This paper is dedicated to my beloved wife Maren and our little Karl.

1. إعداد الأبقار عيون <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> الحصول على عيون البقر مباشرة بعد ذبح الحيوان. </li><li style=";text-align:right;direction:rtl"> نقل وجهة نظر محمية في &quot;Sickel-حل&quot; وسيلة خاص يحتوي على 120 ملي كلوريد الصوديوم، 2 ملي بوكل، 0.1 ملي MgCl 2، 0.15 ملي CaCl 2، 1.5 ملي ناه 2 PO 4، 13.5 ملي نا 2 هبو 4 و 5 ملي الجلوكوز في RT. </li><li style=";text-align:right;direction:rtl"> أداء إعداد الشبكية في ظل ظروف الظلام تكييفها مع ضوء أحمر خافت. </li><li style=";text-align:right;direction:rtl"> إزالة الجزء الأمامي من العين. إجراء شق كاليفورنيا. الاستوائي 4 مم الخلفي لحوف. بعد ذلك إزالة القرنية، القزحية والجسم الهدبي والعدسة في قطعة واحدة. الحفاظ على شبكية العين في Sickel-حل. </li><li style=";text-align:right;direction:rtl"> ميكانيكيا تخفيف المرفقات زجاجي على سطح الشبكية وإزالة الجسم الزجاجي من كأس العين مفتوحة. </li><li style=";text-align:right;direction:rtl"> بعد ذلك تقسيم العين إلى أربعة أجزاء ولكمة من الجولة مناطق من كاليفورنيا. 7 مم باستخدام منقب. </li><li style=";text-align:right;direction:rtl"> فصل بلطف شبكية العينمن الظهارة الصبغية ووضعه على جهاز تسجيل داخل علبة محمية من الضوء. يتكون جهاز التسجيل من معيل البلاستيك مع شبكة في الوسط، وضع شبكية العين على شبكة ومن ثم اصلاحها مع حلقة بلاستيكية مباشرة على الأقطاب الكهربائية. ملاحظة: إن معيل البلاستيك لديها قناتين للسماح لتدفق مستمر من المتوسط. </li></ol> 2. تسجيل في مخطط كهربية الشبكية (أرج) <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> من أجل تسجيل مخطط كهربية الشبكية، واستخدام قطبين الفضة / الفضة كلوريد على جانبي شبكية العين ويروي شبكية العين في سرعة ثابتة نضح من كاليفورنيا. 1 مل / دقيقة ودرجة حرارة ثابتة من 37 درجة مئوية. استخدام &quot;Sickel-حل&quot; مشبع بالأكسجين. </li><li style=";text-align:right;direction:rtl"> قبل البدء في القياس، التكيف مع الظلام شبكية العين (حمايته من الضوء خلال جميع القياسات) واستخدام فترات التحفيز من خمس دقائق. استخدام 1 هرتز واحد أبيض فلاش زينون لتحفيز مع كثافة المقرر أن 6.3 MLX على سطح الشبكية. </لى&gt; <li style=";text-align:right;direction:rtl"> استخدام معايرة مرشحات الكثافة محايدة وحافزا خفيفة من 10 μsec التي يسيطر عليها جهاز توقيت من أجل الحصول على الاستجابات المثلى. </li><li style=";text-align:right;direction:rtl"> لقياس ومعالجة البيانات، تصفية أرج وتضخيمها (100 هرتز تمريرة عالية التصفية، 50 هرتز مرشح الشق، 100،000 س التضخيم) باستخدام العشب RPS312RM مكبر للصوت. محاولة لتصفية الترددات المزعجة المحتملة التي قد تعكر صفو الإشارة. من أجل معالجة البيانات، واستخدام لوحة اكتساب التناظرية إلى الرقمية البيانات على جهاز كمبيوتر سطح المكتب (PC متوافق). </li><li style=";text-align:right;direction:rtl"> بعد فترة التكيف السوداء تحت نضح المستمر، وقياس سعة من الإشارة الكهربائية حتى يتم تسجيل مستقرة سعة ب الموجة. تعتبر مدى التردد مستقرة إذا خمسة قياسات واحدة تصل قيمة المتوسط ​​وتنحرف أقل من 10٪: ملاحظة. ويرد مثال جيد على قياسات واحدة في الشكل 1. </li><li style=";text-align:right;direction:rtl"> لبدء الاختبار، ويحل محل الأكسجين النقي من قبل أي من النيتروجين النقي (عدد من التجارب واحدة، ن = 5) لاختبار لنقص الأكسجةأو 250 ميكرون الغلوتامات (ن = 5). </li><li style=";text-align:right;direction:rtl"> تسجيل الاستجابات الكهربائية كل 5 دقائق لمدة 45 دقيقة. </li><li style=";text-align:right;direction:rtl"> بعد فترة الاختبار، ويروي شبكية العين مع المتوسط ​​القياسي مشبع بالأكسجين لمدة 75 دقيقة وإلقاء نظرة على التغييرات من السعة ب الموجة. وهذه هي المرحلة من الاخفاق. قياس السعة ب-موجة من الحوض الصغير من على الموجة إلى ذروة ب الموجة. </li><li style=";text-align:right;direction:rtl"> لدراسة تأثير نقص الأكسجين أو الغلوتامات على إمكانية مستقبلة للضوء في ظل ظروف ظلامية، قمع ب الموجة بإضافة 1 ملم إلى المحلول المغذي. </li><li style=";text-align:right;direction:rtl"> بعد أن سجل إمكانات مبصرة مستقرة لمدة 30 دقيقة، تنفيذ الإجراء كما كان من قبل، ويعرض شبكية العين 45 دقيقة إلى حلول الري المختلفة مع 1 ملم اسبارتاتي. استخدام نفس الفترة تبييض (خطوة 2.8) كما ذكر في وقت سابق. </li></ol> تحليل 3. البيانات <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> من أجل تقييم البيانات إحصائيا، وضمان التوزيع الطبيعي لجميع البيانات، على سبيل المثال باستخدام كولموغوروف سميرنوف-اختبار 15. </li><li style=";text-align:right;direction:rtl"> حساب الحد من أ ب الموجة سعة في النسب المئوية بعد مرحلة التعرض بالمقارنة مع قياس الأخير قبل المعرض. قارن الحد من ERG-سعة بعد 45 دقيقة - في نهاية فترة المعرض - إلى ERG قياس قبل التطبيق. </li><li style=";text-align:right;direction:rtl"> مقارنة موجة أ- وب- في نهاية مرحلة من الاخفاق إلى السعة المقابلة قبل المعرض لدراسة انتعاش محتمل. </li><li style=";text-align:right;direction:rtl"> للتحليل الإحصائي، استخدام البرنامج أحزاب اللقاء المشترك البرامج الإحصائية SPSS أو البرامج. حساب البيانات في جميع أنحاء كما يعني ± الانحراف المعياري. تقدير أهمية من قبل الاختبار الإحصائي المناسب. ملاحظة: هذه الاختبارات قد تكون مختلفة اعتمادا على نطاق تجريبي. في هذا الإعداد، استخدم تقرن اختبار t الطالب. </li></ol>

