Summary of Research Isomorphic Metaphor as a Tool in Identifying Social Goals and the Quest

合集下载

Meta分析的基本思想及顺序

M e t a分析的思想及步骤Meta分析的前身源于Fisher1920年“合并P值”的思想，1955年由Beecher首次提出初步的概念，1976年心理学家Glass进一步按照其思想发展为“合并统计量”，称之为Meta分析。

1979年英国临床流行病学家ArchieCochrane提出系统评价（systematicreview，SR）的概念，并发表了激素治疗早产孕妇降低新生儿死亡率随机对照试验的系统评价，对循证医学的发展起了举足轻重的作用。

Meta分析国内翻译为“荟萃分析”，定义是“Thestatisticalanalysisoflargecollectionofanalysisresultsfromindividual studiesforthepurposeofintegratingthefindings.”亦即“对具备特定条件的、同课题的诸多研究结果进行综合的一类统计方法。

”Meta从字源来说据考证有“Metalogic：abranchofanalyticphilosophythatdealswiththecriticalexaminationofthebasic conceptsoflogic”；“Metamathematics：thephilosophyofmathematics，especially，thelogicalsyntaxofmathematics.”其中最简洁并且一语中的的是Metascience:：atheoryorscienceofscience，atheoryconcernedwiththeinvestigation?analysis?ordescriptionoftheoryitsel f.”意为一种科学中的科学或理论，一种对原理本身进行调查、分析和描述的原理。

Meta分析有广义和狭义两种概念：前者指的是一个科学的临床研究活动，指全面收集所有相关研究并逐个进行严格评价和分析，再用定量合成的方法对资料进行统计学处理得出综合结论的整个过程；后者仅仅是一种单纯的定量合成的统计学方法。

Meta分析中的异质性(heterogeneity)及其处理原则和方法全文

可编辑修改精选全文完整版Meta分析中的异质性（heterogeneity）及其处理原则和方法Meta 分析又称荟萃分析、汇总分析、整合分析，是对具有相同研究题目的多个医学研究进行综合分析。

meta分析的目的在于增大样本含量，减少随机误差所致的差异，增大检验效能。

一个高质量的Meta 分析相当于开展了一个多中心的研究，理想情况下，Meta分析纳入的各项研究均指向同一个结果，即各研究间具有同质性。

尽管，我们试图通过严格的入选和排除标准，以保证纳入研究的同质性。

然而，实际情况往往不尽如意。

会造成“合并萝卜、白菜、西红柿”的错误，就算是勉强合并统计量，得出的结论也不可信。

meta就没有意义了。

所以，合并效应量之前，一定要进行异质性检验。

可以明确的说，纳入Meta分析的所有研究都存在异质性。

当异质性较大时，超出了随机误差，Meta分析的结果就不太可靠。

我们需要通过适当的方法识别它，对其进行检验，以决定后续的处理策略。

梅斯医学提供有关异质性处理的策略。

我们在做meta分析前，必须要做的事有两件：A 确定文献的纳入和排除标准；B 纳入文章的质量评分，例如jadad评分、QUADAS评分等。

临床异质性、方法学异质性和统计学异质性三者是相互独立又相互关联的，临床或方法学上的异质，不一定在统计学上就有异质性表现，反之亦然。

统计学异质性是指：不同试验间被估计的治疗效应的变异。

其实，我们可以这样理解，A“严格执行文献的纳入和排除标准”可以减少临床异质性的来源；B “纳入文章的质量评分”可以减少方法学异质性的来源。

异质性检验方法异质性检验方法主要有图示法和统计学检验。

比如，大家熟悉的森林图，森林图可显示单项研究和合并效应量及其置信区间，如果单项研究结果的置信区间有很少的重叠或者不重叠，则提示研究间可能存在异质性。

如图，第1项研究和第2、第4项研究的置信区间无重叠，提示研究间可能存在异质性。

统计学异质性的六种检验方法，三种是检验，三种图示，即Q统计量、I2统计量、H统计量、Galbraith图法、L’Abbe图、漏斗图）。

meta分析的写作

益（转换成绝地效应量）。总计不良反应：没有报告严重的不良反应
37
二
Quality of evidence
根据 risk of bias 的评估结果，可直接把 Grade 结果报告出
来，若没有 Grade ，可直接说多少研究是高偏倚风险，多少是低偏倚风险，总体质量的高低。若方法学上有严重的问题，证据强度则很弱
Data collection and analysis ：
e.g. Two review authors independently assessed the identified inclusion. studies to determine eligibility for
23
Main results：
18
Tips： •添加作者时需联系co-authors
•每一个论点都要有出处
•排列出前6个作者etc.或者et al. •杂志需写全名
19
Protocol和Review的写法
Protocol ✔只能用将来时 Review
✔用过去式或者完成时
✔按照标准的方法全面地设计
✔报告实际工作内容
✔不可以删除未完成的
Cochrane要求800字，A4纸12号字，三或四段式结构
1.一般信息
•介绍疾病：关注的临床问题定义（要求1-2句话）
•病因学：关于疾病的临床病学资料
•病理生理学
•疾病的自然发展史
•疾病的危害：对经济、工作、家庭的损失，运用数据说明治
疗此类疾病的重要性
15
2.疾病的当前管理（治疗措施）
第一种写法:
11
一.To coordinator： 1.自我介绍：名字、专业背景、参加过的workshop、感兴趣课题及title、询问是否能够在对方组注册title 2.填注册表（2-3d）：包括研究者一般信息、简化的计划书

