心理干预在儿童功能性再发性腹痛治疗中的应用体会

[目的]探讨心理干预在儿童功能性再发性腹痛治疗中的作用。[方法]应用心理干预结合中药治疗儿童功能性再发性腹痛38例,并与单纯中药治疗30例进行对照分析。[结果]2组有效率比较,治疗组优于对照组,治疗组明显高于对照组(P<0·01)。[结论]心理干预结合中药治疗儿童功能性再发性腹痛疗效显著。     

自体角膜缘干细胞移植与新鲜羊膜移植治疗翼状胬肉临床比较

目的比较自体角膜缘干细胞移植和羊膜移植两种手术方法治疗翼状胬肉的临床效果。方法1组35例胬肉切除联合自体角膜缘干细胞移植,2组26例胬肉切除联合新鲜羊膜移植,术后随访3~24月,比较两种术式术后移植片反应和复发情况。结果1组病例术后7例(20%)1~2周内有结膜水肿增厚,1例(2·8%)12月内复发;2组病例术后12(46%)例出现结膜充血水肿,3例(11·8%)6月内复发;全部患者无术后睑球粘连。结论胬肉切除联合自体角膜缘干细胞移植或新鲜羊膜移植是治疗翼状胬肉的有效方法,可降低复发率,减少术后并发症。自体角膜缘干细胞移植效果更佳。     

1990-2004年上海地区临床分离大肠埃希菌耐药性变迁

目的 了解临床分离大肠埃希菌对抗菌药耐药性变迁情况。方法 对1990至2004年上海地区11所医院的细菌耐药监测资料中大肠埃希菌临床分离株的耐药性变迁情况进行分析，细菌药敏采用Kirby-Bauer法。结果 临床分离大肠埃希菌33495株对21种抗菌药药敏试验结果显示，该菌对大多常用抗菌药的耐药性在15年间呈上升趋势。对氨苄西林、哌拉西林的耐药率自69．0％和30．0％分别增至85．0％和71．4％。对头孢菌素类中的头孢唑啉（24．0％-48．3％）、头孢呋辛（18．0％-45．7％）、头孢克洛（33．3％-46．8％）的耐药率均增长，尤其是头孢噻肟的耐药率自1990年的6.0％增至2004年的35．2％。对氟喹诺酮类的耐药性15年间明显增高，且各品种间呈交叉耐药，自1990年的11．0％增至2004年的55．4％。对庆大霉素的耐药率缓慢上升（44．0％-54．0％）。大肠埃希菌对四环素、氯霉素、磺胺甲晤唑／甲氧苄啶（SMZ／TMP）耐药率始终较高。头孢他啶、头孢吡肟、亚胺培南、阿米卡星、β内酰胺类／β内酰胺酶抑制剂复方、呋喃妥因则保持了对大肠埃希菌的良好抗菌活性。产超广谱B内酰胺酶（ESBL）大肠埃希菌所占比例在2000-2004年间逐渐上升，自14．7％增至36．5％，产ESBL菌株耐药性均明显高于非产ESBL者。结论 临床分离的大肠埃希菌对常用抗菌药的耐药性在1990-2004年的15年间普遍呈明显增高趋势。 床分离的大肠埃希菌对常用抗菌药的耐药性在1990--2004年的15年间普遍呈明显增高趋势。     

