人胎盘基因表达谱芯片的初步研究

目的：制备人胎盘基因表达谱芯片，并用于基因差异表达分析。方法：用基因芯片点样仪将胎盘基因文库探讨打印在氨基包被的玻片上制备表达谱芯片。分别提取对照组与三氧化二砷处理的K562细胞总RNA，纯化mRNA后反转录成cDNA，再以限制性显示技术进行荧光标记，将两组荧光标记的样品混合后与芯片进行杂交，杂交后清洗芯片，干燥后对芯片进行扫描，分析杂交结果。结果：建立了较可靠的制备与检测基因表达谱芯片的方法，并筛选出45个差异表达基因片段，结论：制备的人胎盘基因表达谱芯片可有效地应用于基因的差异表达分析。     

ASSOCIATION OF PLASMA HOMOCYSTEINE LEVEL AND N^5,N^10—METHYLENETETRAHYDROFOLATE REDUCTASE GENE POLYMORPHISM WITH CEREBRAL INFARCTION

OBJECTIVE: To investigate the relationship of plasma homocysteine (Hcy) level to stroke and genetic factor to elevated plasma Hcy level. METHODS: The plasma Hcy level was measured by capillary electrophoresis-ultraviolet detection and the gene polymorphism of N5,N10-methylenetetrahydrofolate reductase (MTHFR) was studied with PCR-RFLP assay in 43 patients with cortical cerebral infarction and 42 healthy control. RESULTS: The plasma Hcy level of the patients (19.3 +/- 6.0 micromol/L) was markedly higher than that of the controls (13.7 +/- 5.4 micromol/L) (t = 4.16, P < 0.001). There are 3 genotypes, C/C, C/T and T/T, about base-variation of MTHFR gene at locus 677. The plasma Hcy level of the subjects with T/T genotype was higher than that of subjects with other genotypes. However, the frequencies of each genotype and allele were not significantly different between the patients and the controls. CONCLUSIONS: The elevated plasma Hcy level is a risk factor for atherothrombotic cerebral infarction, and is related to the C-->T mutation at locus 677 of MTHFR gene.     

经皮穿刺髓核成形术治疗腰椎间盘突出症初步临床报道

目的　寻求一种简单、安全、有效、微创的椎间盘突出症治疗方法。方法　对 1 6例腰椎间盘突出症采用经皮穿刺髓核成形术 (Nucleoplasty)治疗 ,并对其疗效进行观察分析。 结果　全部患者经二周至一个月短期随访 ,症状均有不同程度改善 ,疗效优良率为 93 8% ,有效率为 1 0 0 %。未发现明显并发症。结论　髓核成形术是一种先进、安全、有效的椎间盘突出微创手术 ,具有操作简单、安全、微创、疗效佳、恢复快、无需住院等优点。     

Critical size defect in the canine mandible.

OBJECTIVE: The purpose of this study was to determine the minimum size defect in a canine mandible that would not spontaneously heal during the dog's natural life (the critical size defect). STUDY DESIGN: Sixteen adult female mongrel dogs underwent continuity resection on both sides of the mandible to create bilateral defects. In 8 dogs, mandibular defects ranging from 5 to 20 mm were created with periosteal resection. In the other 8 dogs, mandibular defects ranging from 30 to 60 mm were created preserving the periosteum. The dogs were then killed at 6 months and the defects examined using radiographs and histologic analysis. RESULTS: When the periosteum was removed, mandibular defects greater than 15 mm failed to heal across the entire defect. However, when the periosteum was preserved, mandibular defects needed to be greater than 50 mm in order to fail to heal. CONCLUSION: The critical size defect in a canine mandible model is 15 mm when the periosteum is removed and 50 mm when the periosteum is preserved.     

乳腺良恶性病变的磁共振T2*W首过灌注成像与血管生成相关性研究

Objective： To study the diagnostic value of T2^＊-weighted first-pass perfusion imaging in breast tumors. Methods： We analyzed the magnetic resonance imaging （MRI） information along with the pathological and immunohistochemistry results. Magnetic resonance imaging was performed in 28 patients with breast tumor. The time to signal intensity curves were generated according to the T2^＊-weighted first-pass perfusion imaging. The curve＇s maximal signal intensity drop rate and maximal signal intensity decrease time were analyzed and compared with the pathological diagnoses after surgery. Results： Malignant breast lesions showed higher maximal signal intensity drop rate （44.69% ± 17.07 vs. 17.22% ±7.49, P 〈 0.001） than benign lesions, but there was no significant difference of maximal signal decrease time between those two lesions （23.94 s ± 4.92 vs. 20.02 s ± 6.83, P 〉 0.05）. Conclusion： The T2^＊-weighted first-pass perfusion imaging has enough sensitivity and specificity in breast tumor diagnosis.     