槐花化学成分和药理作用的研究

槐花化学成分和药理作用的研究英文回答：I have conducted extensive research on the chemical composition and pharmacological effects of the Sophora flower. The Sophora flower, also known as the Huaihua flower, is a traditional Chinese medicinal herb that has been used for centuries in various forms of traditional medicine.The chemical composition of the Sophora flower is quite diverse and includes flavonoids, alkaloids, polysaccharides, and volatile oils. These compounds contribute to thevarious pharmacological effects exhibited by the flower.One of the main pharmacological effects of the Sophora flower is its anti-inflammatory properties. The flavonoids present in the flower have been found to inhibit the production of inflammatory mediators, such asprostaglandins and leukotrienes. This makes the flower aneffective natural remedy for conditions such as arthritis and other inflammatory diseases.Furthermore, the Sophora flower has been found to have antioxidant properties. The flavonoids and other compounds in the flower can scavenge free radicals and protect cells from oxidative damage. This antioxidant activity is beneficial for overall health and can help prevent various diseases, including cardiovascular diseases and certain types of cancer.In addition to its anti-inflammatory and antioxidant effects, the Sophora flower has also been found to have antimicrobial properties. The alkaloids and volatile oils present in the flower can inhibit the growth of bacteria, fungi, and viruses. This makes the flower a potential natural remedy for infections and other microbial-related diseases.Moreover, the Sophora flower has been shown to have hepatoprotective effects. The polysaccharides present in the flower can help protect the liver from damage caused bytoxins and other harmful substances. This hepatoprotective activity is particularly important for individuals withliver diseases or those who are exposed to environmental toxins.Overall, the Sophora flower is a valuable medicinalherb with a wide range of pharmacological effects. Itsanti-inflammatory, antioxidant, antimicrobial, and hepatoprotective properties make it a promising natural remedy for various health conditions. Further research is needed to fully understand the mechanisms of action and potential therapeutic applications of the flower.中文回答：我对槐花的化学成分和药理作用进行了广泛的研究。

卢美哌隆治疗成人精神分裂症的有效性和安全性Meta分析

卢美哌隆治疗成人精神分裂症的有效性和安全性Meta分析卢美哌隆治疗成人精神分裂症的有效性和安全性Meta分析引言：精神分裂症是一种严重的精神障碍，患者常常出现幻听、错觉、思维混乱等症状。

卢美哌隆是一种新型的抗精神分裂症药物，已被广泛应用于临床实践。

然而，目前对于卢美哌隆在成人精神分裂症治疗中的有效性和安全性尚有不同意见。

因此，本研究旨在通过进行Meta分析，探讨卢美哌隆在成人精神分裂症治疗中的有效性和安全性。

方法：我们检索了相关的研究文献，共纳入了10个临床试验，涵盖了1800多名患者。

这些研究采用了双盲、随机、安慰剂对照的设计，评估了卢美哌隆与安慰剂在治疗成人精神分裂症中的差异性。

我们使用RevMan软件进行Meta分析，并计算出相关的汇总效应量。

结果：Meta分析结果显示，与安慰剂相比，卢美哌隆在治疗成人精神分裂症中的总有效率显著提高（相对危险度=1.53，95%置信区间1.32-1.77，p<0.001）。

此外，卢美哌隆还能有效减少幻听、错觉等阳性症状（相对危险度=1.34，95%置信区间1.12-1.61，p=0.001）。

然而，卢美哌隆对消极症状的改善效果并不明显（相对危险度=1.08，95%置信区间0.94-1.25，p=0.27）。

在安全性方面，卢美哌隆与安慰剂组没有显著的差异（相对危险度=1.04，95%置信区间0.86-1.24，p=0.72）。

卢美哌隆的常见副作用包括腹泻、失眠和头痛等，但多数症状轻微且可耐受。

讨论：通过Meta分析，我们发现卢美哌隆在治疗成人精神分裂症中具有明显的有效性，并且安全性良好。

卢美哌隆能够显著改善患者的总有效率和阳性症状，但对于消极症状的改善效果并不明显。

此外，卢美哌隆的副作用较轻微且可耐受。

然而，我们的研究还存在一些限制，如研究数量相对较少和研究质量的异质性较高等。

因此，未来还需要更多大规模、高质量的临床试验来验证我们的结果。

结论：基于本Meta分析的结果，我们确认卢美哌隆是一种有效和安全的药物，适用于成人精神分裂症的治疗。

早期胃癌患者化疗前后血清AFP、CEA、CA19-9、CA125水平变化及其对淋巴结转移的预测价值

胃癌是临床常见恶性肿瘤之一，致死率高，死亡原因与癌症细胞的转移扩散密切相关[1]。

胃癌发病往往具有一定的隐匿性，早期没有症状或者症状不典型，常表现为乏力、食欲不振、腹痛腹胀等。

目前临床对于胃癌的治疗尚无明确有效的方法，常采取化疗为主、其他治疗为辅的治疗方式[2]。

血清肿瘤标志物包括血清甲胎蛋白(AFP)、癌胚抗原(CEA)、糖类抗原19-9 (CA19-9)、糖类抗原125(CA125)，是机体癌细胞产生的一种抗原和生物性活性物质，正常组织状态下含量甚微。

AFP是早期诊断原发性肝癌最敏感、最特异的指标，适用于大规模普查；CEA升高常见于大肠癌、胰腺癌、胃癌、乳腺癌等，在心血管疾病、糖尿病、结肠炎等疾病患者中常见CEA升高，常作为辅助指标[3-4]。

上皮性卵巢肿瘤患者中90%可见CA125升高，而血清CA19-9在胃癌患者中也明显升高，对临床诊断和治疗具有重要意义[5]。

本研究旨在观察早期胃癌患者化疗前后血清AFP、CEA、CA19-9、CA125表达水平，并探讨其对发生淋巴结转移的预测价值。

1资料与方法1.1一般资料回顾性分析2020年12月至2022年11月西安医学院附属宝鸡医院收治的56例早期胃癌患者的临床资料。

纳入标准：(1)经胃镜以及胃镜下的活检确诊为早期胃癌，均符合国际抗癌联盟TNM分期[6]中Ⅰ~Ⅱ期胃癌；(2)均首次确诊，预计生存期≥6个月；(3)无脏器功能障碍；(4)病例资料完整，化疗前后均有血清AFP、CEA、CA19-9、CA125等检测数据。

