The influence of environmental and health indicators on premature mortality: An empirical analysis of the City of Toronto's 140 neighborhoods

The objective of this paper was to assess the link between premature mortality and a combination of neighbourhood contextual (environmental and health) and compositional (socioeconomic and demographic) characteristics. We statistically and spatially examined six environmental variables (ultrafine particles, carcinogenic and non-carcinogenic pollutants, pollution released to air, tree cover, and walkability index), six health service indicators (number health providers, breast, colorectal and cervical cancer screening uptake rates, student nutrition program uptake rates, and healthy food index), and eight socioeconomic indicators (total income, Gini coefficient, two age categories – below and above 40 years, proportion of females to males, visible minorities, Indigenous peoples, education, less than grade 9) among 140 neighbourhoods of the City of Toronto in Ontario (Canada). We applied principal component analysis to identify patterns and to reduce the number of explanatory variables into combined component axes that represent unique variation in these confounded and overlapping factors. We then applied regression analysis to model the relationship between the indices of enviro-health and socioeconomics and their potential relationship with premature mortality. Residual spatial analysis was used to investigate any remaining spatial structure (such as neighbourhoods with higher residual premature mortality rates). Neighbourhood Equity Index was correlated with our enviro-health and socioeconomic indices. Premature mortality within neighbourhoods was predicted by poor cancer screenings, pollution, lack of tree canopy, increased uptake of student nutrition programs and high walkability index. A negative association between premature mortality and pollution was associated low walkability index and presence of visible minorities within neighbourhoods. There was some unexplained residual spatial variation in our model of premature mortality - especially along the shores of Lake Ontario and in neighbourhoods with major highways or road corridors: premature mortality in Toronto neighbourhoods was higher than expected along highway-corridor neighbourhoods and shorelines. Our analysis revealed a significant relationship between neighbourhood contextual features – both environmental and health – and premature mortality, suggesting that these contextual components of neighbourhoods can predict rates of urban premature mortality in Toronto.     

树型金银花无公害优质加工技术的研究

目的探讨树型金银花无公害优质加工技术。方法采用树型金银花晾晒和烘烤以及"烤房3段变温烘烤技术"。结果烘干产品比晒干产品具有明显的质量和价格优势,价格高57.1%。烤房3段变温技术第1段烘干温度控制在35～40℃,烘8～9h;第2段将温度提高到50～55℃左右,烘烤6～8h;第3段温度升到60～70℃,烘烤5～6h左右;烘干总时间不超过24h。结论无公害优质加工技术利于规模化生产,获得无公害的绿色产品,增加金银花附加值。     

中药药性量化方法对补虚药功效归类预测的研究

目的对中药药性依其重要性进行更深层次的多值量化分析,将比定性的文字表述和简单的二值量化表示更有意义.方法以补虚药为研究对象,药性为基本特征,在对其进行二值量化和多值量化的基础上,采用应用人工神经网络和决策树等数据库知识发现技术,进行对补虚药功效归类判别结果的影响研究.结论结果表明药性的不同量化方法对补虚药的功效归类预测有一定影响,多值量化比二值量化具有更为理想的判别结果.     

脑缺血时皮层扩布性抑制与心功能障碍

目的 :研究树 鼠句脑缺血时单胺氧化酶 (MAO)活化在脑缺血时心功能障碍以及扩布性抑制中的可能作用。方法 :采用光化学法诱导树 鼠句血栓性脑缺血 ,测定缺血区及血清MAO活性、多巴胺及去甲肾上腺素 (NA)水平 ,经电镜观察脑及肾上腺的超微结构。记录仪检测心率(HR)、左室收缩压峰值 (LVSP) ,左室瞬间收缩与舒张最大速率 (±dp/dtmax) ,左室舒张末期压力 (LVEDP) ,平均动脉压 (MAP)。结果 :树鼠句脑缺血过程中血清NA先升高 (由 11.60± 0 .73ng/ml升高至18.46± 0 .3 9ng/ml,P <0 .0 1) ,72h后降至 8.3 2± 1.86ng/ml;血清MAO活性逐渐升高 ,达 2 10 .1± 2 6.67U/ml(P <0 .0 1) ,72h降低至对照水平 ;心功能指标 (±dp/dtmax,LVSP ) ,尤其是HR明显降低 ,由3 17.0± 98.0 1beat/min降至 2 3 7.4± 3 1.90beat/min(P <0 .0 1) ,于2 4h恢复至对照水平。结论 :血栓性脑缺血时血清NA水平明显取决于MAO活性的变化 ,后者对脑缺血时心脏舒缩功能可能具有调节作用。     

