感谢您对杰西卡希斯协议的建议和贡献的有代表性的数据。特别感谢萨布丽娜Blackledge，劳伦科胡特克和Kerisa谢尔顿展示了这一协议。

1。设置<ol><li>所有研究应该由适当的机构审查委员会或人类受试者审查委员会之前，数据收集的批准。 </li><li>理想的情况下，两房应进行TSST。一个舒适的候车室，应当向与会者提供开始前的TSST在恢复时期。应该使用一个单独的采访室，准备在演讲中，语音性能和数学部分的TSST推出的新颖性和uncontrolability。 </li><li>安排面试室，使参与者都将面临同盟面试官和位置的视频或录音设备，在参与者的视野。应提供实验室外套，主考人穿在TSST期间增加TSST的压力。指示面试者与参与者保持目光接触，不要在TSST情绪的面部表情。 </li><li>仔细考虑日Ë研究问题（S）选择取决于测量时。应激反应的各种测量的分析和出版物的指导方针是由几个来源（心理生理研究协会提供指引，出版和分析<a href="http://www.sprweb.org/journal/index.cfm#guidelines" target="_blank">心理生理</a>措施：http://www.sprweb.org/journal/index。 <a href="http://www.sprweb.org/journal/index.cfm#guidelines" target="_blank">CFM＃指引</a> ），这些资源在实验设计咨询建议。 </li><li>设置需要记录所有设备的TSST的生理，心理或内分泌反应。此设备可能包括（但不仅限于）电极和电子设备和/或软件来记录心率，心血管反应，皮肤电导或响应，眨眼间，肌肉收缩/色调，呼吸频率;纸和铅笔或电子版本如国家特质焦虑INV的心理工具对于本演示 entory; 6管和尿液，血液或唾液样本收集材料;或录像设备，我们将使用三导联心电图（ECG）电极在TSST测量心率，反复的行政管理国家特质焦虑量 ​​表来衡量前后心理应激反应。我们将利用一个基本的录音系统设计来衡量的生理反应（BIOPAC MP36系统）记录心率。 </li><li>如果血液样本（而不是唾液）将收集实验过程中，应努力，尽量减少在收集过程中的疼痛和苦恼。采血程序可以引入更多的身体或心理压力，混杂的TSST。 </li><li>当参与者到达时，欢迎他们到实验室。取得知情同意和座位参与者的舒适。 </li><li>收集人口统计信息，筛选信息或additioNAL的到来，实验所需的措施。验证参与者不消耗食物或饮料（水除外）在过去一小时，如果收集皮质醇测量一个短期内禁食建议，如果你将收集唾液样本进行分析 。 酸性食物或饮料，或可见的污染有关的pH值的变化可干扰精确测量唾液中的标记。 如果利益的措施可能是由药物或其他代谢物污染，可能需要尿毒理学筛查。 因素可能会影响应激反应（如药物，疾病，睡眠，最近的压力事件，社交恐惧症）也应该被认为是当筛选参与者的信息。 </li></ol> 2。预应力测量<ol><li>指示的参与者，在候诊室等待45分钟的舒适。您可以选择阅读材料，如含有EMO杂志，提供参与者tionally中立的内容，或在此期间的另一个情感中立的活动。 </li><li>经过45分钟的等待期，管理国家特质焦虑量 ​​表评估预应力焦虑。此外，可能是在紧张，焦虑或放松状态的变化，旨在评估的其他文书管理（如视觉模拟尺度 ）。 </li><li>收集“预应力”的唾液样本。指示的参与者，用清水冲洗自己的嘴。 5-10厘米的吸管部分和一个干净的，一次性的2.0毫升聚丙烯小瓶，让参与者。指示的参与者，他们的头部倾斜着让唾液池口的地板上，然后通过一根稻草到小瓶的唾液。从参与者收集约1.5-2.0毫升的唾液。另外，唾液可以收集使用吸水牙科灯芯（或类似材料），并指示参与者咀嚼或饱和材料与唾液。如果possible，离开房间提供隐私的参与者。标签和所有唾液样本储存在-20 ° C尽快。 </li><li>记录的预压应力的生理测量5分钟。 </li></ol> 3。该TSST <ol><li>如果您将使用一个单独的面谈室（增加TSST应力的影响），带给参与者从候车室进入面试室。 </li><li>开始TSST讲话的准备期，请阅读下面的脚本参与者：“这是任务的讲话准备的一部分，你在精神上准备一个五分钟的演讲，描述你为什么会是你理想的工作的一个很好的候选人。你的发言将进行录像，并在公众演讲训练的法官小组审查，你有10分钟的准备，现在开始你的时间。“ </li><li>记录在10分钟的演讲准备期的生理测量。设置一个10分钟的数字式计时器，离开房间。 </李&gt; <li> 10分钟后，回到房间，身穿白大褂。阅读下面的脚本参与者：“这是讲话的一部分任务，你要描述你为什么会是你理想的工作的一个很好的候选人发表了演讲，你应该说整个五分钟的时间内。现在开始你的时间。“道具摄像头应打开现在开始，增加评价/性能压力。 </li><li>记录在5分钟的讲话表现期的生理测量。如果参与者停止在演讲中所说，让他或她保持沉默20秒。