胸腔注射尿激酶联合地塞米松治疗结核性胸膜炎的临床效果

目的探讨胸腔注射尿激酶联合地塞米松治疗结核性胸膜炎的疗效与安全性。方法选取2009年4月～2012年6月浙江省温岭市第四人民医院收治的126例结核性胸膜炎患者,将其随机分为A、B、C三组,每组42例。所有患者均通过胸腔给药,A组患者接受尿激酶,B组患者接受地塞米松,C组患者接受尿激酶联合地塞米松。结果 A、B、C三组的胸腔积液消失时间、胸膜厚度、胸膜粘连率分别为：A组：（17.4±3.5）d,（1.92±0.35）mm,26.2%;B组：（17.0±3.7）d,（1.87±0.39）mm,31.0%;C组：（13.5±2.9）d,（1.32±0.29）mm,7.1%。三组患者胸腔积液消失时间、胸膜厚度、胸膜粘连率相比差异有统计学意义（P〈0.05）,C组患者胸腔积液消失时间显著短于A组与B组（P〈0.05）,胸膜厚度显著薄于A组与B组（P〈0.05）,胸膜粘连率显著低于A组与B组（P〈0.05）。三组患者不良反应发生率相比差异无统计学意义（P〉0.05）。结论胸腔注射尿激酶联合地塞米松是治疗结核性胸膜炎的有效方案之一,值得临床应用与推广。     

地塞米松对哮喘小鼠气道炎症反应和外周血单核细胞p38 MAPK表达的影响

目的:探讨支气管哮喘小鼠急性外周炎症反应和血单核细胞p38MAPK表达的变化及地塞米松(DEX)对其的影响。方法:采用蛋白质印迹和ELISA方法检测PBMCs核蛋白p38MAPK的表达及细胞上清液中IL-4、IL-5的蛋白质浓度。结果:哮喘组PBMCs核蛋白p38MAPK表达及细胞上清液中IL-1、IL-6的蛋白质浓度较正常对照组显著升高(P<0.01),DEX处理组核蛋白p38MAPK表达及细胞上清液中IL-1、IL-6的蛋白质浓度较哮喘对照组显著降低(P<0.01)。通过直线相关分析发现,PBMCs核蛋白p38MAPK表达与培养上清液中IL-1、IL-6蛋白质含量之间均呈显著正相关(r分别=0.72、0.56,P<0.01)。结论:地塞米松可在一定程度上减轻哮喘小鼠的气道炎症反应,作用机制可能是通过下调外周血单核细胞p38MAPK过度表达,从而抑制依赖于p38MAPK信号转到通路的急性气道炎症反应。     

地塞米松减少手术后硬膜外吗啡镇痛引起的恶心呕吐

目的　观察静脉注射地塞米松 (Dex)对减少手术后与硬膜外吗啡镇痛有关的恶心呕吐发生率的作用。方法　随机双盲选择 87例在硬膜外麻醉下行腹部手术的女性病人进行观察。所有病人在手术后均接受硬膜外吗啡镇痛。Dex组病人 (n =41)在手术后静注Dex 8mg ,对照组病人 (n=46 )则给予等量生理盐水。结果　在手术后 2 4小时内 ,Dex组病人手术后总的恶心呕吐发生率为2 6 8% ,明显低于对照组病人的 43 5 % (P <0 0 1)。两组病人之间手术后皮肤瘙痒的发生率无明显差异 ,Dex也不影响手术后硬膜外吗啡的镇痛作用。结论　预防性静脉注射Dex是一种减少与硬膜外吗啡镇痛有关的恶心呕吐并发症的有效方法     

