异丙酚和异氟醚对非体外循环搭桥术患者围术期细胞因子的影响

目的:研究异丙酚和异氟醚对非体外循环搭桥术患者围术期炎性与抗炎性细胞因子平衡的影响。方法:择期非体外循环搭桥患者50例,随机分为2组。异丙酚组微量泵输入剂量为4～6mg·kg-·1h-1,异氟醚组吸入浓度为1%～1.5%。检测诱导前、打开心包、旁路血管开放30min,术后2h、24h血清白细胞介素6(IL-6)、白细胞介素10(IL-10)和肿瘤坏死因子α(TNF-α)的浓度。结果:2组患者旁路血管开放后IL-6浓度较术前升高(P<0.01),术后2h达高峰;术后2h异氟醚组高于异丙酚组(P<0.05)。IL-10浓度变化趋势与IL-6相似,旁路血管开放后、术后2h和24h异丙酚组高于异氟醚组(P<0.05)。2组患者TNF-α水平均无显著变化。结论:异丙酚麻醉促进IL-10的产生,抑制IL-6的产生,控制术中应激反应异丙酚优于异氟醚。     

我国医疗器械数字化技术发展中存在的主要问题及原因

本文提出了我国医疗器械产业中数字化技术发展中存在的主要问题，并分析了问题产生的原因。     

不同性别中学生青春期学习成绩变化的研究

目的了解和证实是否客观存在青春期后女生学习能力降低的现象。方法收集分析了青岛市某中学高中毕业的一届学生230名女生和197名男生从初中到高中6年内的各次考试成绩。比较了男女学生每次考试的平均总成绩和成绩排名的平均名次。结果男女生之间初中入学时总成绩没有明显差别，但在初中阶段的历次考试中，女生成绩基本上优于男生，名次领先于男生；高中阶段情况出现倒转，女生成绩和名次逐渐落后于男生，并一直持续到高者．结论在所调查的这届学生中，确实存在女性在青春期前后学习能力下降的现象。     

180篇创伤骨科论文临床疗效研究方法的评估

目的了解目前我国创伤临床病例研究的主要应用手段和研究水平。方法对中华骨科学会创伤学组2002年年会投稿临床病例研究稿件进行总结分析,对稿件论述的研究范围、研究对象、病例数量、骨折分类、研究方法、随访评价、统计分析应用等方面进行统计研究。结果大会收到225篇稿件。其中随访临床病例报告180篇。报告病例1万多例、范围广,包括了当前主要的临床治疗方法。回顾性研究中,对临床资料进行统计学分析的论文仅占少数(6.1%)。对骨折分类方法及临床随访结果评价标准不统一,欠规范。无前瞻性研究报告。结论创伤临床病例研究方法有待进一步改进。     

糖化血红蛋白及糖化血清蛋白与糖尿病肾功能衰竭患者的血糖监测

糖化血红蛋白(Hb)A1c是血糖监测的苇要指标,反映检测前2～3个月的平均血糖水平.慢性肾功能衰竭(CRF)患者存在贫血、酸中毒、氧化应激、胰岛素抵抗、血液透析及促红细胞生成素(EPO)的应用等因素,对HbA1c的测定会造成影响.糖化血清蛋白(GSP)反映检测前2～3周的平均血糖水平,仅受血浆蛋白的影响,几乎不受血红蛋白和EPO治疗等以上因素的影响,且对短时间内的血糖变化更为敏感.将GSP作为糖尿病肾功能衰竭患者血糖监测指标可能比HbA1c更理想.     

便携式多普勒血管探测仪在皮瓣移植中的应用

目的 :研究皮瓣移植前简单、可靠的血管探测的方法。方法 :在皮瓣移植前 ,以 HADECO ES-1 0 0 0 SPM多普勒血管探测仪对皮瓣血管蒂及皮动脉进行探测 ,与术中皮动脉探查结果进行比较 ,考察术前血管探测的准确性和意义。结果 :皮瓣血管蒂及皮动脉术前探测与术中探查结果完全一致。结论 :便携式血管多普勒仪是皮瓣移植前 ,简单、可靠的血管探测的仪器 ,根据探测结果进行皮瓣设计 ,有效地降低了手术失败的风险     

nm23-H1基因转染对人胆管癌细胞系QBC939体外浸润能力的影响

目的：探讨nm23-H1基因转染对人胆管癌细胞系QBC939体外浸润能力的影响。方法：将含有全长nm23-H1 cDNA的真核表达载体通过脂腩体法转染人胆管癌细胞系。结果：转染成功的QBC939细胞，其nm23-Hl基因的mRNA、蛋白表达明显增加，转染nm23-H1基因的胆管癌细胞体外浸润能力下降，穿越matrigel的细胞数明显低于亲本QBC939细胞，代表浸润能力的IV型胶原酶（MMP-9）分泌量下降。结论：nm23-Hl基因可以抑制胆管癌细胞的体外浸润能力。     