树鼩脑干儿茶酚胺神经元的分布

应用FAGLU荧光组化技术观察了树鼩脑干儿茶酚胺神经元(简称CA神经元)的位置分布及其形态特征。结果表明,CA神经元主要分布于下列核区:延髓的腹外侧网状核(LRN),孤束核(Sol);脑桥的面神经核(nVll).脑桥尾侧网状校(PnC),第四脑室顶外侧壁,蓝斑(Lc),脑桥头端与中脑尾端移行部的中缝背核(DR)、中央上核(cs),腹外侧臂旁核(VLPB)、中央灰质腹侧(Vcg);中脑的黑质(SN)、和腹侧被盖区(VTA)。     

Reciprocal heterotopic callosal connections between the two striate areas in Tupaia

Summary WGA-HRP injections were placed into area 17 close to the border with area 18 of Tupaia belangeri in order to study the callosal connections of the striate area in this animal. Most callosal neurons were found in the striate cortex (57.6–86.9%), some in the extrastriate area 18 (10.6–28.1%), and a few in even more temporal regions (2.5–14.3%). Concerning only the area 17, reciprocal homotopic connections could be observed as a strip along the area 17/18 border. Additionally, heterotopic callosal connections could be seen in regions representing the binocular visual field, especially the lower part. The area 17 cells were mostly located in the supragranular layers II and III (94.1–97.2%). But neurons could also be found in the infragranular layers, especially layer VI (2.6–5.2%) and in layer IV (0.2–1.1%). Homotopic projections were mostly seen in layers IIIc and V. The majority of the supragranular and infragranular neurons are pyramidal cells. However, a newly defined subpopulation of neurons, most probably stellate cells, were discovered forming a band in sublayer IIIc, very close to the layer III/IV border.     

树鼩胆固醇酯转运蛋白的cDNA和蛋白质结构分析

目的　获得不易感动脉粥样硬化动物树胆固醇酯转运蛋白 (CETP)的cDNA和蛋白质序列 ,分析其结构特点 ,寻找其可能的抗动脉粥样硬化分子机制。方法　以从树肝脏mRNA反转录获得的cDNA一链为模板 ,应用SMART RACE技术 ,获得了树CETP的cDNA序列 ,并推导出其蛋白质氨基酸序列 ,应用分子生物学软件对该蛋白的一级、二级结构进行分析和比较。结果　获得的树CETPcDNA(在GenBank中的注册号为AF334 0 33)长 16 36bp ,编码 485个氨基酸 ,其成熟蛋白由 477个氨基酸组成 ,比人多一个氨基酸 (Gly318) ,该蛋白与人、家兔的同源性分别为 88%和 82 %。序列中与CETP结合和转运中性脂质功能相关的区域均非常保守 ,但在Asn34 2位的N 糖基化位点缺失 ,可能使其转运胆固醇酯的活性增加 ,利于外周组织和血浆中的胆固醇及其酯的清除。通过对不同种属蛋白序列的比较 ,初步分析了树CETP蛋白与功能相关的结构特点。结论　树CETP糖基化的特点有可能是该动物对动脉粥样硬化具有不易感性的分子机理之一     

On the evolution of chaperones and cochaperones and the expansion of proteomes across the Tree of Life

Across the Tree of Life (ToL), the complexity of proteomes varies widely. Our systematic analysis depicts that from the simplest archaea to mammals, the total number of proteins per proteome expanded ∼200-fold. Individual proteins also became larger, and multidomain proteins expanded ∼50-fold. Apart from duplication and divergence of existing proteins, completely new proteins were born. Along the ToL, the number of different folds expanded ∼5-fold and fold combinations ∼20-fold. Proteins prone to misfolding and aggregation, such as repeat and beta-rich proteins, proliferated ∼600-fold and, accordingly, proteins predicted as aggregation-prone became 6-fold more frequent in mammalian compared with bacterial proteomes. To control the quality of these expanding proteomes, core chaperones, ranging from heat shock proteins 20 (HSP20s) that prevent aggregation to HSP60, HSP70, HSP90, and HSP100 acting as adenosine triphosphate (ATP)-fueled unfolding and refolding machines, also evolved. However, these core chaperones were already available in prokaryotes, and they comprise ∼0.3% of all genes from archaea to mammals. This challenge—roughly the same number of core chaperones supporting a massive expansion of proteomes—was met by 1) elevation of messenger RNA (mRNA) and protein abundances of the ancient generalist core chaperones in the cell, and 2) continuous emergence of new substrate-binding and nucleotide-exchange factor cochaperones that function cooperatively with core chaperones as a network.

