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，     

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。     

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。     

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—     

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。     

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。     

血小板源生生长因子刺激血管平滑肌细胞增殖及其分子机制

目的：探讨血小板源生生长因子（PDGF－BB）刺激血管平滑肌细胞（VSMC）增殖及其分子机制。方法：用Western Blot法测定p44/p42 CCDPK活性。[^3H]脱氧胸腺嘧啶核苷酸掺入测定VSMC DNA合成。原位杂交检测c-myc mRNA的表达。结果：PDGFBB诱导的磷酸化CCDPK蛋白表达和[^3H]脱氧胸腺嘧啶核苷酸掺入呈浓度依赖性,此作用可被PTK抑制剂Genistein,外钙络合剂依他酸和MEK抑制剂PD 98059抑制。PDGF－BB刺激可引起c-myc mRNA的明显表达,此作用可被PD 98059抑制。结论：PDGF－BB通过激活p44/p42 CCDPK,上调c-myc mRNA的表达从而促进VSMC增殖,其作用是由PTK和Ca^2 介导的。     

丝裂素活化的蛋白激酶反义寡核苷酸抑制表皮生长因子诱导体外 …

目的：探讨丝裂素活化的蛋白激酶（ＮＡＰＫ）反义寡核苷（ＯＤＮ）对表皮生长因子（ＥＧＦ）诱导的培养大鼠血管平滑肌细胞增生的抑制作用。方法：用脂质体将Ｐ４２－和Ｐ４４－ＭＡＰＫ ＯＤＮ０．２μｍｏｌˉＬ＾－１转染入大鼠血管平滑肌细胞，设正义及随机ＯＤＮ为对照，用Ｗｅｓｔｅｒｎ Ｂｌｏｔ法结合Ｐ－８１滤纸法以髓磷脂碱性蛋白为底物测定ＭＡＰＫ活性。［＾３Ｈ］胸腺嘧啶核苷酸掺入测定平滑肌细胞ＤＮＡ合成。结果     

缓激肽B2受体拮抗剂艾替班特降低卡托普和对培养新生大鼠心肌细胞 …

AIM: To study whether endogenous kinins are negative modulators in the growth of cardiomyocytes and their possible cellular and molecular mechanisms. METHODS: Cultured neonatal rat cardiomyocytes were used. Intracellular RNA and protein synthesis were measured by [3H]uridine incorporation and [3H]leucine incorporation, respectively. The expression level of proto-oncogene c-myc, c-fos mRNA was observed by Northern blotting. RESULTS: Exposure of cardiomyocytes to captopril (Cap, 100 mumol.L-1) for 48 h inhibited the rates of [3H]Urd and [3H]Leu incorporations by 25% and 26%, respectively, and for 2 h inhibited c-myc, c-fos mRNA expression by 75% and 55%, respectively. Treatment of angiotensin II (Ang II, 1 mumol.L-1) for 48 h significantly increased the rates of [3H]Urd and [3H]Leu incorporations and for 1 h induced c-myc, c-fos mRNA overexpression, which were reduced by pretreatment with Cap (100 mumol.L-1). Icatibant acetate (Hoe 140, a specific antagonist of bradykinin B2 receptor) 0.1-10 mumol.L-1 blocked the effects of Cap in a concentration-dependent manner. CONCLUSION: Endogenous kinins exhibited a negative modulatory effect on growth of cardiomyoctes via BK B2 receptor.     

Effects of berbamine on ATP-induced [Ca2+]i mobilization in cultured vascular smooth muscle cells and cardiomyocytes.

AIM: To study the effects of berbamine (Ber) on [Ca2+]i homeostasis induced by adenosine triphosphate (ATP) in vascular smooth muscle cells (VSMC) of rabbits and cardiomyocytes of rats. METHODS: Both cell types were cultured and loaded with Fura 3-AM. [Ca2+]i was measured by fluorescent intensity (FI) in each cell with confocal microscopy. RESULTS: (1) ATP 30 mumol.L-1 elevated [Ca2+]i in VSMC and cardiomyocytes, FI values reached 660 +/- 258 and 1058 +/- 252 from 250 +/- 84 and 218 +/- 76 at 19 s +/- 5 s and 11.8 s +/- 2.4 s, but FI in nucleus was not changed in VSMC. (2) Ber 30 mumol.L-1 did not affect the resting FI in both cell types, but prolonged the time to peak (P < 0.01) and reduced the FI elevated by ATP (P < 0.01), but not completely inhibited even at 100 mumol.L-1. (3) In D-Hanks' solution or in the presence of egtazic acid (EGTA) 3 mmol.L-1, the inhibitory effect of Ber was not seen (P > 0.05). (4) All effects of Ber on ATP-induced [Ca2+]i mobilization were similar to those of Ver 10 mumol.L-1. CONCLUSION: In VSMC and cardiomyocytes, ATP-induced CA2+ influx was inhibited by Ber and Ver, while the Ca2+ release was not.     