不同液体术前急性高容量血液稀释对深静脉血栓病人血液流变学的影响

Objective To investigate the effects of acute hypervolemic hemodilution (AHH) with different fluids on blood rheology in patients with deep vein (femoral and iliac) thrombosis. Methods Thirty ASA I or II patients aged 40-64 yr who had developed deep vein thrombosis in 48 h and were scheduled for embolectomy were randomly divided into 3 groups ( n = 10 each) ; group I normal saline (NS) ; group II 6 % HES 200/0.5 ( HES) ; group IE gelofusine (GEL). AHH was performed with normal saline, 6% HES or gelofusine infusion at 20 ml·kg-1 ·h-1 for 40 min. MAP, HR and SpO2 were monitored. Blood loss, volume of blood transfusion and fluid infused and urine output during operation were recorded. Anesthesia was induced with fentanyl 3-5 fig/kg, etomidate 0.15-0.30 mg/kg, propofol 1-2 mg/kg and succinylcholine 1-2 mg/kg and maintained with 2% isoflurane and propofol infusion at 5-8 mg·kg-1·h-1 and intermittent iv boluses of vecuronium. The patients were mechanically ventilated (VT 8 ml/kg, RR 12 bpm). PaO2 and PaCO2 were maintained within normal range. Venous blood samples were obtained before and after AHH for measurement of hematocrit (Hct), whole blood viscocity (WBV) at low or high shear rates, plasma viscosity, RBC aggregation and RBC deformation. RBC aggregation index and RBC deformation index were calculated. Results MAP and HR were stable in all patients. The amount of blood transfusion and fluid infused was significantly less in group HES and GEL than in group NS. The WBV at low or high shear rates in group HES and GEL, Hct in all 3 groups and RBC aggregation index in group HES were significantly decreased after AHH, but the RBC deformation index was significantly increased in group HES. Conclusion Colloid is better than crystalloid and HES is better than gelofusine in improving intraoperative hypercoagulability and sluggish blood flow.     

Responses of CDKs and p53 in Delayed Ischemic Neuronal Death

Stroke is a debilitating disease that affects millions each year.While in many cases cerebral ischemic in jury can be limited by effectivw resuscitation or thrombolytic treatment,the injured neurons wither in a process known as delayed neuronal death(DND).Mounting evidence indicates that DND is not simply necrosis played out in slow motion but apoptosis is triggered.Of particular interest are two groups of signal proteins that participate in apoptosis-cyclin dependent kinases(CDKs) and p53-among a myriad of signaling events after an ischemic insult.Recent investigations have shown that CDKs,a family of enzymes initially known for their role in cell cycle regulation,are activated in injured neurons in DND.As for p53,new reports suggest that its up-regulation may represent a failed attempt to rescue in jured neurons,although its up-regulation was previously considered an indication of apoptosis.These observations thus rekindle an old quest to identify new neuroprotective targets to minimize the stroke damage.In this review,the author will examine the evidence that indicates the participation of CDKs and p53 in DND and then introduce pre-clinical data to explore CDK inhibition as a potential neuroprotective target.Finally,using CDK inhibition as an example,this paper will discuss the pertinent criteria for a viable neuroprotective strategy for ischemic in jury.     

地塞米松对布比卡因诱导小鼠神经元毒性的影响

Objective To investigate the effect of dexamethasone on the toxicity of bupivacaine in murine neurons.Methods Murine neuroblastoma cell line N2a was obtained from ATCC cell bank (USA). The cells were cultured in 10% fetal cow serum/MEM culture medium and divided into 4 groups voup I control (Con); group II bupivacaine ( Bup); group Ⅲ dexamethasone (Dex) and group IV Dex + Bup. The culture medium contained bupivacaine 900 μmol/L in group Bup and dexamethasone 1 μmol/L in group Dex respectively. In group Dex + Bup ( IV ) Bup was added to the culture medium with a final concentration of 900 μmol/L at 12 h after pretreatment with Dex 1 μmol/L. The cells were inoculated in 24 well plates (0.5 ml in each well, 24 wells in each group) and 10 cm culture dishes (7 ml in each dish, 4 dishes in each group). The release rate of LDH was calculated and the morphology of the cells and nucleus condensation (by Hoechst 3334224 fluorescent staining) was detected at 9 h of incubation in 24 well plates. The mitochondrial transmembrane potential (by JC-1 assay) and phosphorylation of Akt and ERKs (by Western blot) were measured at 5 h of incubation in 24 well plates and in culture dishes respectively. ResultsBupivacaine caused severe damage to the N2a cells as evidenced by increase in LDH release and nucleus condensation (apoptosis), dephosphorylation of Akt and ERKs, decrease in mitochondrial transmembrane potential and severe morphological changes. Dexamethasone pretreatment significantly attenuated bupivacaine-induced neurotoxicity. Conclusion Dexamethasone can protect N2a cells from bupivacaine-induced neurotoxicity through stabilization of mitochondrial transmembrane potential and inhibition of dephosphorylation of Akt and ERKs.