声波反射测量尿道压力的方法和应用

无论是正常还是病生理条件下女性尿道的闭合机制还未完全了解清楚。近10余年来,尿道压声反射测量(UPR)得以发展并主要应用于女性压力性尿失禁。UPR利用声波反射检测的原理连续测量整个尿道的压力和相应的截面积,其最大优势在于检测时不改变尿道的自然形状和走向,遵循物理定律。这是常用的检测手段如尿道压力分布测定(UPP)难以实现的。本文介绍了该方法和有关UPR的相关研究,在男性和女性其它尿道疾病应用的可能性及其发展趋势。     

CIC对高脂膳食大鼠肝脏氧化应激的影响

目的:研究慢性间断性冷暴露(mild chronic intermittent cold exposure,CIC)对高脂膳食大鼠肝脏氧化应激的影响。方法:轻度CIC已被广泛用于建立冷适应研究的动物模型。本研究通过将大鼠暴露于温和的CIC和/或高脂膳食4w,检测肛温、体重、肝脏重量、ATP和活性氧(ROS)的水平,Western blot检测冷诱导RNA结合蛋白(cold inducible RNA binding protein,Cirbp)和硫氧还蛋白(Thioredoxin,TRX)的蛋白表达。结果:同对照组相比,高脂膳食组体重显著增加,血清和肝脏ROS水平显著升高,ATP水平没有显著影响。同对照组相比,CIC暴露1w后大鼠肛温显著降低,而2w、3w和4w周肛温没有显著差异,ROS水平无显著差异,但ATP水平显著升高;Cirbp和TRX的表达显著升高。同常温高脂膳食组相比,CIC暴露4w后,大鼠体重显著降低,ROS水平无显著差异,而ATP水平显著升高;Cirbp和TRX的表达水平显著升高。这些结果均提示冷适应增强了高脂膳食大鼠肝脏的抗氧化水平,可能是由于冷适应后Cirbp表达升高,继而调控其下游的抗氧化蛋白TRX的表达增加,从而清除ROS的缘故。结论:CIC暴露诱导的冷适应可保护肝脏免于高脂膳食诱导的氧化应激。     

小鼠肝再生过程中ROS及线粒体代谢变化规律的研究

目的:肝脏是维持人体发挥功能的重要器官,同时肝脏再生能力十分强大。本文通过部分肝切除术后小鼠肝再生模型,观察肝再生过程中氧化应激及线粒体代谢变化规律,以期为将来的调控肝再生提供新的干预靶点。方法:选择雄性健康体重均匀的Balb/c小鼠,采用经典70%肝切除模型,随机分为假手术对照组(Sham组)以及70%肝切除组(70%PH组)。肝切除术后6 h、1d、2 d、3 d、5 d、7 d不同时间点取肝组织,制备冰冻切片检测活性氧(ROS)水平,Western blot分别检测细胞增殖相关蛋白PCNA、Cyclin D1;氧化应激相关蛋白SOD1、SOD2、CAT、GPX1;以及线粒体代谢相关蛋白PGC-1α、Nrf1、TFAM、Drp1、Fis1、Mfn1、Mfn2、OPA1的表达并分析其变化规律。结果:70%肝切除术后小鼠肝脏增长迅速,细胞增殖关键蛋白PCNA和Cyclin D1表达显著增加;在此过程中细胞ROS水平呈现先升高后降低的变化,细胞主要抗氧化酶SOD1、SOD2、CAT、Gpx1与ROS相一致出现先升高后降低的变化。线粒体生物合成调控因子PGC-1α、Nrf1、TFAM呈现先降低后升高的趋势,而线粒体分裂蛋白Drp1和Fis1呈现先降低后显著升高的趋势,线粒体融合相关蛋白Mfn1、Mfn2和OPA1总体为先降低后恢复至正常水平。结论:在小鼠70%肝切除再生过程中,存在着明显的氧化应激,线粒体生物合成增加,线粒体分裂/融合平衡偏向分裂,并且这些变化呈现具有一定的时间变化规律,这些变化及规律很可能作为将来调控肝再生的重要的潜在干预靶点。     

