866 resultados para The Dutch Disease
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本文系统研究了沈阳城市森林的布局与结构、城市森林功能、城市森林病虫害发生与树木健康状况和城市自然资源与社会经济状况等指标对沈阳城市森林生态系统健康与管理的影响。同时一,采用2种生态系统健康评价方法对沈阳城市森林生态系统健康状况进行了评价,并提出了沈阳城市森林生态系统健康管理的对策。研究结果如下:1、截至2004年末,沈阳城市森林植被覆盖率已经达到35%,城市森林林地分布基本合理,但需要进一步加强道路林地、居住区林地和城郊大面积生态林建设。2、沈阳城市森林以乔木为主,乔灌株数比为1.7:1,乔灌的覆盖度比约为7:1。3、沈阳城市森林不同类型林地中植物组成不同。公园林地中有74个属,137个种(变种);庭院林地中有53个属,104个种(变种);居住区林地中有45个属,81个种(变种);道路林地中有43个属,94个种(变种);运河风景林地中有75个属,142个种(变种);棋盘山风景林地中有48个属,118个种(变种)。4、公园林地、庭院林地、居住区林地、道路林地和运河风景林地的Shannon一Wiener多样性指数分别为2.78、3.05、3.15、3.18和3.18,均匀度指数分别为0.56、0.66、0.72、0.70和0.64。除了棋盘山风景林地外,沈阳城市森林中栽植总量超过乔木总量5%的乔木树种有7个属,分别为李、柳树、杨树、桧柏、榆树、槐树和银杏,7种树木总量达到了全部乔木总量的82.09%;栽植总量超过灌木总量5%的灌木树种也有7个属,分别为水腊、丁香、李属,小聚、玫瑰、忍冬和连翘,7个属灌木总量达到了全部灌木总量的87.92%。5、公园林地、庭院林地、道路林地和防护林地中OBH<20cm、20cm<DBH<60cm和DBH>60cm树木的比例分别为:57.9%、40.0%、2.1%,49.2%、47.8%、3.0%,65.3%、33.1%、1.6%和64.6%、34.9%、0.5%,表明沈阳城市森林树木的规格总体上偏小。6、经样方调查和CITYgreen模型计算,沈阳城市森林的生态效益约2.0亿USD/yr.。公园林地、庭院林地和风景林地的景观指标相对较高;道路林地和居住区林地的景观效果一般;防护林地的景观效果较差。7、目前已经发现的沈阳城市森林病害约600余种,虫害约700余种,其中杨树主要病虫害39种,柳树的主要病虫害有33种,榆树和槐树的主要病虫害均为,1种。杨柳树腐烂病、光肩星天牛、天幕毛虫、桃红颈天牛和美国白蛾等是近10年来沈阳城市森林中普遍发生和造成严重危害的主要病虫害。沈阳城市森林主要树木的平均健康指数为2.68,处于一般健康状态。8、沈阳城市森林的土壤和水资源状况均不利于树木的健康生长,沈阳的社会经济发展也有待于进一步提高。9、经过生物指示物法(光肩星天牛为生物指示物)、专家权重法、公众问卷调查和对比研究,沈阳城市森林生态系统总体上处于亚健康状态。10、通过对沈阳城市森林资源、管理状况的调查研究和健康状况的评价,本文提出了沈阳城市森林生态系统健康管理的对策,包括合理规划沈阳城市森林林地布局,增加道路林地、居住区林地和城郊林地的面积和植被覆盖率;调整树木种类组成,避免单一或少数树种的大量栽植,提高生物多样性水平;保护大树和古树;增加城市森林管理资金的投入;应用先进技术,采取科学的病虫害防治和植物养护方法,促进树木的健康生长等。This project systematically studied the urban forest ecosystem health and management in Shenyang. The study explored factors, such as urban forest structure, distribution, pests, aesthetic value, ecological benefit, natural resources and socieo-economic status, that affecting the urban forest ecosystem health and management. Two methods were used to evaluate the ecosystem health. This project also proposed Shenyang's urban forest ecosystem health management strategies. The research results can be summarized as follows: 1. As of the end of 2004, urban forest coverage in Shenyang is about 35%, and is in relatively even patch distribution pattern. However, the street trees and roadside forest patches, residential block forest patches should be enhanced. 2. Trees are the major component of the Shenyang s urban forest, followed by shrubs. The quantity ratio of tree to shrub is about 1.7:1, and the coverage ratio of trees to shrub is about 7:1. 3. Species composition varies by location. There are 74 genera, 137 species (including varieties) in the public parks; 53 genera, 104 species (and var.) in the green spaces of the institution (including school), factory, and company; 45 genera, 81 species (var.) in residential blocks; 43 genera, 94 species (var.) in streets and roadside forest patches; 75 genera, 142 species (var.) in the Canal landscape forest patches; 48 genera, 118 species (var.) in the Qipan Mountain recreation forest. 