十二烷氮酮氟尿嘧啶凝胶治疗疣及银屑病150例

443例(男225例,女218例;年龄36±14a)皮肤病患者,其中150例(扁平疣52例、寻常疣55例、银屑病43例)外用含1.8％十二烷氮(艹卓)酮的1％氟尿嘧啶(5-FU)凝胶作为治疗组,148例外用1％5-FU凝胶及145例外用2.5％5-FU霜作为2个对照组。经双盲对照临床试验,结果表明含1.8％十二烷氮(艹卓)酮的1％5-FU凝胶的疗效明显优于2个对照组(P<0.01及P<0.005)。证明氮(艹卓)酮对5-FU确有渗透促进作用。     

MRI同层动态增强对垂体微腺瘤的诊断价值

目的：分析垂体微腺瘤的MPd同层动态增强特征。方法：对40例临床怀疑为垂体微腺瘤的病人行同层动态增强MPd扫描，并绘出时间一信号强度曲线图。结果：40例病人中共检出垂体微腺瘤26例。同层动态增强后垂体微腺瘤的MPd表现为圆或椭圆形的低或稍低信号，似“充盈缺损”；垂体微腺瘤的最大信号强度多出现在注入造影剂后32～96s，以64s最明显。结论：同层MPd动态增强对垂体微腺瘤的诊断有较高价值。     

6种中药制剂治疗急性脑梗死的成本-效果分析

目的：运用药物经济学的方法对在我院应用的6种中药注射液进行成本-效果分析。方法：271例急性脑梗死患者依据药物治疗方案不同分为6组，即血塞通组、舒血宁组、苦碟子组、疏血通组、川芎嗪组、丹红组，分别观察疗效，并运用药物经济学的方法进行成本-效果分析。结果：疏血通组的成本为3 419.90元，总有效率最高（91.84%），6组间增量成本-效果最低。因此疏血通组是较为合理、经济的方案。     

原发性肝癌患者肝切除术前、后免疫细胞表型分析

目的研究原发性肝癌(PrimaryLiverCarcinoma,PLC)患者肝切除术前、后免疫细胞表型的变化。方法采用直接免疫荧光标记,流量血细胞计数法(FlowCytometry,FCM)检测方法,动态观察120例PLC患者肝切除术前后外周血T淋巴细胞亚群、NK细胞和HLA鄄DR含量变化。结果肝切除术前肝功能Child鄄PughB级、OGTTL型和术前施行肝动脉栓塞化疗患者外周血CD8+T细胞含量明显低于正常人组,CD4+/CD8+比值则较高(P<0郾05)。全部肝癌患者肝切除术前、后CD3+CD4+T细胞和NK细胞(CD3-CD16+CD56+)含量无明显差异。术后第1天、第3天、第7天和第2周外周血淋巴细胞CD3+CD8+含量明显低于肝切除术前和术后第3周(P<0.01);而CD4+/CD8+比值则显著高于肝切除术前和术后第3周(P<0郾01)。结论PLC合并肝硬变肝储备功能不足、术前肝动脉栓塞化疗和肝切除术可导致机体细胞免疫功能低下,PLC患者肝切除术前行肝动脉栓塞化疗的价值有待深入研究。     

Ca^＋＋对链霉素抗原—抗体反应的抑制作用

为探讨临床中使用钙制剂抢救链霉素过敏休克病人有良好效果的原因,由被动血凝试验、被动皮肤过敏试验和ELISA法证实,Ca~( )可以抑制链霉素抗原-抗体的反应。这种抑制作用是通过Ca~( )链霉素抗原结合,封闭链霉素抗原决定簇来加以实现的。     

出国务工妇女细菌性阴道病调查结果分析

目的:了解细菌性阴道病在延边地区出国务工妇女中的流行情况。方法:用改良多胺法对延边地区586名出国务工妇女进行细菌性阴道病(BV)检测,同时用常规方法进行滴虫、霉菌检查。结果:586份阴道分泌物标本中,检出BV(+)275例,总阳性率为46.9%,其中单纯BV(+)242例(41.3%)、BV合并滴虫(+)8例(1.3%)、BV合并霉菌(+)25例(4.3%);按年龄分组,33～35岁组BV阳性率最高,为60.3%,≤20岁组最低,为20.0%。结论:延边地区出国务工妇女细菌性阴道病患病率较高,居该人群各种阴道感染的首位,无民族差异(χ2=0.22,P>0.05),但年龄差异显著(χ2=28.72,P<0.05)。因此,建议在出国体检中常规开展BV检查,以便及时发现和治疗,控制疾病传播范围。     