核因子E2p45相关因子2基因在茶多酚调节结肠癌细胞尿苷二磷酸葡萄糖醛酸转移酶1A及其同工酶表达中的作用

目的探讨核因子E2p45相关因子2(Nrf2)基因在茶多酚中的主要化学物质epigallocatechin gallate(EGCG)诱导结肠癌细胞尿苷二磷酸葡萄糖醛酸转移酶(UGT)1A及其同工酶UGT1A8、UGT1A10表达中的调节作用。方法EGCG分别作用Caco-2及HT-29结肠癌细胞12h,逆转录聚合酶链反应(RT-PCR)检测基因表达水平的变化,免疫细胞化学及激光共聚焦显微镜观察细胞内Nrf2蛋白定位的改变。此外,利用RNA干扰技术抑制细胞内Nrf2基因的表达,观察阻断前后EGCG对基因表达水平影响的改变。结果(1)Caco-2及HT-29结肠癌细胞系、结肠癌及癌旁组织中UGT1A、1A8、1A10基因表达水平存在差异。(2)EGCG作用Caco-2及HT-29细胞后Nrf2、UGT1A、1A8、1A10表达升高1.8~9.2倍(均P<0.05),免疫细胞化学及激光共聚焦显微镜检测到Nrf2蛋白向细胞核内聚集。(3)酶切分析和测序证实成功构建了RNA干扰真核表达载体pSilence-Nrf2-A、B、C、D及随机序列对照pSilence-CON。(4)pSilence-Nrf2-B质粒转染可显著抑制Nrf2基因的表达,在Caco-2及HT-29细胞中抑制率分别为81.46%±1.68%及84.72%±2.08%(实验重复3次);稳定筛选建立的Nrf2低表达的细胞系Caco-2-siNrf2、HT-29-siNrf2,不仅基础UGT1A酶的表达水平降低,而且EGCG作用后酶诱导表达的作用消失。结论Nrf2基因参与了EGCG诱导UGT1A及其同工酶表达的过程并在其中起关键作用,为进一步论证EGCG在结肠癌化学预防中的作用及其可能的机制提供了新的论据。     

长期服抗精神病药病人的隐性运动障碍

目的：评估抗精神病药对迟发性运动障碍（ＴＤ）的掩盖,即隐性运动障碍（ｃｏｖｅｒｔ ｄｙｓｋｉｎｅ－ｓｉａ）状况。方法应用Ｓｉｍｐｓｏｎ运动障碍评分表评定ＴＤ。入组的６９例病人有２３例病人完成了减药之前、停药三周后和再服药四个月后的ＴＤ评定,６９例次检查都给于隶像,并且两个评定者按照录像独立评定ＴＤ是否存在,评定ＴＤ的一致性良好（ＩＣＣ＝０．７５）。结果完成整个调查的２３例病人中,减药前ＴＤ出现率为     

拉呋替丁鼠伤寒沙门氏菌基因回复突变试验

目的　体外观察拉呋替丁能否诱发鼠伤寒沙门氏菌组氨酸营养缺陷型突变株的回复突变。方法　Ames试验用TA97、TA98、TA10 0、TA10 2菌株并分加与不加肝微粒体酶活化系统( +/ -S9)试验。结果　拉呋替丁对四个菌株各剂量组的回复菌落数都未超过自然回复菌落数,Ames试验结果为阴性。结论　未见拉呋替丁致突变性。     

海洛因依赖性人格概念的建构及其与心理健康的关系

目的:了解海洛因依赖性人格的概念结构,建立海洛因依赖性人格量表。方法:对10 5名海洛因戒除者的海洛因依赖性人格问卷的测试数据进行验证性因素分析。结果:(1)海洛因依赖性人格由海洛因渴求感和戒除效能感两个维度构成,二维模型对样本数据的拟合度较好;(2 )海洛因渴求感α=0 .86 6 ,戒断效能感α=0 . 92 3,所有项目与所属因素因子分的相关系数在0. 6 81- 0 . 876之间,P <0 .0 0 1,两个分量表的相关系数r =- 0 4 4 2 ,P <0 . 0 0 1;(3)海洛因渴求感和戒除效能感与自尊、孤独、抑郁的相关系数的绝对值在0 . 2 2 1- 0. 5 11之间,达到显著性水平;回归分析的结果显示,戒断效能感可解释自尊、孤独和抑郁14 . 4 %、10 . 8%和2 6 . 2 %的变异。结论:海洛因依赖性人格的概念的构想合理,其量表具有良好的项目区分度、内部一致性信度和效度。     

从我院药品盘点工作的改进浅析医院药品的管理

运用医院电脑信息系统的盘点程序来进行药品盘点工作,使盘点准确率大大提高,为药剂科完成实时库存的管理打下了扎实的基础     

Metabolic activation of fluoropyrrolidine dipeptidyl peptidase-IV inhibitors by rat liver microsomes.