All cellular life is thought to have stemmed from the last universal common ancestor (LUCA) (1, 2), that emerged more than 3.6 billion y ago. Two major kingdoms of life diverged from LUCA: bacteria and archaea, which about 2 billion y later merged into the eukaryotes (3). Since the beginning of biological evolution, life’s volume has increased on a grand scale: The average size of individual cells has increased ∼100-fold from prokaryotes to eukaryotes (4), the number of cell types has increased ∼200-fold from unicellular eukaryotes to humans (5), and average body size has increased ∼5,000-fold from the simplest sponges to blue whales (6).This expansion in organismal complexity and variability was accompanied by an expansion in life’s molecular workforce, proteomes in particular, which in turn presented a challenge of reaching and maintaining properly folded and functional proteomes. Most proteins must fold to their native structure in order to function, and their folding is largely imprinted in their primary amino acid sequence (7–9). However, many proteins, and especially large multidomain polypeptides, or certain protein types such as all-beta or repeat proteins, tend to misfold and aggregate into inactive species that may also be toxic (10). Life met this challenge by evolving molecular chaperones that can minimize protein misfolding and aggregation, even under stressful out-of-equilibrium conditions favoring aggregation (11, 12). Chaperones can be broadly divided into core and cochaperones. Core chaperones can function on their own, and include ATPases heat shock protein 60 (HSP60), HSP70, HSP100, and HSP90 and the adenosine triphosphate (ATP)-independent HSP20. The basal protein holding, unfolding, and refolding activities of the core chaperones are facilitated and modulated by a range of cochaperones such as J-domain proteins (13–15).Starting from LUCA, as proteomes expanded, so did the core chaperones and their respective cochaperones. Indeed, chaperones have been shown to facilitate the acquisition of destabilizing mutations and thereby accelerate protein evolution (16–18). However, the coexpansion of proteomes and of chaperones, underscoring a critical balance between evolutionary innovation and foldability, remains largely unexplored. We thus embarked on a systematic bioinformatics analysis that explores the evolution of both proteomes and chaperones, and of both core and their auxiliary cochaperones, along the Tree of Life.     

野生树鼩肠道蠕虫感染调查及分析

目的调查野生树鼩(Tupaia belangeri Chinensis)感染肠道蠕虫的主要种类并进行鉴定,为今后树鼩寄生虫检测提供形态学参考,为实验树鼩寄生虫控制提供依据。方法采集203只野外来源的树鼩新鲜粪便,虫卵采用常规粪便直接涂片以及孵化后显微镜观察;绦虫采用压片、固定染色,以及线虫经透明后体视镜观察,虫卵与成虫相对应鉴定。结果野生树鼩肠道蠕虫的总感染率为75.86%,主要感染种类有3种,经鉴定为长膜壳绦虫、奇口线虫和粪类圆线虫,感染率分别为27.67%,30.06%和51.52%。三种蠕虫的混合感染率为4.55%。两种线虫虫卵在树鼩粪便中多为含胚胎形态。结论野生树鼩肠道蠕虫的感染率较高。对野外引入的新种源必须隔离检疫,进行针对性的药物治疗,才能有效地控制肠道寄生虫病的传播。     

人乙型肝炎病毒感染与原发性肝癌──—在树忽的实验研究

用人乙肝病毒（ＨＢＶ）接种树的，建立ＨＢＶ感染动物模型，实现连续传代感染，并用乙肝疫苗预防其感染。以此模型研究ＨＢＶ及（或）黄曲霉毒素Ｂ１（ＡＦＢ１）在诱发肝癌中的作用。结果肝癌诱发率在同时接受两种因子者显著高于单一因子者，癌前病变的发生与肝癌诱发率相关，被感染树的肝组织及（或）肝癌中检出ＨＢＶＤＮＡ可整合于宿主肝ＤＮＡ。提示ＨＢＶ和ＡＦＢ１起协同致癌作用并支持ＨＢＶ与肝癌的病因学关系。