如果他或她不会继续讲，提示参与者继续说，指示他们：“你还有剩余的时间。” </li><li>在5分钟的讲话表现期结束时，参与者阅读下面的脚本：“在最后五分钟，你将被要求按顺序从1022减去13号任务的数学部分，你会口头上。LY报告你的答案大声，并要求从1022开始，如果是一个错误。你的时间，现在开始“，如果参与者犯错，提示他们：”这是不正确的的，请从1022开始“设置为5分钟的数字计时器。 </li><li>记录在5分钟的数学表现期的生理测量。 </li><li>在数学履行期限的TSST年底，收集“后讲”的唾液样本。 </li><li>管理后的应力状态特质焦虑量表。 </li></ol> 4。后强调恢复测量<ol><li>与会者返回到原来的候车室。在第一个恢复时期，指示参与者舒适的等待20分钟。设置一个20分钟的数字式计时器，离开房间。 </li><li> 20分钟后返回候车室，并收集了“恢复1”唾液样本。 </li><li>在第二个恢复期，指示参与者，再等待20分钟舒适。设置一个20分钟的数字式计时器，离开房间。 </li><li> 20分钟后返回候车室，并收集了“复苏2”唾液样本。 </li><li>指导参与完成的“复苏”的国家特质焦虑量表。 </li><li>汇报的参与者，以实验的真实性质。通知他们的表现是不是没有分析其辞或数学成绩将进行记录和参与者。到参与者，他们提出的任务是不合理的困难并没有反映参与者的资质或能力时解释。 </li></ol> 5。数据分析<ol><li>要分析心理的措施，每个国家特质焦虑量 ​​表得分从预压应力，应力和恢复时间点。 6 </li><li>分析生理措施，为每5分钟平均心率评分“预应力计算，”讲话准备“，”讲话“表现”和“MATH“的TSST的时期。此外，计算平均分数TSST或TSST在离散时间点的测量心率为每分钟。 </li><li>分析神经内分泌措施，检测唾液激素浓度的样品，使用市售的环境影响评估套件。 </li></ol> 6 可选：附加唾液皮质醇含量的协议信息（转载Salimetrics唾液皮质醇检测试剂盒插入） <ol><li>至室温，将所有的唾液检测试剂盒。 </li><li>准备洗涤缓冲液，按试剂盒说明。 </li><li>确定到适当的水井在重复板布局和移液器25μL标准和控制。 </li><li>解冻唾液样本，涡在1500 XG（3000转）离心15分钟。 </li><li>吸取25μL的离心样品的透明液体，为在适当的井板（一式两份）。 </li><li>酶标记物，并吸取200微升到所有井准备。 </li&gt; <li>混合盘5分钟500转，并孵育一个额外的55分钟。 </li><li>洗净，吸干板缓冲液洗4次。 </li><li>加入200μL的四甲基联苯胺，每孔（TMB）解决方案，采用多道移液器。 </li><li>混合板5分钟500转，在黑暗中孵育一个额外的25分钟。 </li><li>添加50μL到每口井的一站式解决方案和混合3分钟500转，停止反应。 </li><li>用板底部清洁，并在450 nm处读取板块在酶标仪添加一站式解决方案的10分钟内。 </li><li>要计算皮质醇浓度，计算平均光密度为所有重复的井。减为零，标准，控制和样品孔的平均光密度的非特异性结合井的平均光密度。 </li><li>计算每个标准，控制和样品的断言这些井的平均光密度（B）除以势必％（B / BO）岁零井（博）的光密度。确定使用的物流功能的软件插值的控制和样品的浓度。 </li></ol> 7。代表性的成果： 这里介绍的数据代表是编制审查期间与健康成年男性参与者下午，在我们的实验室进行的文学和两项研究。 这些数据是为了约表示，可能会发现使用本文提出的协议的结果 。 这TSST协议（图1）诱导自我报告的焦虑程度的增加（由国家特质焦虑量表测量图2），心率（图3），和唾液皮质醇浓度（图4）。如图1所示的实验方案是提供各种测量过程中可能会与TSST的数据收集会议的一个例子。 measuremen时机TS和列入不同的措施，将取决于具体的研究问题。如果使用，目的是减少焦虑和/或应激反应，在这些措施的减弱或减毒增加预测的干预。 <img alt="图1" src="/files/ftp_upload/3238/3238fig1.jpg" /> 图1。实验协议注：特里尔社会压力测试（TSST）;国家特质焦虑量 ​​表（STAI），5分钟前应力期（PS）; 10分钟提前应激期（讲话筹备）（）; 5分钟的讲话期间。 （S），5分钟的数学期（M）。 <img alt="图2" src="/files/ftp_upload/3238/3238fig2.jpg" /> 图2。代表状态焦虑分数注：国家焦虑评分从20 iten状态焦虑状态特质焦虑量 ​​表（STAI）测量计算代表分数反映在我们的实验室收集的数据，在文学出版。 图3。代表心率数据 注 ：心脏每分钟节拍数（BPM）的速度代表值，反映在我们的实验室收集的数据，在文学出版。 <img alt="图4" src="/files/ftp_upload/3238/3238fig4.jpg" /> 图4。代表唾液皮质醇数据 注 ：UL / DL中的皮质醇浓度 。代表值反映了在我们的实验室收集的数据，在文学出版。

