c-myc反义寡核苷酸对低氧内皮细胞条件培养液诱导的肺血管周细胞增殖的影响

应用细胞培养、核酸斑点杂交、~３Ｈ－胸腺嘧啶核苷（~３Ｈ－ＴｄＲ）掺入、免疫细胞化学、图像分析等技术观察ｃ－ｍｙｃ反义寡核苷酸（ＯＤＮｓ）对低氧内皮细胞条件培养液（ＨＥＣＣＭ）诱导的大鼠肺血管周细胞ｃ－ｍｙｃ ｍＲＮＡ表达、增殖细胞核抗原（ＰＣＮＡ）表达及~３Ｈ－ＴｄＲ掺入量的影响。结果表明,ＨＥＣＣＭ显著促进周细胞 ｃ－ｍｙｃ ｍＲＮＡ表达、ＰＣＮＡ表达（Ｐ＜０．０１）及~３Ｈ－ＴｄＲ掺入量增加（Ｐ＜０．０１）,反义ＯＤＮｓ显著阻抑 ＨＥＣＣＭ诱导的周细胞ｃ－ｍｙｃ ｍＲＮＡ表达、ＰＣＮＡ表达（Ｐ＜０．０１）及~３Ｈ－ＴｄＲ掺入量增加（Ｐ＜０．０５）,而同义ＯＤＮｓ无上述作用（Ｐ＞０．０５）。结果提示,ＨＥＣＣＭ可通过上调ｃ－ｍｙｃ基因表达促进肺血管周细胞增殖,反义ＯＤＮｓ通过下凋ｃ－ｍｙｃ基因表达,抑制ＨＥＣＣＭ诱导的肺血管周细胞增殖。     

基因工程人生长激素的纯化及鉴定

将在中国仓鼠卵巢细胞（ＣＨＯ）中基因克隆表达的人生长激素（ｈＧＨ）培养物经Ｏｃｔｙｌ－ＳｅｐｈａｒｏｓｅＣＬ－４Ｂ疏水层析，ＳｅｐｈａｄｅｘＧ－１００凝胶过滤层析，ＤＥＡＥ－ＣｅｌｌｕｌｏｓｅＤＥ５２离子交换层析，得到了较纯的ｈＧＨ。通过ＳＤＳ－聚丙烯酰胺凝胶电泳（ＳＤＳ－ＰＡＧＥ），Ｎ－末端氨基酸分析及放免分析，证明基因工程ｈＧＨ与天然ｈＧＨ性质相符。     

The Possible Mechanism of Inhibiting Smooth Muscle Cell Proliferation by Emodin

ＴｈｅＰｏｓｓｉｂｌｅＭｅｃｈａｎｉｓｍｏｆＩｎｈｉｂｉｔｉｎｇＳｍｏｏｔｈＭｕｓｃｌｅＣｅｌｌＰｒｏｌｉｆｅｒａｔｉｏｎｂｙＥｍｏｄｉｎＣＨＥＮＹｕａｎ－ｙｕａｎ（陈源源）；ＧＵＯＤａｎ－ｊｉｅ（郭丹杰）；ＸＵＣｈｅｎｇ－ｂｉｎ（徐成斌）（Ｄｅｐａ...     

蜂窝哈夫尼亚菌脂多糖核心区的免疫学特征

用单克隆抗体和多克隆抗血清对８株Ｈａｆｎｉａａｌｖｅｉ（Ｈ．ａｌｖｅｉ）的脂多糖核心区进行了测定，结果如下：①用ＫＤＯ－特异性单克隆抗体（克隆１４和２０）分别在６株和５株Ｈ．ａｌｖｅｉ的脂多糖中检测到α－连接的ＫＤＯ侧链，②Ｅ．ｃｏｌｉ核心型（Ｒ＿１～Ｒ＿４）特异性单克隆抗体和吸收后单一特异性抗血清均不能与Ｈ．ａｌｖｅｉ的脂多糖核心发生反应。③Ｅ．ｃｏｌｉ－Ｒｃ（化学型）核心特异性单克隆抗体（ＷＮ１２２２－５）能与所有（８株）测试的Ｈ．ａｌｖｅｉ的脂多糖发生反应。结果表明，Ｈ．ａｌｖｅｉ含有类似于Ｅ．ｃｏｌｉ－ＫＤＯ侧链和Ｒｃ（化学型）核心的抗原结构，但两者己糖区核心型（Ｒ＿１～Ｒ＿４）抗原不同。     

