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.     

川芎嗪和维拉帕米纠正阿霉素对小鼠艾氏腹水癌的抗药性

阿霉素(adriamycin,ADR)广泛应用于肿瘤临床,但易产生抗药性及多药抗药性(multidrug resistance,MDR),从而限制了其临床疗效的发挥。MDR与细胞表型改变有关。抗ADR的人乳腺癌细胞和小鼠SEWA癌细胞内,谷胱甘肽-S-转移酶(GST)的活性增高。ADR的MDR可被钙拮抗剂逆转,但是否与GST有关尚未见报道。     

Potent Vinblastine C20′ Ureas Displaying Additionally Improved Activity Against a Vinblastine-Resistant Cancer Cell Line

相似文献   

Inhibition of P-glycoprotein by natural products in human breast cancer cells

Multidrug resistance (MDR) is one of the most significant obstacles in cancer chemotherapy. One of the mechanisms involved in the development of MDR is the over-expression of P-glycoprotein (P-gp). It is widely known that natural compounds found in vegetables, fruits, plant-derived beverages and herbal dietary supplements not only have anticancer properties, but may also modulate P-gp activity. Therefore, the purpose of this investigation was to examine the effects of naturally occurring products on P-gp function in human breast cancer cell lines, MCF-7 (sensitive) and MCF-7/ADR (resistant). The accumulation of daunomycin (DNM), a P-gp substrate, was greater in the sensitive cells compared to the resistant cells, while the efflux of DNM was higher in the resistant cells compared to the sensitive cells over a period of 2 h. The IC50 value of DNM in the resistant cells was about 22 times higher than that in the sensitive cells, indicating an over-expression of P-gp in the resistant cells, MCF-7/ADR. All of the compounds tested, with the exception of fisetin, significantly decreased the IC50 value of DNM. Biochanin A showed the greatest increase in [3H]-DNM accumulation, increasing by 454.3 +/- 19.5% in the resistant cells, whereas verapamil, the positive control, increased the accumulation by 229.4 +/- 17.6%. Also, the accumulation of [3H]-DNM was increased substantially by quercetin and silymarin while it was reduced by fisetin. Moreover, biochanin A, silymarin, and naringenin significantly decreased DNM efflux from MCF-7/ADR cells compared with the control. These results suggest that some flavonoids such as biochanin A and silymarin may reverse MDR by inhibiting the P-gp function.     

Characterization of a Chinese hamster ovary cell line with acquired resistance to the bisdioxopiperazine dexrazoxane (ICRF-187) catalytic inhibitor of topoisomerase II

A Chinese hamster ovary (CHO) cell line highly resistant to the non-cleavable complex-forming topoisomerase II inhibitor dexrazoxane (ICRF-187, Zinecard^®) was selected. The resistant cell line (DZR) was 1500-fold resistant (IC₅₀ = 2800 vs 1.8 μM) to continuous dexrazoxane exposure. DZR cells were also cross-resistant (8- to 500-fold) to other bisdioxopiperazines (ICRF-193, ICRF-154, and ICRF-186), and somewhat cross-resistant (4- to 14-fold) to anthracyclines (daunorubicin, doxorubicin, epirubicin, and idarubicin) and etoposide (8.5-fold), but not to the other non-cleavable complex-forming topoisomerase II inhibitors suramin and merbarone. The cytotoxicity of dexrazoxane to both cell lines was unchanged in the presence of the membrane-active agent verapamil. DZR cells were 9-fold resistant to dexrazoxane-mediated inhibition of topoisomerase II DNA decatenation activity compared with CHO cells (IC₅₀ = 400 vs 45 μM), but were only 1.4-fold (IC₅₀ = 110 vs 83 μM) resistant to etoposide. DZR cells contained one-half the level of topoisomerase II protein compared with parental CHO cells. However, the specific activity for decatenation using nuclear extract topoisomerase II was unchanged. Etoposide (100 μM)-induced topoisomerase II-DNA complexes in DZR cells and isolated nuclei were similarly one-half the level found in CHO cells and in isolated nuclei. However, the ability of 500 μM dexrazoxane to inhibit etoposide (100 μM)-induced topoisomerase II-DNA covalent complexes was reduced 4- to 6-fold in both DZR cells and nuclei compared with CHO cells and nuclei. In contrast, there was no differential ability of aclarubicin or merbarone to inhibit etoposide-induced topoisomerase II-DNA complexes in CHO compared with DZR cells and isolated nuclei. It was concluded that the DZR cell line acquired its resistance to dexrazoxane mainly through an alteration in the topoisomerase II target.     