VAD方案治疗多发性骨髓瘤疗效观察

 目的 评估VAD方案治疗多发性骨髓瘤（MM）的疗效。方法 24例Ⅲ期MM,采用VAD方案,即长春新碱0.5 mg／d（或长春地辛1 ~ 2 mg／d）缓慢静脉注射,第1～4天;多柔比星（或表柔比星）10 ~ 20 mg／d缓慢静脉注射,第1～4天;地塞米松40 mg／d口服,第1～4天,第9～12天,第17～20天,28 d为1疗程。连续应用2疗程以上评估疗效。观察项目包括：血清M蛋白、肝肾功能、尿蛋白、骨髓穿刺、血象等,记录毒副反应。MM疗效标准,分为完全缓解（CR）、部分缓解（PR）、未缓解（NR）。结果 CR8例（33.3 %）,PR12例（50 %）,NR4例（16.7 %）,总有效率为83.3 %。结论 VAD方案治疗Ⅲ期MM的临床疗效显著,临床症状改善明显。     

地塞米松对老龄大鼠术后认知功能的影响

目的 评价地塞米松对老龄大鼠术后认知功能的影响.方法 雄性SD大鼠180只,18 ～ 20月龄,体重400 ～ 600 g,采用随机数字表法,将大鼠随机分为3组(n=60)∶对照组(C组)、手术组(S组)和地塞米松组(D组).采用大鼠剖腹探查手术模型.D组于麻醉开始时腹腔注射地塞米松10 mg/kg.C组不进行手术,腹腔注射生理盐水2 ml/kg.于术后3h、7d时测定海马OX42(小胶质细胞激活特异性标志物)的表达水平;于术后3h、1d、3d和7d时测定海马IL-1β mRNA和TNF-α mRNA的表达水平.采用Morris水迷宫实验和条件恐怖适应实验检测大鼠术后认知功能.结果 与C组比较,S组和D组逃逸潜伏期延长,穿越原平台次数减少,术后僵直时间缩短,海马OX42表达、IL-1β mR-NA和TNF-α mRNA表达上调(P＜0.05或0.01);与S组比较,D组逃逸潜伏期缩短,穿越原平台次数增多,术后僵直时间延长,海马OX42、IL-1β mRNA和TNF-α mRNA表达下调(P＜0.05或0.01).结论 地塞米松可抑制海马小胶质细胞过度激活,减轻炎性反应,从而改善老龄大鼠术后认知功能.     

Glial Fibrillary Acidic Protein and Vimentin Expression Is Regulated by Glucocorticoids and Neurotrophic Factors in Primary Rat Astroglial Cultures

The neurotrophic factors epidermal growth factor (EGF), basic fibroblast growth factor, (bFGF), insulin‐like growth factor I (IGF‐I) and insulin (INS) regulate neural and astroglial cell functions. Glucocorticoids may influence the metabolism of astroglial compartment and are key hormones in neurodegenerative events. This study was designed to assess the interactions between growth factors and dexamethasone (DEX) on cytoskeletal proteins (GFAP and vimentin) expression in 25 days in vitro (DIV) astrocyte cultures. An increase in GFAP and vimentin expression was observed after 12 h pretreatment with bFGF and subsequent treatment for 60 h with DEX. GFAP immunoreactivity was decreased after 24 h progression growth factors (EGF, IGF‐I and INS) addition, when compared to control 36 h DEX and bFGF‐pretreated cultures for the last 12 h. Vimentin immunoreactivity was decreased after 12 h bFGF pretreatment and subsequent 60 h DEX addition in astrocyte cultures compared to 12 h bFGF‐pretreated ones. Pretreatment for 36 h with DEX plus bFGF in the last 12 h and subsequent treatment for 24 h with DMEM (Dulbecco's modified Eagle medium; DMEM) + BSA (bovine serum albumine) (harvesting), or with progression growth factors (EGF, IGF‐I or INS) alone or two of them together, stimulated GFAP expression, compared to untreated controls. Immunochemical analysis of the mitogen‐activated protein kinase ERK2 suggests an involvement of this enzyme in the control of GFAP expression. The above findings support the view of an interactive and complex dialogue between growth factors and glucocorticoids during astroglial cell proliferation and maturation in culture. This may have implications in therapeutic approach of neurologic disorders associated with astrogliosis, including cerebrovascular disease.     