排除标准：(1)因胃癌并发症如出血、穿孔或梗阻等情况行急诊手术者；(2)具有严重的肝肺脏器疾病者；(3)胃间质瘤、胃肉瘤或胃淋巴瘤者；(4)资料不全者。

56例患者中男性44例，女性12例；年龄60~82岁，平均(69.38±10.26)岁；小胃癌16例，微小胃癌30例，点状癌10例。

通过腹部增强CT、肿瘤标志物检测和病理检查观察患者淋巴结转移情况，按患者是否有淋巴结转移分为转移组9例和未转移组47例。

meta分析范文

meta分析范文Meta-analysis is a statistical technique used to combine the results of multiple studies in order to provide a more comprehensive and accurate understanding of a particular research question. It allows researchers to synthesize the findings of various studies and draw more reliable conclusions than any single study could provide.In this paper, we will discuss the process of conducting a meta-analysis, its advantages, and its potentiallimitations.The first step in conducting a meta-analysis is todefine the research question and establish inclusion and exclusion criteria for the studies to be included in the analysis. This involves identifying the relevant literature, searching for studies that meet the criteria, and then selecting the studies that will be included in the analysis. Once the studies have been selected, the next step is to extract the relevant data from each study and convert itinto a common format that can be used for analysis.After the data has been extracted, the next step is to analyze the data using statistical techniques. Thistypically involves calculating effect sizes, which measure the strength of the relationship between variables, andthen combining the effect sizes from the individual studies to produce an overall estimate of the effect. This estimate can then be used to draw conclusions about the research question and to assess the overall strength of the evidence.One of the key advantages of meta-analysis is that it allows researchers to synthesize the findings of multiple studies, which can provide a more comprehensive andreliable understanding of a particular research question.By combining the results of multiple studies, researchers can increase the statistical power of their analysis and draw more reliable conclusions than any single study could provide. This can be particularly useful when individual studies have produced conflicting results, as meta-analysis can help to identify the sources of the discrepancies and provide a more accurate estimate of the true effect.Another advantage of meta-analysis is that it can help to identify patterns and trends that may not be apparent in individual studies. By combining the results of multiple studies, researchers can identify consistent findings and explore potential sources of variation across studies. This can help to generate new hypotheses and guide future research in the field.Despite its many advantages, meta-analysis also has some potential limitations that should be considered. One potential limitation is publication bias, which occurs when studies with positive results are more likely to be published than studies with negative results. This can lead to an overestimation of the true effect, as the published literature may not accurately reflect the full range of findings on a particular research question. To address this limitation, researchers can use statistical techniques such as funnel plots to assess the presence of publication bias and adjust their estimates accordingly.Another potential limitation of meta-analysis is the risk of including low-quality studies, which can bias theoverall estimate of the effect. To address this limitation, researchers can use inclusion criteria to select only high-quality studies for inclusion in the analysis and conduct sensitivity analyses to assess the robustness of their findings.In conclusion, meta-analysis is a powerful tool that can provide a more comprehensive and reliable understanding of a particular research question by synthesizing the findings of multiple studies. By combining the results of individual studies, researchers can increase thestatistical power of their analysis, identify patterns and trends, and draw more reliable conclusions than any single study could provide. However, it is important to consider the potential limitations of meta-analysis and take steps to address them in order to ensure the reliability and validity of the findings.。

库恩研究范式英文

库恩研究范式英文1. Research:研究2. Paradigm:范式3. Scientific:科学的4. Theory:理论5. Hypothesis:假设6. Experiment:实验7. Data:数据8. Analysis:分析9. Conclusion:结论10. Observation:观察11. Variables:变量12. Control:控制13. Replication:复制14. Validity:有效性15. Reliability:可靠性16. Bias:偏见17. Sample:样本18. Population:总体19. Correlation:相关性20. Causation:因果关系21. Inductive reasoning:归纳推理22. Deductive reasoning:演绎推理23. Peer review:同行评议24. Publication:发表1. Research is a systematic process of inquiry.（研究是一种系统的探究过程。

）2. The scientific paradigm is the framework within which researchers operate.（科学范式是研究人员工作的框架。

）3. Theories are proposed explanations for observed phenomena.（理论是对观察到的现象提出的解释。

）4. Researchers often start with a hypothesis, which is a testable prediction.（研究人员通常从一个假设开始，这是一个可验证的预测。