Effects of psoralen from <Emphasis Type="Italic">Psoralea corylifolia</Emphasis> on quinone reductase,ornithine decarboxylase,and JB6 cells transformation promotion

The cancer chemopreventive effect of psoralen isolated from the seeds of Psoralea corylifolia was investigated in the induction of quinone reductase (QR) activity, intracellular detoxification enzyme, inhibition of 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced ornithine decarboxylase (ODC) activity, a key regulatory enzyme for polyamine metabolism, and tumor promotion in mouse epidermal JB6 cells, sensitive to tumor promoters (clone 415a P+ cells), which are related to suppress multistage carcinogenesis including initiation and promotion. Psoralen was isolated and identified from the ethyl acetate-soluble fraction of the methanolic extract from the seeds. Psoralen was active in induction of QR activity, the concentration of psoralen required to induce 1.5 fold QR activity was 14.8 μg/mL. Also, this pure compound inhibited TPA-induced ODC activity by 50% (designated IC₅₀) at the concentration 15.6 μg/mL and exhibited inhibition of TPA-induced tumor promotion in mouse epidermal JB6 cells with an IC₅₀ value of 17.1 μg/mL. Therefore, it is extrapolated that psoralen has the potential capable of inhibiting the initiation and/or promotion stage of carcinogenesis by induction of QR activity, inhibition of TPA-induced ODC activity and mouse epidermal JB6 cells tumor promotion.     

干扰素与维拉帕米逆转乳腺癌细胞耐药作用的研究

目的:研究α-干扰素与维拉帕米对体外培养的乳腺癌细胞多药耐药(MDR)的逆转作用。方法:以对药物敏感的人乳腺癌细胞系MCF-7和经阿霉素(ADM)诱导具有MDR表型的人乳腺癌耐药细胞系MCF-7/ADR为体外试验模型,分别单用及联用α-干扰素与维拉帕米对细胞系进行处理,MTT法检测各组细胞存活率,计算半数抑制浓度(IC50)、耐药倍数和逆转倍数;流式细胞术定量检测细胞表面P-170的表达。结果:α-干扰素与维拉帕米联用后使乳腺癌细胞耐ADM的IC50降低为0.32μmol·L-1,优于二者单用(2.29、1.23μmol·L-1),逆转倍数升高到51.88(二者单用为7.25、13.49),P-170表达低于二者单用。结论:单独应用α-干扰素、维拉帕米均可达到部分逆转MCF-7/ADR对ADM的耐药作用,但二者联用效果更强。     

Effects of verapamil enantiomers and major metabolites on the cytotoxicity of vincristine and daunomycin in human lymphoma cell lines

Summary Verapamil, a calcium channel blocker, is used as the racemate. Recently, racemic verapamil has been shown to increase the cytotoxicity of vinca alkaloid and anthracycline derivatives in several resistant tumour cell lines. With respect to its cardiovascular activity S-verapamil is an order of magnitude more potent than R-verapamil. Since it was not known whether the effect on multidrug resistance was also enantioselective a comparison has been made of the potency of the R and S enantiomers and racemic verapamil in their ability to increase the cytotoxicity of vincristine and daunomycin in sensitive (MOLT 4B) and drug resistant human T-lymphoma cell lines (MOLT/VCR-5×9, MOLT/DAU-8 and VCR 1000, a highly resistant subline of CCRF-CEM). Two major metabolites, norverapamil and D617 were tested in the same system.(+)-R, (–)-S-, racemic verapamil, norverapamil and D617 alone had no effect on cell growth in sensitive or resistant cell lines in concentrations up to 20 M. In combination with vincristine, verapamil and norverapamil but not D617 produced a concentration dependent increase in the sensitivity of the resistant lines. Racemic verapamil, its individual enantiomers and norverapamil were equipotent. The concentration of the modifiers required to elicit 50% of the maximum effect (EC₅₀) was of the order of 0.5 M. No significant difference in the slopes of the concentration-effect curves were observed. The effect of verapamil and norverapamil was additive. In the sensitive MOLT 4B cell line both enantiomers and norverapamil increased sensitivity towards vincristine. However, the EC₅₀ values were at least an order of magnitude higher (2.5–8 M) than in the resistant cell lines. In contrast to the vincristine resistant cell lines, no effect on the potentiation of daunomycin cytotoxicity was observed in sensitive and daunomycin-resistant cells in the presence of a modifier. Since the activity of verapamil as a modifier of drug resistance is not enantioselective, the weaker calcium antagonist R-enantiomer appears to be better suited for clinical trials. Because of its lesser cardiovascular activity much higher doses could be given, and a higher plasma concentration would be achieved. As norverapamil, the major plasma metabolite formed during first pass elimination, is as potent as the parent drug as a modifier of drug resistance, the oral route of administration is preferable to i. v. administration in clinical trials employing R-verapamil as a modifier.Presented in part at the 30^th Spring Meeting of the Deutsche Gesellschaft für Pharmakologie und Toxikologie, Mainz, 1989, and at the IV. World Conference on Clinical Pharmacology and Therapeutics, Mannheim-Heidelberg, 1989     