4. The Shannon-Woener indices varies in parks, in institution, factory, and company yards, in streets and roadside forest patches, in residential blocks.there are 2.78, 3.05, 3.18, 3.15, 3.18, respectively; and the evenness indices are 0.56, 0.66, 0.70, 0.72, 0.64, respectively. Besides the Qipan Mountain forest patches, trees of 7 genera, Prunus spp., Salix spp., Populus spp., Sabina spp., Ulmus spp., Robinia spp. and Ginkgo biloba are of more than 5% the total urban trees, respectively. In fact, trees from these 7 genera are about 82% of all trees in Shenyang's urban forests. In terms of shrubs, species of 7 genera, Ligustrum spp., Syringa spp., Prunus spp., Berberis spp., Rosa spp., Lonicera spp., and Forsythia spp. are more than 5% the total urban shrubs, respectively. 88% of all the shrubs in Shenyang s urban forest are from these 7 genera. 5. The diameter class of DBH<20cm, 20cm
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禾谷孢囊线虫严重影响禾谷类作物的产量,在小麦中由禾谷孢囊线虫引起的产量损失可达30-100%。尤其在澳大利亚、欧洲、印度和中东危害严重,目前禾谷孢囊线虫已成为危害我国作物的主要病源。控制禾谷孢囊线虫的方法主要有:作物轮作、杀线虫剂、寄主抗性等等,其中基因工程方法培育抗线虫小麦品种被认为是最经济有效的方法。分离抗禾谷类孢囊线虫基因对揭示抗性基因结构与功能及其表达调控具有重要意义。 尽管小麦是重要的粮食作物,在小麦中已发现的抗禾谷孢囊线虫的基因很少,而比其近缘属如节节麦、易变山羊草、偏凸山羊草中含有丰富的抗源。目前已鉴定出禾谷孢囊线虫抗性位点Cre,并发现了9个禾谷孢囊线虫抗性基因(Cre1,2, 3, 4, 5, 6, 7, 8, and R) ,其中只有Cre1和Cre8直接从普通小麦中获得。从节节麦中获得的Cre3基因能最有效的控制线虫数量,其次是Cre1和Cre8。这些基因的克隆对于了解禾谷孢囊线虫抗性机制及进一步的育种应用都是非常关键的。然而,目前为止仅有Cre3基因通过图位克隆的方法从节节麦中被分离得到。该基因已被克隆得到的多数线虫抗性基因一样均属于核苷酸结合位点区(NBS)-亮氨酸重复序列区(LRR)基因家族。目前,已有很多抗性基因被分离,这些已知的NBS-LRR类抗性基因的保守序列为应用PCR的方法克隆新的抗性基因提供了可能。 因此本课题的目的是采用保守区同源克隆、3′RACE 和5′RACE 等方法从抗禾谷孢囊线虫小麦-易变山羊草小片段易位系E10 中克隆小麦抗禾谷孢囊线虫基因全序列,进而通过半定量PCR 和荧光定量PCR 研究该基因的表达模式。同时通过mRNA 差别显示技术和任意引物PCR(RAP-PCR)技术分离克隆植物禾谷孢囊线虫抗性基因及其相关基因,为阐明植物抗病性分子机制以及改良作物抗病性和作物育种提供基础,为通过分子标记辅助育种和基因工程方法实现高效、定向转移抗病基因到优良小麦品种奠定了重要的理论和物质基础。主要研究结果: 1. 本实验根据此前从抗禾谷孢囊线虫材料E-10 扩增得到的与来自节节麦的抗禾谷孢囊线虫Cre3 基因及其他的NBS-LRR 类抗性基因的NBS 和LRR 保守区序列设计了两对特异性引物,从E10 中扩增到532bp 和1175bp 的两个目标条带,它们有一个32bp 的共同序列,连接构成总长为1675bp 的NBS-LRR 编码区(命名为RCCN)。根据RCCN设计引物,利用NBS-LRR区序列设计引物,通过5′RACE 和3′RACE 技术采用3′-Full RACE Core Set(TaKaRa)和5'-Full RACE Kit (TaKaRa)试剂盒,反转录后通过嵌套引物GSP1 和GSP2 分别进行两轮基因特异性扩增,分别将NBS_LRR 区向5′端和3′端延伸了1173bp 和449bp,并包含了起始密码子和终止密码子。根据拼接的得到的序列重新设计引物扩增进行全基因扩增的结果与上面获得的一致。拼接后得到全长2775 bp 的基因序列(记作CreZ, GenBank 号:EU327996)。CreZ 基因包括完整的开放阅读框,全长2775 bp,编码924个氨基酸。序列分析表明它与已知的禾谷孢囊线虫抗性基因Cre3的一致性很高,并且它与已经报到的NBS-LRR 类疾病抗性基因有着相同的保守结构域。推测CreZ基因可能是一个新的NBS-LRR 类禾谷孢囊线虫抗性基因,该基因的获得为通过基因工程途径培育抗禾谷孢囊线虫小麦新品种奠定了基础,并为抗禾谷孢囊线虫基因的调控表达研究提供了参考。 2. 通过半定量PCR和SYBR Green荧光定量PCR技术对CreZ基因的相对表达模式进行了研究。以α-tubulin 2作为参照,采用半定量PCR 分析CreZ 基因在不同接种时期1d, 5d, 10, 15d 的E-10的根和叶的的表达情况。在内参扩增一致的条件下,CreZ 在E-10的根部随着侵染时间的增加表达量有明显的增加,在没有侵染的E-10的根部其表达量没有明显变化,而在叶中没有检测表达,说明该基因只在抗性材料的根部表达。SYBR Green定量PCR分析接种前后E10根部基因CreZ基因的表达水平为检测CreZ基因的表达建立了一套灵敏、可靠的SYBRGreen I 荧光定量PCR 检测方法。接种禾谷孢囊线虫后E10根内CreZ基因的相对表达水平显著高于接种前。随接种时间的延长持续增加,最终CreZ基因的相对表达量达到未接种的对照植株的10.95倍。小麦禾谷孢囊线虫抗性基因CreZ的表达量与胁迫呈正相关,表明其与小麦的的禾谷孢囊线虫抗性密切相关,推测CreZ基因可能是一个新的禾谷孢囊线虫候选抗性基因。 3. 针对小麦基因组庞大、重复序列较多,禾谷孢囊线虫抗性基因及其相关基因的片断难以有效克隆的问题,通过mRNA 差别显示技术及RAP-PCR 技术分离克隆植物禾谷孢囊线虫抗性及其相关基因。试验最终得到154 条差异表达条带,将回收得到的差异条带的二次PCR 扩增产物经纯化后点到带正电的尼龙膜上,进行反向Northern 杂交筛选,最终筛选得到102 个阳性差异点。