）5. Experiments are conducted to gather data and test hypotheses.（实验旨在收集数据并测试假设。

突变基因与呼吸系统疾病的联系

突变基因与呼吸系统疾病的联系突变基因是指在个体遗传物质DNA序列中发生突变，导致基因功能的改变。

这些突变可能与许多疾病的发生和发展有着密切的联系，尤其是与呼吸系统疾病相关的基因突变。

本文将探讨突变基因与呼吸系统疾病之间的关联。

1. 突变基因与哮喘哮喘是一种慢性炎症性呼吸系统疾病，其特征是支气管高反应性、气道炎症和气流受限。

研究表明，多个基因突变与哮喘的遗传易感性密切相关。

例如，人类第5号染色体上的Cys-Leu突变与阻塞性空气道疾病（包括哮喘）的发生有关。

此外，Toll样受体4基因（TLR4）的D299G和T399I突变与哮喘的风险增加相关。

2. 突变基因与慢性阻塞性肺疾病（COPD）慢性阻塞性肺疾病是一种气道慢性炎症反应导致的进行性气流受限性呼吸系统疾病。

研究发现，一些突变基因与COPD的发生和发展相关。

例如，人类第6号染色体上的α1-抗胰蛋白酶（α1-antitrypsin）基因的突变导致该蛋白的缺乏，增加了COPD的风险。

3. 突变基因与肺癌肺癌是最常见的恶性肿瘤之一，并且与吸烟、环境污染等因素密切相关。

然而，研究表明，某些突变基因也与肺癌的发生有关。

例如，表皮生长因子受体（EGFR）基因突变可以导致癌细胞的无限增殖和肿瘤的发展。

此外，KRAS和TP53等基因的突变也与肺癌发生有关。

4. 突变基因与囊性纤维化囊性纤维化是一种影响多个器官的遗传性疾病，最常见的受累部位是肺部。

该疾病是由囊性纤维化转膜调节子（CFTR）基因的突变导致的。

不同的突变会导致CFTR蛋白的结构和功能发生改变，从而引起黏液的增加和器官功能损害。

总结起来，突变基因与呼吸系统疾病之间存在着紧密的联系。

这些基因突变可能会影响呼吸系统的发育和功能，导致呼吸系统的疾病发生和发展。

深入研究突变基因与呼吸系统疾病之间的关联有助于我们更好地理解这些疾病的发病机制，并为相关疾病的预防和治疗提供新的思路和方法。

参考文献：1. Marinho S, Simpson A. Cracking the case of childhood wheeze: could genetics hold the key? Archives of disease in childhood. 2019;104(2):195-196.2. Zhou H, Zhang L, Chen D, et al. Toll-like receptor 4 D299G andT399I polymorphisms are associated with increased risk of asthma: An updated meta-analysis. Medicine. 2020;99(14):e19677.3. Müller T, Müller G, Steinbach L, Fehrenbach H, Fühner T. Decoding the role of α1-antitrypsin deficiency in chronic obstructive pulmonary disease. Annals of the American Thoracic Society. 2016;13 Suppl 4:S317-s325.4. Shi J, Hua X, Zhu B, Ravichandran S, Wang M, Nguyen C. Lung cancer epidemiology, risk factors, and prevention. J Thorac Dis.2016;8(9):E981-e989.5. Alton EW, Stern M, Farley R, et al. Cystic fibrosis gene therapy: a new era in treatment for the UK CF gene therapy consortium. human gene therapy. 2013;24(5):440-452.。

色氨酸羟化酶基因多态性与单相抑郁症关系的Meta分析

码控制５一ＨＴ合成、释放、摄取和代谢或受体活性有关的基因成为研究抑郁症的候选基因，如色氨酸羟化酶（ＰＴＨ）基因、５一Ｔ转运体基因、５一ＨＨＴ受体基因和单胺氧化酶基因等Ｊ。色氨酸羟化酶是５一羟
色胺合成的限速酶，它将色氨酸羟化为５一色酚后羟
ＷＮＧＭｅ— ｉ，ＨＮＡｉｘａＺＡＧＱ，，ＺＵＱ —ｚｅ，ＴＮＤ一ｘｏｅａｔｅｔｆＩｏｍｔｎＥｇｎｅｎ，ｉｎｄａｏｅｅＨｉｈｎＩｙ，Ａｉ，ＤｐｒｎｎｒａｉｎｉｅｉｇＪｎｇＭｅｉｌｌｇ，ａｍｏｆｏｒｉＣｌ
吕少妮任淑敏王美霞张庆朱启贞田永晓
日９７８６２６２）
（济宁医学院信息工程学院
［摘要］以色氨酸羟化酶（ＰＴＨ）基因和单相抑郁症应关系病倒对照的国内外文献为研究对象，应用Ｒｖｅ．
Ｍａ．ｎ５０对数据统计分析，综合评价色氨酸羟化酶基因多态性与单相抑郁症的关系。结果表明色氨酸羟化酶
ｂｏｄａｓａｃｂｃｓｓｇｔｏｗｒｏｅＭａ．，ｈａｅｏｐｅｅｓｅｖｌａｓｈｌｉｎｅｅｎｒＨｇｎｏ — ｒｓｒｅｒｈｏｊｔ。ｕｉｅｓｆａｆｖｎ５０ｔｅｐｐｒｍｒｎｉｌｅａｕｔｅｒａｏｓｔｅＰｅｅｌａｅｅｎｈｔｅＲｃｈｖｙｅｔｅｔｂｗｐｙ
［作者简介］吕少妮，讲师，发表论文１；通讯作者：６篇

7原核基因表达调控

原核基因表达调控总论之特点
转录终止阶段的调控一般包括抗终止子作用和弱化作用。
当操纵子被阻遏，RNA合成被终止时，起终止转录信号作用的那一段核苷酸被称为弱化子。
原核基因表达调控总论之特点
操纵子的调控
乳糖操纵子色氨酸操纵子
主要特点
转录起始的调控
σ因子
转录终止的调控
抗终止作用弱化作用
转录后调控
翻译和翻译后微调
DNA
原核基因表达调控
前言
自然界中，原核生物及单细胞真核生物直接暴露在变幻莫测的环境中，能量供应常常没有保障，它们只有适应不同的环境来合成各种不同的蛋白质，使代谢过程适应环境的变化，才能维持自身的生存和繁衍。
It is well established that aesthetic appreciation is related with activity in several different brain regions. The identification of the neural correlates of beauty or liking ratings has been the focus of most prior studies.
1
Part ONE
原核基因表达调控总论
Summary of previous work, It is well established that aesthetic appreciation is related with activity in several different brain regions.
乳糖操纵子与负控诱导系统
lac 操纵子的本底水平表达
乳糖操纵子与负控诱导系统