丝裂素活化蛋白激酶反义寡核苷酸对血管紧张素Ⅱ诱导的大鼠心肌？…

AIM: To investigate the inhibitory effect of down-regulating mitogen activated protein kinase (MAPK) on c-myc gene expression and further on cardiac fibroblast proliferation. METHODS: Cultured neonatal rat cardiac fibroblasts was pretreated with a phosphorothioate-protected 17-mer antisense MAPK oligodeoxynucleotide (ODN) directed against the initiation of translation sites of the p42 and p44 MAPK isoforms by liposomal transfection. A 17-mer sense and mismatch sequence MAPK ODN were used as controls. After liposomal transfecting, cells were exposed to angiotensin II (Ang II) 10 nmol.L-1 for 5 min and then harvested in lysis buffer. MAPK activity was measured by Western blot and P-81 phosphocellulose filter paper method by using [gamma-32P]ATP and myelin basic protein as substrates. c-myc mRNA expression stimulated by Ang II for 30 min was measured by Northern blot. DNA synthesis and collagen protein synthesis induced by Ang II for 24 h were measured by [3H]thymidine incorporation and [3H]Proline incorporation, respectively. RESULTS: Antisense ODN 0.2 mumol.L-1 reduced Ang II-induced MAPK activities by 72%, MAPK protein expression by 80%, and suppressed c-myc mRNA expression by 97%, respectively. [3H]thymidine incorporation and [3H]proline incorporation in Ang II-induced cardiac fibroblast were inhibited by 59% and 58%, respectively. CONCLUSION: A 17-mer MAPK antisense oligonucleotide directed againsts the initiation of translation sites of MAPK could specifically inhibit Ang II-stimulated cultured neonatal rat cardiac fibroblast proliferation through down-regulating MAPK activity and further depleting c-myc mRNA expression.     

糖基化终产物对培养的大鼠主动脉平滑肌细胞增殖及胞浆游离钙含…

目的：研究糖基化终产物（ＡＧＥＰ）对主动脉平滑肌细胞增殖的影响及其与［Ｃａ＾２＋］ｉ的关系。方法：采用同位素掺入法分别测定ＤＮＡ和蛋白质合成；Ｆｕｒａ２－ＡＭ测定［Ｃａ＾２＋］ｉ。结果：ＡＧＥＰ以浓度、时间相关的方式促进［＾３Ｈ］ＴｄＲ与［＾Ｈ］Ｌｅｕ掺入细胞，随ＡＧＥＰ作用时间、糖化时间延长，掺入率增加明显，ＡＧＥＰ增加［Ｃａ＾２＋］ｉ，与时间、浓度相关，但随ＡＧＥＰ作用时间延长（４０分钟后）而     

酪氨酸激酶参与α1A肾上腺素受体介导的人胚胎肾细胞浆游离？…

AIM: To determine the role of protein-tyrosine kinase (PTK) in alpha 1A-adrenoceptor-mediated increase of [Ca2+]i (intracellular calcium) in human embryo kidney (HEK) 293 cells expressed alpha 1A-adrenoceptor. METHODS: Effects of two PTK inhibitors: genistein and tyrphostin, were investigated on the increase of [Ca2+]i by using Fura-2, The activity of PTK was measured and the accumulation of [3H] InsPs were observed. RESULTS: Norepinephrine stimulated a rapid increase in [Ca2+]i to (371 +/- 31) nmol.L-1 in HEK 293 cells. Norepinephrine-induced increase of [Ca2+]i was inhibited by the tyrosine kinase inhibitors quercetin and tyrphostin by 23.8% and 21.4%, respectively, but the accumulation of [3H]InsPs induced by norepinephrine was not. The activity of the plasma-associated tyrosine kinase was increased to (1.73 +/- 0.72)-fold over the control by norepinephrine 10 mumol.L-1. The norepinephrine-activated PTK was inhibited by calphostin C and depletion of intra- and extra-cellular Ca2+. CONCLUSION: The PTK participates in mobilization of Ca2+ mediated by alpha 1A-adrenoceptors in HEK 293 cell lines.     

小檗碱对培养大鼠神经细胞内游离Ca^2＋的影响

以Ｆｕｒａ２／ＡＭ为细胞内钙离子的荧光指示剂，用ＡＲＣＭＭＩＣ阳离子测定系统，直接测定了体外培养的新生大鼠神经细胞内游离钙（［Ｃａ２＋］ｉ）值，并观察了小檗碱（Ｂｅｒ）的影响。结果表明，Ｂｅｒ对神经细胞静息［Ｃａ２＋］ｉ无明显影响，Ｂｅｒ１～１００μｍｏｌ·Ｌ－１能剂量依赖地抑制去甲肾上腺素和Ｈ２Ｏ２引起的［Ｃａ２＋］ｉ升高，其ＩＣ５０分别为３９．９和１７．９μｍｏｌ·Ｌ－１。高剂量Ｂｅｒ（１０～１００μｍｏｌ·Ｌ－１）能抑制高Ｋ＋引起的［Ｃａ２＋］ｉ升高。姐果提示，Ｂｅｒ对去甲肾上腺素，高Ｋ＋及Ｈ２Ｏ２引起的［Ｃａ２＋］ｉ升高的抑制作用可能是其抗脑缺血作用机制之一。