关注阿片类急性中毒的抢救

阿片依赖者常常循环于戒毒--复吸--再戒毒--再复吸的怪圈之中,在强烈"渴求"的支配下,经常过量用药而发生急性中毒事件,若得不到及时抢救,可造成死亡.因此,阿片类急性中毒的抢救应引起社会和广大医护工作者的关注.     

放射线联合p53基因及内皮抑素治疗小鼠前列腺癌皮下移植瘤

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.     

神经症与路径依赖

美国精神病学会于1980年出版的《精神障碍诊断统计手册,第三版》(DSM-III)取消了神经症(Neurosis)这个术语和概念。说得更详细一些,在类别命名上,不再使用神经症这个术语,在分类方法上,不再使用神经症这个概念。这一做法已逐渐为英语精神病学出版物所接受,尽管ICD-10(1992)还是     

叉头蛋白、p66shc与长寿

p66shc是原癌基因shc编码的蛋白，敲除p66shc增加由H202和紫外线诱发的细胞凋亡的抵抗。P66shc^-／-小鼠可增加对百草枯的抵抗和寿命延长。FKHRL1和DAF16是叉头蛋白转录因子家族成员，适当增加叉头蛋白的转录活性可延长寿命，而它的磷酸化可抑制其转录活性。氧化应激可导致浓度依赖的FKHRL1的磷酸化。p66shc^-／-细胞在H202处理后FKHRL1的磷酸化无明显改变，表明氧化应激修饰的叉头蛋白的磷酸化的调节需要p66shc的参与。     

原位杂交法检测BP1基因在乳腺癌组织中表达

目的探讨BP1同源盒基因在乳腺癌中的表达及其与临床病理指标的关系。方法收集165例乳腺癌临床和病理资料,采用原位杂交法检测BP1的表达,同时用二步法进行ER、p53、PCNA、bcl2、cerbB2免疫组化染色。结果BP1基因表达率为67.88%,免疫组化:ER70.30%、p5349.09%、PCNA74.55%、bcl253.33%、cerbB275.52%。BP1与bcl2具有相关性(P<0.01),且均与ER相关(P<0.05),与p53呈负相关(P<0.05)。BP1与PCNA、cerbB2、患者年龄、组织学类型、淋巴结转移等无相关性。结论BP1可能通过某种非依赖p53基因调控机制,与bcl2、ER协同抑制肿瘤细胞的凋亡而参与乳腺癌的发生。     

胆碱酯酶抑制剂-激素-大剂量血浆置换联合治疗重症肌无力的评价

重症肌无力（MG）是一组以病态疲劳为主要临床表现的自身免疫性疾病，其发病机制为横纹肌终板受乙酰胆碱受体抗体（AchRab）损害，从而造成终板AchR数量下降，功能降低。因此，AchRab在MG发病中占主要地位，血浆置换（PE）是以健康人血浆及血浆代用品替换患者血浆，快速去除患者血浆中AchRab及免疫复合物，从而使乙酰胆碱能正常与AchR结合，达到治疗目的。本研究通过观察接受及未接受PE治疗的MG患者病情转归，评价PE在MG治疗中的价值。     

机械通气并发呼吸机依赖的预防护理进展

呼吸机依赖是由于长期机械通气的病人已习惯了被动辅助呼吸，对呼吸机有所依赖，脱离呼吸机后不能自行调节呼吸，干扰并延长脱机的过程。作为一种呼吸支持疗法，临床发现一般呼吸机使用超过2周，就会产生呼吸机的依赖性。而正确的有针对性的护理措施可以在预防呼吸机依赖的发生中起到重要的作用，现根据文献报道，将发生呼吸机依赖的常见因素及其预防的护理措施归纳如下。     

那格列奈临床应用进展

那格列奈是一种新型的口服速效型餐后降血糖药。1999年8月首次在日本上市，2000年12月22日食品药品管理局（FDA）批准本品作为治疗2型糖尿病的口服降糖药，我国已开始生产，如正大晴天生产的贝加等。那格到奈用于饮食和锻炼控制无效的2型糖尿病的治疗，或与α-葡萄糖苷酶抑制剂联用能较好的控制餐后血糖。     

5型磷酸二酯酶抑制剂对勃起功能障碍和心血管疾病的治疗作用

Ravipati等对5型磷酸二酯酶抑制剂进行了回顾性研究。自从1989年高选择性的5型磷酸二酯酶（PDE-5）受体抑制剂西地那非被研发以来，另有两种PDE-5抑制剂上市，他达拉非和伐地那非，这两种抑制剂均能安全和有效的治疗勃起功能障碍（ED）。PDE家族中的酶成员可以催化细胞内的信号分子环磷酸腺苷（cAMP）和环磷酸鸟苷（cGMP）的水解，这两种信号分子又是一氧化氮（NO）的第二信使和平滑肌舒张、血管扩张的一个主要调控因子。