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H., Hellhammer, J. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Attenuation+of+the+hypothalamic-pituitary-adrenal+axis+responsivity+to+the+Trier+Social+Stress+Test+by+the+benzodiazepine+alprazolam.">Attenuation of the hypothalamic-pituitary-adrenal axis responsivity to the Trier Social Stress Test by the benzodiazepine alprazolam.</a> Psychoneuroendocrinology. 31, 1278-1288 (2006).</li><li>Kudielka, B. M., Fischer, J. 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D., Roy, M., Peretz, I., Lupien, S. J. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Effects+of+relaxing+music+on+salivary+cortisol+level+after+psychological+stress.">Effects of relaxing music on salivary cortisol level after psychological stress.</a> Ann. NY Acad. Sci. 999, 374-376 (2003).</li><li>Balodis, I. M., Wynne-Edwards, K. E., Olmstead, M. C. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=The+other+side+of+the+curve:+Examining+the+relationship+between+pre-stressor+physiological+responses+and+stress+reactivity.">The other side of the curve: Examining the relationship between pre-stressor physiological responses and stress reactivity.</a> Psychoneuroendocrinology. 35, 1363-1373 (2010).</li><li>Shultheiss, O. C., Stanton, S. J., Harmon-Jones, E., Beer, J. S. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Assessment+of+salivary+hormones.">Assessment of salivary hormones.</a> Methods in Social Neuroscience. , 17-44 (2009).</li><li>Kudielka, B. M., Hellhammer, D. H., W&#252;st, S. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Why+do+we+respond+so+differently?+Reviewing+determinants+of+human+salivary+cortisol+responses+to+challenge.">Why do we respond so differently? Reviewing determinants of human salivary cortisol responses to challenge.</a> Psychoneuroendocrinology. 34, 2-18 (2009).</li><li>Buske-Kirschbaum, A., Jobst, S., Wustmans, A., Kirschbaum, C., Rauh, W., Hellhammer, D. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Attenuated+free+cortisol+response+to+psychosocial+stress+in+children+with+atopic+dermatitis.">Attenuated free cortisol response to psychosocial stress in children with atopic dermatitis.</a> Psychosom. Med. 59, 419-426 (1997).</li></ol>

没有利益冲突的声明。

在这篇文章中，我们演示了如何在一个健康的志愿者进行特里尔社会压力测试。 TSST是一个标准化的实验室社会应激诱导强大而可靠的心理，生理和神经内分泌措施增加。 TSST是一个有用的替代物理压力，如在寒冷的压测试或跑步机上行走，并抄录在评价观众面前表现更自然的心理压力。 的TSST的许多方面可以进行修改，以满足各种研究方案的需求。本文所演示的测量时间点代...

<table border="1"><tbody><tr><th>设备名称/供应</th><th>公司</th><th>目录编号</th></tr><tr><td> BSL心理生理学的Mac OS系统，包括MP36数据采集单元和三导联心电图电极</td><td> BIOPAC系统公司</td><td> BSLPSY - M </td></tr><tr><td>状态特质焦虑量表</td><td>心灵花园，公司</td><td>沉静- B </td></tr><tr><td>唾液皮质醇酶免疫检测试剂盒</td><td> Salimetrics </td><td> 1-3002 </td></tr><tr><td> 2.0毫升的聚丙烯小瓶</td><td> Fisher Scientific则</td><td> 05 40B 146 </td></tr><tr><td> BioRad公司酶标仪，680型，与微孔板Manager软件</td><td> BioRad公司</td><td>酶标仪：168 1000软件：1706800 </td></tr></tbody></table>

