黄连解毒汤加味治验四则

笔者自 2 0 0 1年 10月～ 2 0 0 2年 10月采用黄连解毒汤加味治疗流行性感冒 6例 ,急性扁桃体炎 14例 ,急性胃肠炎 3例 ,急性阑尾炎 2例 ,急性肺炎 3例。均收到满意疗效 ,今举验案四则 ,以资佐证。1　方药组成方由黄芩、黄柏、黄连、淡豆豉、栀子、麻黄、石膏 7味药组成。加减 :流行性感冒加荆芥、防风 ;急性扁桃体炎去麻黄、淡豆豉 ,加夏枯草、板蓝根 ;急性胃肠炎加神曲、砂仁 ;急性阑尾炎去石膏、麻黄、淡豆豉 ,加大黄、牡丹皮、厚朴 ;急性肺炎加鱼腥草。成人每日 1剂 ,分 3次煎服 ,儿童酌减。2　病案举例例 1　急性扁桃体炎　于某 ,女 ,4…     

睾丸表皮样囊肿继发睾丸畸胎瘤恶变一例报告

<正> 睾丸肿瘤多为恶性,良性仅占2～4％,睾丸表皮样囊肿罕见,而睾丸表皮样囊肿继发睾丸畸胎瘤恶变更为罕见,至今尚无报告。我们收治1例,报告如下。 患者,33岁。2年前左阴囊有轻微下坠感体检发现左睾丸肿大而于1988年10月第1次入院。查体:左睾丸内侧中部触及2.0cm×2.0cm×2.0cm肿物,质硬、光滑、无压痛。“B”超:左睾丸内侧探及1.5cm×1.5cm圆型低回声区,界限清楚。手术见睾丸内侧肿物有完整包膜,境界清楚,行单纯肿物摘除术。病理报告:睾丸表皮样囊肿。术后痊愈出院。18个月后再次发现左睾丸肿大,伴有坠痛感于1990年2月再次入院。体     

银染mRNA差异显示方法的建立和吗啡诱导基因的克隆

目的：建立非同位素银染ｍＲＮＡ差异显示方法，分离吗啡相关基因。方法：以吗啡处理的ＳＨＳＹ５Ｙ细胞中提取的总ＲＮＡ为模板，用５’ｄＴ１２ＭＧ锚定引物和两条随机引物组合进行ＤＤＲＴＰＣＲ扩增。经测序凝胶电泳分离后，用银染方法显示差异ＤＮＡ条带，在直视下从凝胶中回收差异条带并进行再扩增，扩增产物克隆入ｐＧＥＭＴ载体。结果：建立了非同位素的银染ｍＲＮＡ差异显示方法，分离和克隆了一些吗啡诱导的差异表达基因。结论：建立的非同位素银染差异显示方法是简单快捷和高效的分离差异表达基因的方法     

长时间给予高选择性μ激动剂抑制μ阿片受体基因表达

目的：观察长时间给予μ阿片受体肽类激动剂DAGO及非肽类激动剂OMF对μ受体基因表达的影响，并比较这两者作用的差异性。方法：采用反转录-聚合酶链反应（RT－PCR）方法。结果：（1）DAGO使μ受体mRNA水平显著降低，作用持续48h；而OMF作用只持续24h；（2）DAGO在10－8mol·L-1时即可使μ受体的mRNA水平显著降低，而OMF在10－7mol·L-1时才有效。结论：长时间给予肽类及非肽类μ激动剂均可以显著抑制μ受体的基因表达；DAGO作用较强，时程较长。     

电针刺激能诱发大鼠脊髓原癌基因c-fos的表达

原癌基因c-fos在中枢的表达被视为伤害性刺激的标志物。本文首次报道电针刺激亦可在大鼠脊髓诱发c-fos的表达。我们采用c-fos的蛋白产物Fos抗体的免疫反应活性(Fos-like immunoreactivity,FLI)来间接反映c-fos的表达。实验在雌性Wistar大鼠上进行。给予大鼠一侧后肢“三阴交”穴位100 Hz电针30分钟(1-3 mA),2小时后灌流、固定动物,取脊髓腰     

妊娠阑尾炎并发卵巢囊肿蒂扭转坏死1例报告

<正>1 病历摘要 患者女性,23岁。因右下腹痛2天于1994年6月13日入院。患者入院前2天无明显诱因,突发上腹部疼痛,后转移到右下腹部持续性疼痛,逐渐加重。伴恶心、呕吐、发热、恶寒、乏力、食欲不佳。二便正常。在当地治疗无好转而来我院。既往健康。停经3个月。查体:T36.6,P78,Bp12/8。一般情况好,急性病容。心、肺未见异常。下腹部轻度膨隆,右下腹部及下腹部肌紧张、压痛及反跳痛均存在。以右下腹部压痛、肌紧张、反跳痛更甚。结肠充气试验阳性,腰大肌试验阴性。无移动性浊音。WBC14.0×10~9, S0.79,L0.21,尿常规正常。B超报妊娠3个月。诊断妊娠合并阑尾炎。行阑尾切除术。术中见阑尾浆膜高度充血水肿,表面附有脓苔。术后病理回报:急性化脓性阑尾炎。术后病人腹痛未完全缓解。伴有腹胀、恶心,时有发热、恶寒,下腹部仍有压痛、肌紧及反跳痛。数次B超追踪观查提示腹腔内有10.3cm×8.0cm边界清楚之囊性肿物。经妇科会诊及消炎对症治疗无好转。再次手术探查,见右卵巢囊肿蒂扭转,卵巢囊肿大小约16.0cm×14.0cm,全囊襞发黑坏死,囊内吸出大量炎性液体。囊肿位于肠管后方,前襞全部被小肠肠管遮盖,部分粘     

