癫痫患者执行功能损害特点及影响因素研究

目的分析癫痫患者执行功能损害的特点及相关影响因素。方法1999年1月～2006年4月在我院癫痫专病门诊就诊或长期随访的109例成年癫痫患者和75例正常对照者进行神经认知心理测验，包括语义流畅性试验、数字广度测验、数字符号测验、色词干扰测验和连线试验检查。结果癫痫患者组语义流畅性显著差于正常对照组，数字广度、数字符号亦显著低于正常对照组．癫痫组连线时间、Stroop试验反应时显著延长，Stroop试验错误数显著增加（P〈0．01）。颞叶癫痫患者数字广度低于额叶癫痫患者。多元线性回归显示：文化程度高、非颞叶癫痫对语义流畅性有保护作用：文化程度高、单一抗癫痫药物治疗、病程短、年龄大对数字广度有保护作用；病程短、文化程度高和颅内无病灶对数字符号有保护作用。结论癫痫患者在多项执行功能方面均存在损害．文化程度高的患者执行功能相对较好；颞叶癫痫患者语义流畅性差；病程、药物、年龄对数字广度有影响：病程、有无病灶对数字符号有影响。     

腺苷对突触体^45Ca摄取的抑制作用

用同位素标记~(15)Ca法测定大鼠突触体内游离钙的浓度,探讨了腺苷对高钾、N-甲基-D-天冬氨酸(NMDA)谷氨酸(Glu)等刺激所致的Ca~(2 )内流增加的影响。结果发现腺苷在10nmol/L～0.1μmol/L范围内对高钾、NMDA、Glu等刺激所致的Ca~(2 )内流有抑制作用,并呈剂量依赖关系,最大抑制率分别为41.68±7.68％、31.32±6.17％、37.52±2.29％。这可能是腺苷对缺血性脑损伤保护作用的机理。     

甲襞微循环观测辅助诊断的初步研究

甲襞微循环观测辅助诊断的初步研究胡金麟＊田牛＊刘凤英＊宋欣＊李向红＊规范化的甲襞、球结膜、舌、口唇、牙龈、耳廓、皮肤、子宫颈、阴茎头微循环观测方法标志着我国临床微循环的研究与应用已进入了一个新的阶段［１，２］。临床微循环观测结果的数学公式表达，促进了...     

HMME在不同溶液中光漂白反应动力学规律

目的 分析国产光敏剂血卟啉单甲醚（HMME）在不同溶液中光漂白反应动力学规律，加深对光漂白反应复杂反应过程的理解，并为HMME-PDT治疗微血管病变的数学建模研究提供实验依据和参数。 方法 根据光化学反应动力学原理，从理论上推导出在单纯溶液和复杂溶液（含可被光氧化的底物）中，单态氧介导的光漂白反应动力学方程，通过对实验测定的漂白数据（不同时间点的HMME浓度）进行拟合，进一步验证理论推导出光漂白反应动力学方程。 结果 HMME在单一溶液体系（PBS、DMSO）中的光漂白符合1级反应动力学过程，在含底物的复杂体系（白蛋白缓冲液、细胞悬液）中符合2级反应动力学过程。 结论 HMME在不同溶液体系中的光漂白遵循不同的反应动力学规律。根据化学反应动力学原理进行光漂白等复杂光化学反应过程的数学模拟是可行的，并有利于对复杂光化学反应过程的深入理解。     

异丙酚对大鼠海马神经元NMDA受体通道电流的影响

目的 研究异丙酚对大鼠海马神经元N-甲基-D-天冬氨酸（NMDA）受体通道电流的影响。方法 体外培养新生Wistar大鼠海马神经元8—12d，采用全细胞膜片钳技术和压力喷射给药方式，钳制电压为-80mV，记录3、48μg∥ml异丙酚对100μmol／LNMDA诱发NMDA受体通道电流的影响；然后用7-氨基丁酸（GABA）受体拮抗剂荷包牡丹碱100μmol／L阻断GABA．受体，观察3、48μg／ml异丙酚对NMDA受体通道电流的影响。结果 3、48μg／ml异丙酚抑制自发兴奋性突触后电流并直接激动GABA．受体，使Cl．内流，产生外向超极化的GABA电流，从而间接抑制NMDA受体通道电流。用荷包牡丹碱100μmol／L阻断GABA．受体后，3、48μg∥ml异丙酚仍可抑制100μmol／LNMDA诱发的NMDA受体通道电流（P〈0．05）。结论 异丙酚通过激活GABA．受体影响NMDA受体通道电流，对NMDA受体通道也有直接抑制作用。     

Treatment of singultus following craniocerebral injury★ Intranasal cavity drip infusion versus intramuscular injection of aminazine

