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。     

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。     

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。     

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。     

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，     

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—     

茶叶提取的咖啡因的重金属和易炭化物的检查法

我国茶叶资源丰富，利用茶叶生产的下脚料提取天然咖啡因满足国际市场需要的厂家越来越多。该产品出口一般要求符合美国药典22版规定，而从茶叶中提取的天然咖啡因，由于条叶色素的影响，带有淡黄绿色，在检查重金属和易炭化物时影响比色，易错判结果。对此我们做了一些消除试验，以保证判断的准确性。现将实验结果报告于下。1．重金属检查：美国药典22版咖啡团的重金属限度为0．001％［1］，在检查实验中，由于供试品带有淡黄绿色，使得供试液与对照液的颜色不一致。焦糖溶液也无法把两种溶液的颜色调节接近，使限度检查难于进行。故拟以下…     

语言的可听度与稳定度的适用的原则

语言的可听度与稳定度的适用的原则阮前英编译（北京铁路总医院耳鼻喉科北京市１０００３８）科研人员付出了巨大努力，制定出满足于适合耳聋患者听力的助听设备的适用原则。这个原则已经与多种助听设备的适用原则十分接近。目前存在的较流行的助听设备适用原则，只是适用...     

药师是专业的、可爱的、快乐的

常有人问我,你的职业是什么?我总是自豪的回答:我是一名医院药师.一提到药师,人们自然会想到神农披荆斩棘遍尝百草;想到药王孙思邈大医精诚,普救众生;想到李时珍辨疑正误,精修本草.这些先辈先哲给我们留下了宝贵的财富.而作为今天的药师,我们肩负着怎样的历史使命呢?     

Effect of 3,6-dimethamidodibenzopyriodonium citrate on Ca2+ in rabbit platelet in vitro.

AIM: To study the effect of 3,6-dimethamidodibenzopyriodonium citrate (I-65) on the cytoplasmic free Ca2+ ([Ca2+]i) concentration in rabbit platelet. METHODS: Measurement of the cytosolic Ca2+ of platelets in vitro by using Quin 2-AM fluorescence technique. RESULTS: In the presence of CaCl2 1 mmol.L-1, I-65 (10, 20, and 30 mumol.L-1) reduced the rise in [Ca2+]i induced by thrombin and calcimycin from 142 +/- 22 nmol.L-1 and 124 +/- 18 nmol.L-1 to 118 +/- 20, 78 +/- 12, 40 +/- 10 nmol.L-1, respectively and 108 +/- 15, 77 +/- 14, 37 +/- 14 nmol.L-1, respectively. In the presence of egtazic acid 2 mmol.L-1, I-65 (10, 20, and 30 mumol.L-1), reduced the Ca2+ release induced by thrombin from 52 +/- 11 nmol.L-1 to 34 +/- 9, 19 +/- 6, and 11 +/- 5 nmol.L-1, respectively. In addition, I-65 (10, 20, and 30 mumol.L-1) also reduced the Ca2+ influx induced by thrombin from 91 +/- 13 nmol.L-1 to 84 +/- 15, 58 +/- 15, and 28 +/- 19 nmol.L-1, respectively. CONCLUSION: I-65 inhibited not only the Ca2+ release, but also the influx of Ca2+ in activation platelet.     

血小板释放的ADP通过稳定细胞内钙浓度而稳定PAF诱导的兔血小板 …

AIM: To examine whether platelet-released adenosine diphosphate (ADP) would contribute to the stabilization of rabbit platelet aggregation induced by platelet activating factor (PAF). METHODS: Rabbit platelet aggregation induced by PAF was measured turbimetrically. ADP release from rabbit platelets stimulated by PAF was determined by HPLC. Intracellular Ca2+ was measured using Ca(2+)-sensitive fluorescent indicator Fura 2-AM. RESULTS: PAF > or = 1 nmol.L-1 induced full platelet aggregation, which did not deaggregate over 5 min after aggregation reached peak. Platelet aggregation was deaggregated in a concentration-dependent manner by subsequent addition of ADP scavenger ATP-diphosphohydrolase (apyrase) at 5-100 mg.L-1. PAF 3 nmol.L-1 stimulated release of ADP (29% vs 6% of control), and elicited a rapid rise in intracellular calcium ([Ca2+]i) which peaked at approximately 15 s. Then the [Ca2+]i gradually decayed from 585 +/- 80 nmol.L-1 within 100 s to a low level (364 +/- 82 nmol.L-1). Apyrase 100 mg.L-1, added 2 min after PAF, reduced [Ca2+]i to a lower level (171 +/- 29 nmol.L-1). CONCLUSION: Platelet-released ADP stabilizes PAF-induced rabbit platelet aggregation by stabilizing [Ca2+]i at elevated level.     

