神经科门诊血压记录表的设计及应用

<正>中国是脑卒中高发区,高血压与脑卒中的发生关系密切,18岁以上居民高血压患病率为18.8%,而且呈逐年增高的趋势,血压水平越高,脑卒中再次发生危险越大[1],控制高血压可以减少脑卒中的发生率。但是长期以来,由于患者对监测疾病情况相关知识的重视程度不够,影响了高血压的诊治效果。目前,大部分医院对出院后门诊高血压患者血压数据缺乏规范、连续性的记录管理,只在每次来医院就诊时在门诊病历上记录上     

顽固性癫痫的外科治疗

目的：探讨术中在皮质和深部脑电图监测下顽固性癫痫的致痫灶定位及术式选择。方法：38例患者根据术前致痫灶的定位和术中皮质及深部电极的监测，分别采用不同的术式：(1)单纯致痫灶切除2例；(2)多软膜下横切术(multiple subpial transection，MST)8例；(3)致痫灶切除4-MST18例；(4)前颞叶、杏仁核-海马切除5例，神经导航下选择性杏仁核-海马切除1例；(5)胼胝体切开4-MST4-皮质热灼4例。结果：38例患者经3～30个月的随访，满意12例(31．6％)，显著改善10例(26．3％)，良好6例(15．8％)，效差4例(10．5％)。无改善6例(15．8％)。总有效率73．7％，治愈率达31．6％。无一例致残或死亡。结论：术中在皮质和深部脑电图监测下，对致痫灶准确的定位和采用不同的术式切除是治疗顽固性癫痫的有效途径。     

Decay-Accelerating Factor Suppresses Complement C3 Activation and Retards Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient Mice

Decay-accelerating factor (DAF; CD55) is a membrane protein that regulates complement pathway activity at the level of C3. To test the hypothesis that DAF plays an essential role in limiting complement activation in the arterial wall and protecting from atherosclerosis, we crossed DAF gene targeted mice (daf-1^−/−) with low-density lipoprotein-receptor deficient mice (Ldlr^−/−). Daf-1^−/−Ldlr^−/− mice had more extensive en face Sudan IV staining of the thoracoabdominal aorta than Ldlr^−/− mice, both following a 12-week period of low-fat diet or a high-fat diet. Aortic root lesions in daf-1^−/−Ldlr^−/− mice on a low-fat diet showed increased size and complexity. DAF deficiency increased deposition of C3d and C5b-9, indicating the importance of DAF for downstream complement regulation in the arterial wall. The acceleration of lesion development in the absence of DAF provides confirmation of the proinflammatory and proatherosclerotic potential of complement activation in the Ldlr^−/− mouse model. Because upstream complement activation is potentially protective, this study underlines the importance of DAF in shielding the arterial wall from the atherogenic effects of complement.Complement, a complex cascade of serine proteases, is well characterized as playing a pivotal role in inflammation and in bridging innate and adaptive immunity.¹ Currently, complement is understood to be triggered by three proximal cascades, the classical, alternative, and mannose-binding lectin pathways, which converge on C3 at the central hub of the system. Cleavage of C3 leads to the generation of down-stream proinflammatory mediators, including the anaphylatoxins C3a and C5a and the membrane attack-complex C5b-9. Although the assembly and insertion of C5b-9 into cell membranes may lyse non-nucleated cells, sublytic levels can activate proliferation and/or proinflammatory gene expression.²There is increasing interest in dissecting the possible roles of complement in atherosclerosis in vivo.^3,4 Theoretically, many factors might activate complement in the arterial wall, including Igs, cholesterol crystals, enzymatically-modified low-density lipoprotein (LDL) and apoptotic cells.^{5,6,7,8,9,10,11,12} However, enzymatically-modified LDL is likely to be the most abundant stimulus for complement activation in atherosclerosis, and may act via the alternative pathway and also via direct binding of C1q and C-reactive protein.^8,9,13,14,15 In addition, the classical and alternative pathways are capable of low grade “tick-over” activity.^16,17Previous experimental work has focused on the effects of natural or experimental deficiency of individual complement pathway components. Relevant studies are as follows: (1) rabbits with natural deficiency of C6 have been shown to be protected from diet-induced atherosclerosis^18,19; (2) although C5 deficiency has been found to have no effect on lesion development in high fat diet-fed ApoE^−/− mice,²⁰ a recent study has shown protective effects of an anti-C5 antibody in ApoE^−/− mice deficient in both Cd59a and Cd59b genes²¹; (3) C3 deficient mice crossed with Ldlr^−/− single knock-out mice have been found to have increased aortic lipid deposition with impaired lesion development beyond the foam cell stage²²; (4) crossing Factor B deficient mice with ApoE^−/−Ldlr^−/− double-knock-outs had no effect, arguing against an important role for the alternative pathway in that model²³; and (5) more recently, we have reported that low fat diet-fed Ldlr^−/− mice deficient in classical pathway activity through gene-targeting of C1q (C1qa^−/−) show accelerated atherosclerosis with increased lesion complexity.²⁴ The increased lesion size and complexity in low fat diet-fed C1qa^−/−Ldlr^−/− mice was associated with an increase in lesional apoptotic cells, consistent with previous studies that have demonstrated a direct role for C1q in apoptotic cell clearance, independent of terminal pathway activation.^25,26 Recently, the role of the lectin pathway has also been shown to have atheroprotective functions in mice,²⁷ in line with the involvement of mannose-binding lectin in apoptotic cell clearance and also with the association of mannose-binding lectin deficiency with accelerated atherosclerosis in humans.^28,29Complement activity is tightly regulated by a number of fluid-phase and membrane-bound inhibitors, including the two glycosylphosphatidylinositol-anchored membrane proteins decay-accelerating factor (DAF, CD55) and protectin (CD59). Although CD59 inhibits insertion of C9 into cell membranes and thus the development of C5b-9 membrane attack complexes, DAF binds to C3, thereby accelerating the decay of the two C3 convertases, C3Bb (alternative pathway) and C4b2a (classical and mannose-binding lectin pathways).^30,31,32 Structurally, DAF is a multidomain protein comprising a proximal serine/threonine-rich region and four complement control protein (CCP) domains, of which CCP2 and CCP3 dissociate C3Bb and C4b2a oligomers into constituent proteins. The catalytic mechanism of DAF activity is not fully clear, but the crystal structure and substitution mutants identify Bb (Tyr338), DAF-CCP2 (Arg69, Arg96) and DAF-CCP3 (Phe148 Leu171) as key residues.^33,34The mouse has two DAF genes encoding glycosylphosphatidylinositol-anchored and trans-membrane forms, respectively, with the former being more representative of human DAF.³⁵ Gene-targeting of the glycosylphosphatidylinositol-anchored form has led to the generation of a knock-out strain that is healthy but shows exaggerated inflammation in models of renal, autoimmune, and nervous system diseases.^36,37,38,39 Recently, no protection or exacerbation of atherosclerosis was observed after crossing these mice with the ApoE^−/− strain.⁴⁰Observations that the classical pathway exerts atheroprotective effects without terminal pathway activation suggest the importance of a strong complement regulatory system in the arterial wall.^14,24 Consistent with this, we and others have recently published evidence that CD59 deficiency leads to an acceleration of atherosclerosis in Ldlr^−/− and ApoE^−/− mouse models, establishing the proatherogenic potential of the terminal complement pathway and highlighting the importance of CD59 in its regulation.^21,40,41 In this article, we show that DAF also plays a role in the regulation of atherosclerosis in the Ldlr^−/− model.     

