扩大经蝶入路进入海绵窦内侧腔的应用显微解剖

目的为临床开展扩大经蝶入路进入海绵窦内侧腔手术提供解剖学依据。方法用50例成人头颅标本．在显微镜下对蝶窦外侧壁、蝶鞍、海绵窦及周围结构进行解剖学观察并测量。模拟扩大经蝶入路磨除海绵窦腹侧骨质，切开海绵窦内侧壁，显露海绵窦内侧腔。结果颈内动脉（ICA）明显隆起于蝶窦侧壁的占58％，蝶窦内隆起呈管型占3％。鞍底硬膜分为2层，海绵窦内侧壁的上部南垂体硬膜构成，无骨性结构支撑；下部由骨周硬膜构成，有蝶窦侧壁骨质支撑。两侧海绵窦内侧壁的距离为（14．8±2．7）mm。海绵窦内侧腔位于C4段ICA与垂体之间，腔内为丰富的静脉丛，最宽可达7mm，但常因ICA扭曲而闭塞。无颅神经穿越海绵窦内侧腔，ICA是扩大经蝶入路探查海绵窦遇到的第一个主要结构。结论扩大经蝶入路进入海绵窦内侧腔是安全可行的。     

颈内动脉大型和巨大型动脉瘤的手术策略

目的探讨颈内动脉巨大动脉瘤的特点和手术策略。方法回顾性分析48例颈内动脉大型和巨大型动脉瘤的手术经验。手术均采用翼点人路，床突旁动脉瘤病例预先暴露颈部颈内动脉以备临时阻断。从硬脑膜内磨除前床突、视神经管上壁以及外侧嵴，以显露动脉瘤的近侧角。术中采用逆向抽吸法使动脉瘤塌陷，如动脉瘤内含机化血栓，则在临时阻断后切开瘤体，用CUSA和取瘤镊去除瘤内血栓，再将动脉瘤夹闭并达到视神经减压的目的。术中监测脑电图和体感诱发电位，并采用术中超声多普勒检查动脉血流。结果46例动脉瘤直接夹闭，2例海绵窦段动脉瘤行动脉瘤孤立并分别做颞浅动脉-大脑中动脉和大隐静脉移植颈外动脉-大脑中动脉搭桥手术。43例术后行DSA检查，绝大多数动脉瘤夹闭满意。按GOS评分术后良好为41例（85．4％），差为5例，死亡2例。结论充分显露、合理应用临时阻断技术、有效的动脉瘤减压，以及术中应用电生理监测和超声多普勒检查等辅助措施，能够取得动脉瘤的满意夹闭。     

影响飞行员掩饰性心理家庭多因素分析

目的 探讨飞行员夫妻双方掩饰性与心理健康及婚姻质量的关系.方法 采用症状自评量表、艾森克个性问卷的掩饰分量表和Olson婚姻质量问卷对288名空军飞行员夫妻双方进行评定,采用SPSS 15.0进行相关分析、回归分析.结果 发现飞行员以及妻子的掩饰特质与自身的心理健康9个因子:躯体化、强迫症状、人际关系敏感、焦虑、抑郁、敌对、恐怖、偏执、精神病性具有显著负相关性,前者相关系数在-0.219～-0.306之间,后者在-0.127～-0.391之间.飞行员以及妻子的掩饰特质与自身婚姻质量的12因子中的6(相关系数0.151～0.232)、7(相关系数0.123～0.309)项有显著正相关性;飞行员以及妻子的掩饰特质与对方的婚姻质量各有4项存在显著相关性,前者相关系数在0.127～0.251之间,后者在0.129～0.203之间.多因素分析揭示,对丈夫掩饰特质贡献最大的因素依次为妻子的焦虑情绪、妻子的恐怖情绪、丈夫的敌对情绪、妻子的婚姻满意度、丈夫的角色平等性;对妻子掩饰特质贡献最大的因素依次为妻子的敌对情绪、经济安排、性格相客性,丈夫的性生活、与亲友关系等.结论 开展飞行员心理健康教育,进行婚姻家庭心理咨询时,提高夫妻双方的掩饰性是非常有必要的.     

