眩晕的的手术治疗

耳源性眩晕是耳科临床常见的症状性诊断,其病变部位大致分为前庭末梢感受器和前庭神经系两部分。传统的药物只能控制一部分患者的眩晕发作,因此,手术治疗眩晕已运用到临床。国内从80年代开展了梅尼埃尔病的手术治疗,至今尚未见到前庭神经微血管减压术治疗耳源性眩晕的报告,本文将我科1986年以来6例外耳源性眩晕的手术治疗进行了总结,报告如下。1 临床资料:6例患者男2例,女4例,年龄32岁—45岁。病史2年—4年。其中临床诊断梅尼埃尔病5例,桥小脑角微血管压迫症1例。梅尼埃尔病5例均有反复发作性眩晕伴恶心呕吐,耳鸣及耳内胀感。纯音测听传导性聋1例,感音性聋3例,听力正常2例。纯音测听(非隔音室)平均语言频率听阈小于30dB1耳,41—     

看得见的与看不见的

我有时也与一些投资公司聊天,他们一般会问三个标准问题。问题一：网上卖药对实体药店有没有影响？答：当然有影响,尤其是安全套、家用医疗器械。经过类别分析,实体店里药食同源类商品增长较快,处方药与OTC有一定增长,而安全套与器械类没有增长,保健品似乎是负增长。这显然是网上药店的冲击所致。     

丹参的药理作用的研究进展

丹参作为活血化瘀的代表药物之一,因有广泛而确切的药理作用受到重视,相关制剂也逐步地应用于临床。论文阐述近年来有关丹参的药理作用研究进展,以供广大药学及临床人员参考。     

天然的是不是最好的

西方国家政府已认识到有必要管理传统草药的使用。欧盟2001／83指令对引入欧盟的药物及其使用作出了法律。修订的2004／24指令规定了传统草药的注册、上市及制造，使其能与常规西药一样得到管理。     

贫穷的和富有的

有的人永远贫穷。我认识一家人，买什么东西都不肯落后，就是这不肯落后，害得他一直闹经济危机你永远听他抱怨钱不够用，因为缺钱，永远牢骚满腹。我们谈到西方发达国家，常说那里的老百姓喜欢消费在前，凡事都预支，动不动就贷款。我认识的这家人，新潮的消费观念似乎也像发达国家的老百姓，有理无理，也是先享受起来再说，     

妇科急腹症的的临床研究

目的探讨妇科急腹症的临床特征,提高对该类疾病发展规律的认识,提高其诊断救治能力。方法回顾性分析2002年1月至2007年12月急腹症102例患者的临床资料。结果引起妇科急腹症的病因:内出血性疾病,感染性疾病及其他,内出血性和肿瘤并发症性手术治疗280例。感染性疾病及部分异位妊娠保守治疗者120例,全部患者均获痊愈出院,住院时间7～19d.平均(8.7±1.3)d。结论在妇科急腹症病因复杂,但均以常见病,多发病为主,各自具有病史、体检、HCG、后穹窿穿刺、盆腔B超特点可资鉴别。     

中药饮片的煎煮方法与疗效的关系的探讨

煎剂(又称汤剂)是指中药饮片加水煎煮提取有效成分的液体药剂。在我国已有几千年的历史记载，在民间及中医药界广为采用，至今不衰。为了更好地发挥中药的最佳疗效，除药材必须货真价实，质量合格外，还应有正确的加工使用方法，在煎煮过程中应注意一些不可忽视的要点，简述如下。     

对罹患急性乙型肝炎的母亲的幼儿的处理

Nelson医生问:近两周来,我们地区有3名内科医师在诊所发现,一些8～18月龄婴幼儿的母亲罹患实验室确诊的急性乙型肝炎。与这些母亲密切接触的幼儿应该接受乙型肝炎免疫球蛋白(HBIG)和乙型肝炎疫苗吗?对这些婴儿及其母亲应进行哪些实验室试验? Krugman医生(纽约大学医学中心)答:回答这一问题需要了解实验室确诊的急性乙型肝炎的自然史。急性乙型肝炎病人的传染期为潜伏期后期到急性肝炎或黄疸出现后的两周至3或4个月。血中出现乙型肝炎表面抗原(HBsAg)是潜在传染性的证据。大约90%病人于HBsAg消失后3个月不再具有传染性。在这些情况下,密切的家庭接触者应该接受HBIG,肌肉注射0.06ml/kg,0.5～1.0ml的HBIG可使8～18月龄幼儿被动获得抗-HBs约3个月。     

PgP介导的多药耐药的逆转的研究进展

肿瘤的化疗是其综合治疗的一个重要方面,而多药耐药（MDR）的影响是导致化疗失败的重要原因。国内外对逆转MDR也进行了很多研究工作,在各种引起MDR的机制中,以P糖蛋白（PgP）介导的MDR占重要方面,针对逆转PgP介导的MDR的研究也较多,主要包括化学逆转剂、单克隆抗体和基因水平调控等方面,本文是对PgP介导的MDR的逆转的研究进展做一个简要综述。     