白藜芦醇抑制胆囊癌细胞生长与诱导细胞凋亡的实验研究

目的:探讨白藜芦醇(Res)对胆囊癌细胞(GBC)和正常成纤维细胞(3T3)体外增殖的影响,进而观察Res对GBC和3T3细胞凋亡的影响.方法:MTT法测定肿瘤细胞生长抑制率;流式细胞术分析细胞周期,检测细胞凋亡;SABC法检测细胞bcl-2、c-myc、p53蛋白表达.结果:Res呈浓度依赖性抑制GBC细胞的生长与增殖(P＜0.01),抑制率最高可达54%.Res能明显诱导GBC细胞凋亡,凋亡率最高为30.52%;处理组较对照组G1期细胞由34.88%上升至55.47±3.95%,S期细胞减少8.41%～17.54%,呈明显的G0/G1期阻滞现象.GBC细胞的bcl-2、c-myc基因蛋白表达降低,而p53基因蛋白表达增强.结论:Res能通过诱导GBC细胞凋亡而抑制其生长与增殖,但对3T3细胞无此作用.     

黄芪建中汤对胃黏膜损伤模型大鼠MMP-2及TIMP-1表达的影响

目的:观察黄芪建中汤对胃黏膜损伤模型大鼠基质金属蛋白酶-2(MMP-2)及其抑制因子-1(TIMP-1)表达的影响。方法:将健康SD大鼠随机分为4组:假手术组、模型组、黄芪建中汤组、生胃酮组,每组10只。采用改良Okabe法复制动物模型。胃黏膜MMP-2、TIMP-1表达水平检测采用免疫组织化学法。结果:模型组MMP-2表达较假手术组显著升高(P<0.01),各治疗组MMP-2表达水平显著低于模型组(P<0.01);模型组TIMP-1表达较假手术组显著降低(P<0.05,P<0.01),各治疗组TIMP-1表达水平显著高于模型组(P<0.01);黄芪建中汤组较生胃酮组MMP-2表达水平显著降低(P<0.01),TIMP-1表达水平显著升高(P<0.01)。结论:黄芪建中汤通过调控MMP-2、TIMP-1的表达水平,修复胃黏膜损伤。     