Clinical Study of Effect of Yizhi Capsule(益智胶囊)on Senile Vascular Dementia

Ｃｌｉｎｉｃａｌ　Ｓｔｕｄｙ　ｏｆ　Ｅｆｆｅｃｔ　ｏｆ　Ｙｉｚｈｉ　Ｃａｐｓｕｌｅ（益智胶囊）ｏｎ　Ｓｅｎｉｌｅ　Ｖａｓｃｕｌａｒ　ＤｅｍｅｎｔｉａＣＨＥＮＫａｉ（陈揩），ＣＨＥＮＫｅ－ｊｉ（陈可冀），ＺＨＯＵＷｅｎ－ｑｕａｎ（周文泉），ｅｔａｌ（Ｇ...     

损毁伏隔核多巴胺神经末梢对二氢埃托啡偏爱效应的影响

目的：研究伏隔核中多巴胺神经末梢在二氢埃托啡精神依赖性中的作用。方法：采用条件性位置偏爱实验反映ＤＨＥ的精神生。结果：ＤＨＥ（０．５μｇ．ｋｇ＾－１，ｓｃ）单独给药产生显著的位置偏爱效应。用６－羟多巴胺（６－ＯＨＤＡ）选择性损毁ＮＡｃ的ＤＡ能神经元末梢后，大鼠则不能对ＤＨＥ形成偏爱效应。结论：ＮＡｃ中ＤＡ神经元的完整性是ＤＨＥ产生偏爱效应所必需的。     

HIGH DENSITY CULTIVATION OF GENETICALLY-ENGINEERED CHO CELL LINES WITH MICROCARRIER CULTURE SYSTEMS

ＨＩＧＨＤＥＮＳＩＴＹＣＵＬＴＩＶＡＴＩＯＮＯＦＧＥＮＥＴＩＣＡＬＬＹ－ＥＮＧＩＮＥＥＲＥＤＣＨＯＣＥＬＬＬＩＮＥＳＷＩＴＨＭＩＣＲＯＣＡＲＲＩＥＲＣＵＬＴＵＲＥＳＹＳＴＥＭＳ￥ＸｉａｏＣｈｅｎｇｚｕ；（肖成祖）；ＨｕａｎｇＺｉｃａｉ（黄子才）；Ｌｉ...     

抗人氧化修饰低密度脂蛋白单克隆抗体的制备和生物学性质

用经Ｃｕ￣（２＋）氧化修饰４ｈ和２４ｈ的小鼠低密度脂蛋白（ｍｕｒｉｎｅＯ－ＬＤＬ）混合物免疫的ＢＡＬＢ／ｃ小鼠，于融合前３天用经Ｃｕ￣（２＋）氧化修饰４ｈ和２４ｈ人低密度脂蛋白（ｈｕｍａｎＯ－ＬＤＬ）的混合物加强免疫，取免疫鼠脾细胞和小鼠骨髓瘤ＳＰ－（２／０）细胞融合，获得５株抗人氧化修饰低密度脂蛋白单克隆抗体，命名为ＨＯＬ－１、ＨＯＬ－２、ＨＯＬ－３、ＨＯＬ－４、ＨＯＬ－５。这些单抗均有较高的抗体效价，抗体类型为ＩｇＧ－（２ａ），单克隆抗体相加实验表明，ＨＯＬ－１、ＨＯＬ－３、ＨＯＬ－４识别Ｏ－ＬＤＬ的同一抗原位点，ＨＯＬ－２识别另一个，ＨＯＬ－５识别第３个。竞争性ＢＡ－ＥＬＩＳＡ实验显示：ＨＯＬ－１能够识别丙二醛修饰的ＬＤＬ（ＭＤＡ－ＬＤＬ）、乙酰化修饰的ＬＤＬ（Ａｃｅｔｙｌ－ＬＤＬ）和各种修饰度的Ｏ－ＬＤＬ，但与未修饰ＬＤＬ（ｎ－ＬＤＬ）无交叉反应。     