普鲁托品对兔血小板内钙的影响

AIM: To study the influence of protopine (Pro) on the cytoplasmic free Ca2+ concentration ([Ca2+]i) in rabbit platelets. METHODS: Measurement of [Ca2+]i of platelets in vitro by Fura 2-AM fluorescence technique. RESULTS: In the presence of CaCl2 1 mmol.L-1, Pro 10, 20, and 40 mumol.L-1 attenuated the rise in [Ca2+]i evoked by ADP from (420 +/- 57) to (320 +/- 26), (264 +/- 21), and (180 +/- 14) nmol.L-1, respectively, by arachidonic acid (AA) from (280 +/- 36) to (210 +/- 17), (184 +/- 21), and (143 +/- 16) nmol.L-1, respectively, and by platelet-activating factor (PAF) from (350 +/- 42) to (282 +/- 31), (223 +/- 30), and (165 +/- 15) nmol.L-1, respectively. In the presence of egtazic acid 1 mmol.L-1, Pro 10, 20, and 40 mumol.L-1 reduced the Ca2+ release induced by ADP, AA, and PAF, respectively. Pro 10, 20, and 40 mumol.L-1 also decreased ADP-, AA-, and PAF-induced Ca2+ influx. CONCLUSION: Pro inhibited not only Ca2+ release but also the influx of Ca2+.     

Characterization of endothelin receptors in the anesthetized ferret: a novel model for investigating the functional ET(B) receptor subtypes.

The pharmacology of endothelin (ET)-1, big ET-1, ET-3, and S6c were characterized in the anesthetized ferret to assess whether this species would provide a new and suitable nonrodent model to be used in characterization of endothelin antagonists. Unlike other species such as dog, rabbit, and rat, the ferret exhibited a dose-dependent pressor response to both ET-1 and big ET-1 with no preceding vasodilatory response. The median effective concentration (ED50) values were 0.047+/-0.009 and 0.469+/-0.003 nmol/kg for ET-1 and big ET-1, respectively. ET-3 and S6c, however, were found to elicit a transient vasodilatory response preceding the pressor response, with ED50 values of 0.23+/-0.09 and 0.18+/-0.03 nmol/kg, respectively. The rank potency of the agonists for the pressor response was found to be ET-1 > S6c > big ET-1 > ET-3. The ET(A)-specific antagonist BQ-123 was shown to block only partially the ET-1 and big ET-1 pressor response with median antagonistic dose (AD50) of 0.24+/-0.11 and 0.015+/-0.005 mg/kg, i.v., respectively, and blockade of the ET(A) receptor did not uncover an ET(B)-induced vasodilation. The dual ET(A/B) antagonist L-754,142 completely antagonized the ET-1 and big ET-1 pressor responses with AD50 values of 0.195+/-0.063 and 0.019+/-0.006 mg/kg, respectively. The ET(B) antagonist BQ-788 blocked the depressor response of S6c entirely but was unable to antagonize the pressor response completely. BQ-123 was shown to antagonize the S6c pressor response partially, suggesting a possible interaction between the ET(A) and ET(B) receptors in the ferret. The unexpected absence of an ET-1-mediated depressor response but the presence of ET-3 and S6c vasodilation in this species supports the theory that there may be subtypes of the ET(B) receptor. These studies demonstrate that the anesthetized ferret provides a suitable model for assessing the physiological potencies of the endothelins and may provide a tool for further understanding of the diversity of the ET(B) receptor.     

cGMP介导以注入L—精氨酸诱导的大鼠血管加压素释放效应

目的：探讨ｃＧＭＰ是否介导Ｌ－精氨酸（一氧化氮合酶物）引起的血管加压素（ＡＶＰ）释放增多效应。方法：用放射免疫法测定大鼠血浆中ＡＶＰ水平。结果：侧脑室分别注射Ｌ－精氨酸和８－溴－ｃＧＭＰ（一种可透过膜的ｃＧＭＰ衍生物）能刺激血浆ＡＶＰ水平增加［分别从（３．２±０．５）升至（５．８±１．４）ｎｇ·Ｌ＾－１，从（２．６±０．３）升至６６．６±０．４）ｎｇ·Ｌ＾－１，Ｐ〈０．０１］，同时注射Ｌ－精氨酸和     

眼镜蛇毒因子对大鼠血小板的激活作用(英文)