Studies on Toxicity of Nitroquine-Dapsone Compound and Therapeutic Effects of Folic or Folinic Acid on Toxicated Animals

The toxic effects of nitroquine-dapsone compound(NQD)in mice and dogs were studied.The therapeutic index of NQDin mice is 1911,the greatest among the 6 antimalarials tested.Thetoxic effects of NQD(50 mg/kg/day for 3 days per os)and nitro-quine in dogs were manifested by injuries on the adrenal cortexand intestinal epithelium.When folic acid(4 mg/kg/day for 4 days)or calcium leucovorinum(0.3 mg/kg/day for 4 days)were usedconcomitantly with NQD,the death rate and the incidence of dia-rrhea in the toxicated dogs were greatly reduced,the injury on theintestinal epithelium was much milder,and the goblet cells weremuch more numerous than those without treatment.The results suggestthat folic acid and calcium leucovorinum can protect the undifferen-tiated cells in the intestinal crypts from being injured by NQD.     

超声电丛刺治疗后急性脑梗死患者神经功能缺损及实验室相关指标的变化

目的:观察超声电丛刺头穴丛刺法治疗急性脑梗死的效果,以及治疗前后体感诱发电位指标及血液生化指标变化。方法:①选择2003-01/2005-06在沈阳脑科医院神经内科住院的急性脑梗死患者261例,男160例,女101例。均为首次患病,且对治疗方案知情同意。将上述患者随机分为2组:丛刺治疗组131例,对照组130例。②丛刺治疗组:采用超声电丛刺治疗仪于头部电丛刺顶区(运动区),以100～200Hz疏密波电针通过6～8h,1次/d,1个疗程30次。对照组:均予以常规脑血管病药物同等治疗。丛刺治疗组和对照组均干预30d。两组疗效判定标准:治疗后神经功能缺损评分减少91%～100%为基本恢复,减少46%～90%为显著进步,减少18%～45%为进步。③采用酶联免疫法测定血浆α-颗粒膜蛋白水平;应用放射免疫法测定血浆血栓素A2水平;采用酶联免疫吸附法双抗体夹心法测定血浆D-二聚体水平;采用免疫透射比浊方法测定脂蛋白(a)水平。应用神经电生理检测仪检测体感诱发电位。④计数和计量资料差异比较采用χ2检验和t检验。结果:急性脑梗死患者261例均进入结果分析。①丛刺治疗组131例中:基本恢复31例,显著进步80例,进步15例,总有效率为96%(126/131);对照组130例:基本恢复14例,显著进步68例,进步12例,总有效率为72%(96/130);丛刺治疗组总有效率明显高于对照组(P<0.01)。②丛刺治疗组治疗后血浆α-颗粒膜蛋白、血栓素A2、D-二聚体和脂蛋白(a)含量较治疗前明显降低(P<0.01)。③丛刺治疗组治疗后体感诱发电位的波潜伏期与传导时间较治疗前明显缩短(P<0.01)。结论:超声电丛刺治疗急性脑梗死效果显著,可显著改善急性脑梗死患者体感诱发电位指标及血液生化指标。     

危重患者经外周静脉置入中心静脉导管的临床研究——前瞻性随机对照研究

目的 比较经外周静脉置入中心静脉导管(peripherally inserted central catheter,PICC)与经锁骨下静脉中心静脉置管在危重患者中的临床应用.方法 通过前瞻性随机对照研究方法,将80例ICU危重患者分为PICC组(40例)和锁骨下静脉组(40例),观察两组穿刺成功率、穿刺时间、穿刺不良反应发生率等.结果 PICC组较锁骨下静脉组一次穿刺成功率高(92.5%vs 75.0%,χ2=4.501,P=0.034),穿刺时间短[(15.7±5.3)min vs(23.9±6.3)min,t=-6.263,P=0.000],总不良反应发生率低(10.0%vs 27.5%,χ2=4.021,P=0.045).结论 PICC穿刺简便易行,危险性小,在危重患者中PICC置管优于锁骨下静脉置管.     

Genetics of epilepsy: epilepsy research foundation workshop report.

The Sixth Epilepsy Research Foundation workshop, held in Oxford in March 2006, brought together basic scientists, geneticists, epidemiologists, statisticians, pharmacologists and clinicians to consider progress, issues and strategies for harnessing genetics to improve the understanding and treatment of the epilepsies. General principles were considered, including the fundamental importance of clear study design, adequate patient numbers, defi ned phenotypes, robust statistical data handling, and follow-up of genetic discoveries. Topics where some progress had been made were considered including chromosomal abnormalities, neurodevelopment, hippocampal sclerosis, juvenile myoclonic epilepsy, focal cortical dysplasia and pharmacogenetics. The ethical aspects of epilepsy genetics were reviewed. Principles and limitations of collaboration were discussed. Presentations and their matched discussions are produced here. There was optimism that further genetic research in epilepsy was not only feasible, but might lead to improvements in the lives of people with epilepsy.