狂犬病诊治进展

人类的狂犬病是一种中枢神经系统病毒感染性疾病,常由患狂犬病动物的唾液污染伤口而传染;一旦出现症状,病人基本上100%死亡,从狂犬病后康复的病例极为罕见,仅有3例报道。临床表现为特有的恐水怕风、咽肌痉挛、进行性瘫痪等。狂犬病在87个国家有流行,主要流行于东南亚、非洲及拉     

布洛芬对乙酰氨基酚退热疗效对比

长期以来,发热是儿科关注的问题,发热程度有助于判断病情,儿童多因与病情不成比例,轻微疾病即可出现发烧,父母常常不了解这一现象而引起不必要的恐慌,随意应用退热药即成为儿科普遍的现象[1].采用安全有效的退热药物值得临床探讨.     

Establishment of a mouse model of cancer cachexia with spleen deficiency syndrome and the effects of atractylenolide I

Cancer cachexia is a multifactorial metabolic syndrome that affects～50%–80%of cancer patients,and no effective therapy for cancer cachexia is presently available.In traditional Chinese medicine,a large portion of patients with cancer cachexia was diagnosed as spleen deficiency syndrome and treated with tonifying TCMs that produce clinic benefits.In this study we established a new animal model of spleen deficiency and cancer cachexia in mice and evaluated the therapeutic effects of atractylenolide I,an active component of tonifying TCM BaiZhu,in the mouse model.Cancer cachexia was induced in male BALB/c mice by inoculation of mouse C26 colon adenocarcinoma cells,whereas spleen deficiency syndrome was induced by treating the mice with spleen deficiency-inducing factors,including limited feeding,fatigue,and purging.The mouse model was characterized by both cachexia and spleen deficiency characteristics,including significant body weight loss,cancer growth,muscle atrophy,fat lipolysis,spleen,and thymus atrophy as compared with healthy control mice,cancer cachexia mice,and spleen deficiency mice.Oral administration of atractylenolide I(20 mg·kg?1per day,for 30 days)significantly ameliorated the reduction in body weight and atrophy of muscle,fat,spleen,and thymus in mice with spleen deficiency and cachexia.The established model of spleen deficiency and cancer cachexia might be useful in the future for screening possible anticachexia TCMs and clarifying their mechanisms.     

精于颐养走过百年——许德珩的长寿要诀

许德珩一生精于摄生颐养,享年100岁.他的养生要诀主要有如下几条: 重视饮食条理 许老的饮食以清淡为主,定时定量,不饱食,不偏食,不挑食.早餐一般是一碗稀饭,一个小馒头,少许咸菜;午餐以蔬菜为主,加上少许牛肉(晚年不食猪肉),主食100克;晚餐则以素为主.一日三餐既不随意增减,更不暴饮暴食.饮酒微量,只喝一点果酒,不饮白酒等烈性酒.爱吃新鲜水果,不吃甜食.     

浅谈如何加强医疗器械的管理

医疗器械的应用在疾病的诊断、治疗及预防等各个环节都发挥着不可替代的作用,其质量的好坏直接关系到人民群众的身体健康和生命安危.2000年国务院颁布了第一部医疗器械监管法规-<医疗器械监督管理条例>,标志着我国医疗器械监管正式走上了法制化轨道,但是由于种种原因,目前我国在医疗器械的生产、经营以及使用等各个环节都存在着较为普遍和严重的问题,其监管已显得相对滞后,成为食品药品部门监管中的一个"软肋",以至于频频出现像钢板等植入性器械断裂现象和发生举国震惊的"眼球事件".本文就我县医疗器械的经营、使用现状和如何加强对医疗器械的监管作以下分析和探讨.     

黑米:滋肾补胃益气血

黑米因外皮乌黑而得名,又称补血糯米、贡米、黑珍珠,是一种具有诸多保健功效的珍贵稻米.黑米含有淀粉、蛋白质、脂肪、多种维生素,又含钙、磷、镁、铁、锌、钼、硒等多种矿物质和微量元素.黑米所含蛋白质不但比普通大米高37%,而且其中氨基酸的含量亦比白米高25.4%,人体所需的赖氨酸、精氨酸、氮氨酸、色氨酸等,黑米中也都具有,营养价值很高.     