目的:研究补体激活剂眼镜蛇毒因子(CVF)对大鼠血小板的作用及其细胞机制。方法:比浊法测富血小板血浆内血小板聚集并同步记录ATP释放;生色底物法测血小板表面凝血酶原酶活性;用钙离子荧光指示剂Fura-2 AM负载血小板测细胞内游离钙;放免法测细胞内cAMP含量。结果:CVF在19.5-617nmol·L~(-1)范围内浓度依赖性地诱导血小板聚集和ATP释放,195nmol·L~(-1)诱导的ATP释放不依赖于聚集,且明显弱于凝血酶1U/ml的作用。CVF195nmol·L~(-1)时间依赖性地增加血小板表面凝血酶原酶活性。抗血小板膜糖蛋白Ⅰb/Ⅸ、Ⅲa、Ⅱb的单克隆抗体SZ-1、SZ-21、SZ-22抑制CVF诱导的血小板聚集。CVF 195nmol·L~(-1)使血小板内游离钙从静息态的(141±46)nmol·L~(-1)升高到(240±64)nmol·L~(-1),在61.7-617nmol·L~(-1)范围内轻度降低血小板内的cAMP。结论:补体激活剂CVF能诱导大鼠血小板聚集、ATP释放,增加血小板表面凝血酶原酶活性,其激活血小板的作用与血小板表面纤维蛋白原受体及血小板内游离钙升高、cAMP下降有关。     

蛋白酪氨酸磷酸化在血小板激活因子诱导血小板信号传导中的调节 …

AIM: To study the role of protein tyrosine phosphorylation (PTP) in platelet activating factor (PAF)-induced platelet signal transduction cascade. METHODS: Washed rabbit platelets were used to test the inhibitory effect of genistein (Gen) on platelet aggregation and serotonin secretion. Intracellular Ca2+ ([Ca2+]i) and pH (pHi) were measured by a dual wavelength fluorophotometer with Fura 2-AM and BCECF-AM. PTP was determined with a specific anti-phosphotyrosine monoclonal antibody by Western blotting. RESULTS: Pretreatment with Gen (100 and 200 mumol.L-1) inhibited PAF (20 nmol.L-1)-stimulated platelet serotonin release by 23.7% +/- 2.0% and 41% +/- 8%, respectively. Similar inhibitory effects of Gen were observed on PAF-evoked increase of [Ca2+]i and intracellular alkalization. PAF also elicited a pronounced increase in PTP of several bands with M(r) 70,000, 60,000, 50,000, 42,000/40,000, and 34,000, which were suppressed markedly by Gen 200 and 400 mumol.L-1. Pretreatment with staurosporine (Sta) 20 nmol.L-1, BAPTA 200 mumol.L-1, and egtazic acid 2 mmol.L-1 to inhibit PKC activation, [Ca2+]i elevation, and Ca2+ influx respectively, also showed an inhibitory effects on the formation of PTP. CONCLUSION: PTP is involved in multiple signal transduction pathways induced by PAF, on which PKC activation and calcium mobilization play a regulatory role.     

Cell proliferation and Ca(2+)-calmodulin dependent protein kinase activation mediated by alpha 1A- and alpha 1B-adrenergic receptor in HEK293 cells

AIM: To examine the ability of alpha 1-AR subtypes on proliferation and Ca(2+)-calmodulin dependent protein kinase (CCDPK, formerly called MAPK) activation in transfected human embryo kidney 293 (HEK293) cells. METHODS: pREP8/alpha 1A-AR, pREP4/alpha 1B-AR, and pREP9/alpha 1D-AR were transfected, respectively, into HEK293 cells by calcium phosphate precipitation. The expression of alpha 1-AR was detected by radioligand binding assays. DNA synthesis was measured by [3H]thymidine incorporation. CCDPK activity was determined by immunoprecipitation method and myelin basic protein was used as substrate. RESULTS: Three clonal HEK293 cell lines stably expressing alpha 1A- or alpha 1B- or alpha 1D-AR were chosen and characterized by radioligand binding assay with receptor densities of about 0.6 nmol.g-1. Treatment with norepinephrine (NE) in the presence of propranolol for 24 h increased DNA synthesis in HEK293/alpha 1A- or HEK293/alpha 1B-AR cells concentration-dependently, with EC50 values of 48.8 nmol.L-1 (95% confidence limits 9.7-246 nmol.L-1) and 8.4 nmol.L-1 (95% confidence limits 2.1-32.9 nmol.L-1), respectively. The increase of DNA synthesis induced by NE 10 mumol.L-1 was 201% +/- 28% and 269% +/- 44% of basal, and the activation of CCDPK was 171% +/- 84% and 292% +/- 92% of basal in HEK293/alpha 1A-AR and HEK293/alpha 1B-AR cells, respectively. Preincubation with prazosin completely abolished NE-induced CCDPK activation in HEK293/alpha 1A- and alpha 1B-AR cells. Those changes were not found in HEK293/alpha 1D-AR cells. CONCLUSION: The activation of alpha 1A- or alpha 1B-AR but not alpha 1D-AR induces cell proliferation.