苏合香吸嗅对炎症抑郁小鼠行为学影响及初步机制研究

目录中文摘要 (1)英文摘要 (4)英文缩写 (8)研究论文苏合香吸嗅对炎症抑郁小鼠行为学影响及初步机制研究前言 (9)第一部分苏合香吸嗅抗抑郁焦虑活性的实验研究材料与方法 (11)结果 (14)附图 (15)讨论 (17)小结 (17)第二部分苏合香吸嗅对炎症致抑郁小鼠的作用材料与方法 (18)结果 (20)附图 (21)讨论 (24)小结 (25)第三部分苏合香吸嗅抗抑郁作用机制研究材料与方法 (26)结果 (28)附图 (29)讨论 (32)小结 (34)结论 (35)参考文献 (36)综述苏合香对中枢神经系统调控作用的研究进展 (41)致谢 (49)个人简历 (50)苏合香吸嗅对炎症抑郁小鼠行为学影响及初步机制研究目的：明确苏合香吸嗅对炎症刺激致抑郁小鼠行为的影响，并进一步探究苏合香吸嗅对抑郁小鼠的作用途径。

方法：本研究运用脂多糖（lipopolysaccharide,LPS）腹腔注射诱导炎症应激的方法建造小鼠抑郁模型，应用10%苏合香精油进行干预，观察其效果，并使用硫酸锌滴鼻灌洗的方式建造小鼠嗅觉障碍模型探讨苏合香吸嗅对抑郁小鼠的影响是否通过嗅觉进行介导。

小鼠行为学测试方法：利用悬尾测试（Tail suspension test,TST）和强迫游泳测试（Forced swimming test,FST）评价小鼠抑郁样行为；旷场测试（Open field test,OFT）和新颖抑制摄食测试（Novelty suppressed feeding test,NSFT）评价小鼠焦虑行为；埋藏食物小球测试（Buried food test, BFT）评价小鼠嗅觉功能。

苏合香吸嗅干预方法：用20mL10%的苏合香精油混悬液浸湿棉球，将浸湿的棉球放入网状铁丝球中，置于苏合香吸嗅专用长方体塑料盒中，供小鼠吸嗅，每次吸嗅后及时更换棉球。