云南罗平医院PM调查的分析与对策

文章以云南罗平医院为研究对象,调查了65名一般员工和21名科主任级中层领导,使用PM量表对该医院的高层及中层领导行为进行评估,对情景因素与领导行为的内在联系进行探讨,并提出改进对策。目的是了解员工需求,促进人力资源合理配置,从而提高医院的管理水平。     

宋《本草图经》草木部所述植物药主要产地及药材集散地考略

1 宋代社会经济、医事制度与历史地理 1.1 宋代的社会经济 宋朝是我国历史上继唐朝之后,社会经济发展、科技文化进步的一个历史时期,后世有"治隆唐宋"之说.公元960年陈桥兵变,赵匡胤(宋太祖)"黄袍加身"以后,遂代周而自立,是为宋朝,史称北宋.当时的社会在经历了五代十国的战乱之后而趋于安定,经济逐渐恢复,科学也日益发达.     

The effects of chymase on matrix metalloproteinase-2 activation in neointimal hyperplasia after balloon injury in dogs.

Chymase is known to generate angiotensin II in the vascular wall. In this study we investigated a novel role for chymase other than angiotensin II production in vascular proliferation after balloon injury. Chymase promoted the migration of vascular smooth muscle cells in the matrix-coated invasion chambers and activated promatrix metalloproteinase-2 obtained from the culture medium of vascular smooth muscle cells. Two weeks after balloon injury, significant neointimal formation was found in dog carotid arteries. After injury, active matrix metalloproteinase-2 was increased in parallel with the augmentation of chymase activity that was seen in the proliferating region of the vascular wall. The oral administration of NK3201 (1 mg/kg per day), a chymase inhibitor, prevented neointimal formation and significantly suppressed both active matrix metalloproteinase-2 and chymase activities 2 weeks after injury. These results suggest that chymase inhibitors can prevent the development of intimal hyperplasia via the inhibition of matrix metalloproteinase-2 activation in balloon-injured arteries.     

Fidgetin-like 1 gene inhibited by basic fibroblast growth factor regulates the proliferation and differentiation of osteoblasts.

The FIGNL1 gene was proven to be a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). In this in vitro study, the AAA proteins inhibited osteoblast proliferation and stimulated osteoblast differentiation. We showed that FIGNL1 may play some regulatory role in osteoblastogenesis. INTRODUCTION: The fidgetin-like 1 (FIGNL1) gene encodes a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). Although the FIGNL1 protein localizes to both the nucleus and cytoplasm, the function of FIGNL1 remains unknown. In a previous study, we identified several genes that mediate the anabolic effects of basic fibroblast growth factor (bFGF) on bone by using microarray data. FIGNL1 was one of the genes that downregulated >2-fold in MC3T3-E1 cells after treatment with bFGF. Therefore, this study was aimed to identify and confirm the function of FIGNL1 on osteoblastogenesis. MATERIALS AND METHODS: We examined the effect of the FIGNL1 gene on proliferation, differentiation, and apoptosis in mouse osteoblast cells (MC3T3-E1 and mouse primary calvarial cells) using flow cytometry, RT-PCR, cell proliferation assay, and cell death assay. MC3T3-E1 cells and mouse calvarial cells were transfected with small interfering RNA (siRNA) directed against the FIGNL1 or nontargeting control siRNA and examined by cell proliferation and cell death assays. Also, FIGNL1 was fused to enhance green fluorescent protein (EGFP), and the EGFP-fused protein was transiently expressed in MC3T3-E1 cells. RESULTS: Reduced expression of FIGNL1 by bFGF and TGF-beta1 treatment was verified by RT-PCR analysis. Overexpression of FIGNL1 reduced the proliferation of MC3T3-E1 and calvarial cells, more than the mock transfected control cells did. In contrast, siFIGNL1 transfection significantly increased the proliferation of osteoblasts, whereas overexpression of FIGNL1 did not seem to alter apoptosis in osteoblasts. Meanwhile, overexpression of FIGNL1 enhanced the mRNA expression of alkaline phosphatase (ALP) and osteocalcin (OCN) in osteoblasts. In contrast, siFIGNL1 decreased the expression of ALP and OCN. A pEGFP-FIGNL1 transfected into MCT3-E1 cells had an initially ubiquitous distribution and rapidly translocated to the nucleus 1 h after bFGF treatment. CONCLUSIONS: From these results, we proposed that FIGNL1, a subfamily member of the AAA family of proteins, might play some regulatory role in osteoblast proliferation and differentiation. Further analyses of FIGNL1 will be needed to better delineate the mechanisms contributing to the inhibition of proliferation and stimulation of osteoblast differentiation.