the trier social stress test protocol for inducing psychological stress

本文演示了在实验室环境中使用的心理压力协议。协议，使研究人员研究在健康和疾病的应激反应的生物途径是在紧张和焦虑的研究进展的基础。[1]虽然众多的协议，在实验室中诱导应激反应存在，许多忽视提供自然背景或纳入社会和心理压力方面。心理压力协议，荟萃分析表明，特里尔社会压力测试（TSST）的应激激素的反应性。研究，在原来的TSST描述是最有用和最适当的的标准化协议，研究人员试图设计和评估的程序能够诱导可靠的应激反应，在大多数健康志愿者3这些研究人员发现，在心率，血压和几个内分泌应激米的海拔高度arkers的TSST（心理应激）相比，生理盐水注射液（物理应激）。，虽然TSST已被修改，以满足不同的研究小组的需求，它一般由一个到达后的等待期，预期讲话算术准备，演讲表现，口头表现时期，由一个或多个恢复时期。 TSST要求与会者准备并发表讲话，并口头回应一个具有挑战性的算术问题，在一个社会评价的观众。社会评价和不可控性已被确定为关键部件的压力感应的 TSST。使用4十多年来，TSST的目标任务的过程中，有系统地诱导应激反应，以衡量不同反应，焦虑和激活下丘脑 - 垂体 - 肾上腺（HPA）或交感神经 - 肾上腺髓质（SAM）轴1 Researc她一般评估自我报告的焦虑的变化，生理的措施（如心率），和/或神经内分泌指标（如应激激素皮质醇）的TSST。许多研究者通过对应激标志物，如皮质醇和α-淀粉酶（植物神经系统激活的标志）作为替代采血，血液收集技术，以减少混杂强调的唾液取样。除了​​TSST完成个人所经历的变化，研究人员可以比较不同的治疗组（如临床与健康对照样本）或压力减少干预的有效性的变化1。

Watch this Scientific Journal Video about The Trier Social Stress Test Protocol for Inducing Psychological Stress at JoVE.com

The Trier Social Stress Test Protocol for Inducing Psychological Stress

本文介绍了诱导参与者的心理压力，这使研究人员能够测量单个参与者或群体之间的心理，生理和神经内分泌反应强调了协议。

特里尔社会压力诱发心理应激的测试协议

This article demonstrates a psychological stress protocol for use in a laboratory setting.  Protocols that allow researchers to study the biological ...

the-trier-social-stress-test-protocol-for-inducing-psychological

Research

JoVE Journal

Medicine

55.6K 次观看.  Northern Arizona University. 本文介绍了诱导参与者的心理压力，这使研究人员能够测量单个参与者或群体之间的心理，生理和神经内分泌反应强调了协议。

视频: The Trier Social Stress Test Protocol for Inducing Psychological Stress

Using Visual and Narrative Methods to Achieve Fair Process in Clinical Care

The Institute of Medicine has targeted patient-centeredness as an important area of quality improvement. A major dimension of patient-centeredness is respect for patient's values, preferences, and expressed needs. Yet specific approaches to gaining this understanding and translating it to quality care in the clinical setting are lacking. From a patient perspective quality is not a simple concept but is best understood in terms of five dimensions: technical outcomes; decision-making efficiency; amenities and convenience; information and emotional support; and overall patient satisfaction. Failure to consider quality from this five-pronged perspective results in a focus on medical outcomes, without considering the processes central to quality from the patient's perspective and vital to achieving good outcomes. In this paper, we argue for applying the concept of fair process in clinical settings. Fair process involves using a collaborative approach to exploring diagnostic issues and treatments with patients, explaining the rationale for decisions, setting expectations about roles and responsibilities, and implementing a core plan and ongoing evaluation. Fair process opens the door to bringing patient expertise into the clinical setting and the work of developing health care goals and strategies. This paper provides a step by step illustration of an innovative visual approach, called photovoice or photo-elicitation, to achieve fair process in clinical work with acquired brain injury survivors and others living with chronic health conditions. Applying this visual tool and methodology in the clinical setting will enhance patient-provider communication; engage patients as partners in identifying challenges, strengths, goals, and strategies; and support evaluation of progress over time. Asking patients to bring visuals of their lives into the clinical interaction can help to illuminate gaps in clinical knowledge, forge better therapeutic relationships with patients living with chronic conditions such as brain injury, and identify patient-centered goals and possibilities for healing. The process illustrated here can be used by clinicians, (primary care physicians, rehabilitation therapists, neurologists, neuropsychologists, psychologists, and others) working with people living with chronic conditions such as acquired brain injury, mental illness, physical disabilities, HIV/AIDS, substance abuse, or post-traumatic stress, and by leaders of support groups for the types of patients described above and their family members or caregivers.

This paper illustrates an innovative visual approach (photovoice or photo-elicitation) to achieve fair process in clinical care for patients living with chronic health conditions, illuminate gaps in clinical knowledge, forge better therapeutic relationships, and identify patient-centered goals and possibilities for healing.

利用视觉和叙事方法，以实现公平的进程中，在临床护理

The Institute of Medicine has targeted patient-centeredness as an important area of quality improvement. A major dimension of patient-centeredness is ...

