抗角蛋白抗体、抗核周因子和抗环瓜氨酸肽抗体联合检测幼年类风湿关节炎：早期诊断及治疗评估意义

目的:评价抗角蛋白抗体、抗核周因子和抗环瓜氨酸肽抗体联合检测在幼年类风湿关节炎诊断及病情评估中的意义。方法:①观察对象及分组:选择2003-01/2005-12首都医科大学附属北京儿童医院风湿免疫病房住院治疗的76例幼年类风湿关节炎患儿及54例非幼年类风湿关节炎患儿,正常对照30例(家属均知情同意)。②检测上述人员血清抗角蛋白抗体、抗核周因子抗体和抗环瓜氨酸肽抗体水平;观察两组患儿出现临床症状、体征例数及实验室检测数据。③对幼年类风湿关节炎诊断的敏感性、特异性,阳性似然比、阴性似然比进行评价,并对幼年类风湿关节炎患儿中3种抗体联合检测阳性组阴性组的临床症状、体征及实验室检查方面的指标进行比较,资料作统计学分析。结果:两组患儿130例,正常儿童30例,全部进入结果分析。①两组患儿临床症状、体征例数及实验室检测值差异没有显著性意义。②抗角蛋白抗体、抗核周因子抗体和抗环瓜氨酸肽抗体联合检测对幼年类风湿关节炎组早期诊断缺乏有效性。③抗角蛋白抗体( )/抗核周因子抗体( )/抗环瓜氨酸肽抗体( )病例与抗角蛋白抗体(-)/抗核周因子抗体(-)/抗环瓜氨酸肽抗体(-)病例相比,关节强直病例明显增多,差异有显著性(较正χ2=3.902,P=0.048),抗链球菌溶血素“O”和C-反应蛋白均显著增高,差异有显著性(χ2=2.616,3.557,P=0.025,0.001)。结论:抗角蛋白抗体、抗核周因子抗体、抗环瓜氨酸肽抗体联合检测对幼年类风湿关节炎缺乏早期诊断意义及特异性,联合检测对判断疾病的活动性、病理损害程度和预后有临床意义。     

有氧运动延缓衰老线粒体DNA突变的机制

目的:线粒体DNA突变在衰老过程中起核心作用。总结有氧运动在延缓机体衰老过程中对线粒体DNA突变的影响,探讨有氧运动延缓衰老的机制。资料来源:应用计算机检索Medline数据库1996-01/2006-01期间关于线粒体DNA突变与有氧运动延缓衰老的文章,检索词为"aerobics exercise,aging,mtDNA mutation",限定文章语言种类为English。同时计算机检索中国期刊全文数据库、万方数据库1994-01/2006-12期间的有氧运动、衰老和线粒体DNA突变相关的文章,检索词"衰老,线粒体DNA突变,有氧运动",并限定文章语言种类为中文。资料选择:对资料进行初审,纳入标准:①有氧运动延缓衰老关系的理论研究。②线粒体DNA突变与衰老关系的基础与临床研究。③有氧运动对线粒体DNA突变的影响研究。资料提炼:共收集到36篇线粒体DNA突变与有氧运动延缓衰老相关的文献,均为全文,32篇符合纳入标准,排除4篇重复性研究。资料综合:①有氧运动可以通过减少线粒体DNA突变,从而达到延缓机体的衰老。有氧运动可能通过影响自由基及抗氧化系统、细胞凋亡、线粒体的结构和功能,对衰老进程产生重要影响。②线粒体DNA突变随增龄而积累,达到一定阈值后,可导致细胞能量供应的严重障碍,从而造成组织器官生理功能的减退。③长期有氧运动可通过刺激心肌、骨骼肌线粒体的生成及蛋白质的合成而延缓线粒体形态结构的改变,有利于维持线粒体功能以满足机体对其能源的需求。结论:中、低强度有氧运动可以提高机体有氧工作能力,增进线粒体氧化磷酸化的功能,对延缓衰老具有一定的积极作用。有氧运动可以减少心肌、骨骼肌等线粒体DNA突变,提示有氧运动在延缓衰老机制中,减少线粒体DNA突变是可能机制之一。     

大鼠眼外肌成肌细胞的增殖及分化特征

目的:完善眼外肌成肌细胞体外培养、鉴定的方法及观察其生物学特性。方法:实验于2005-02/08在青岛大学医学院附院中心实验室(省级实验室)完成。取出生后3～7d的大鼠,通过大鼠眼外肌细胞的取材、分离、消化、培养等技术,观察细胞的形态、生长曲线、细胞融合率,观察大鼠眼外肌卫星细胞的增殖与分化能力,利用成肌细胞标记物α-横纹肌肌动蛋白、中间丝结蛋白免疫细胞化学染色对所获得的细胞进行鉴定。结果:①成肌细胞的生长情况:在生长培养基作用下,细胞增殖旺盛;在分化培养基条件下,细胞分化良好,可融合成肌管。②成肌细胞融合率:在24h和48h融合率提高明显,72h达高峰,之后不再变化。③细胞免疫化学检测结果:α-横纹肌肌动蛋白和中间丝结蛋白免疫细胞化学染色阳性。结论:体外培养的大鼠眼外肌卫星细胞具有良好的增殖与分化能力,其生物学特征同骨骼肌卫星细胞。     