The current study evaluated the potential for two dipeptidyl peptidase-IV (DPP-IV) inhibitor analogs (1S)-1-(trans-4-([(4-trifluoromethoxyphenyl)sulfonyl]amino)cyclohexyl)-2-[(3S)-3-fluoropyrrolidin-1-yl]-2-oxoethanaminium chloride and (1S)-1-(trans-4-([(2,4-difluorophenyl)sulfonyl]amino)cyclohexyl)-2-[(3S)-3-fluoropyrrolidin-1-yl]-2-oxoethanaminium chloride (MRL-A and MRL-B), containing a fluoropyrrolidine moiety in the structure, to undergo metabolic activation. The irreversible binding of these tritium-labeled compounds to rat liver microsomal protein was time- and NADPH-dependent and was attenuated by the addition of reduced glutathione (GSH) or N-acetylcysteine (NAC) to the incubation, indicating that chemically reactive intermediates were formed and trapped by these nucleophiles. Mass spectrometric analyses and further trapping experiments with semicarbazide indicated that the fluoropyrrolidine ring had undergone sequential oxidation and defluorination events resulting in the formation of GSH or NAC conjugates of the pyrrolidine moiety. The bioactivation of MRL-A was catalyzed primarily by rat recombinant CYP3A1 and CYP3A2. Pretreatment of rats with prototypic CYP3A1 and 3A2 inducers (pregnenolone-16alpha-carbonitrile and dexamethasone) enhanced the extent of bioactivation which, in turn, led to a higher degree of in vitro irreversible binding to microsomal proteins (5- and 9-fold increase, respectively). Herein, we describe studies that demonstrate that the fluoropyrrolidine ring is prone to metabolic activation and that GSH or NAC can trap the reactive intermediates to form adducts that provide insight into the mechanisms of bioactivation.     

A mechanistic basis for the role of cycle arrest in the genetic toxicology of the dietary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP).

The heterocyclic amine 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), formed during the cooking of meat, induces tumors of the prostate, colon, and mammary gland when fed to rats. PhIP is readily absorbed and efficiently metabolized to a genotoxic derivative by CYP1 enzymes. Although metabolism and mutational potential of PhIP have previously been well characterized, the intervening cellular and genomic responses to the chemical are not fully understood. We have examined the cellular response to PhIP exposure in human mammary epithelial MCF10A cells, which retain characteristics of normal breast epithelial cells. Because these cells fail to activate PhIP, they were cocultured with a human lymphoblastoid cell line MCL-5, which constitutively expresses CYP1A1, and have been transfected to express human CYPs1A2, 2A6, 3A4, and 2E1. The MCL-5 cells were irradiated (2,000 rads) prior to coculture, rendering them unable to replicate yet still retaining metabolic competency. MCF10A cells were treated (in the presence of MCL-5 cells) with PhIP (1-100 microM) and harvested at various time-points. Compared to DMSO control, treatment (24 or 48 h) with PhIP resulted in a significant dose-dependent fall in cell number. Cells treated for 48 h then cultured in the absence of PhIP (and MCL-5 cells) for a further 6 days showed a much greater dose-dependent reduction in cell number. Flow cytometric analysis indicated that PhIP treatment (48 h) resulted in a dose-dependent accumulation of cells in the G1 population. Western blotting revealed elevated expression of p53 and the cyclin dependent kinase inhibitor p21WAF1/CIP1 after PhIP treatment. Levels of MDM2, a negative regulator of p53, and the hypophosphorylated form of RB were also elevated, consistent with the triggering of G1 cell cycle checkpoint. These cell cycle effects are critical, as they enable cells to effect genome repair, accept mutation, or eliminate excessively damaged cells.