捕捉蛛丝马迹,让恶性肿瘤早现身——常见恶性肿瘤发病的早期信号(二)

痣 痣可发生在皮肤的任何部位,如面部、手掌、脚底、腰部、前胸、后背和阴囊等处.痣如出现下述现象,可能是癌变信号:反复发生感染;突然有痒感,不由自主地用手搔抓,甚至抓破出血;表面潮湿或有结痂形成;原为棕色,逐渐颜色变深变黑;有出血倾向,稍微触碰即发生出血;周围有炎性红晕,触之有痛感;痣上原有毛发突然自行脱落;痣的中央部出现硬结或自发性出血、溃疡形成和周围出现散在的呈卫星状小黑痣.     

克隆病并穿孔1例

1病例介绍病人,女,35岁,因突发下腹部疼痛半小时就诊,病史诉说欠清,(家属补充,腹痛时间约4～5年),查体:脉搏96次/分,血压84/60 mmHg,表情淡漠、四肢湿冷。全腹压痛呈板状腹,叩诊移动浊音可疑,以脐下压痛明显,B超提示腹腔内有少许积液,右侧卵巢囊肿,约44 cm大小。实验室检查白细胞16×109/L,中性0.80。考虑腹腔脏器穿孔,在全麻下行剖腹探查,取下腹正中切口进腹,腹腔内有臭味溢出,吸出浑浊性液体约250 ml,有食物残渣,距回盲部约50 cm处,向上见约45 cm长的回肠充血水肿     

刺五加注射液致过敏反应2例报告

例1:患者男性,51岁,因患冠心病人院治疗.给予刺五加注射液60mL加5%葡萄糖250mL中静脉注射.输人约50mL时,患者面色潮红,瘙痒感,开始发现前臂有散在的米粒大小的红色小点,继而遍及颈、四肢部以及全身出现点状红色皮疹,甚痒.立即停药,给予扑尔敏、Vc、葡萄糖酸钙口服无效.改为肌注盐酸肾上腺素、静滴地塞米松,1天后上述症状逐渐减轻.     

小便带血,源于结石

市运动会就要开幕了,体校的学生都在紧张地"备战",准备在运动会上崭露头角.小董一直是学校的"尖子生",这段时间练得更加刻苦.可是,最近每次锻炼小董都会感到小腹疼痛难忍,而且小便常常带血,他又怕去医院会耽误比赛,一直不敢告诉老师和家人.后来,还是同宿舍的小张告诉了老师.老师得知这种情况后,马上带着小董到了医院.医生做了X线摄片检查,才知道小董是患了尿路结石.     

Chlorpyrifos induces apoptosis in human monocyte cell line U937

In order to investigate chlorpyrifos-induced cell death and its underlying mechanism in human immune cells, a human monocyte like cell line (U937) was treated with chlorpyrifos at 4.45-570microM for 0.5-24h at 37 degrees Celsius in a 5% CO(2) incubator. We first found that chlorpyrifos induced cell death of U937 in a dose- and time-dependent manner, as shown by LDH and MTT assays and PI uptake. Then, we investigated if chlorpyrifos-induced cell death consisted of apoptosis, as determined by analysis of Annexin-V staining and the intracellular level of active caspase-3 by flow cytometry, and DNA fragmentation analysis. We found that chlorpyrifos induced apoptosis in U937 in a time- and dose-dependent manner, as shown by Annexin-V staining. DNA fragmentation was detected when cells were treated with 71 to 284microM chlorpyrifos for 4 or 6h. Chlorpyrifos also induced an increase of intracellular active caspase-3 in U937 cells in a dose-dependent manner, and a caspase-3 inhibitor, Z-DEVD-FMK, significantly inhibited the chlorpyrifos-induced apoptosis. These findings indicate that chlorpyrifos can induce apoptosis in U937 cells, and this effect is partially mediated by activation of intracellular caspase-3.     