科研

医学

Development of a Unilaterally-lesioned 6-OHDA Mouse Model of Parkinson's Disease

The unilaterally lesioned 6-hyroxydopamine (6-OHDA)-lesioned rat model of Parkinson's disease (PD) has proved to be invaluable in advancing our understanding of the mechanisms underlying parkinsonian symptoms, since it recapitulates the changes in basal ganglia circuitry and pharmacology observed in parkinsonian patients1-4. However, the precise cellular and molecular changes occurring at cortico-striatal synapses of the output pathways within the striatum, which is the major input region of the basal ganglia remain elusive, and this is believed to be site where pathological abnormalities underlying parkinsonian symptoms arise3,5.
In PD, understanding the mechanisms underlying changes in basal ganglia circuitry following degeneration of the nigro-striatal pathway has been greatly advanced by the development of bacterial artificial chromosome (BAC) mice over-expressing green fluorescent proteins driven by promoters specific for the two striatal output pathways (direct pathway: eGFP-D1; indirect pathway: eGFP-D2 and eGFP-A2a)8, allowing them to be studied in isolation. For example, recent studies have suggested that there are pathological changes in synaptic plasticity in parkinsonian mice9,10. However, these studies utilised juvenile mice and acute models of parkinsonism. It is unclear whether the changes described in adult rats with stable 6-OHDA lesions also occur in these models. Other groups have attempted to generate a stable unilaterally-lesioned 6-OHDA adult mouse model of PD by lesioning the medial forebrain bundle (MFB), unfortunately, the mortality rate in this study was extremely high, with only 14% surviving the surgery for 21 days or longer11. More recent studies have generated intra-nigral lesions with both a low mortality rate &gt;80% loss of dopaminergic neurons, however expression of L-DOPA induced dyskinesia11,12,13,14 was variable in these studies. Another well established mouse model of PD is the MPTP-lesioned mouse15. Whilst this model has proven useful in the assessment of potential neuroprotective agents16, it is less suitable for understanding mechanisms underlying symptoms of PD, as this model often fails to induce motor deficits, and shows a wide variability in the extent of lesion17, 18.
Here we have developed a stable unilateral 6-OHDA-lesioned mouse model of PD by direct administration of 6-OHDA into the MFB, which consistently causes &gt;95% loss of striatal dopamine (as measured by HPLC), as well as producing the behavioural imbalances observed in the well characterised unilateral 6-OHDA-lesioned rat model of PD. This newly developed mouse model of PD will prove a valuable tool in understanding the mechanisms underlying generation of parkinsonian symptoms.

Development of a Unilaterally-lesioned 6-OHDA Mouse Model of Parkinson&#039;s Disease

A protocol for performing unilateral 6-OHDA lesions of the medial forebrain bundle in mice is described. This method has a low mortality rate (13.3 %) with 89% of the surviving animals showing &#62;95% loss of striatal dopamine and 90.63&#177;-4.02 % ipsiversive rotational bias towards the side of the lesion.

1单侧损毁6  - 羟基多巴胺帕金森病小鼠模型的发展

The unilaterally lesioned 6-hyroxydopamine (6-OHDA)-lesioned rat model of Parkinson's disease (PD) has proved to be invaluable in advancing our ...

Implantation of a Carotid Cuff for Triggering Shear-stress Induced Atherosclerosis in Mice

It is widely accepted that alterations in vascular shear stress trigger the expression of inflammatory genes in endothelial cells and thereby induce atherosclerosis (reviewed in 1 and 2). The role of shear stress has been extensively studied in vitro investigating the influence of flow dynamics on cultured endothelial cells 1,3,4 and in vivo in larger animals and humans 1,5,6,7,8. However, highly reproducible small animal models allowing systematic investigation of the influence of shear stress on plaque development are rare. Recently, Nam et al. 9 introduced a mouse model in which the ligation of branches of the carotid artery creates a region of low and oscillatory flow. Although this model causes endothelial dysfunction and rapid formation of atherosclerotic lesions in hyperlipidemic mice, it cannot be excluded that the observed inflammatory response is, at least in part, a consequence of endothelial and/or vessel damage due to ligation.
In order to avoid such limitations, a shear stress modifying cuff has been developed based upon calculated fluid dynamics, whose cone shaped inner lumen was selected to create defined regions of low, high and oscillatory shear stress within the common carotid artery 10. By applying this model in Apolipoprotein E (ApoE) knockout mice fed a high cholesterol western type diet, vascular lesions develop upstream and downstream from the cuff. Their phenotype is correlated with the regional flow dynamics 11 as confirmed by in vivo Magnetic Resonance Imaging (MRI) 12: Low and laminar shear stress upstream of the cuff causes the formation of extensive plaques of a more vulnerable phenotype, whereas oscillatory shear stress downstream of the cuff induces stable atherosclerotic lesions 11. In those regions of high shear stress and high laminar flow within the cuff, typically no atherosclerotic plaques are observed.
 
In conclusion, the shear stress-modifying cuff procedure is a reliable surgical approach to produce phenotypically different atherosclerotic lesions in ApoE-deficient mice.

The constricting cuff presented in this article is designed to induce atherosclerosis in the murine common carotid artery. Due to the conical shape of its inner lumen the implanted cuff generates well-defined regions of low, high and oscillatory shear stress triggering the development of atherosclerotic lesions of different inflammatory phenotypes.

植入小鼠触发剪应力致动脉粥样硬化的颈袖

It is widely accepted that alterations in vascular shear stress trigger the expression of inflammatory genes in endothelial cells and thereby induce ...

