛋白表达量分别为3.40±0.84,5.80±0.55和6.40±0.45。MT干预组肺组织损伤得到改善,MIP-2 mRNA表达分别为ANP相应时间点的87%,77%和84%,MIP-2蛋白表达分别为2.20±0.84.4.20±0.45和5.20±0.50,与ANP相应时间点比较,相差显著(P<0.05)。结论MIP-2在ANP相关肺损伤发病中起一定作用,MT可能通过下调MIP-2的表达以减轻ANP相关肺损伤的程度。     

Acute type a aortic dissection complicated with acute inferior myocardial infarction following aortic valve replacement

Acute aortic dissection complicated with acute myocardial infarction (AMI) is the most fatal situation. We experienced the successful treatment for acute type A aortic dissection complicated with inferior AMI following aortic valve replacement (AVR). A 60-year-old man had had AVR for aortic regurgitation. Sixteen months after the AVR, he had a sudden onset of severe chest pain with complete atrioventricular block. Immediately, temporary pacing and cardiac catheterization were conducted, showing the occlusion of the right coronary artery due to acute type A aortic dissection. On his way to our hospital, direct current shock was conducted 3 times for ventricular fibrillation. We replaced the ascending aorta combined with coronary artery bypass grafting and the postoperative course was uneventful. The key to treat acute aortic dissection complicated with AMI is early accurate diagnosis, prompt temporary pacing for bradycardia, defibrillation for lethal arrhythmia and insertion of a perfusion catheter if possible. These preoperative hemodynamic stabilization gives us the chance to save these patients.     

降纤酶对ACI患者血清sCRP的影响及改善神经缺损的作用

目的:探讨降纤酶对急性脑梗死(ACI)患者血清超敏C反应蛋白(sCRP)水平的影响及其在改善神经功能缺损方面的作用。方法:46例ACI患者随机分为2组,对照组23例,静脉滴注曲克芦丁注射液,0.6g/d;治疗组23例,入院后立即给予降纤酶10IU溶入250ml生理盐水静脉滴注,1~1.5h滴完,第3、5天各给予降纤酶5IU,其他用药同对照组;应用免疫比浊法检测2组治疗前及治疗后第7天、14天的血清sCRP水平变化,并对神经功能缺损进行评分。结果:2组sCRP水平在治疗后第7天最高,随后逐渐降低。治疗组治疗前血清sCRP水平和治疗前、第7天的神经功能缺损总分与对照组比较差异无统计学意义(P>0.05),治疗组治疗后第7天、14天sCRP水平分别为(7.73±2.16)、(2.92±2.24)mg/L,对照组分别为(10.18±3.16)、(4.66±2.42)mg/L,治疗组明显低于对照组(P<0.05~0.01);第14天治疗组神经功能缺损总分为(10.68±4.08)分,明显低于对照组[(16.81±4.86)分](P<0.01)。结论:降纤酶能明显降低ACI患者血清sCRP水平,有利于减轻炎症反应,改善神经功能缺损程度。     

实时荧光定量PCR检测PML-RARα融合基因的临床应用研究

目的 利用PML-RARα融合基因作为标志物,应用实时荧光定量PCR技术,监测急性早幼粒细胞白血病(APL)微小残留病(minimal residual disease,MRD)患者体内病毒的状态,探讨预测APL复发风险的方法.方法 利用本实验室建立的定量检测APL患者PML-RARα融合基因的方法,对25例处于初诊、完全缓解(complete remission,CR)、复发等不同阶段的APL患者进行了PML-RARα融合基因的定量检测,并对其中6例患者的MRD状态进行了动态监测.结果 应用荧光定量PCR技术分析患者初诊、CR和复发状态的PML-RARα基因对数值(lg)水平,结果 显示有统计学意义(x2=6.847,P＜0.05);随访期患者的PML-RARα对数值(lg)水平变化较大:初诊时较高(-0.61±0.79),CR时下降(-1.31±0.62),复发时又出现上升(-0.57±0.44),提示若该患者在CR时的对数值呈现上升趋势,患者复发的机率大.结论 应用实时荧光定量(RQ)-PCR技术定量检测PML-RARα融合基因,对监测APL患者MRD状态具有临床适用性,随访期的MRD动态追踪监测具有预后价值.     

苯丙胺急性中毒患者的急救及护理

笔总结了2000年5月-2002年3月收治的9例口服苯丙胺中毒患救护成功的体会。（1）及早，彻底，反复洗胃，有效清除消化吸收的毒物，洗胃过程中做好安全约束措施，使洗胃能顺利完成，对中毒较深的病人结合床边血液透析，以提高疗效。（2）迅速建立静脉通路，合理使用安定，利尿剂，激素，加强对症处理。（3）严密观察病情变化，保持呼吸道通畅。（4）做好基础护理，安全保护及心理护理，9例患均治愈出院。     

用金标法快速测定血清中cTn-Ⅰ在急性心肌梗死诊断上的应用

为探讨急性心肌梗死和疑为心梗病人血中 c Tn I的敏感性和特异性 ,采用金标法对 5 2例就诊病人测定其血中 c Tn- 和酶学法测定 CK- MB两个指标 ,结果发现急性心肌梗死组病人血中的 c Tn- 敏感度高于 CK- MB,但二者无显著性差异 ;而疑为心梗病人血中的 c Tn- 敏感度高于 CK- MB且具有显著的特异性。c Tn- 的测定对急性心肌梗死病人的诊断和治疗具有特别重要的意义     

An uncommon cause of acute right ventricular failure and high mixed venous oxygen saturation

Ruptured sinus of Valsalva aneurysms are rare. We report a case in which the usual clinical manifestations were not present and the patient was initially treated as an acute pulmonary embolus. Despite three negative echocardiograms an intra-cardiac shunt was suspected because of a persistently elevated mixed venous oxygen saturation. Cardiac catheterisation confirmed the diagnosis. Surgical repair was performed and post operative recovery was uneventful.     

Interdigestive small bowel motility and duodenal bacterial overgrowth in experimental acute pancreatitis

The objective of this study is to investigate the effects of an acute necrotizing pancreatitis (ANP), without biliary obstruction, on the migrating motor complex (MMC), small bowel bacterial overgrowth (SBBO), bacterial translocation (BT) and infection of the pancreas simultaneously. Rats were divided into four groups: mild pancreatitis, control, ANP and sham operated control. Jejunal myoelectrodes were used to measure MMCs. Blood, peritoneal fluid, bile, and abdominal organs were harvested for microbial culturing 72 h after induction of pancreatitis. The splenic portion of the pancreas was taken for histology. During ANP the MMC cycle length was significantly increased from 14.1 +/- 0.2 to 22.4 +/- 1.9 min (P < 0.05). The duodenum of ANP rats was in contrast with the other groups characterized by Enterobacteriacae (> 3 log 10 CFU g-1 in seven of 12 rats, P < 0.05). A positive correlation (r = 0.78, P < 0.01) existed between duodenal Gram-negative and anaerobic flora and the MMC cycle. Correlation between MMC cycle length and BT to the pancreas was positive as well (r = 0.70, P < 0.01). A positive correlation (r = 0.85, P < 0.01) was found between the severity of pancreatitis and duodenal bacterial overgrowth. During ANP without biliary obstruction, the jejunal MMC is disturbed and consequently SBBO occurs. The correlation between the severity of pancreatitis, the disturbance of the MMC and SBBO suggests an important pathophysiological role of the proximal small bowel in the infection of pancreatic necrosis.