南沙参多糖对四氯化碳损伤原代培养大鼠肝细胞保护作用的研究

目的:探讨南沙参多糖(RAPS)对四氯化碳(CCl4)损伤原代培养大鼠肝细胞的保护作用及其机制。方法:通过原位灌流法分离大鼠肝细胞,培养36h后加入RAPS,同时造成CCl4损伤,分别于损伤24h和48h时检测培养液中丙二醛(MDA)的含量、丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)的活性,48h后用MTT法测定肝细胞存活率。结果:RAPS对CCl4引起的ALT、AST活力的升高有抑制作用,同时抑制MDA的产生及肝细胞损伤造成的SOD活性及GSH-PX活性的降低。而且能明显改善肝细胞存活率。结论:RAPS能有效抑制CCl4造成的原代培养大鼠肝细胞损伤,机制可能与其抗氧化作用有关。     

肝细胞生长因子对四氯化碳损伤原代培养大鼠肝细胞的保护作用

采用大鼠离体肝细胞原代培养24 h，并利用CCl₄造成急性肝细胞损伤模型，检定肝细胞生长因子(HGF)对肝细胞损伤的影响. 结果表明：HGF可显著降低中毒肝细胞及细胞膜脂质过氧化物水平, 抑制肝细胞脂质过氧化, 并降低谷丙转氨酶和谷草转氨酶水平, 稳定质膜；显著促进中毒肝细胞RNA和DNA的合成；超微病理证实HGF能减轻CCl₄对肝细胞质膜，染色质, 线粒体, 内质网及核蛋白体的损害.     

丹酚酸A抗四氯化碳中毒致大鼠肝损伤和肝纤维化的作用

目的：研究丹酚酸Ａ（ＳＡ－Ａ）抗肝损伤、肝纤维化作用。方法：采用ＣＣｌ４诱导大鼠肝损伤及肝纤维化，期间予ＳＡ－Ａ灌胃治疗，另设秋水仙碱（Ｃｏｌ）组、丹参组作对照，６周后进行肝组织病理学和Ｉ、Ⅲ型胶原免疫组化观察，肝组织羟脯氨酸（Ｈｙｄ）、丙二醛（ＭＤＡ）含量及血清ＡｌａＡＴ、ＡｓｐＡＴ和白蛋白含量测定。结果：ＳＡ－Ａ降低血清ＡｌａＡＴ、ＡｓｐＡＴ水平及肝组织ＭＤＡ、Ｈｙｄ含量，减轻肝纤维化程度，抑     

白细胞介素—1阻滞剂CK—119和CK—122地成纤维样细胞增生的抑制

AIM: To study potent and nontoxic agents to inhibit fibroblast proliferation. METHODS: Fibroblast-like corneal and conjunctival cells were cultured and inhibited by interleukin-1 (IL-1) blockers, dihydropyridazino-pyridazines CK-119 and CK-122. The cell growth and syntheses of DNA, RNA, and protein after IL-1 blocker incubation were determined. RESULTS: CK-119 and CK-122 inhibited cell growth of corneal fibroblast at 30 mg.L-1. DNA and RNA syntheses in corneal fibroblasts were markedly inhibited by CK-119 and CK-122 whereas protein synthesis was either unaffected or mostly enhanced at 30-100 mg.L-1 and 100-300 mg.L-1, respectively. Similar results were obtained in conjunctival cell cultures by CK-119 and CK-122 at 3-10 mg.L-1 and 30-100 mg.L-1, respectively. CONCLUSION: CK-119 and CK-122 are potent IL-1 blockers to inhibit cell growth of fibroblast-like corneal and conjunctival cells mainly through the inhibition of DNA and RNA syntheses but not protein synthesis.     

Protective effect of S-adenosyl-L-methionine against CCl4-induced hepatotoxicity in cultured hepatocytes

Effect of S-adenosyl-L-methionine disulfate tosylate salt (SAMe-ST) and L-methionine (L-Met) on primary cultured rat hepatocytes were studied. In cultured hepatocytes treated with CCl4, SAMe-ST and L-Met suppressed the decrease in urea-nitrogen secretion as well as the leakages of GOT and GPT. The membrane-protective action of these two compounds was verified by the histological data. Failure of SAMe-ST to counteract CCl4-induced reduction of radioactive leucine incorporation into the trichloroacetic acid-insoluble materials in hepatocytes indicates that the observed effects of SAMe-ST or L-Met do not involve acceleration of protein synthesis. The present results indicate that SAMe-ST remarkably protects hepatocytes from CCl4-induced hepatotoxicity, probably by either changing the structure or compositions of membrane phospholipids or by modifying the interaction of CCl4 with the intracellular drug-metabolizing enzyme systems.     