两种不同入路手术治疗海绵窦区肿瘤

目的探讨海绵窦区肿瘤切除的手术入路,以提高手术全切率,降低残障率.方法对14例海绵窦内肿瘤行硬膜下入路切除5例,行硬膜外入路切除9例,比较两种入路的方法及疗效.结果行硬膜下入路者中全切除2例,大部切除3例;术后出现新的神经功能障碍4例.行硬膜外入路者中全切除5例,次全切除3例,大部切除1例;术后出现新的脑神经功能障碍3例,其中1例完全恢复.结论针对不同类型的肿瘤及生长特性,选择适当的手术入路和显微神经外科技术,可有效提高全切率,降低残障率.     

肌电引导治疗仪的设计

介绍一种操作简单、成本较低、便于医生确定靶肌肉的肌电引导治疗仪.该仪器经过临床初步试验,效果良好.     

原发性脑淋巴瘤的MRI表现特点与诊断

目的：分析颅内原发性淋巴瘤的MRI表现特点，为临床诊断与治疗提供资料。方法：回顾分析28例经病理证实颅内原发性淋巴瘤的MRI资料，所有病例均行平扫及增强扫描。结果：病灶单发6例，多发22例，分布于幕上14例，幕下4例，幕上幕下同时存在10例，大多位于深部脑白质，病灶多呈圆形或不规则形，T1WI呈低信号，T2WI呈等或高信号，瘤周水肿较轻，增强扫描病灶均呈团块状显著强化。结论：颅内淋巴瘤的MRI表现缺乏特异性，需手术或活检才可作出定性诊断。     

Different ion channel mechanisms between low concentrations of capsaicin and high concentrations of capsaicin and nicotine regarding peptide release from pulmonary afferents

Vagal nerve stimulation (1 Hz for 1 min), capsaicin (10^-8 M and 10^-6 M), resiniferatoxin (3 × 10^-10 M) and nicotine (10^-4 M) evoked a non-cholinergic bronchoconstriction in the isolated perfused guinea-pig lung preparation. Simultaneously there was an increase in the perfusate levels of calcitonin gene-related peptide-like immunoreactivity, suggesting release from sensory nerves. Both the bronchoconstriction and peptide release evoked by a low concentration of capsaicin (10^-8 M) and that evoked by nerve stimulation were depressed by tetrodotoxin, suggesting involvement of Na⁺ channel dependent depolarization. Since the effects of capsaicin (10^-8 M) and vagal nerve stimulation were inhibited by ω-conotoxin but not influenced by nifedipine, the Ca²⁺-channel involved is probably of N-type. Furthermore, the capsaicin analogue resiniferatoxin also evoked ω-conotoxin sensitive peptide release and bronchoconstriction. At the higher capsaicin concentration (10^-6 M), the functional response was only slightly inhibited by wconotoxin or tetrodotoxin indicating that capsaicin at this concentration evoked peptide release and functional effects through other mechanisms, probably involving Ca²⁺ fluxes in the non-selective cation channel associated with the proposed capsaicin receptor. The nicotine (10^-4 M) evoked peptide release and bronchoconstriction were only marginally influenced by ω-conotoxin or tetrodotoxin. It is concluded that the ion-channel mechanisms underlying the peptide releasing properties of antidromic nerve stimulation and low concentrations of capsaicin are similar and depend on action potential propagation, whereas capsaicin in high, toxic concentration and nicotine mainly act via receptor operated channels.     