Effect of Dexamethasone Treatment on Oxidative Energy Metabolism in Rat Liver Mitochondria During Postnatal Developmental Periods

Dexamethasone — a potent synthetic glucocorticoid — has multiple therapeutic applications and, used in all age groups, as well as for antenatal and perinatal treatments. However, side‐effects of dexamethasone treatment, including those on development, are becoming increasingly apparent. Since developmental processes are energy‐dependent, we examined the effects of chronic dexamethasone treatment on oxidative energy metabolism in liver mitochondria from rats belonging to different developmental age groups. Dexamethasone treatment adversely affected the state 3 respiration rates in 2‐ and 3‐week groups and in the adults with glutamate as the substrates, whereas for pyruvate + malate, the adverse effects were seen for the 3 week rats and the adult groups. Oxidation of succinate was severely impaired in all the age groups rats. For ascorbate + TMPD as the substrate, elevated respiration was noted for the 5‐week group and the impaired oxidation was observed in adults. Dexamethasone treatment also resulted in site‐specific uncoupling with the effect being seen predominantly in the 3‐ and 5‐week and adult animals. The activity of dehydrogenases decreased in a manner comparable to the respiration rates. The mitochondrial cytochromes decreased in an age‐dependent manner. The ATPase activity also decreased significantly. The results thus emphasize the adverse effects of dexamethasone treatment on mitochondrial energy metabolism especially in critical age groups.     

The in-vitro and in-vivo characterization of PLGA:L-PLA microspheres containing dexamethasone sodium phosphate

Dexamethasone sodium phosphate (DSP) is a widely used corticosteroid in the treatment of brain oedema associated with brain tumours. DSP has many side effects that limit its usage at an effective concentration. The objective of this study was to minimize these side effects by encapsulating DSP using biodegradable synthetic polymers, to extend the release time from microspheres and to evaluate the effectiveness in the treatment of brain oedema. Microspheres containing 5% DSP were formulated by the solvent evaporation method by using a 1:1 mixture of two synthetic polymers, poly(lactic-co-glycolic acid) and L-polylactic acid (PLGA and L-PLA). The surface morphologies and particle size distribution of the microspheres were investigated. The in-vitro     

补肾方剂拮抗地塞米松促骨髓基质细胞向成脂细胞分化的实验研究

目的观察补肾方剂对地塞米松促骨髓基质干细胞成脂作用的影响。方法从成年SD大鼠分离出骨髓基质干细胞体外培养,取第三代细胞用于实验。分别在培养液其中加入1×10^-7mol·L^-1的地塞米松（A组）、1×10^-7mol·L^-1的地塞米松和80mg·L^-1的补肾方剂（B组）,C组为对照组。分别应用MTT、碱性磷酸酶活性与三酰甘油含量法检测MSCs增殖与分别向成骨和成脂方向分化的能力。结果实验组（A组和B组）的MSCs增殖能力较对照组明显降低（P〈0.05）,但A组与B组之间差异无显著意义（P〉0.05）;B组MSCs硷性磷酸酶活性较A组增高（P〈0.05）,而三酰甘油含量低于A组（P〈0.05）。结论补肾方剂不能干预地塞米松对MSCs增殖的抑制作用,但具有抑制地塞米松促进MSCs向成脂方向分化的作用。     

评价地塞米松和甘露醇合用对急性重症脑血管病脑保护作用的疗效

目的：分析探讨地塞米松和甘露醇合用对急性重症脑血管病脑保护作用的疗效。方法整群选取该院2011年8月-2013年8月收治的急性重症脑血管病患者88例,随机分为对照组和观察组,对照组患者采用甘露醇治疗,观察组患者采用地塞米松联合甘露醇治疗。比较两组患者的颅内压(ICP),并发症和格拉斯哥昏迷(GCS)评分。结果观察组患者不同时间段ICP恢复正常例数所占比率与对照组比较差异有统计学意义,P<0.05;两组患者治疗期间并发症发生率比较差异无统计学意义,P>0.05;治疗后第3个月,观察组患者的GCS评分明显优于对照组,P<0.05,具有统计学意义。结论地塞米松与甘露醇合用治疗急性重症脑血管疾病,患者ICP恢复速度快,患者预后情况良好,且不会增加治疗期间的并发症,能够有效降低颅内压、保护脑细胞、减轻脑水肿,值得临床大力推广。