1.急性应激小鼠行为学实验：30只小鼠随机分为溶媒组、苏合香吸嗅10分钟组和苏合香吸嗅30分钟组。

META分析文字版

AbstractBackground: Whether depression causes increased risk of the development of breast cancer has long been debated. We conducted an updated meta-analysis of cohort studies to assess the association between depression and risk of breast cancer. Materials and Methods: Relevant literature was searched from Medline, Embase, Web of Science (up to April 2014) as well as manual searches of reference lists of selected publications. Cohort studies on the association between depression and breast cancer were included. Data abstraction and quality assessment were conducted independently by two authors. Random-effect model was used to compute the pooled risk estimate. Visual inspection of a funnel plot, Begg rank correlation test and Egger linear regression test were used to evaluate the publication bias. Results: We identified eleven cohort studies (182,241 participants, 2,353 cases) with a follow-up duration ranging from 5 to 38 years. The pooled adjusted RR was 1.13(95% CI: 0.94 to 1.36; I2=67.2%, p=0.001). The association between the risk of breast cancer and depression was consistent across subgroups. Visual inspection of funnel plot and Begg’s and Egger’s tests indicated no evidence of publication bias. Regarding limitations, a one-time assessment of depression with no measure of duration weakens the test of hypothesis. In addition, 8 different scales were used for the measurementof depression, potentially adding to the multiple conceptual problems concerned with the definition of depression. Conclusions: Available epidemiological evidence is insufficient to support a positive association between depression and breast cancer.IntroductionDepression is highly prevalent in the general population, and it is estimated that 5.8% of men and 9.5% of women will experience a depressive episode in a 12-month period. The lifetime incidence of depression has been estimated at more than 16% in the general population (World Health Organization, 2001; Kessler et al., 2003; World Health Organization, 2008). Breast cancer is by far the most commom cancer in women (International Agency for Research on Cancer, 2008), the global burden of breast cancer measured by incidence and mortality is substantial and on the increase (Benson et al., 2012). There are an estimated 1.5 million cases diagnosed annually and almost 0.5 million died from this disease, representing 14% of female cancer deaths in the worldwide (Jemal et al., 2011; Benson et al., 2012). Many factors have been shown to be associated with the occurrence of breast cancer, such as having a first degree relative with breast cancer, bearing the first child at a late age, alcohol consumption and long term use of menopausal estrogen replacement therapy (Kampert et al., 1988; Gail et al., 1989;Slattery et al., 1993). However, it has long been debated that whether depression is an increased risk of the development of breast cancer. Depression may affect the endocrine and immune function (Kowal et al., 1955; Miller et al., 1993), which may have influence on cancer initiation and progression, including breast cancer. Importantly, women themselves widely believed that depression was a risk factor in the development of their breast cancer (Mitchell et al., 1995). However epidemiology evidences on the association between depression and breast cancer incidence are mixed and inconclusive.A great many of studies have assessed the association between depression and subsequent risks of breast cancer. A previous meta-analysis (Oerlemans et al., 2007) focusing on breast cancer pooled results from 7 prospective studies published before 2003 as a secondary analysis and reported a pooled relative risk estimated of 1.59 (95% confidence intervals, 0.74-3.44). Since then some cohort studies have been published, which provide stronger evidence of the association between depression and breast cancer. Therefore, we conducted a meta-analysis of cohort studies to describe the association between depression and risk of breast cancer.Materials and MethodsSearch strategyWe conducted a systematic literature search (up toApril 2014) of Medline, Embase, Web of Science for studies describing the association between depression and breast cancer. We used the following terms “depression”or “depressive disorder” or “major depressive disorder”or “depressive symptoms” and “breast cancer” or “breast carcinoma” combined with “cohort study” or “prospective study” or “follow-up study” or “longitudinal study”.In addition, studies from reference lists of all relevant publications and reviews were searched to identify potential pertinent studies.Study selectionStudies meeting the following criteria would be included in this meta-analysis: i) the study was a cohort design (prospective cohort or historical cohort); ii) the exposure was depression symptoms or depressive disorder which were measured by self-reported scales or structured clinical interview or clinician diagnosis; iii) the endpoint was diagnosis or report of breast cancer, all participants were free of any subtypes of cancer at the beginning of the study; iv) the study reported the RR or hazard risk(HR) with corresponding 95% CIs for the association between depression and breast cancer; and v) study was publishedin English. If multiple independent published reports were from a same cohort, only the latest one was included. Study selection was independently performed by two authors (S.H.L and D.X.X) and conflicts were resolved through discussion with the third reviewer (L.Z.X).Data extractionWe extracted the following information fromeach retrieved article: name of the first author, yearof publication, study location, characteristics of study population at baseline, duration of follow-ups, sample size, numbers of cases, depression and breast cancer measurements, adjusted effect estimate and corresponding 95% CIs, and variables used in multivariable analysis. Quality assessment was performed according to the Newcastle-Ottawa quality assessment scale for cohort studies (Wells et al., 2006) by two investigators (S.H.L and D.X.X). This scale allocates a maximum of nine points for quality of selection (0-4 points), comparability (0-2 points), exposure and outcome of study participants (0-3 points). The two authors discussed the implementationof this assessment tool and agreed on a method of implementation before their independent assessments ofstudies. The level of agreement between the two reviewers was calculated by another investigator (L.Z.X).Statistical analysisThe RRs were used as the common measure of association across studies, and the hazard ratios (HRs) were considered equivalent to RRs. Forest plot was produced to visually assess the RRs and corresponding 95% CIs across studies. Statistical heterogeneity across studies was estimated by I2 statistic. I2 values of 25%, 50%, 75% are regarded as cut-off points for low, moderate and 2003). The RRs were pooled using the fixed-effect modelif no or low heterogeneity was detected, or random-effect model otherwise (DerSimonian et al., 1986). In sensitivity analyses, we conducted leave-one-out analysis (Wallaceet al., 2009) for each study to examine the magnitude of influence of each study on pooled risk estimates. Subgroup analyses for study location, number of participants and cases, follow-up time, exposure measurement, smokingor alcohol drinking and study quality were conductedto examine the robustness of the primary results. Visual inspection of a funnel plot and Begg rank correlation test, Egger linear regression test (Begg et al., 1994;Egger et al., 1997) were used to evaluate the potential publication bias. The Duval and Tweedie nonparametric trim-and-fill procedure(Duval et al., 2000) was used to further assess the possible effect of publication bias. All statistical analyses were performed with STATA version 11.0 (StataCorp, College Station, Texas, USA). All tests were two sided with a significance level of 0.05.ResultsEligible studiesTotally 1705 articles were identified from the Medline, Embase, Web of Science. After the first round of screening based on titles and abstracts with aforementioned criteria, 1682 articles were excluded. Examining the articles remained in more details, nine articles (Hahn et al.,1988; Jacobs et al., 2000; Dalton et al., 2002; Nyklicek et al., 2003; Goldacre et al., 2007; Gross et al., 2010; Chen et al., 2011; Liang et al., 2011; Lemogne et al., 2013) met the inclusion criteria. The detailed reasons for exclusion were shown in Figure 1. Besides, one article (Schuurman et al., 2001) was found from the previous meta-analysis (Oerlemans et al., 2007) and one (Knekt et al., 1996) was identified by searching the reference lists. In total, elevenarticles were included in this meta-analysis.Study characteristicsCharacteristics of the eleven articles were showedin Table 1. These studies were published between 1988 and 2013. The sample size of studies varied from 1,533to 57,320, with a total of 182,241, and the number of breast cancer cases ranged from 20 to 728, with a totalof 2,353. With regard to study location, three studies were conducted in the USA, two studies in Taiwan, twoin Netherlands, one in France, one in the UK, one in Denmark, and one in Finland. In four of eleven studies, depression was measured by self-reported scales which were the Center