将其中81 个进行测序,并将序列提交到Genbank 中的dbEST 数据库,分别获得登录号(FE192210 -FE192265,FE193048- FE193074 )。序列比对分析发现,其中26 个序列与已知功能的基因序列同源;有28 条EST 序列在已有核酸数据库中未找到同源已知基因和EST,属新的ESTs 序列;另外27 个EST 序列与已知核酸数据库中的ESTs 具有一定相似性,但功能未知。其所得ESTs 序列补充了Genbank ESTs 数据库,为今后进一步开展抗禾谷类孢囊线虫基因研究工作打下了基础。结合本试验功能基因的相关信息,对小麦接种禾谷孢囊线虫后产生的抗性机制进行了探讨。接种禾谷孢囊线虫后植物在mRNA 水平上的应答是相当复杂的,同时植物的抗病机制是一个复杂的过程,涉及到多个代谢途径的相互作用。 The cereal cyst nematode (CCN), Heterodera avenae Woll, causes severe yieldreductions in cereal crops. The losses caused by CCN can be up to 30-100% in somewheat fields. At present, cereal cyst nematode has become the major disease sourcein China and it also damaged heavily in Australia, Europe, India and Middle East.The damage caused by CCN can be mitigated through several methods, includingcrop rotation, nematicide application, cultural practice, host resistance, and others.Of these methods, incorporating resistance genes into wheat cultivars and breedingresistant lines is considered to be the most cost-effective control measure forreducing nematode populations. Although wheat is an economically important crop around the world, far fewergenes resistant to CCN were found in wheat than were detected in its relatives, suchas Aegilops taucchi, Aegilops variabilis and Aegilops ventricosa. Cloning these genesis essential for understanding the mechanism of this resistance and for furtherapplication in breeding. Because of the huge genome and high repeat sequencescontent, the efficient methods to clone genes from cereal crops, are still lacking. A resistance locus, Cre, has been identified and 9 genes resistant to CCN (designatedCre1, 2, 3, 4, 5, 6, 7, 8, and R) have been described, in which Cre1 and Cre8 werederived directly from common wheat. The Cre3 locus, which was derived from Ae.tauschii, has the greatest impact on reducing the number of female cysts, followed byCre1 and Cre8. Cloning these genes is essential for understanding the mechanism ofthis resistance and for further application in breeding. However, to this point, only Cre3, a NBS-LRR disease resistance gene, has been obtained through mappingcloning in Ae. tauschii. The majority of nematode resistance genes cloned so far belong to a super familywhich contains highly conserved nucleotide-binding sites (NBS) and leucine-richrepeat (LRR) domains. To date, many NBS-LRR resistance genes have been isolated.The conserved sequences of these recognized NBS-LRR resistance genes provide thepossibility to isolate novel resistance genes using a PCR-based strategy. The aim of the present study was to clone the resistance gene of CCN fromWheat/Aegilops variabilis small fragment chromosome translocation line E10 whichis resistant to CCN and investigate the espression profiles of this gene withsemi-quantitative PCR and real-time PCR. Another purpose of this study is cloningthe relational resistance gene for CCN by mRNA differential display PCR andRAP-PCR. These works will offer a foundation for disease defence of crop andbreeding and directional