Biomarkers in an Animal Model for Revealing Neural, Hematologic, and Behavioral Correlates of PTSD

Identification of biomarkers representing the evolution of the pathophysiology of Post Traumatic Stress Disorder (PTSD) is vitally important, not only for objective diagnosis but also for the evaluation of therapeutic efficacy and resilience to trauma. Ongoing research is directed at identifying molecular biomarkers for PTSD, including traumatic stress induced proteins, transcriptomes, genomic variances and genetic modulators, using biologic samples from subjects' blood, saliva, urine, and postmortem brain tissues. However, the correlation of these biomarker molecules in peripheral or postmortem samples to altered brain functions associated with psychiatric symptoms in PTSD remains unresolved. Here, we present an animal model of PTSD in which both peripheral blood and central brain biomarkers, as well as behavioral phenotype, can be collected and measured, thus providing the needed correlation of the central biomarkers of PTSD, which are mechanistic and pathognomonic but cannot be collected from people, with the peripheral biomarkers and behavioral phenotypes, which can.
Our animal model of PTSD employs restraint and tail shocks repeated for three continuous days - the inescapable tail-shock model (ITS) in rats. This ITS model mimics the pathophysiology of PTSD 17, 7, 4, 10. We and others have verified that the ITS model induces behavioral and neurobiological alterations similar to those found in PTSD subjects 17, 7, 10, 9. Specifically, these stressed rats exhibit (1) a delayed and exaggerated startle response appearing several days after stressor cessation, which given the compressed time scale of the rat's life compared to a humans, corresponds to the one to three months delay of symptoms in PTSD patients (DSM-IV-TR PTSD Criterian D/E 13), (2) enhanced plasma corticosterone (CORT) for several days, indicating compromise of the hypothalamopituitary axis (HPA), and (3) retarded body weight gain after stressor cessation, indicating dysfunction of metabolic regulation.
The experimental paradigms employed for this model are: (1) a learned helplessness paradigm in the rat assayed by measurement of acoustic startle response (ASR) and a charting of body mass; (2) microdissection of the rat brain into regions and nuclei; (3) enzyme-linked immunosorbent assay (ELISA) for blood levels of CORT; (4) a gene expression microarray plus related bioinformatics tools 18. This microarray, dubbed rMNChip, focuses on mitochondrial and mitochondria-related nuclear genes in the rat so as to specifically address the neuronal bioenergetics hypothesized to be involved in PTSD.

We describe a rat model of post traumatic stress disorder (PTSD) that reveals the persistent alterations in neuroendocrine function and the delayed long-term, exaggerated fear response, characteristic of PTSD patients. The animal model and methods described here are useful for correlating biomarkers in brain nuclei, which are mechanistic but cannot be measured in patients, with biomarkers in peripheral white blood cells, which can.

在动物模型揭示神经，血液，创伤后应激障碍和行为相关因素的生物标志物

Identification of biomarkers representing the evolution of the pathophysiology of Post Traumatic Stress Disorder (PTSD) is vitally important, not only for ...

Cardiac Stress Test Induced by Dobutamine and Monitored by Cardiac Catheterization in Mice

Dobutamine is a &beta;-adrenergic agonist with an affinity higher for receptor expressed in the heart (&beta;1) than for receptors expressed in the arteries (&beta;2). When systemically administered, it increases cardiac demand. Thus, dobutamine unmasks abnormal rhythm or ischemic areas potentially at risk of infarction. 
Monitoring of heart function during a cardiac stress test can be performed by either ecocardiography or cardiac catheterization. The latter is an invasive but more accurate and informative technique that the former.
Cardiac stress test induced by dobutamine and monitored by cardiac catheterization accomplished as described here allows, in a single experiment, the measurement of the following hemodynamic parameters: heart rate (HR), systolic pressure, diastolic pressure, end-diastolic pressure, maximal positive pressure development (dP/dtmax) and maximal negative pressure development (dP/dtmin), at baseline conditions and under increasing doses of dobutamine.
As expected, in normal mice we observed a dobutamine dose-related increase in HR, dP/dtmax and dP/dtmin. Moreover, at the highest dose tested (12 ng/g/min) the cardiac decompensation of high fat diet-induced obese mice was unmasked.

We describe the protocol to perform a cardiac stress test induced by dobutamine and monitored by cardiac catheterization in normal mice. Also we show its application to unmask subclinical cardiac disease in high fat diet-induced obese mice.

多巴酚丁胺诱导的心脏压力测试和监控通过在小鼠心脏导管插入术

Dobutamine is a &beta;-adrenergic agonist with an affinity higher for receptor expressed in the heart (&beta;1) than for receptors expressed in the ...