Novel Quinazoline Derivatives Bearing Various 4‐Aniline Moieties as Potent EGFR Inhibitors with Enhanced Activity Against NSCLC Cell Lines

A class of novel quinazoline derivatives bearing various C‐4 aniline moieties was synthesized and biologically evaluated as potent epidermal growth factor receptor (EGFR) inhibitors for intervention of non‐small‐cell lung cancer (NSCLC). Most of these inhibitors are comparable to gefitinib in inhibiting these cancer cell lines, and several of them even displayed superior inhibitory activity. In particular, analogue 5b with an IC₅₀ of 0.10 μm against the EGFR wild‐type A431 cells and 5c with an IC₅₀ of 0.001 μm against the gefitinib‐sensitive HCC827 cells (EGFR del E746‐A750) was identified as highly active EGFR inhibitors. It was also significant that the discovered analogue 2f , not only has high potency against the gefitinib‐sensitive cells (IC₅₀ = 0.031 μm ), but also possesses remarkably improved activity against the gefitinib‐resistant cells. In addition, the enzymatic assays and the Western blot analysis for evaluating the effects of the typical inhibitors indicated that these molecules strongly interfere with the EGFR target.     

Antitumor activity and antioxidant property of Curcuma caesia against Ehrlich’s ascites carcinoma bearing mice

Abstract

Context: Curcuma caesia Roxb. (Zingiberaceae), commonly known as “Kala Haldi” in Bengali, has been traditionally used for the treatment of cancer, bruises, inflammation and as an aphrodisiac.

Objective: To evaluate the antitumor activity and antioxidant status of the methanol extract of Curcuma caesia (MECC) rhizomes on Ehrlich’s ascites carcinoma (EAC)-treated mice.

Materials and methods: In vitro cytotoxicity assay of MECC was evaluated by using Trypan blue method. Determination of in vivo antitumor activity was performed after 24?h of EAC cells (2?×?10⁶?cells/mouse) inoculation; MECC (50 and 100?mg/kg i.p.) was administered daily for nine consecutive days. On day 10, half of the mice were sacrificed and the rest were kept alive for assessment of increase in lifespan. Antitumor effect of MECC was assessed by the study of tumor volume, tumor weight, viable and non-viable cell count, hematological parameters and biochemical estimations. Furthermore, antioxidant parameters were assayed by estimating liver and kidney tissue enzymes.

Results: MECC showed direct cytotoxicity (IC₅₀ 90.70?±?8.37?μg/mL) on EAC cell line. MECC exhibited significant (p?<?0.01) decrease in tumor volume, tumor weight, viable cell count and percentage increased the lifespan (57.14 and 88.09%) of EAC-treated mice. Hematological profile, biochemical estimation, tissue antioxidant assay significantly (p?<?0.01) reverted to normal level in MECC-treated mice.

Conclusion: MECC possesses potent antitumor activity that may be due to its direct cytotoxic effect or antioxidant properties. Further research is in progress to find out the active principle(s) of MECC for its antitumor activity.     

屈洛苷芬对K562耐阿霉素细胞株耐药性的逆转作用

目的：研究屈洛昔芬（DRO）对耐阿霉素（ADR）K562细胞株（K562／A02)多药耐药性（MDR）的逆转作用及逆转机制。方法：用DRO分别处理K562／A02和K562敏感株。MTT法观察DRO影响K562／A02对ADR化学敏感性的变化。DRO 10μmol/L处理K562／A02前后,通过RT－PCR和免疫细胞化学染色,分析MDR1、GSTπ基因表达的变化,采用流式细胞技术测定细胞内ADR浓度的变化。结果：DRO显著逆转K562／A02的MDR,在20,10和5μmol/L浓度时,对ADR的化学敏感性分别增加到14、13和4倍,逆转活性与维拉帕米相当。MDR1和GSTπ的mRNA和蛋白表达在DRO 10μmol/L处理后第2天开始下降,第5天明显降低。用20、10和5μmol/L浓度的DRO处理两株细胞,K562／A02细胞内ADR积累分别增加到2．9、2．3和1．5倍。但DRO不能明显增加K562细胞内的ADR的浓度。结论：DRO对K562／A02的MDR有较强的逆转活性,逆转强度与维拉帕米相当,其逆转机制有多种不同的途径。