不同浓度的右美托咪定对老年腰椎术患者的镇静效果、氧化应激和血流动力学的影响

目的:探讨不同浓度的右美托咪定对老年腰椎术患者的镇静效果、氧化应激和血流动力学的影响。方法:选取2013年3月-2018年4月期间我院收治的老年腰椎术患者90例为研究对象。根据随机数字表法将患者分为对照组(n=30)、低浓度组(n=30)以及高浓度组(n=30)。低浓度组麻醉诱导前输注0.5μg/kg右美托咪定,高浓度组输注1μg/kg右美托咪定,对照组不输注右美托咪定。比较给药前(T0)、给药后10 min(T1)、给药后30 min(T2)、给药后60 min(T3)的听觉诱发电位指数(AAI)、改良/镇静视觉评分(OAA/S)。比较T0、T3、手术后24h(T4)的三组患者丙二醛(MDA)、超氧化物歧化酶(SOD)水平。比较T0-T3时间点三组患者的心率(HR)、平均动脉压(MAP)情况。观察三组患者术后不良反应发生情况。结果:与T0时间点比较,三组T1-T3时间点AAI、OAA/S均显著降低(P0.05);与对照组相比,低浓度组与高浓度组T1-T3时间点AAI、OAA/S均较低,且高浓度组低于低浓度组(P0.05)。与T0时间点比较,三组T3、T4时间点MDA均显著升高,T3时间点SOD显著降低(P0.05);与对照组相比,低浓度组与高浓度组T3、T4时间点MDA均降低,且高浓度组低于低浓度组(P0.05);高浓度组T3、T4时间点SOD高于低浓度组和对照组(P0.05)。与T0时间点比较,三组T2、T3时间点HR、MAP均降低(P0.05);与对照组相比,低浓度组、高浓度组T2、T3时间点HR均降低,且高浓度组低于低浓度组(P0.05);与对照组相比,低浓度组、高浓度组T2、T3时间点MAP均降低,但高浓度组高于低浓度组(P0.05)。三组患者术后不良反应总发生率比较差异无统计学意义(P0.05)。结论:1μg/kg右美托咪定对老年腰椎术患者的镇静效果较好,可有效维持血流动力学稳定,减轻氧化应激反应。     

神经内镜辅助下经鼻蝶窦入路术对垂体瘤患者血清E, NE, R及ATⅡ的影响及其临床疗效

目的:研究神经内镜辅助下经鼻蝶窦入路术对垂体瘤的临床观察及对肾上腺素(epinephrine,E)、去甲肾上腺素(Norepinephrine,NE)、肾素(Renin,R)、血管紧张素(Angiotensin,ATⅡ)的影响。方法:收集2015年3月-2017年3月我院收治的60例垂体瘤患者,随机分为实验组和对照组,每组30例,实验组采用神经内镜辅助下经鼻蝶窦入路术治疗,对照组采用经口鼻下鼻中隔垂体瘤切除术治疗。观察并比较两组治疗疗效,手术时间、术中出血量、住院时间,血清E、NE、R及ATⅡ水平,激素下降程度、肿瘤残留、肿瘤体积减少程度、复发率及不良反应。结果:实验组总有效率显著高于对照组(P0.05);手术时间、术中出血量、住院时间均显著小于对照组(P0.05);E、NE、R、ATⅡ水平显著低于对照组(P0.05);激素下降程度、肿瘤残留、肿瘤体积减少程度、复发率显著低于对照组(P0.05);不良反应总发生率显著低于对照组(P0.05)。结论:神经内镜辅助下经鼻蝶窦入路术对垂体瘤的疗效显著,可减少应激反应,提高肿瘤全切除率,可减少术后并发症,利于患者预后。     

硬膜外复合全身麻醉对开胸手术患者血流动力学和应激反应的影响研究

目的:研究硬膜外复合全身麻醉对开胸手术患者血流动力学和应激反应的影响。方法:选取120例我院2015年1月到2016年1月收治的开胸手术患者,按照随机数字表法将患者分为研究组和对照组,对照组给予单纯全麻,研究组给予硬膜外复合全身麻醉,比较两组苏醒时间、苏醒期收缩压、舒张压、心率及烦躁情况,并比较两组术前、术后72 h血糖、皮质醇以及肾上腺素水平。结果:两组苏醒时间比较无统计学意义(P0.05),苏醒期研究组收缩压、舒张压及心率、烦躁发生率均较对照组降低(P0.05);两组术前血糖、皮质醇及肾上腺素比较无统计学差异(P0.05);术后72 h,两组血糖、皮质醇及肾上腺素均升高(P0.05);研究组血糖、皮质醇及肾上腺素均较对照组降低(P0.05)。结论:硬膜外复合全身麻醉应用于开胸手术能显著提高患者苏醒期苏醒质量,稳定血流动力学,改善其应激反应。     