Doppler超声时间指标评价高血压病、冠心病左室功能

采用Ｄｏｐｐｌｅｒ超声测量ＣＨＤ、ＨＤ、ＨＣＤ－ＣＨＤ及ｓ四组ＡＴ、ＥＴ、ＡＴ／ＥＴ、ＩＣＴ、ＰＥＰ／ＥＴ、ＰＥＰ、ＩＶＲＴ、ＡｃＴＥ、ＡｃＴＥ／ＭＶＯＴ，结果ＣＨＤ、ＨＤ、ＨＣＤ－ＣＨＤ三组ＩＶＲＴ明显升高（Ｐ＜０．０１），ＨＤ、ＣＨＤ与ＨＣＤＣＨＤ之ＩＶＲＴ差异有显著性（Ｐ＜０．０１），ＮＳ、ＣＨＤ、ＨＤ与ＨＣＤ－ＣＨＤ组ＰＥＰ／ＥＴ、ＩＣＴ、ＰＥＰ差异均有显著性（Ｐ＜０．０５），ＨＣＤ－ＣＨＤ组ＰＥＰ／ＥＴ、ＩＣＴ、ＰＥＰ值升高，ＮＳ、ＨＤ与ＣＨＤ、ＨＣＤ－ＣＨＤ、ＡＴ／ＥＴ差异有显著性（Ｐ＜０．０５），ＣＨＤ及ＨＣＤ－ＣＨＤ组ＡＴ／ＥＴ下降，ＨＲ、ＡＴ、ＥＴ、ＡＣＴＥ各组间差异均无显著性（Ｐ＞０．０５），Ｄｏｐｐｌｅｒ超声时间指标评价左室功能具有一定价值。     

C-Ha-ras Oncogene in Oral Leukoplakia Tissues

Ｃ（程鹏）（李辉奉）（杨平）（谭云）Ｃ－Ｈａ－ｒａｓＯｎｃｏｇｅｎｅｉｎＯｒａｌＬｅｕｋｏｐｌａｋｉａＴｉｓｓｕｅｓＣＨＥＮＧＰｅｎｇ（ＤｅｐａｒｔｍｅｎｔｏｆＳｔｏｍａｔｏｌｏｇｙ．ＴｏｎｇｊｉＨｏｓｐｉｔａｌ，ＴｏｎｇｊｉＭｅｄｉｃａｌＵｎｉｖｅ...     

自由基在卡那霉素内耳中毒中的作用

探讨自由基在卡那霉素（ＫＭ）内耳中毒中的作用，方法：豚鼠６６只，分正常对照组，ＫＭ组，ＫＭ＋尼莫地平（ＮＤ）组，ＫＭ＋超氧化物歧化酶（ＳＯＤ）组，连续用药１２ｄ，停药４ｄ后，分别测试听性脑干反应（ＡＢＲ）阈移，血清ＳＯＤ和耳蜗组织丙二醛（ＭＤＡ），同时也对耳蜗组织作扫描电镜观察，结果：ＫＭ组ＡＢＲ阈移和耳蜗ＭＤＡ显著高于对照组，ＮＤ和ＳＯＤ组（Ｐ〈０．０１），其血清ＳＯＤ明显低于对照组（Ｐ〈０．０     

Adeno-associated virus-mediated Bcl-xL prevents aminoglycoside- induced hearing loss in mice

Background Recent studies showed that aminoglycosides destroyed the cochlear cells and induced ototoxicity by producing reactive oxygen species, including free radicals in the mitochondria, damaging the membrane of mitochondria and resulting in apoptotic cell death. Bcl-XL is a well characterized anti-apoptotic member of the Bcl-2 family. The aim of this study was to determine the potential cochlear protective effect of Bcl-XL as a therapeutic agent in the murine model of aminoglycoside ototoxicity. Methods Serotype 2 of adeno-associated virus （AAV2） as a vector encoding the mouse Bcl-XL gene was injected into mice cochleae prior to injection of kanamycin. Bcl-XL expression in vitro and in vivo was examined with Western blotting and immunohistochemistry separately. Cochlear dissection and auditory steady state responses were checked to evaluate the cochlear structure and function. Results The animals in the AAV2-Bcl-XL/kanamycin group displayed better auditory steady state responses hearing thresholds and cochlear structure than those in the artificial perilymph/kanamycin or AAV2-enhanced humanized green fluorescent protein/kanamycin control group at all tested frequencies. The auditory steady state responses hearing thresholds and cochlear structure in the inoculated side were better than that in the contralateral side. Conclusions AAV2-Bcl-XL afforded significant preservation of the cochlear hair cells against ototoxic insults and protected the cochlear function. AAV2-mediated BCI-XL might be an approach with respect to potential therapeutic application in the cochlear degeneration.     