药对“蛇床子一补骨脂”与乳腺癌骨转移裸鼠体重变化与骨代谢的量效关系研究

目的 从调节破骨细胞分化的主要途径护骨素(OPG)/细胞核因子κB受体活化因子配体(RANKL)/细胞核因子κB受体活化因子(RANK)系统研究蛇床子—补骨脂温肾药对抑制乳腺癌骨转移的作用机制.方法 将42只乳腺癌骨转移裸鼠随机分为模型组、唑来磷酸组、蛇床子组、补骨脂组、2:2配比组、1:3配比组、3:1配比组,每组6只;另备正常裸鼠6只作为正常组.分别给予相应的药液灌胃,唑来磷酸组皮下注射,正常组给予生理盐水灌胃,持续6周.观察裸鼠的体重、骨转移灶病理和OPG、RANKL mRNA表达水平变化.结果 3:1配比组和2:2配比组体重下降率明显低于其他配比组,而2:2配比组低于3:1配比组;不同比例配伍组的骨抗酒石酸酸性磷酶(TRAP)(+)细胞数差异均有统计学意义,2:2配比组优于1:3配比组(P＜0.05);不同配比的蛇床子—补骨脂可不同程度地上调OPG基因表达,下调RANKL基因表达,从基因方面调节OPG/RANKL的分泌比例,其中2:2配比组的疗效优于其他配比组.结论 不同配比的蛇床子—补骨脂均具有一定的抑制乳腺癌骨转移作用,其中2:2配比组疗效最突出,其作用机制可能是调节了OPG/RANKL基因分泌比例.     

阔叶十大功劳根中生物碱组分体外抗流感病毒试验研究

利用鸡胚试验技术研究了阔叶十大功劳根中生物碱成分在体外对流感病毒的抑制作用。试验结果表明，阔叶十大功劳根中生物碱成分在20mg／ml时对鸡胚无毒性，0．25mg／ml时仍显示出对甲1型流感病毒较强的抑制作用。     

不同干燥方法对桂枝药材中苯丙素类成分的影响及评价

目的:研究不同干燥方法对桂枝药材中苯丙素类(香豆素、肉桂醇、肉桂酸、桂皮醛、邻甲氧基肉桂醛)化学成分的影响,为桂枝适宜干燥方法的确定提供依据。方法:以苯丙素类化学成分含量为评价指标,分别对晒干、阴干及3种现代加工干燥方法后桂枝的质量进行评价,通过SPSS软件进行主成分分析,利用主成分得分进行综合评价。结果:不同干燥处理方法后有效成分含量差异较大,其中微波干燥使有效成分损失最多,阴干、晒干、低温热风干燥有利于桂枝有效成分的保留。结论:以干燥时间、化学成分含量、外观性状、气味等为评价指标,确定热风干燥50℃为桂枝药材较为适宜的现代干燥加工方法。     

2016—2020年我国中药资源学学科建设及科学研究进展与展望

中药资源学学科建设主要包涵中药资源学相关专业建设、教材体系建设、人才团队建设,以及中药资源学理论与方法技术创新、成果转化及服务社会等方面。中药资源领域的科学研究主要涉及中药资源调查研究、中药材规范化生产、中药资源有效利用、中药资源保护、中药资源产业发展等方面。在以往连续报道的基础上,对2016―2020年我国中药资源学学科建设及科学研究进展等进行归纳整理,基本反映了本领域的发展概况和广大科技工作者、企业家及管理者的代表性贡献,以期为中药与天然药物资源领域的学科建设、人才培养、科学研究、社会服务及中药产业发展起到相互借鉴的作用,共同致力于我国中医药事业和中药资源产业的高质量发展。     

李海松教授从瘀、虚论治慢性前列腺炎经验

慢性前列腺炎是男科较为常见的疾病,其病因病机复杂,单纯从某一病机论治通常难以取得良好的效果。李海松教授临床经验丰富,指出精室具有易虚易瘀的重要特征,所以慢性前列腺炎也应当从瘀、虚论治。其中,瘀既是核心病机又是病理产物,可以分为络脉瘀阻、因郁致瘀、痰湿致瘀、因火致瘀; 虚为基本病机和病理趋势,可分为肾气亏虚和脾气亏虚。瘀和虚二者关系紧密,相互作用,从瘀、虚论治慢性前列腺炎拓宽了诊疗思路。