Gnidilatimonoein from<Emphasis Type="Italic">Daphne mucronata</Emphasis> induces differentiation and apoptosis in leukemia cell lines

Gnidilatimonoein is a new diterpene ester, recently isolated from the leaves of Daphne macronata with potent anti-tumoral and anti-metastastic activities (Yazdanparast et al., 2004). Promyeloblastic (KG1), promyelocytic (NB4) and promonocytic (U937) cells were cultured in the presence of various concentrations of the drug (0.5-3.0 microM) for 3 days. Herein, we report that gnidilatimonoein induces differentiation and apoptosis in KG1, NB4 and U937 cells. The drug inhibited growth and proliferation of KG1, NB4 and U937 cells with IC50 values of 1.5, 1.5 and 1.0 microM, respectively, after 72 h of treatment. Cell viability was also decreased by 18%, 20% and 23%, respectively, after 72 h treatment with the drug. NBT reducing assay revealed that the inhibition of proliferation is associated with differentiation especially toward monocytes-like morphology. Indeed, the drug at 0.5-1.5 microM induced differentiation by 5-50% in the cells. Acridine orange/ethidium bromide (AO/EtBr) double staining and DNA fragmentation assays revealed that apoptosis occurred after differentiation of the cells. Based on the present data, it seems that the new compound is a good candidate for further evaluation as an effective chemotherapeutic agent acting through induction of differentiation and apoptosis.     

Ziram induces apoptosis and necrosis in human immune cells

Ziram as a dithiocarbamate fungicide is widely used throughout the world in agriculture and as an accelerating agent is used in latex production. In order to investigate ziram-induced apoptosis/necrosis and its underlying mechanism in human immune cells, a human monocyte-like cell line (U937) was treated with ziram at 0.0312–2 μM for 2–24 h at 37°C in a 5% CO₂ incubator. Apoptosis/necrosis induced by ziram was determined by analysis of FITC-Annexin-V/PI staining and the intracellular level of active caspase-3 by flow cytometry and DNA fragmentation analysis. We found that ziram induced apoptosis/necrosis in U937 in a time- and dose-dependent manner, as shown by FITC-Annexin-V/PI staining. DNA fragmentation was detected when cells were treated with 0.5, 1, or 2 μM ziram for 24 h. Ziram also induced an increase in intracellular active caspase-3 in U937 cells in a dose-dependent manner, and a caspase-3 inhibitor, Z-DEVD-FMK, significantly inhibited the ziram-induced apoptosis. Moreover, it was found that ziram induced mitochondrial cytochrome c release in U937 cells. These findings indicate that ziram can induce apoptosis/necrosis in U937 cells, and this effect is partially mediated by activation of intracellular caspase-3 and mitochondrial cytochrome c release.     

新型组蛋白去乙酰化酶抑制剂致U251细胞周期阻滞、凋亡及其机制的研究

目的探讨新型组蛋白去乙酰化酶抑制剂(HDACi)2,2,3,3-四甲基环丙酰硫脲(TCCT)诱导人脑胶质瘤U251细胞周期阻滞、凋亡及其作用机制。方法以不同药物浓度与U251细胞共同培养48 h后,采用MTT法检测药物作用48 h后肿瘤细胞的增殖。药物作用24 h后,采用RT-PCR检测肿瘤细胞的p21WAF1/CIP1与Cyclin D1 mRNA的表达,Western blot检测HDAC3、HDAC4、Cyclin D1与p21WAF1/CIP1蛋白的表达,PI单染法分析细胞周期,Annexin V-PI双染法检测肿瘤细胞凋亡。结果 TCCT对U251细胞增殖具有明显抑制作用,药物干预48 h时的IC50为(0.461±0.108)mmol·L-1,并呈现剂量依赖性。TCCT药物干预24 h后U251细胞p21WAF1/CIP1mRNA表达上调,Cyclin D1 mRNA下调;组蛋白去乙酰化酶3(HDAC3)和组蛋白去乙酰化酶4(HDAC4)表达下调,Cyc-lin D1蛋白表达弱下调,p21WAF1/CIP1蛋白表达上调;S期细胞比例明显提高(P<0.05);细胞凋亡率明显增高(P<0.01)。结论 TCCT对U251细胞增殖有明显的抑制作用,引起肿瘤细胞S期阻滞和凋亡。其作用机制可能与其下调HDAC3、HDAC4表达,促进组蛋白乙酰化,而影响p21WAF1/CIP1和Cyclin D1的基因、蛋白的表达有关。     

