NO在脊髓痛觉传递过程中的作用

一氧化氮(nitric oxide,NO)是神经元细胞内一种新型的神经递质,它参与多种生命活动,包括脊髓水平的伤害性信息传递过程。研究NO在伤害性信息传递过程中的作用及其机制,有利于阐明痛觉生理和发现疼痛治疗的新手段。本文将NO在慢性痛脊髓伤害性信息传递中的作用及其机制的相关研究进展作一综述。     

ZSM-5(38)/Al-MCM-41复合分子筛对纤维素催化热解的影响

以纤维素为原料,以自制的不同硅铝比ZSM-5(38)/Al-MCM-41微-介孔复合分子筛为催化剂,在固定床反应器上进行了催化热解实验。采用XRD表征分子筛,采用GC-MS分析生物油成分,考查了催化剂的改变对生物质热解产物及生物油成分的影响。实验结果表明:添加催化剂后,生物油产率降低,且其含水率也有所增加。与未添加催化剂相比,生物油中D L-2,3-丁二醇有明显提高。其中,ZSM-5(38)/Al-MCM-41(20)最有利于苯酚、愈创木酚(2-甲氧基-苯酚)的生成。此外,这几种催化剂均有利于小分子化合物的生成,其中,ZSM-5(38)有利于C4~C5化合物的生成,微-介孔复合分子筛则有利于C6~C8化合物的生成。     

超声波对猪胰脂肪酶催化活性影响的机理研究

猪胰脂肪酶(porcine pancreas Lipase,PPL)反应系统经适宜参数的超声波处理,催化活性提高了11.22%～24.42%。PPL经超声波处理后,其动力学参数Km和Vmax都变小,酶分子的紫外吸收光谱不变,荧光发射光谱不变。而酶分子经超声波处理后,其紫外差示光谱出现了明显的正峰或负峰。探讨了超声波影响PPL活性的作用机理。     

鳞片状细胞癌抗原Ⅰ与乙型肝炎病毒的结合受反应位点环域疏水性的影响

鳞片状细胞癌抗原Ⅰ (SCCA1)是丝氨酸蛋白酶抑制剂 (serpin)超家族的成员 ,具有多种变异体。有报道其中的两种(BP和AJ515706 )能通过乙型肝炎病毒 (HBV)的前S1抗原促进表达SCCA1的细胞与HBV的结合。本研究从HepG2细胞中扩增出的一株SCCA1(A1)却不具备HBV结合能力。将A1的C末端与BP的C末端互换 ,获得的A1-BP能够结合HBV ,而BP-A1却不能。A1与BP的C末端仅有 3个氨基酸的差异 ,其中 2个位于反应位点环域。一级结构分析发现在该区域内 ,A1的疏水性较弱 ,而BP和AJ515706的疏水性较强。将A1的aa349位的弱疏水性的谷氨酸突变为强疏水性的缬氨酸 ,则可获得HBV结合能力。反之 ,将BP同一位点的缬氨酸突变为谷氨酸 ,则会丧失HBV结合能力。这些结果提示SCCA1与HBV的结合受反应位点环域的疏水性的影响。     

中国倍唇螺属一新种记述(前鳃亚纲,中腹足目,环口螺科)

笔者对我国已记载的倍唇螺属Diplommatina Benson,1849种类进行了厘订,并对馆藏的该属标本进行整理和鉴定,发现1新种,即兴义倍唇螺Diplommatina xingyinensis sp.nov.,新种隶属前鳃亚纲、中腹足目、环口螺科、倍唇螺属.对新种形态特征、栖息环境进行了记述,并对其近似种进行了讨论.     

寄生于杜氏泛树蛙多盘虫属单殖吸虫一新种记述

于云南屏边县杜氏泛树蛙Polypedates dugritei David膀胱内检获单殖吸虫多盘科多盘虫属1新种:屏边多盘吸虫Polystoma pingbianensis sp.nov.,对其形态结构及宿主特异性问题进行了初步研究.据宿主膀胱内寄生的产卵成虫测量形态分类数据和描述鉴定特征.虫体全长平均9.428 mm,后吸器大小平均0.869 mm×0.784 mm,后吸器吸盘的直径平均434.4μm,后吸器上两个中央大钩全长平均403.2μm.朝向外侧肠管无盲突,朝向内侧肠管每侧形成13～14个盲突,有1个或无过腹中线的肠联合,肠管于后端合并向后延伸至后吸器内,不形成盲突.卵巢较小,位于单个睾丸之前,卵巢长平均711.52 μm.卵相对较大,卵长平均306.6μm,卵宽平均164.6μm.     