transferring resistance gene into wheat with geneengineering. Primary results as following: 1.According to the conversed motif of NBS and LRR region of cereal cystnematode resistance gene Cre3 from wild wheat (Triticum tauschlii) and the knownNBS-LRR group resistance genes, we designed two pairs of specific primers for NBSand LRR region respectively. One band of approximately 530bp was amplified usingthe specific primers for conversed NBS region and one band of approximately 1175bpwas amplified with the specific primers for conversed LRR region. After sequencing,we found that these two sequences included 32bp common nucleotide having 1675bpin total, which was registered as RCCN in the Genbank. Based on the conservedregions of known resistance genes, a NBS-LRR type CCN resistance gene analog wasisolated from the CCN resistant line E-10 of the wheat near isogenic lines (NILs), by5′RACE and 3′ RACE.designated as CreZ (GenBank accession number: EU327996) .It contained a comlete ORF of 2775 bp and encoded 924 amino acids. Sequencecomparison indicated that it shared 92% nucleotide and 87% amino acid identitieswith those of the known CCN-resistance gene Cre3 and it had the same characteristic of the conserved motifs as other established NBS-LRR disease resistance genes. 2. Usingα-tubulin 2 as exoteric reference, semi-quantitative PCR and real-timePCR analysis were conducted. The expression profiling of CreZ indicated that it wasspecifically expressed in the roots of resistant plants and its relative expression levelincreased sharply when the plants were inoculated with cereal cyst nematodes. therelative expression level of the 15days-infected E10 is the 10.95 times as that ofuninfected E10,ultimately. It was inferred that the CreZ gene be a novel potentialresistance gene to CCN. 3.We cloned the relational resistance gene for CCN by mRNA differentialdisplay PCR and arbitrarily primed PCR fingerprinting of RNA from wheat whichpossess huge and high repeat sequence content genomes. Total 154 differentialexpression bands were separated and second amplified by PCR. The products werenylon membrane. The 102 positive clones were filtrated by reverse northern dot blotand 81 of those were sent to sequence. The EST sequences were submitted toGenbank (Genbank accession: FE192210 - FE192265, FE193048 - FE193074). Thesequences alignment analysis indicated 26 of them were identical with known genes;28 were not found identical sequence in nucleic acid database; another 27 ests wereidentical with some known ests, but their functions were not clear. These ESTsenriched Genbank ESTs database and offered foundation for further research ofresistance gene of CCN.