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR

Injection of Algisyl-LVR, a treatment under clinical development, is intended to treat patients with dilated cardiomyopathy. This treatment was recently used for the first time in patients who had symptomatic heart failure. In all patients, cardiac function of the left ventricle (LV) improved significantly, as manifested by consistent reduction of the LV volume and wall stress. Here we describe this novel treatment procedure and the methods used to quantify its effects on LV wall stress and function.
Algisyl-LVR is a biopolymer gel consisting of Na+-Alginate and Ca2+-Alginate. The treatment procedure was carried out by mixing these two components and then combining them into one syringe for intramyocardial injections. This mixture was injected at 10 to 19 locations mid-way between the base and apex of the LV free wall in patients.
Magnetic resonance imaging (MRI), together with mathematical modeling, was used to quantify the effects of this treatment in patients before treatment and at various time points during recovery. The epicardial and endocardial surfaces were first digitized from the MR images to reconstruct the LV geometry at end-systole and at end-diastole. Left ventricular cavity volumes were then measured from these reconstructed surfaces.
Mathematical models of the LV were created from these MRI-reconstructed surfaces to calculate regional myofiber stress. Each LV model was constructed so that 1) it deforms according to a previously validated stress-strain relationship of the myocardium, and 2) the predicted LV cavity volume from these models matches the corresponding MRI-measured volume at end-diastole and end-systole. Diastolic filling was simulated by loading the LV endocardial surface with a prescribed end-diastolic pressure. Systolic contraction was simulated by concurrently loading the endocardial surface with a prescribed end-systolic pressure and adding active contraction in the myofiber direction. Regional myofiber stress at end-diastole and end-systole was computed from the deformed LV based on the stress-strain relationship.

This article describes procedures for implanting a novel hydrogel in failing hearts and quantifying its effect on left ventricular wall stress and function. These procedures have been successfully applied in dogs and humans.

左室壁应力和改进功能衰竭心脏使用Algisyl LVR减少

Injection of  Algisyl-LVR, a treatment under clinical development, is intended to treat  patients with dilated cardiomyopathy. This treatment was recently ...

A Mouse Tumor Model of Surgical Stress to Explore the Mechanisms of Postoperative Immunosuppression and Evaluate Novel Perioperative Immunotherapies

Surgical resection is an essential treatment for most cancer patients, but surgery induces dysfunction in the immune system and this has been linked to the development of metastatic disease in animal models and in cancer patients. Preclinical work from our group and others has demonstrated a profound suppression of innate immune function, specifically NK cells in the postoperative period and this plays a major role in the enhanced development of metastases following surgery. Relatively few animal studies and clinical trials have focused on characterizing and reversing the detrimental effects of cancer surgery. Using a rigorous animal model of spontaneously metastasizing tumors and surgical stress, the enhancement of cancer surgery on the development of lung metastases was demonstrated. In this model, 4T1 breast cancer cells are implanted in the mouse mammary fat pad. At day 14 post tumor implantation, a complete resection of the primary mammary tumor is performed in all animals. A subset of animals receives additional surgical stress in the form of an abdominal nephrectomy. At day 28, lung tumor nodules are quantified. When immunotherapy was given immediately preoperatively, a profound activation of immune cells which prevented the development of metastases following surgery was detected. While the 4T1 breast tumor surgery model allows for the simulation of the effects of abdominal surgical stress on tumor metastases, its applicability to other tumor types needs to be tested. The current challenge is to identify safe and promising immunotherapies in preclinical mouse models and to translate them into viable perioperative therapies to be given to cancer surgery patients to prevent the recurrence of metastatic disease.

A mouse tumor model of surgical stress is used to explore how postoperative immune suppression promotes metastatic disease and to evaluate immunostimulatory perioperative therapies.

手术应激探索术后免疫抑制的机制和评估新围手术期免疫疗法的小鼠肿瘤模型

Surgical resection is an essential treatment for most cancer patients, but surgery induces dysfunction in the immune system and this has been linked to ...

A Modified In vitro Invasion Assay to Determine the Potential Role of Hormones, Cytokines and/or Growth Factors in Mediating Cancer Cell Invasion

Blood serum serves as a chemoattractant towards which cancer cells migrate and invade, facilitating their intravasation into microvessels. However, the actual molecules towards which the cells migrate remain elusive. This modified invasion assay has been developed to identify targets which drive cell migration and invasion. This technique compares the invasion index under three conditions to determine whether a specific hormone, growth factor, or cytokine plays a role in mediating the invasive potential of a cancer cell. These conditions include i) normal fetal bovine serum (FBS), ii) charcoal-stripped FBS (CS-FBS), which removes hormones, growth factors, and cytokines and iii) CS-FBS + molecule (denoted &#8220;X&#8221;). A significant change in cell invasion with CS-FBS as compared to FBS, indicates the involvement of hormones, cytokines or growth factors in mediating the change. Individual molecules can then be added back to CS-FBS to assay their ability to reverse or rescue the invasion phenotype. Furthermore, two or more factors can be combined to evaluate the additive or synergistic effects of multiple molecules in driving or inhibiting invasion. Overall, this method enables the investigator to determine whether hormones, cytokines, and/or growth factors play a role in cell invasion by serving as chemoattractants or inhibitors of invasion for a particular type of cancer cell or a specific mutant. By identifying specific chemoattractants and inhibitors, this modified invasion assay may help to elucidate signaling pathways that direct cancer cell invasion.