白首乌化学成分与药理活性研究进展

白首乌类植物含有C21甾体酯甙类、磷脂类、苯乙酮甙类等化学成分,具有抗氧化、调节免疫功能、抗肿瘤、抗缺氧、降血脂等多种药理活性.主要综述了近年来白首乌类植物化学成分及药理活性研究进展概况.     

柴胡属植物化学成分及药理研究新进展

介绍了近十年来国内外柴胡属植物化学成分及主要化学部位药理研究新进展.为进一步研究开发柴胡提供了依据.     

Epithelial neutrophil-activating peptide (ENA-78), acute coronary syndrome prognosis, and modulatory effect of statins

Endothelial inflammation with chemokine involvement contributes to acute coronary syndromes (ACS). We tested the hypothesis that variation in the chemokine gene CXCL5, which encodes epithelial neutrophil-activating peptide (ENA-78), is associated with ACS prognosis. We also investigated whether statin use, a potent modulator of inflammation, modifies CXCL5's association with outcomes and characterized the in vitro effect of atorvastatin on endothelial ENA-78 production. Using a prospective cohort of ACS patients (n = 704) the association of the CXCL5 -156 G>C polymorphism (rs352046) with 3-year all-cause mortality was estimated with hazard ratios (HR). Models were stratified by genotype and race. To characterize the influence of statins on this association, a statin*genotype interaction was tested. To validate ENA-78 as a statin target in inflammation typical of ACS, endothelial cells (HUVECs) were treated with IL-1beta and atorvastatin with subsequent quantification of CXCL5 expression and ENA-78 protein concentrations. C/C genotype was associated with a 2.7-fold increase in 3-year all-cause mortality compared to G/G+G/C (95%CI 1.19-5.87; p = 0.017). Statins significantly reduced mortality in G/G individuals only (58% relative risk reduction; p = 0.0009). In HUVECs, atorvastatin dose-dependently decreased IL-1beta-stimulated ENA-78 concentrations (p<0.0001). Drug effects persisted over 48 hours (p<0.01). CXCL5 genotype is associated with outcomes after ACS with potential statin modification of this effect. Atorvastatin lowered endothelial ENA-78 production during inflammation typical of ACS. These findings implicate CXCL5/ENA-78 in ACS and the statin response.     

Quantitative-Trait Loci Influencing Body-Mass Index Reside on Chromosomes 7 and 13: The National Heart, Lung, and Blood Institute Family Heart Study

Obesity is a risk factor for many chronic diseases, including glucose intolerance, lipid disorders, hypertension, and coronary heart disease. Even though the body-mass index (BMI) is a heterogeneous phenotype reflecting the amount of fat, lean mass, and body build, several studies have provided evidence of one or two major loci contributing to the variation in this complex trait. We sought to identify loci with potential influence on BMI in the data obtained from National Heart, Lung, and Blood Institute Family Heart Study. Two complementary samples were studied: (a) 1,184 subjects in 317 sibships, with 243 markers typed by the Utah Molecular Genetics Laboratory (UMGL) and (b) 3,027 subjects distributed among 401 three-generation families, with 404 markers typed by the Mammalian Genotyping Service (MGS). A genome scan using a variance-components-based linkage approach was performed for each sample, as well as for the combined sample, in which the markers from each analysis were placed on a common genetic map. There was strong evidence for linkage on chromosome 7q32.3 in each sample: the maximum multipoint LOD scores were 4.7 (P<10-5) at marker GATA43C11 and 3.2 (P=.00007) at marker D7S1804, for the MGS and UMGL samples, respectively. The linkage result is replicated by the consistent evidence from these two complementary subsets. Furthermore, the evidence for linkage was maintained in the combined sample, with a LOD score of 4.9 (P<10-5) for both markers, which map to the same location. This signal is very near the published location for the leptin gene, which is the most prominent candidate gene in this region. For the combined-sample analysis, evidence of linkage was also found on chromosome 13q14, with D13S257 (LOD score 3.2, P=.00006), and other, weaker signals (LOD scores 1.5-1.9) were found on chromosomes 1, 2, 3, 5, 6, 14, and 15.