GPC3对肝癌细胞糖酵解的调控作用研究

目的:探讨GPC3(glypican 3)在肝癌细胞糖酵解中的调控作用。方法:采用si RNA(small interfering RNA)干扰肝癌细胞中GPC3的表达后,采用q PCR(quantitative PCR)与Western blot实验检测肿瘤糖酵解关键调控分子Glut1(glucose transporter-1)、HK2(hexokinase 2)与LDH-A(Lactate Dehydrogenase A)的表达,通过检测培养液中葡萄糖的减少量分析GPC3对细胞葡萄糖摄取情况,通过检测培养液中乳酸含量与PH值分析GPC3对细胞乳酸产生的影响,通过检测细胞的氧耗速率,分析GPC3对线粒体氧化磷酸化功能的影响。结果:干扰肝癌细胞中GPC3的表达可抑制糖酵解关键调控分子Glut1、HK2与LDH-A表达,降低肝癌细胞葡萄糖摄取速率和细胞氧耗速率,且细胞培养液PH升高,乳酸产生减少。结论:肝癌细胞中GPC3高表达通过上调糖酵解关键调控分子Glut1、HK2与LDH-A表达而促进肝癌细胞糖酵解效应,同时抑制线粒体氧化磷酸化活性。这些结果进一步提示糖代谢重编程可能是GPC3促进肝癌增殖与转移的重要机制。     

The oxygen concentration in cultures modulates protein expression and enzymatic antioxidant responses in Metarhizium lepidiotae conidia

Conidia from Metarhizium spp. are used for integrated pest control; however, environmental factors diminish the effectivity of these programs. Several approaches tried to improve conidia resistance to overcome this limitation, although little is known about the mechanisms involved in this effect. Here we measured the activity of antioxidant enzymes and conidia virulence, comparing the proteomic profiles of Metarhiziumlepidiotae CP-OAX conidia produced under normal (21% O₂) and high oxygen atmospheres (pulses with 30% O₂). We detected a higher virulence against Tenebrio molitor larvae, in addition to an increase in ultraviolet light tolerance in conidia produced under 30% O₂, which correlates with increased glutathione reductase activity. Two-dimensional gel electrophoresis (2D SDS–PAGE) of proteins extracted in conidia harvested from both experimental conditions revealed a group of proteins that was observed only in conidia from oxidant atmospheres. Some of those proteins were directly involved in oxidative stress responses, whereas others were involved in conidial virulence, thermo-tolerance, and the central metabolism. Thus, a high atmospheric oxygen concentration (30%) activates antioxidant defence and general stress response mechanisms involved in conidia resistance to adverse environmental factors, which can ultimately translate into higher effectivity for the use of entomopathogenic fungi conidia in pest control.     

Redox-active trace metal-induced release of high mobility group box 1(HMGB1) and inflammatory cytokines in fibroblast-like synovial cells is Toll-like receptor 4 (TLR4) dependent

Rheumatoid arthritis (RA) is a chronic autoimmune systemic inflammatory disease that is characterized by synovial inflammation and bone erosion. We have investigated the mechanism(s) by which essential trace metals may initiate and propagate inflammatory phenotypes in synovial fibroblasts. We used HIG-82, rabbit fibroblast-like synovial cells (FLS), as a model system for potentially initiating RA through oxidative stress. We used potassium peroxychromate (PPC, Cr⁺⁵), ferrous chloride (FeCl_2, Fe⁺²), and cuprous chloride (CuCl, Cu⁺) trace metal agents as exogenous pro-oxidants. Intracellular ROS was quantified by fluorescence microscopy and confirmed by flow cytometry (FC). Protein expression levels were measured by western blot and FC, while ELISA was used to quantify the levels of cytokines. Trace metal agents in different valence states acted as exogenous pro-oxidants that generate reactive oxygen species (ROS), which signal through TLR4 stimulation. ROS/TLR4- coupled activation resulted in the release of HMGB1, TNF-α, IL-1β, and IL-10 in conjunction with upregulation of myeloid-related protein (MRP8/14) inflammatory markers that may contribute to the RA pathophysiology. Our results indicate that oxidant-induced TLR4 activation can release HMGB1 in combination with other inflammatory cytokines to mediate pro-inflammatory actions that contribute to RA pathogenesis. The pathway by which inflammatory and tissue erosive changes may occur in this model system possibly underlies the need for functioning anti-HMGB1-releasing agents and antioxidants that possess both dual trace metal chelating and oxidant scavenging properties in a directed combinatorial therapy for RA.