低氧训练对下丘脑-垂体-肾上腺皮质轴内分泌相关激素的影响

目的:总结低氧训练对下丘脑-垂体-肾上腺皮质轴内分泌相关激素的影响,为科学运动训练提供依据。资料来源:应用计算机检索中国期刊全文数据库1994-01/2006-10的相关文章,检索词"低氧,低氧训练,下丘脑-垂体-肾上腺,激素",并限定文章语言种类为中文。并应用计算机检索美国国立医学图书馆NCBI1980-01/2006-10的相关文章,检索词"Hypoxic Training,organism endocrine system,hormone",并限定文章语言种类为English。资料选择:对资料进行初审,选取低氧训练与下丘脑-垂体-肾上腺分泌的相关激素有关的文献,并作初步分类,同类文献首选近年发表的核心期刊文章。排除重复及综述类文献。资料提炼:共收集到95篇相关文章,其中56篇属于重复及综述类文献,对符合标准38篇文献进行分析整理。资料综合:①高海拔状态下机体对低氧产生应激反应,表现为下丘脑-垂体-肾上腺皮质轴的适应性运转,血中促肾上腺皮质激素浓度增加,以调节机体对应激刺激的适应能力,同时使促肾上腺皮质激素释放因子分泌增加。②高原训练后,睾酮和皮质醇的变化都较明显,其总体变化均趋于降低,睾酮/皮质醇值有升有降,从一定意义上反映了机体的机能状况与疲劳积累程度。③低氧还引起大鼠血浆β-内啡肽浓度升高,可使心房钠尿素增加、前列腺素增加、血管内皮素分泌增加及抑制血管内皮舒张因子的分泌。结论:激素对机体的新陈代谢、生长发育、各种功能活动以及维持内环境稳态等方面发挥重要的调节作用,低氧训练对机体激素的影响一直应该受到人们的关注。     

甲氨蝶呤的卷积极谱法测定和电极还原机理的研究

用高阶导数卷积极谱法研究了针剂和尿液中抗肿瘤药物甲氨蝶呤的微量测定法。在9.0×10^-8～1.6×10^(-5)mol/L内波高与浓度有线性关系。最低检测限为1.8×10^-8mol/L。与英国药典(1980)的标准方法进行了比较,极谱法具有更高的灵敏度。研究了甲氨蝶呤的电极还原机理。在Britton—Robinson缓冲溶液中甲氨蝶呤产生两个还原波。第一个波为可逆的2e—2H⁺电极还原过程,可供定量测定。第二个波为不可逆波。     

Genetic polymorphisms and drug interactions modulating CYP2D6 and CYP3A activities have a major effect on oxycodone analgesic efficacy and safety

Background and purpose:

Thrombus formation is commonly associated with pulmonary arterial hypertension (PAH). Thrombin may thus play an important role in the pathogenesis and pathophysiology of PAH. Hence, we investigated the contractile effects of thrombin and its mechanism in pulmonary artery.

Experimental approach:

The cytosolic Ca²⁺ concentrations ([Ca²⁺]_i), 20 kDa myosin light chain (MLC20) phosphorylation and tension development were evaluated using the isolated porcine pulmonary artery.

Key results:

Thrombin induced a sustained contraction in endothelium-denuded strips obtained from different sites of a pulmonary artery, ranging from the main pulmonary artery to the intrapulmonary artery. In the presence of endothelium, thrombin induced a transient relaxation. The contractile effect of thrombin was abolished by either a protease inhibitor or a proteinase-activated receptor 1 (PAR₁) antagonist, while it was mimicked by PAR₁-activating peptide (PAR₁AP), but not PAR₄AP. The thrombin-induced contraction was associated with a small elevation of [Ca²⁺]_i and an increase in MLC20 phosphorylation. Thrombin and PAR₁AP induced a greater increase in tension for a given [Ca²⁺]_i elevation than that obtained with high K⁺-depolarization. They also induced a contraction at a fixed Ca²⁺ concentration in α-toxin-permeabilized preparations.

Conclusions and implications:

The present study revealed a unique property of the pulmonary artery. In contrast to normal arteries of the systemic circulation, thrombin induces a sustained contraction in the normal pulmonary artery, by activating PAR₁ and thereby increasing the sensitivity of the myofilament to Ca²⁺. This responsiveness of the pulmonary artery to thrombin may therefore contribute to the pathogenesis and pathophysiology of PAH.     

TRILINOLEIN INHIBITS THE ADHESION OF NEUTROPHILS TO ENDOTHELIAL CELLS

1. Trilinolein is a triacylglycerol with linoleic acid as the only type of fatty acid in all three esterified positions of glycerol. It was recently reported to have a myocardial protective effect in coronary ligated rats. We now study its effect on the adhesion of human neutrophils to cultured bovine endothelial cells. 2. Pretreatment of an endothelial monolayer with trilinolein at concentrations ranging from 10^-10 to 10^-6 mol/L significantly inhibited neutrophil adhesion to endothelial cells. Trilinolein was less potent than sodium nitroprusside in inhibiting neutrophil adhesion. 3. The inhibitory effect of trilinolein was antagonized by methylene blue and N^G-nitro-L-arginine methyl ester. The inhibitory effect of trilinolein was not mediated through linoleic acid because linoleic acid did not inhibit neutrophil adhesion. 4. Pretreatment of neutrophils with trilinolein did not reduce neutrophil adhesion. However, in neutrophils activated with N-formyl-methionyl-leucyl-phenylalanine, trilinolein inhibited the neutrophil adhesion to endothelial cells. 5. We conclude that trilinolein inhibits neutrophil adhesion to the endothelial monolayer by stimulating the nitric oxide and cyclic GMP pathways in endothelial cells. It may also inhibit neutrophil adhesion by scavenging free radicals. The inhibitory effect of trilinolein on neutrophil adhesion may play a role in its myocardial protective activity.