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Emotion is one of the most popular spots in recent decision making research, while regret is always being considered as the most relevant emotion with decision making. Current article firstly reviewed the literature of regret theory to date to profile the relation between regret and decision making under uncertainty through three mainlines: experienced regret, anticipated regret and regret orientation, respectively. And then, based on the theory of regret regulation raised by Zeelenberg recently, we came up with a theory of risk preference regulated by regret. Then three studies were conducted under the current framework, by using experiment, survey, and quasi experiment design. The major findings were below: In study 1, when playing ultimatum game, risk preference in decision making can be determined by experienced regret and anticipated regret of risk aversion, which made individual risk taking; In study 2, survey showed that risk orientation was negatively related with risk taking (health/safety, recreational and social); In study 3, when asked the Asian Disease Problem, risk preference can be determined by the coherence of the risk preference between the past decision and the current alternative. Individuals much more like alternative with the same risk preference of the past decision. A two way interaction was found, regret orientation, as a personality, was found as a moderator. Individuals with high regret orientation were more sensitive to the coherence of the risk preference than those with low regret orientation. Three studies provide fruitful evidences for the theory of risk preference regulated by regret in different prospective, show us the function of regret in decision making.
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The extremes of exercise capacity and health are considered a complex interplay between genes and the environment. In general, the study of animal models has proven critical for deep mechanistic exploration that provides guidance for focused and hypothesis driven discovery in humans. Hypotheses underlying molecular mechanisms of disease, and gene/tissue function can be tested in rodents in order to generate sufficient evidence to resolve and progress our understanding of human biology. Here we provide examples of three alternative uses of rodent models that have been applied successfully to advance knowledge that bridges our understanding of the connection between exercise capacity and health status. Firstly we review the strong association between exercise capacity and all-cause morbidity and mortality in humans through artificial selection on low and high exercise performance in the rat and the consequent generation of the "energy transfer hypothesis". Secondly we review specific transgenic and knock-out mouse models that replicate the human disease condition and performance. This includes human glycogen storage diseases (McArdle and Pompe) and α-actinin-3 deficiency. Together these rodent models provide an overview of the advancements of molecular knowledge required for clinical translation. Continued study of these models in conjunction with human association studies will be critical to resolving the complex gene-environment interplay linking exercise capacity, health, and disease.