水杨酸钠对庆大霉素耳毒性拮抗作用的机制研究

目的：探讨水杨酸钠（sodium salicylate,NaSA）对庆大酶素（gentamicin,GM）耳毒性作用的影响及其机制。方法：豚鼠随机分为对照组、GM组、NaSA组和GM＋NaSA组,每组9只。采用听性脑干反应（acoustic brainstem response,ABR）、耳蜗铺片及透射电镜技术,观察用药前后听反应阈及形态变化,检测血清尿素氮、肌苷以及GM浓度,同时测定组8kHzABR平均阈移达55dB,GM NaSA组平均阈移为23dB,差异显（P＜0．05）。形态学改变与听力变化一致。GM＋NaSA组耳蜗组织丙二醛和秩离子较GM组明显减少（P＜0．05）,GM＋NaSA组和GM组超氧化物岐化酶活性明显高于另两组（P＜0．05）,GM＋NaSA组和NaSA组前列环素水平显低于另两组（P＜0．05）。NaSA对GM血药浓度没有影响。结论：自由基和铁离子在GM的耳毒性中起重要作用,NaSA能有效减轻GM耳毒性,有望成为临床庆大霉素耳毒性的预防药物。     

卡那霉素内耳中毒对豚鼠外淋巴液中SOD含量的影响

目的：通过对过豚鼠实验性卡那霉素（ＫＭ）内耳中毒时血清及耳蜗外淋巴液中ＳＯＤ含量的检测，以探讨ＫＭ耳毒性内耳损伤自由基产生与可能的作用机制。方法：用放射免疫法和硫代巴比妥酸荧光法测定豚鼠实验性ＫＭ内耳中毒时血清和耳蜗外淋巴液中ＳＯＤ及耳蜗组织中丙二醛（ＭＤＡ）的含量，测定了内耳中毒有后脑干诱发电位（ＡＢＲ）阈移变化。结果：应用ＫＭ１２ｄＡＢＲ阈移明显增高的豚鼠ＭＤＡ含量也相应明显增高，而血清及外淋     

白藜芦醇在豚鼠耳蜗中的抗自由基作用

目的:观察白藜芦醇(Res)的抗自由基作用.方法:将豚鼠随机分为3组:庆大霉素组(GM组);Res GM组;空白对照组,每组动物10只.测定听性脑干反应(ABR)、耳蜗铺片、动物血清中丙二醛(MDA)和超氧化物歧化酶(SOD)含量及GM血药浓度,观察Res对自由基的影响.结果:GM Res组血液中MDA较GM组明显减少(P＜0.05);GM Res组SOD活性明显高于GM组(P＜0.05).Res对GM的血药浓度无影响.耳蜗铺片结果显示空白对照组毛细胞排列整齐,无损伤;GM组底圈毛细胞损伤严重,向上逐渐减轻,与听阈升高的程度相平行.而GM Res组的毛细胞部分消失,与GM组比较损伤较轻.结论:Res能对豚鼠体内自由基含量产生很明显的影响,对GM引起的耳毒性有保护作用.     

Partial protection by lipoic acid against carboplantin-induced ototoxicity in rats

To investigate the alterations in auditory brainstem evoked responses (ABRs) and the changes of carboplatin-induced ototoxicity in the cochlear oxidant/antioxidant systems and otoprotection by an antioxidant lipoate. Methods Male wistar rats were divided into four groups and treated as follows: 1) vehicle (saline) control, 2) carboplatin (256 mg/kg, i.p.), 3) lipoate (100 mg/kg, i.p.), 4) lipoate carboplatin. Post-treatment ABRs were performed after four days and rats were sacrificed with their cochleae harvested and analyzed. Results Carboplatin significantly elevated ABR threshold above the pretreatment thresholds. Lipoate carboplatin treated rats showed decreased elevation of hearing threshold. Carboplatin significantly depleted cochlear reduced to oxizized glutathione (GSH/GSSG) ratio, whereas lipoate carboplatin treatment increased GSH/GSSG ratio. Carboplatin significantly decreased cochlear copper zinc-superoxide dismutase (CuZn-SOD) catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR) and glutathione-S-transferase (GST) activities and enzyme protein expressions and a significant increase in Mn-SOD activity, protein expression and malondialdehyde (MDA) level. Cochlear antioxidant enzyme activities, enzyme protein expressions and MDA level were partially restored in lipoate carboplatin treated rats, compared to carboplatin alone. Conclusion Carboplatin-induced ototoxicity is related to impairment of cochlear antioxidant system and otoprotection conferred by lipoate is associated with partial sparing of the cochlear antioxidant defense system.     