Effects of arotinoid acid on induction of apoptosis and differentiation and telomerase activity and cell cycle in the HL～60 cell line

Objective To investigate the effects of arotinoid acid (Ro13-7410) on the morphological and functional alterations of leukemia HL-60 cell line and compared with those of RA.Methods Differentiation of HL-60 cells was assessed by morphology and by NBT reduction.Trypan blue exclusion was used to determine viability.Apoptosis was assessed by changes in cell morphology and by measurement of fragmented DNA using the PCD-assay-kit.Telomerase PCR ELISA-kit tested telomerase activity.The cell cycle was analyzed by flow cytometry.Results Incubation of the HL-60 cells with 10(-6)-10(-8) mol/L Ro13-7410 resulted in suppression of cell growth.Apoptotic cells were detected following exposure to 10(-6) mol/LRo13-7410 for 3 hours by measurement of the 'in situ' enzymatic labeling of DNA breaks with biotinylated dUTP.Ultrastructural examination of Ro13-7410-treated samples showed cells with chromatin compaction and cytoplasm condensation and the presence of 'apoptotic bodies'.Cells induced into apoptosis were accompanied by increase of intracellular free Ca[2+].Percentage of HL-60 cells reduced NBT following incubation with Ro13-7410 was lower than with all-trans retinoic acid (RA) (27% vas 85%).Telomerase PCR-ELISA assay showed that HL-60 cells cultured in the absence of inducing agents had significant telomerase activity.Telomerase activity declined gradually after 10(-6) mol/L Ro13-7410 treatment, and changes becoming evident at 1 day.The inhibition of telomerase activity at day 5 of treatment with Ro13-7410 was less effective than with RA.DNA flow cytofluorimetric analysis revealed that Ro13-7410 caused partial cell arrest in the G(2)/M phase after a 2-day treatment and the percentage of cells arrested in the G(2)/M phase increased after 4-days treatment.With RA-treated cells, a reduction in the percentage of cells in the G(2)/M phase was observed after 2-day of treatment.Conclusion Our study shows that Ro13-7410 suppresses HL-60 cells growth mainly via the induction of apoptosis and is less effective than RA in induction differentiation.Ro13-7410 dramatically inhibits telomerase activity during the course of induction and results in G(2)/M arrest within 2 days.These findings suggest that Ro13-7410 is worthy of further study for its effects on leukemic cells.     

亚硝基谷胱甘肽对大鼠肝微粒体谷胱甘肽转移酶的激活及机制

目的　探索一氧化氮供体亚硝基谷胱甘肽(GSNO)能否在体外通过S 亚硝酰化机制激活大鼠肝微粒体谷胱甘肽转移酶 (mGST)。方法　微粒体粗提物与GSNO体外共孵育 ,测定mGST催化动力学改变 ,结合N 乙基马来酰亚胺 (NEM )再激活实验和二巯基苏醇 (DTT)逆转实验 ,以及酶蛋白游离巯基和酶S 亚硝酰化蛋白的改变 ,研究酶的激活机制。结果　GSNO在 0 .12 5～ 2mmol·L- 1浓度范围内呈浓度和时间 (3～ 15min)依赖性地激活mGST ,NEM对酶的再激活效应消失 ,DTT可以逆转上述激活作用 ,同时酶蛋白游离巯基浓度依赖性减少 ,而S 亚硝酰化蛋白浓度依赖性增多。结论　GSNO体外可激活大鼠肝mGST ,激活机制可能与mGST第 4 9位半胱氨酸 (Cys4 9)的巯基被亚硝酰化形成S 亚硝基硫醇结构有关。     

上海郊区老年痴呆症病人α-雌激素受体及芳香烃受体基因多态性

目的：探索上海地区农民人群中α-雌激素受体基因(ER-α)及芳香烃受体基因(Ahr)不同基因形态和老年痴呆症高发风险的可能联系．方法：分别以PCR—RFLP和AS—PCR方法分析一组老年痴呆症患者(n=52)ER-α基因及Ahr基因的多态位点，同一地区的健康人群(n=125)为对照．结果：Alzheimer症病人ER-α基因两个位点突变形态频率显著高于对照人群(Pvu Ⅱ位点：P=0．023，OR=2．94，95％CI 1．13—7．71；Xba I位点：P=0．046，0R=2．28，95％ CI 1．003—5．17)．Ahr G1721A位点基因型频率在病人组和对照组间无显著差异．结论：ER-α基因多态性可能与Alzheimer症易感性个体差异有关，本工作不支持Ahr基因多态性与老年痴呆症高发风险间的可能关联．