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Projeto de Pós-Graduação/Dissertação apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Ciências Farmacêuticas
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Projeto de Pós-Graduação/Dissertação apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Ciências Farmacêuticas
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Projeto de Pós-Graduação/Dissertação apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Ciências Farmacêuticas
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The neurodegenerative disease Friedreich's ataxia (FRDA) is the most common autosomal-recessively inherited ataxia and is caused by a GAA triplet repeat expansion in the first intron of the frataxin gene. In this disease, transcription of frataxin, a mitochondrial protein involved in iron homeostasis, is impaired, resulting in a significant reduction in mRNA and protein levels. Global gene expression analysis was performed in peripheral blood samples from FRDA patients as compared to controls, which suggested altered expression patterns pertaining to genotoxic stress. We then confirmed the presence of genotoxic DNA damage by using a gene-specific quantitative PCR assay and discovered an increase in both mitochondrial and nuclear DNA damage in the blood of these patients (p<0.0001, respectively). Additionally, frataxin mRNA levels correlated with age of onset of disease and displayed unique sets of gene alterations involved in immune response, oxidative phosphorylation, and protein synthesis. Many of the key pathways observed by transcription profiling were downregulated, and we believe these data suggest that patients with prolonged frataxin deficiency undergo a systemic survival response to chronic genotoxic stress and consequent DNA damage detectable in blood. In conclusion, our results yield insight into the nature and progression of FRDA, as well as possible therapeutic approaches. Furthermore, the identification of potential biomarkers, including the DNA damage found in peripheral blood, may have predictive value in future clinical trials.
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Aquaporin-4 (AQP4) has recently been implicated in the pathogenesis of neuromyelitis optica(NMO) where it has been identifed as the first defined autoantigen pertinent to an infammatory demyelinating disorder of the human CNS. Furthermore, a recent case report has shown a lack of AQP4 expression in the spinal cord lesions of NMO. However, the pattern of AQP4 expression in multiple sclerosis (MS) tissues has not been well-defned. In the present investigation we have confirmed a lack of expression of AQP4 in optic and spinal cord lesions in NMO which contrasted sharply with the increased levels of AQP4 expression seen in MS lesions. Furthermore a detailed immunohistochemical and semi-quantitative analysis is used to describe the expression pattern of AQP4 on well-characterized tissue microarray samples of MS and control white matter. Anatomically AQP4 was more highly expressed in all categories of MS tissue compared to normal control tissues with the most abundant expression in active lesions. Within active lesions AQP4 expression was significantly correlated with expression of the pro-infammatory cytokine osteopontin. At the cellular level dual-labelling immunofluoresence demonstrated that increased expression of AQP4 was most pronounced at the astrocytic endfeet but was also associated with the cell bodies of astrocytes in the tissue parenchyma. The finding of increased AQP4 expression in MS lesions in contrast to the lack of expression in NMO lesions may suggest different mechanisms of initiation and progression between the two disease states.
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Background: Cough is a prominent symptom across a range of common chronic respiratory diseases and impacts considerably on patient health status.
Methods: We undertook a cross-sectional comparison of scores from two cough-specific health-related quality of life (HRQoL) questionnaires, the Leicester Cough Questionnaire (LCQ), and the Cough Quality of Life Questionnaire (CQLQ), together with a generic HRQoL measure, the EuroQol. Questionnaires were administered to and spirometry performed on 147 outpatients with chronic cough (n = 83), COPD (n = 18), asthma (n = 20), and bronchiectasis (n = 26).
Results: There was no significant difference in the LCQ and CQLQ total scores between groups (p = 0.24 and p = 0.26, respectively). Exploratory analyses of questionnaire subdomains revealed differences in psychosocial issues and functional impairment between the four groups (p = 0.01 and p = 0.05, respectively). CQLQ scores indicated that chronic coughers have more psychosocial issues than patients with bronchiectasis (p = 0.03) but less functional impairment than COPD patients (p = 0.04). There was a significant difference in generic health status across the four disease groups (p = 0.04), with poorest health status in COPD patients. A significant inverse correlation was observed between CQLQ and LCQ in each disease group (chronic cough r = - 0.56, p < 0.001; COPD r = - 0.49, p = 0.04; asthma r = - 0.94, p < 0.001; and bronchiectasis r = - 0.88, p < 0.001). There was no correlation between cough questionnaire scores and FEV1 in any group, although a significant correlation between EuroQol visual analog scale component and FEV1 (r = 0.639, p = 0.004) was observed in COPD patients.