丹参对GSH-Px/MDA比值的影响及其在人肝细胞胶原合成中的作用

利用四氯化碳（CCl4）造成肝细胞脂质过氧化损伤，测定原代培养人胚肝细胞匀浆中羟脯氨酸（Hyp）含量及培养液中Ⅲ型前胶原（PCⅢ）、脂质过氧化物（MDA）、谷胱甘肽过氧化物酶（GSH－Px）活性水平．观察丹参对GSH－Px／MDA比值的影响及其与PCⅢ、Hyp水平的关系。结果：与损伤模型组比较，丹参（1mg／ml）预作用4h，可明显减少受损肝细胞产生PCⅢ、Hyp及MDA，提高GSH－Px活性，GSH－Px／MDA比值增加非常显著（P＜0．01）。提示丹参可抑制CCl4所致人胚肝细胞胶原合成。     

Inhibitory effects of dexamethasone on epidermal growth factor-induced DNA synthesis and proliferation in primary cultures of adult rat hepatocytes

We investigated the effects of dexamethasone on epidermal growth factor (EGF)-induced DNA synthesis and proliferation in serum-free primary cultures of adult rat hepatocytes. Isolated hepatocytes were cultured at a density of 3.3 × 10? cells/cm2 in Williams' medium E containing 5% bovine calf serum and various concentrations of dexamethasone for 1, 2 and 3 h. After the 3-h attachment period, the medium was changed, and cells were cultured in serum-free and dexamethasone-free Williams' medium E with or without glucocorticoid receptor antagonists. The growth-stimulating effects of EGF (20 ng/ml) on the primary cultured hepatocytes were time- and concentration-dependently inhibited by dexamethasone added to the culture medium. The mineral corticoid aldosterone (10?? M) did not produce the same growth-inhibitory effects as dexamethasone (10?? M). The inhibitory effects of dexamethasone were reversed by treatment with the glucocorticoid receptor antagonist mifepristone (RU486, 10?? M) or a monoclonal antibody against glucocorticoid receptor (100 ng/ml). In addition, the growth-inhibitory effects of dexamethasone did not affect EGF-induced p42 mitogen-activated protein (MAP) kinase phosphorylation. These results indicate that dexamethasone concentration-dependently delays and inhibits the EGF-induced DNA synthesis and proliferation through its own intracellular receptor in primary cultures of adult rat hepatocytes.     

Effect of estrogen on liver plasma membrane in rats.

The effect of estrogen on plasma membrane was investigated using the primary cultured rat hepatocytes treated with carbon tetrachloride (CCl4) and the isolated plasma membrane of rat liver. 17 beta-Estradiol (E2), at concentrations of 10(-10) M to 10(-4) M, 10(-8) M to 10(-6) M and 10(-12) M to 10(-4) M, had an inhibitory effect on the CCl4-induced leakage of glutamic oxaloacetic transaminase, glutamic pyruvic transaminase and lactate dehydrogenase, respectively from primary cultured rat hepatocytes. Diethylstilbestrol, which caused inhibition at a dose of 10(-4) M, did not inhibit any enzyme leakage at any further concentrations of 10(-12) M to 10(-6) M. In the isolated plasma membrane of rat liver, Mg(2+)- and Na+,K(+)-adenosine triphosphatase activity was increased by E2 treatment at concentrations of 10(-6) M and 10(-4) M.     

龙眼参多糖对四氯化碳诱导大鼠原代肝细胞损伤的保护作用

目的:研究龙眼参多糖(LYS)对大鼠原代肝细胞损伤的保护作用及其机制。方法:用四氯化碳(CCl4)体外诱导大鼠原代肝细胞损伤,检测培养上清液中天门冬氨酸转移酶(AST)和丙氨酸氨基转移酶(ALT)水平,测定肝细胞中丙二醛(MDA)和谷胱甘肽(GSH)含量,四甲基偶氮唑盐(MTT)法检测细胞活性。结果:与模型组比较,LYS组AST和ALT水平及肝细胞MDA含量明显降低,肝细胞存活率和GSH含量升高。结论:LYS对大鼠原代培养肝细胞损伤有直接保护作用,机制可能与其抗氧化作用有关。     

二至丸提取物对体外肝细胞损伤的保护作用

 目的：研究二至丸乙酸乙酯提取物(ethyl acetate extractsof Erzhi pill,EAEP)对体外肝细胞损伤的保护作用及其机理。方法：培养L-O2型肝细胞,采用CCl4和H2O2体外分别诱导肝细胞损伤,检测培养上清液中天门冬氨酸转换酶(AST)和丙氨酸氨基转换酶(ALT)水平,测定上清液中丙二醛(MDA)的含量和过氧化物岐化酶(SOD)活力及谷胱甘肽过氧化物酶(GSH-Px)活性,MTT法检测细胞存活和增殖活性。结果：① EAEP(0.32～40 μg?mL-1)剂量组可明显降低由CCl4所致肝细胞培养上清液中AST和ALT水平及MDA含量的升高,还可提高由H2O2所致肝细胞存活率和SOD活力及GSH-Px活性的降低。② EAEP(0.32～40 μg?mL-1)剂量组可使H2O2升高的肝细胞培养上清液中ALT和ALT水平及MDA含量明显降低或恢复,还可提高CCl4降低的肝细胞存活率和SOD活力及GSH-Px活性。结论：提示AEEP对体外肝细胞损伤有直接保护作用,该作用可能与其抗氧化作用有关。