for Epidemiologic Studies Depression Scale (CES-D), General Health Questionnaire (GHQ), Minnesota Multiphasic Personality Inventory(MMPI), and Ediburgh Depression Scale (EDS). Two studies used the Diagnostic Interview Schedule (DIS) and one used International Classification of Health Problems in Primary Care (ICHPPC) to define depression. The other four studies defined depression according to the International Classification of Disease, Ninth Revision, Clinical Modification or International Classification of Disease,Eighth Revision, Clinical Modification (ICD-9-CM or ICD-8-CM). The outcome of studies was ascertained by medical records or death certificates in seven studies, by self-report in two studies, and by combining self-report with medical records in the rest two studies. The eleven articles were assessed and were of moderate quality with a mean score of 6.9 (ranging from 6-8).All the included studies provided adjusted RRs. The major confounding factors adjusted included age, family history of breast cancer, cigarette smoking, alcohol intake, obesity, social status, and complications.Association between depression and risk of breast cancer The association between depression and breastcancer risk was shown in Figure 2. The majority of allthe eleven studies indicated a positive trend between depression and breast cancer (RR>1), but only two of them were statistically significant. At the same time one article (Nyklicek et al., 2003) reported that depression could reduce the risk of breast cancer in middle-aged women. With a moderate to high heterogeneity (I2=67.2%, p=0.001), the pooled analysis from random-effect model revealed that depression was not associated with breastcancer risk (RR,1.13; 95% CI 0.94 to 1.36).Subgroup analyses and sensitivity analysesTable 2 showed the results of subgroup analyses. We conducted subgroup analyses by study characteristics, such as study locations, number of study of participants and cases, duration of follow-up, exposure levels and study quality, while the results were not statistically significant. In addition, we conducted subgroup analyses according to the results whether or not adjusted by alcohol consumption or smoking, and neither alcohol consumption nor smoking altered the association.one showed that Jacobs et al’s study (Jacobs et al., 2000) and Goldacre et al’s study (Go ldacre et al., 2007) imposed the largest influence on the results. The pooled RRs were 1.24 (95%CI: 0.95-1.61) and 1.06 (95%CI 0.92-1.22) after excluding the two studies, respectively.Publication biasVisual inspection of funnel plot revealed some asymmetry (see supplementary Figure 1A). However,the Begg rank correlation test, Egger linear regressiontest provide no evidence of substantial publication bias (Begg’s test Z=1.25, p=0.213; Egger’s test t=-0.39,p=0.709). A sensitivity analysis using the trim-and-fill method was performed with 3 imputed studies, which produced a symmetrical funnel plot (see supplementary Figure 1B). The pooled RR incorporating the three hypothetical studies was smaller than the original results, but it still did not reach the statistically significant (RR, 1.04; 95% CI, 0.84-1.27).DiscussionThe study results were derived from eleven cohort studies which reported association between depression and risk of breast cancer. In all, our meta-analysis involved 2,353 cases of breast cancer and 182,241 participants.No significant association between depression and risk of breast cancer was found (RR, 1.13; 95%CI, 0.94 to 1.36) after adjustment for potential confounders. Furthermore, the association between depression and breast cancer persisted across subgroup analyses.Taking into account the impact of ethnic and geographic on the incidence of breast cancer, subgroup analyses by locations (European countries vs. USA vs. Taiwan) were conducted but no significant difference was found. As we know, different levels of exposure mayhave different effects on the study outcome. Therefore,we conducted subgroup analysis by exposure levels (depression symptoms vs. depressive disorder) which showed no statistically significant association between depression and breast cancer risk. Given that a long period was required to develop a detective tumor, subgroup analysis by the duration of follow-up were conductedand the results were not statistically significant as well, though the RR was elevated in the cohorts of more than10 years of follow-up. There were studies identifiedthat depression individuals may engage more unhealthy behaviors that predispose them to further onset of cancer, such as smoking, alcohol consumption, lack of physical activity (Son et al., 1997; Strine et al., 2008). But the subgroup analyses according to the results that whetheror not adjusted by smoking and alcohol consumption didnot find significant association.A meta-analysis conducted by Marjolein EJ Oerlemanset al. (2007) in 2007 investigated the relationship between depression and overall cancer risk. The previous metaanalysis also identified association between depressionand breast cancer as a secondary analysis. The secondaryanalysis included seven prospective studies which involved 111756 participants and 1601 cases and reported no significant association (RR, 1.59; 95%CI, 0.74-3.44). Our meta-analysis, with four more cohort (Goldacre et al., 2007; Chen et al., 2011; Liang et al., 2011; Lemogne et al., 2013) studies and one update study (Gross et al., 2010), demonstrates no evidence of association between depression and breast cancer, which is consistent with the previous meta-analysis. However, we noticed that the previous review found depression might be a risk factor for breast cancer (RR, 2.5; 95%CI, 1.06-5.91) if study population were followed more than 10 years. In our review, this association in subgroup analysis by follow-up more than 10 years was not proved. To our knowledge, the larger size of participants, the stronger evidence of the study. The combined results of our meta-analyses are more credible with relatively narrow confidence intervals. Considering the limited number of the included studiesof the previous meta-analysis, we can not conclude that there is significant association between depression and breast cancer.Experimental animal studies, human studies andclinical evidence suggest that depression may put an influence on the development of breast cancer through several mechanisms, such as impairing immune function, causing an aberrant activity of the hypothalamic-pituitary- adrenal axis and inhibiting DNA repairmechanisms (Kiecolt-Glaser et al., 2002; Reiche et al., 2005; Soygur et al., 2007). However, epidemiological research evidences did not indicate the presence of sucha relationship between depression and breast cancer. The and epidemiological studies may be explained by two reasons. On the one hand, the strength of experimental evidence may be compromised due to species differences, inconsistent of laboratory conditions and the measurement of biomarker. Some experiments could not be replicated by different investigators. On the other hand, epidemiological studies may have some methodological flaws, such as insufficient follow-up duration, different definitions and measurement of exposure, the size of sample and so on. Overall, evidence supporting that depression increases the risk of breast cancer are insufficient.There are two strengths in our meta-analysis. Firstly,all studies in the present analyses were cohort studies,which minimized the selection and recall bias. Although our review is an updated meta-analysis, it provides robust and credible conclusion for the association between depression and breast cancer. Secondly, most of studies included in this meta-analysis had average follow-up times more than 10 years. Sufficiently long follow-up duration is necessary because most cancers have a latent period of a few years or even decades (Spratt et al., 1996; Friberget al., 1997). Thus, our results based on long follow-up duration studies could indicate that the depression might not increase the risk of breast cancer.Limitations: A few limitations of our meta-analysis should be acknowledged. Firstly, depression was only measured on the basis of a single baseline measure, which was clearly not identical to depression diagnosis. During the follow-up duration, the exposure intensity of subjects would change. Penninx et al (1998) (Penninx et al., 1998) proved that repeated assessment of depressive symptoms yielded positive association with later developmentof some cancers, in contrast to single measurements. Therefore, a one-time assessment of depression withno measure of duration weakens the test of hypothesis.Secondly, no less than 8 different scales were used for the measurement of depression in the 11 original studies. It may add to the multiple conceptual problems concerned with the definition of depression (Buntinx et al., 2004), which could increase the heterogeneity in our metaanalyses. In conclusion, available epidemiological evidencesare insufficient to support association between depression and the development of breast cancer. Given the high prevalence and morbidity of depression and breast cancer, the results of this meta-analysis not only can act as the clue of the etiology, but can provide the evidence to women who believed that depression could increase the risk of breast cancer.Acknowledgements。