低O2高CO2致大鼠海马超微结构改变及川芎嗪的保护作用

目的：观察慢性低O2高CO2对大鼠海马超微结构的影响及川芎嗪注射液的保护作用。方法：雄性SD大鼠30只，随机分为正常对照组、低O2高CO2 4周组（模型组）、低O2高CO2 4周＋川芎嗪治疗组（川芎嗪组）。通过电镜观察海马超微结构并测定超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量。结果：慢性低O2高CO2使海马神经元和神经胶质细胞水肿、SOD活性降低、MDA含量升高，川芎嗪干预可使上述指标的异常变化明显减轻。结论：川芎嗪对慢性低O2高CO2大鼠海马神经细胞结构损害有保护作用，其机制可能与抗氧化作用有关。     

川芎嗪预处理对大鼠肾脏缺血再灌注损伤的保护作用

目的:探讨川芎嗪预处理对大鼠肾脏缺血再灌注损伤的保护作用及机制。方法:30只SD大鼠被随机分为3组(n=10):假手术组、缺血再灌注损伤(ischemia reperfusion injury,IR)组、川芎嗪预处理组(ligus-trazine injection preconditioning group,LI)。建立大肾脏缺血再灌注损伤模型,测定血清肌酐(Scr)与尿素氮(BUN)含量、肾组织匀浆中SOD(黄嘌呤氧化酶法)、GSH_Px(二硫代二硝基甲苯法)的活性及MDA(硫代巴比妥酸盐法)含量。结果:与缺血再灌注损伤(IR)组比较,川芎嗪预处理(PFI)组Scr(P<0.01)、BUN(P<0.05)、MDA(P<0.05)含量显著下降。而SOD(P<0.01)、GSH_Px(P<0.05)活力显著升高。结论:SOD、GSH_Px是重要的内源性保护物质,川芎嗪可增加SOD、GSH_Px的活性、增加机体抗氧化和清除自由基的能力,从而发挥对肾缺血再灌注损伤的预防和保护作用。     

Aminoglycoside ototoxicity in three murine strains and effects on NKCC1 of stria vascularis

Background After establishing a murine model of aminoglycoside antibiotic （AmAn） induced ototoxicity, the sensitivity of AmAn induced ototoxicity in three murine strains and the effect of kanamycin on the expression of Na-K-2Cl cotransporter-1 （NKCC1） in stria vascularis were investigated. Methods C57BL/6J, CBA/CaJ, NKCC1^＋/- mice （24 of each strain） were randomly divided into four experimental groups： A： kanamycin alone; B： kanamycin plus 2,3-dihydroxybenzoate; C： 2,3-dihydroxybenzoate alone; and D： control group. Mice were injected with kanamycin or/and 2,3-dihydroxybenzoate twice daily for 14 days. Auditory brainstem response （ABR） was measured and morphology of cochlea delineated with succinate dehydrogenase staining. Expression of NKCC1 in stria vascularis was detected immunohistochemically. Results All three strains in groups A and B developed significant ABR threshold shifts （P〈0.01）, which were accompanied by outer hair cell loss. NKCC 1 expression in stria vascularis was the weakest in group A （A cf D, P〈0.01） and the strongest in groups C and D （P〈0.05）. CBA/CaJ mice had the highest sensitivity to AmAn. Conclusions Administration of kanamycin established AmAn induced ototoxicity. Kanamycin inhibited the expression of NKCC1 in stria vascularis. 2, 3-dihydroxybenzoate attenuated AmAn induced ototoxicity-possibly by enhancing the expression of NKCC 1. Age related hearing loss did not show additional sensitivity to AmAn induced ototoxicity in murine model.