BACKGROUND: Craniocerebral injury always accompanies with singultus, while frequent singultus may cause increased intracranial pressure. Simultaneously, respiratory alkalosis and cerebral hypoxia induced by respiratory disorder may aggravate craniocerebral injury. OBJECTIVE: To observe the therapeutic effects of intranasal cavity drip infusion of aminazine and intramuscular injection on singultus following craniocerebral injury. DESIGN: Contrast observation. SETTING: Department of Neurosurgery, Xi'an Aerospace General Hospital. PARTICIPANTS: A total of 102 patients with singultus following craniocerebral injury were selected from the Department of Neurosurgery, Xi'an Aerospace General Hospital from June 2001 to June 2006. Patients with craniocerebral injury were diagnosed with CT examination and randomly divided into nasal cavity medication group (n =62) and intramuscular injection group (n =40). There were 44 males and 18 females in the nasal cavity medication group and their mean age was (33±4) years; while, there were 26 males and 14 females in the intramuscular injection group and their mean age was (29±4) years. All patients and their relatives provided the confirmed consent. METHODS: Patients in the nasal cavity medication group were slowly dripped aminazine solution into bilateral nasal cavity with the dosage of 12.5 mg (0.5 mL). Patients who had no obvious effect or had mild improvement received the treatment once every 6 hours. The treatment was stopped if symptoms were also observed after the fifth medication. In addition, patients in the intramuscular injection group received intramuscular injection of 50 mg aminazine. Patients who had no obvious effect or had mild improvement received the treatment once every 6 hours. The treatment was changed if symptoms were also observed after the fifth medication. MAIN OUTCOME MEASURES: Therapeutic effects of different medications in the two groups. RESULTS: All 102 patients were involved in the final analysis. Effective rate in the nasal cavity medication group was higher than that in the intramuscular injection group, and there was significant difference (χ2= 11.882, P < 0.01). At 6 hours after onset of singultus, effective rate in the nasal cavity medication group was higher than that in the intramuscular injection group, and there was significant difference (χ2 =8.188, P < 0.01). CONCLUSION: Therapeutic effects of intranasal cavity drip infusion of aminazine on singultus following craniocerebral injury are superior to those of intramuscular injection.     

定君生胶囊用于妊娠期细菌性阴道病的临床观察

目的调查妊娠期细菌性阴道病(BV)的发病情况,观察定君生胶囊治疗细菌性阴道病的有效性。方法采用珠海市银科生物技术应用研究所生产的细菌性阴道病快速检测卡,对不同孕周的1500名孕妇进行BV筛查,确定妊娠期细菌性阴道病的发病率。对确诊为BV的孕妇266例,随机分为两组。定君生组:136例,给予定君生胶囊(乳杆菌活菌胶囊)阴道给药治疗;孚舒达组:130例,给予孚舒达栓(复方甲硝唑栓)阴道给药治疗。两组均连续用药10d,停药7d后复查。结果妊娠期BV的检出率为17.73%。定君生胶囊治疗BV的总有效率为92.65%,孚舒达栓治疗BV的总有效率为91.53%,二者差异无显著性(P>0.5)。结论妊娠期BV的发病率较高。定君生胶囊能有效改善阴道内生态环境,治疗妊娠期细菌性阴道病安全、有效,易为孕妇所接受。     

应用荧光探针H2DCF-DA检测光照致细胞内活性氧产生的初步研究

目的应用荧光显微镜及新型荧光探针H2DCF-DA检测在光源照射过程中人脐静脉血管内皮细胞(ECV304)内活性氧的产生情况。方法将ECV304细胞接种于35mm培养皿中,24h后加入H2DCF-DA,使其终浓度为10μmol/L,孵育30min。利用荧光显微镜的激发光源作为照射光源,在采集荧光图像的同时完成光源照射,光源输出波长范围为460～490nm,功率密度约为100mW/cm2。连续采集DCF的荧光图,观察细胞内DCF荧光的变化情况,采用计算机图像处理和分析技术,求得细胞内不同照射时间点DCF平均荧光强度,进而得到平均荧光强度-时间曲线。另外,使用线粒体特异标记探针MitoFluorRed589与H2DCF-DA共同孵育细胞,分别采集同一细胞的DCF的荧光图和MitoFluorRed589的荧光图,并利用像素-荧光强度分析方法来确定DCF荧光在细胞内的分布位置。结果在光源照射的开始阶段,ECV304细胞内的DCF荧光强度迅速增加,在第10s时便上升至第2s时的2.2倍,但是随着照射时间逐渐延长,荧光强度增幅逐渐变小,到第60s时上升至第2s时的4.7倍。观察时间进一步延长,DCF的荧光强度的变化似乎进入平台期,继而开始出现下降。考察DCF荧光在ECV304细胞内的分布位置主要通过比较细胞内不同区域的I1/I2值,通过图像分析与计算得到线粒体区、细胞核区以及细胞质非线粒体区内I1/I2值分     

Pharmacological action of Adenophora polysaccharides

Adenophora polysaccharides (AP), is an active principle extracted from the root of Adenophorae Potaninii Korsh originated in Gansu Province and isolated with boiling water(1). AP is isolated and purified from the crude drug by DEAE-cellulose and Sephadex G-200 column, with a white powder and mean molecular weight of 8.3 × 104 , and [α]D20of AP is 68(1). AP is only composed of glucose judging from the analysis of it with patina chromatography (PC) and gas chromatography-mass spectrometer (GC-MS) methods.The methylation analysis showed that AP is composed of (1→6) linked glucose residues. The measure of nuclear magnetic resonance imaging (NMR) 1H NMR and 14C NMR techniques further proved that AP is α(l→6) linked by Dglucose. The structure of AP is as follows: -[→6]α-D-Glu(1-)n→ (2).