中西医结合治疗阿尔茨海默病疗效的meta分析

中西医结合治疗阿尔茨海默病疗效的meta分析梁娟芳;郭君伟;付宝;刘越泽【摘要】目的评价中西医联合治疗阿尔茨海默病的疗效是否优于单一疗法.方法计算机检索CNKI、Wanfang、VIP数据库,纳入所有关于阿尔茨海默病/老年痴呆的随机对照试验,并对纳入文献进行质量评价.数据统计分析采用RevMan5.0软件进行.结果共纳入15个随机对照试验(RCT),其中对照组为单纯服用西药的RCT为13个,患者共计937例;对照组为单纯服用中药的RCT为2个,患者共计87例.Meta分析结果显示:与对照组比较,中药和西药联合治疗阿尔茨海默病的疗效优于任一单一疗法.结论中西医联合治疗阿尔茨海默病的疗效优于单一中药或西药疗法.【期刊名称】《山西医科大学学报》【年(卷),期】2014(045)003【总页数】4页(P209-212)【关键词】中西医结合;阿尔茨海默病;meta分析【作者】梁娟芳;郭君伟;付宝;刘越泽【作者单位】山西医科大学图书馆,太原030001;山西医科大学第三医院;山西中医学院附属医院人事科;山西医科大学第三医院【正文语种】中文【中图分类】R741.05阿尔茨海默病(Alzheimer disease，AD)，又叫老年性痴呆，是一种渐进性神经功能退行性疾病，主要表现为渐进性记忆障碍、认知功能障碍、人格改变及语言障碍等神经精神症状，严重影响社交、职业与生活功能［1］。

目前该病病因尚不明确，普遍认为是一种与遗传、环境等多种因素相关的神经系统变性疾病。

治疗方面目前对痴呆尚无特效疗法，主要是药物治疗、心理或社会行为治疗［2］。

某临床实践指南中指出，目前还缺乏西药联合中药治疗痴呆疗效优于单一疗法的研究证据［3］。

本研究对中西医结合治疗AD的随机对照试验(randomized clinical trial，RCT)进行meta分析，以期为临床决策提供证据支持。

1 资料与方法1.1 研究对象中西医结合治疗AD患者的RCT文献。

1、下载文档前请自行甄别文档内容的完整性，平台不提供额外的编辑、内容补充、找答案等附加服务。
2、"仅部分预览"的文档,不可在线预览部分如存在完整性等问题,可反馈申请退款(可完整预览的文档不适用该条件!)。
3、如文档侵犯您的权益，请联系客服反馈,我们会尽快为您处理(人工客服工作时间：9:00-18:30)。

Paper Number:PA061396
Paper Title:Isomorphic Metahor as a Tool in Identifying Social Goals and the Quest for Wholeness
Author(s):
Robb Shoaf, The United Methodist Church in Madison, Madison, NJ, USA
Summary of Research
Isomorphic Metaphor as a Tool in Identifying Social Goals and the Quest for Wholeness.
Summary:
The present proposal involves building a theory of social goal setting action as a direct result of the insights of metaphorical isomorphism. It is a qualitative approach based on the assumptions of chaos and complexity theory that mechanistic understanding of phenomenon and the linear regressiveness of quantitative analysis and prediction are limited and limiting in scope. The cross-disciplinary isomorphic tendencies of metaphors will help envision reality differently by examining multiple dimensions as a way to better identify, seek and achieve social goals.
Description
Isomorphic Metaphor as a Tool in Identifying Social Goals and the Quest for Wholeness.
The qualitative work of building theory differs from most quantitative work of testing theory. Quantification of data and the linear function of predictability provides much insight into phenomenon in the world. Yet as complexity and chaos research has shown, mechanistic and linear predictions often miss the forest for the trees. Yet, the need for quantitative analysis is obvious, for what good is seeing a forest if nothing of significance can be said of the individual trees? Yet a “gestalt” eludes us and we are left with trying to put humpty dumpty together by his parts alone.
The present paper seeks to understand phenomenon in terms of a systemic appreciation of wholeness. This completeness is a matter of appreciative inquiry; replacing a methodology of control and dissection with appreciation for the mysterious nature of reality and the humble realization that complete understanding is beyond our grasp even though we fool ourselves to believe it is within our reach. Nowhere is this better illustrated than in the work of Kurt Gödel in proving the inconsistency and incompleteness of formal mathematical systems. This was examined metaphorically in Douglas R. Hofstadter’s important work Gödel,Escher, Bach: an Eternal Golden Braid, which uses recursive processes as a model to better understand human consciousness.
The methodology of the present research is one of examining the possibilities of isomorphic metaphor as a tool to envision and understand broad social goals. Recognizing the complexity of reality will open us up, not necessarily to better predictions in the short-run, but a better understanding in the long-run. An example may suffice. Within the human community, no relationship between individuals or institutions functions well without a level of trust. Trust may be understood as the ability to share one’s vulnerability (or weakness) with another. Within the realm of simple mathematics, the rule that two negatives will equal a positive number illustrates this nicely. What is more important is the insight from such a problem that two negatives added do not reveal anything positive, they must be multiplied. This may provide isomorphic insight into the nature of partnerships; collaboration is multiplicative rather than additive in nature. Again, we come back to the simple equation of gestalt; the whole is greater than the sum of its parts. We will ask the question: What does it mean to be a complete individual, what brings completeness to a community and the broader collection of communities? And can wholeness not eliminate distinctions of thought , action and life, but actually fortify them? And how?
References:
Byrne, David. 1998. Complexity and the Social Sciences. London: Routledge Golding, Christina. 2002. Grounded Theory. London: Sage Publications. Goldstein, Rebecca. 2005. Incompleteness: The Proof and Paradox of Kurt Gödel.
New York. W.W. Norton & Company, Inc.
Hofstadter, Douglas R. 1979. Gödel,Escher,Bach: an Eternal Golden Braid. New York: Basic Books.
Holland, John D. 1998. Emergence: From Chaos to Order. Cambridge Massachusetts: Perseus Books.
Waldrop, M. Mitchell. 1992. Complexity: The Emerging Science at the Edge of Order And Chaos. New York: Touchstone.。