通关藤对U937细胞凋亡相关基因表达谱的影响

目的利用细胞凋亡基因芯片比较通关藤作用前后U937细胞基因表达谱的改变,探讨通关藤诱导U937细胞凋亡的可能机制。方法利用流式细胞仪检测细胞凋亡率。提取经和未经50μL/mL通关藤处理的U937细胞的mRNA,逆转录为cDNA,然后用含89个目的基因的细胞凋亡基因芯片(APH-012)进行杂交,GEArray软件分析,通过比较得到通关藤处理前后表达有差异的基因。结果通关藤作用前后表达有差异的基因共36条(占芯片基因总数的44.4%),其中28条(28/89,31.5%)基因表达上调,8条(8/89,8.9%)基因表达下调。这些改变的基因主要包括肿瘤坏死因子配体和受体家族、bcl-2家族、caspase家族、P53家族成员。结论通关藤主要通过上调促凋亡基因及下调凋亡抑制基因来诱导U937细胞凋亡,其中死亡受体途径活化可能在凋亡过程中发挥重要作用。     

白藜芦醇对髓系白血病干细胞增殖和凋亡的影响及其与allo-NK细胞的联合杀伤作用

目的探讨白藜芦醇(RES)对髓系白血病干细胞(CD34+CD38-KG1a细胞,以下简写为KG1a细胞)增殖和凋亡的影响,并初步探讨RES增强allo-NK细胞对KG1a细胞杀伤作用的机制。方法免疫磁珠分选法分选人外周血单个核细胞(PBMCs)中的CD16+CD56+CD3-NK细胞(以下简写为NK细胞)。流式细胞术检测细胞表面分子CD34、CD38、CD3、CD15和CD56。MTT法、甲基纤维素克隆形成实验检测RES对KG1a细胞增殖抑制作用。DAPI染色法和流式细胞术检测RES对KG1a细胞凋亡的影响。使用IC50的RES作用KG1a细胞24 h后清洗离心获得RES/KG1a细胞。LDH释放法检测NK细胞对KG1a细胞和RES/KG1a 2种细胞的杀伤能力。流式细胞术检测KG1a细胞和RES/KG1a细胞的表面配体ULBP1、ULBP2、ULBP3、MICA和MICB。结果免疫磁珠分选后,外周血单个核细胞中的NK细胞比例为(90.5±3.2)%;KG1a细胞纯度为(91.2±3.9)%。RES对KG1a细胞的增殖抑制作用具有时间和剂量依赖性,24 h的IC50=24.0μmol·L-1;48 h的IC50=13.7μmol·L-1。RES抑制KG1a细胞的克隆形成能力并诱导细胞凋亡,具有剂量依赖性(P<0.05)。NK细胞对RES/KG1a细胞的杀伤能力比其对KG1a细胞的杀伤能力强(P<0.05)。与KG1a细胞比较,RES/KG1a细胞表面配体ULBP1、ULBP2、ULBP3表达明显上调(P<0.05),MICA和MICB变化不明显。结论 RES能够抑制KG1a细胞增值抑制并诱导细胞凋亡,联合NK细胞对KG1a细胞具有协同杀伤作用,这可能与KG1a细胞表面的ULBP1、ULBP2、ULBP3表达上调相关。     

Deguelin inhibits expression of IκBα protein in Raji and U937 cells

AIM: To determine whether deguelin can regulate the expression of nuclear factor kappa B (NF-kappaB) binding protein (IkappaBalpha) in U937 human leukemia cells and Raji human B lymphoma cells. METHODS: The localization of IkappaBalpha protein was investigated by using an immunofluorescence method. The expression of IkappaBalpha and NF-kappaB /p65 proteins in Raji and U937 cells were investigated by using Western blotting. Apoptosis was detected through annexin V/PI double-labeled cytometry. RESULTS: IkappaBalpha localized in the cytoplasm in untreated and deguelin-treated cells. After treatment with tumor necrosis factor alpha (TNF-alpha) or deguelin plus TNF-alpha for 15 min, there was a substantial reduction in the amount of IkappaBalpha protein. The expression of IkappaBalpha was downregulated by deguelin in Raji and U937 cells. Deguelin induced apoptosis in U937 cells. CONCLUSION: Deguelin inhibited the expression of IkappaBalpha protein in U937 and Raji cells. The anti-proliferative activity of deguelin is related to the signal pathway of NF-kappaB.     