A Modified In vitro Invasion Assay to Determine the Potential Role of Hormones, Cytokines and/or Growth Factors in Mediating Cancer Cell Invasion

This video article describes a modified in vitro method to examine the role of hormones, cytokines and/or growth factors in driving cancer cell invasion.

一种改进<em&gt;在体外</em&gt;入侵检测，以确定激素，在调节肿瘤细胞侵袭的细胞因子和/或生长因子的潜在作用

Blood serum serves as a chemoattractant towards which cancer cells migrate and invade, facilitating their intravasation into microvessels. However, the ...

Glutamate and Hypoxia as a Stress Model for the Isolated Perfused Vertebrate Retina

Neuroprotection has been a strong field of investigation in ophthalmological research in the past decades and affects diseases such as glaucoma, retinal vascular occlusion, retinal detachment, and diabetic retinopathy. It was the object of this study to introduce a standardized stress model for future preclinical therapeutic testing.
Bovine retinas were prepared and perfused with an oxygen saturated standard solution, and the ERG was recorded. After recording stable b-waves, hypoxia (pure N2) or glutamate stress (250 &#181;m glutamate) was exerted for 45 min. To investigate the effects on photoreceptor function alone, 1 mM aspartate was added to obtain a-waves. ERG-recovery was monitored for 75 min.
For hypoxia, a decrease in a-wave amplitude of 87.0% was noted (p &#60;0.01) after an exposition time of 45 min (decrease of 36.5% after the end of the washout p = 0.03). Additionally, an initial decrease in b-wave amplitudes of 87.23% was recorded, that reached statistical significance (p &#60;0.01, decrease of 25.5% at the end of the washout, p = 0.03).
For 250 &#181;m glutamate, an initial 7.8% reduction of a-wave amplitudes (p &#62;0.05) followed by a reduction of 1.9% (p &#62;0.05). A reduction of 83.7% of b-wave amplitudes (p &#60;0.01) was noted; after a washout of 75 min the reduction was 2.3% (p = 0.62). In this study, a standardized stress model is presented that may be useful to identify possible neuroprotective effects in the future.

With this study, we introduce a standardized stress model for the isolated superfused bovine retina for future preclinical therapeutic testing. The effect of either hypoxia (pure N2) or glutamate stress (250 &#181;M glutamate) on retinal function represented by a- and b-wave amplitudes was evaluated.

谷氨酸和缺氧作为离体脊椎动物视网膜应力模型

Neuroprotection has been a strong field of investigation in ophthalmological research in the past decades and affects diseases such as glaucoma, retinal ...

Induction and Analysis of Oxidative Stress in Sleeping Beauty Transposon-Transfected Human Retinal Pigment Epithelial Cells

Oxidative stress plays a critical role in several degenerative diseases, including age-related macular degeneration (AMD), a pathology that affects ~30 million patients worldwide. It leads to a decrease in retinal pigment epithelium (RPE)-synthesized neuroprotective factors, e.g., pigment epithelium-derived factor (PEDF) and granulocyte-macrophage colony-stimulating factor (GM-CSF), followed by the loss of RPE cells, and eventually photoreceptor and retinal ganglion cell (RGC) death. We hypothesize that the reconstitution of the neuroprotective and neurogenic retinal environment by the subretinal transplantation of transfected RPE cells overexpressing PEDF and GM-CSF has the potential to prevent retinal degeneration by mitigating the effects of oxidative stress, inhibiting inflammation, and supporting cell survival. Using the Sleeping Beauty transposon system (SB100X) human RPE cells have been transfected with the PEDF and GM-CSF genes and shown stable gene integration, long-term gene expression, and protein secretion using qPCR, western blot, ELISA, and immunofluorescence. To confirm the functionality and the potency of the PEDF and GM-CSF secreted by the transfected RPE cells, we have developed an in vitro assay to quantify the reduction of H2O2-induced oxidative stress on RPE cells in culture. Cell protection was evaluated by analyzing cell morphology, density, intracellular level of glutathione, UCP2 gene expression, and cell viability. Both, transfected RPE cells overexpressing PEDF and/or GM-CSF and cells non-transfected but pretreated with PEDF and/or GM-CSF (commercially available or purified from transfected cells) showed significant antioxidant cell protection compared to non-treated controls. The present H2O2-model is a simple and effective approach to evaluate the antioxidant effect of factors that may be effective to treat AMD or similar neurodegenerative diseases.

Induction and Analysis of Oxidative Stress in Sleeping Beauty Transposon-Transfected Human Retinal Pigment Epithelial Cells

We present a protocol for the development and use ofan oxidative stress-model by treating retinal pigment epithelial cells with H2O2, analyzing cell morphology, viability, density, glutathione, and UCP-2 level. It is a useful model to investigate the antioxidant effect of proteins secreted by transposon-transfected cells to treat neuroretinal degeneration.

睡眠美人转座转染人视网膜色素上皮细胞氧化应激的诱导与分析

Oxidative stress plays a critical role in several degenerative diseases, including age-related macular degeneration (AMD), a pathology that affects ~30 ...