美国国家卫生与医学博物馆的发展启示

美国国家卫生与医学博物馆（National Museum of Health and Medicine）隶属于武装部队病理学研究所，原名为军队医学博物馆，在美国是少数几个具有悠久历史的国家级博物馆之一。该馆成立于1862年，收藏和展出战争对人体创伤以及疾病的遗骸和文件档案。这个博物馆为法医学、人类学、病理学和军事医学提供了丰富的研究资料。解剖标本的收藏起着研究、展览、教育的作用，数百名国内外研究者来博物馆从事研究工作。     

白藜芦醇诱导前列腺癌细胞系PC-3凋亡的实验研究

目的探讨白藜芦醇（resveratroi，Res）诱导人前列腺癌细胞系PC-3凋亡及其机制。方法应用四甲基偶氮唑蓝（MTT）比色法、软琼脂集落生长试验和流式细胞术测定Res对PC-3的增殖抑制、集落生长抑制、周期阻滞和诱导凋亡作用，应用逆转录-聚合酶链反应（RT—PCR）方法检测对凋亡相关基因bcl-2和bax表达的影响。结果Res具有时间和剂量依赖性增殖抑制、G0／G1期阻滞和诱导凋亡作用，作用72hIC50为0．39g／L，Res0．1g／L作用2天对PC-3细胞集落生长抑制率为88．9％，Res0．5g／L作用2天G0／G1期细胞比例从42．30％增高至75．20％。Res可以下调beb2基因／蛋白，上调bax的表达。结论Res可能通过抑制PC-3细胞的集落生长、增殖抑制、G0／G1期阻滞、下调bcl-2基因，上调bax基因表达等作用机制诱导前列腺癌细胞凋亡。     

Effects of nuclear translocation of tissue transglutaminase and the release of cytochrome C on hepatocyte apoptosis

Objective To assess the effects of nuclear translocation of tissue transglutaminase (TTG) and the release of cytochrome C on hepatocyte apoptosis and to reveal the mechanism of signal transcluction of early apoptosis in injured hepatocytes.Methods Hepatocytes isolated from tissue transglutaminase gene knock-out mice and rats were stimulated with ethanol. Proteins from whole cell, cytoplasm and nuclei were extracted for determination of TTG activity by ^14C-putrescine incorporation. Distribution of TTG throughout the entire cell, as well as just nucleus was observed under a confocal scanning microscope. The amount of cytochrome C released from mitochonclria was determined by ELISA. Cell apoptosis was observed by fluorescent cytochemistry.Results TTG activity in whole cells and nuclei was significantly increased after the hepatocytes were treated with ethanol. Cytochrome C release was remarkably increased in the cells isolated from rat and wild-type mouse after treatment with ethanol but not in TTG gene knock-out mice. Cellular apoptosis appeared in hepatocytes isolated from rats and wild-type mice but not in the hepatocytes from TTG gene knock-out mice after stimulation with ethanol.Conclusions Increased TTG in hepatocytes can be translocated into the nucleus and promote release of mitochonclrial cytochrome C into the cytoplasm. Passing through a series of signal pathways, hepatocyte apoptosis is induced eventually.     

IDENTIFICATION OF SPECIFIC PEPTIDE LIGANDS FOR B-LYMPHOMA CELL AND ITS EFFECT ON TYROSINE PHOSPHORYLATION AND CELL APOPTOSIS

Objective To search novel method for diagnosis and therapy of B-lymphoma, specific small molecular peptide ligands against binding site of tumor cells were screened and its effects on signal transduction and cell apoptosis were tested. Methods Specific peptide hgands were screened by binding with site of human B lymphoma cell (OC1LY8) using peptide-bead libraries. The identified peptides were characterized with responsible cells by rebinding test. The role of tyrosine phosphorylation of peptide ligand was tested by Western blot;and its apoptosispromoting role was observed by confocal fluorescent microscope. Results Specific peptide ligand was able to bind specifically to site on cell surface and enter into cytoplasm. Tetrameric peptide ligand was able to strongly trigger signal transduction resulting in tyrosine phosphorylation and cellular apoptosis in OC1LY8 cell line. Conclusion Screened peptide ligand can effectively bind with OC1LY8 cell, stimulate cellular tyrosine phosphorylation and induce cellular apoptosis.