线粒体通路和死亡受体通路在中华眼镜蛇毒组分诱导KG1a细胞凋亡中的作用

目的研究线粒体通路和死亡受体通路在中华眼镜蛇毒组分(naja naja actra venom component,NNAVC)诱导KG1a细胞凋亡过程中的作用。方法以人急性髓系白血病细胞株KG1a细胞为研究对象,采用Annexin V-FITC/PI荧光染色法进行凋亡细胞的形态学观察,流式细胞仪检测细胞凋亡率,分光光度法检测Caspase-9、Caspase-8和Caspase-3的活性,ELISA法检测胞质内细胞色素C的表达水平,流式细胞仪分析TRAIL死亡受体(DR4、DR5)和诱骗受体(DcR1、DcR2)的改变。结果 NNAVC作用后,荧光显微镜下可见明显的凋亡细胞,细胞凋亡率随药物作用浓度的增加而升高;Caspase-9、Caspase-8和Caspase-3蛋白被激活,胞质内细胞色素C的表达明显增加;流式细胞仪检测结果显示,NNAVC具有降低死亡受体DR4和诱骗受体DcR1的表达率,而提高DR5和DcR2的表达水平的作用。结论线粒体凋亡通路和死亡受体通路均参与NNAVC诱导KG1a细胞凋亡的过程,这可能是NNAVC发挥抗白血病作用的机制之一。     

沙利度胺对人慢性粒细胞白血病细胞株K562细胞凋亡的影响研究

目的:研究沙利度胺对人慢性粒细胞白血病细胞株K562细胞凋亡的影响。方法:将K562细胞分为对照(未加药)组和沙利度胺低、中、高剂量(0·5、1·0、2·0mmol·L-1)组,加入相应药物分别作用24、48、72、96h后,MTT法检测各组细胞生长抑制率,Wright-Giemsa染色观察各组细胞形态变化,AnnexinⅤ-FITC/PI双染法流式细胞仪检测各组细胞凋亡率。结果:K562细胞的生长抑制率和凋亡率与沙利度胺浓度和作用时间均呈正相关;与对照组比较,沙利度胺3个剂量组作用72、96h后细胞的生长抑制率明显升高(P<0·05),4个时间点的细胞凋亡率均明显升高(P<0·01)。沙利度胺3个剂量组作用72h后,K562细胞出现细胞体积缩小等凋亡形态。结论:沙利度胺能够抑制K562细胞的增殖,呈一定的浓度和时间依赖性,并能够诱导K562细胞的凋亡。     

脂多糖与干扰素α联用诱导白血病U937细胞凋亡及其机制

目的：探讨Toll样受体配体内毒素脂多糖（LPS）与干扰素(IFN)-α联用对白血病U937细胞凋亡的作用及其机制。方法：将200 μg/L的LPS和（或）2000 U/mL的IFN-α作用于U937细胞,MTT检测细胞生长抑制率,流式细胞术（FCM）检测细胞凋亡率,半定量逆转录-聚合酶链反应(RT-PCR) 法检测作用48 h后U937细胞中caspase-8 mRNA的表达。结果：LPS与IFN-α联用较单用LPS、IFN-α能明显抑制U937细胞增殖、增加细胞凋亡率（P<0.01）,且各药物组较对照组均有统计学意义（P<0.01）。LPS与IFN-α联用作用48h后,caspase-8mRNA的表达水平较IFN-α组、LPS组和对照组升高（P<0.01）。结论：LPS与IFN-α联用能有效抑制白血病细胞的增殖并诱导其凋亡,其机制可能与caspase-8的激活有关。