Conclusion: Cough adversely affects health status across a range of common respiratory diseases. The LCQ and CQLQ can each provide important additional information concerning the impact of cough.
Resumo:
Raman microscopy is used to investigate the spectral features of selected compounds known to be involved in the development of the eye disease age-related macular degeneration (AMD). Diagnostic features were identified in synthetic samples of these compounds and in a biological matrix. The study demonstrates the potential of Raman microscopy for the development of diagnostic markers of the onset of AMD. Copyright (C) 2008 John Wiley & Sons, Ltd.
Resumo:
As biological invasions continue, interactions occur not only between invaders and natives, but increasingly new invaders come into contact with previous invaders. Whilst this can lead to species replacements, co-existence may occur, but we lack knowledge of processes driving such patterns. Since environmental heterogeneity can determine species richness and co-existence, the present study examines habitat use and its mediation of the predatory interaction between invasive aquatic amphipods, the Ponto-Caspian Dikerogammarus villosus and the N. American Gammarus tigrinus. In the Dutch Lake IJsselmeer, we found broad segregation of D. villosus and G. tigrinus by habitat type, the former predominating in the boulder zone and the latter in the soft sediment. However, the two species co-exist in the boulder zone, both on the short and longer terms. We used an experimental simulation of habitat heterogeneity and show that both species utilize crevices, different sized holes in a plastic grid, non-randomly. These amphipods appear to optimise the use of holes with respect to their 'C-shape' body size. When placed together, D. villosus adults preyed on G. tigrinus adults and juveniles, while G. tigrinus adults preyed on D. villosus juveniles. Juveniles were also predators and both species were cannibalistic. However, the impact on G. tigrinus of the superior intraguild predator, D. villosus, was significantly reduced where experimental grids were present as compared to absent. This mitigation of intraguild predation between the two species in complex habitats may explain the co-existence of these two invasive species.
Resumo:
Nursing research leans heavily towards naturalism, with phenomenology commonly adopted. The three main schools of phenomenology used are Husserl's descriptive approach, Heidegger's interpretive hermeneutic approach and the Dutch Utrecht School of phenomenology which combines characteristics of both. Husserl's approach--the description of ordinary human experiences as perceived by each individual--involves four main steps: bracketing, intuiting, analysing and describing. Many phenomenological nurse researchers consciously decide to adopt a Heideggerian approach because of the perceived difficulties in achieving bracketing. This paper examines the concept of bracketing (epoché) and outlines some of the practical considerations when attempting to achieve it.
Resumo:
Zoonotic infections are among the most common on earth and are responsible for >60 per cent of all human infectious diseases. Some of the most important and well-known human zoonoses are caused by worm or helminth parasites, including species of nematodes (trichinellosis), cestodes (cysticercosis, echinococcosis) and trematodes (schistosomiasis). However, along with social, epidemiological and environmental changes, together with improvements in our ability to diagnose helminth infections, several neglected parasite species are now fast-becoming recognized as important zoonotic diseases of humans, e.g. anasakiasis, several fish-borne trematodiasis and fasciolosis. In the present review, we discuss the current disease status of these primary helminth zoonotic infections with particular emphasis on their diagnosis and control. Advances in molecular biology, proteomics and the release of helminth genome-sequencing project data are revolutionizing parasitology research. The use of these powerful experimental approaches, and their potential benefits to helminth biology are also discussed in relation to the future control of helminth infections of animals and humans.
Resumo:
To use protein kinase C (PKC) d-knockout mice to investigate the role of PKCd in lesion development and to understand the underlying mechanism of the vascular disease.