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The authors have nothing to disclose.

في هذه الدراسة، تم العثور على تأثير كبير على السعة ب-موجة بعد 45 دقيقة من نقص الأكسجة. لا يزال هذا انخفاض كبير بعد مرحلة الغسل. ويمكن ملاحظة تأثير مماثل على إمكانية مبصرة. معتمدة النتائج وفقا لبيانات أخرى نشرت 16 وتعطينا الفرص?...

وكانت العصبية حقل قوي من التحقيق في الأبحاث لطب العيون في العقود الماضية. شبكية العين هي شبكة الخلايا العصبية الحساسة للغاية التي تعتمد بشكل كبير على الأوكسجين وتتأثر بشدة عملية التمثيل الغذائي للخلايا المحيطة بها. أمراض العين الرئيسية المتعلقة تلف الخلايا العصبية هي انسداد الأوعية الدموية في شبكية العين، والزرق، وانفصال الشبكية. في شبكية العين انسداد الشريان، كمثال لشبكية العين انسداد الأوعية الدموية، ويؤدي إلى فقدان مفاجئ للرؤية بسبب نقص الأكسجين في شبكية العين الداخلية 1. وغالبا ما تترافق مع أمراض الأوعية الدموية العامة (2) ويؤدي إلى فقدان البصر المستمرة 1، مع 8٪ فقط من المرضى يتعافى حدة البصر بشكل ملحوظ 1. وعلى الرغم من انحلال الفيبرين الشرياني وقد اقترح كخيار العلاج، لا يمكن أن تظهر فائدة في تجربة سريرية عشوائية 3. الزرق وانفصال الشبكيةعلى حد سواء وزيادة في تركيز الصوديوم 4-6. واجه الغلوتامات في ظل الظروف الفسيولوجية باعتبارها مثير الارسال في جميع أنحاء الجهاز العصبي المركزي كله، وشبكية العين 7،8 الداخلي. تم العثور على مستويات مرتفعة الغلوتامات ليس فقط في الزرق وانفصال الشبكية 5،6 ولكن أيضا في اعتلال الشبكية السكري التكاثري 9. زيادة في الغلوتامات ربما يؤدي إلى التحفيز الزائدة، وبالتالي تلف الخلايا العصبية 10. في معظم حالات انفصال الشبكية، وفي بعض الحالات من التكاثري جراحة اعتلال الشبكية السكري على الشبكية (الجزء المسطح استئصال الزجاجية) ضرورية. خلال الجزء المسطح استئصال الزجاجية التلاعب الميكانيكية، والضوء الساطع من الألياف البصرية أو إجهاد القص التي كتبها معدلات تدفق عالية من حلول الري المبذولة خلال عمليات طويلة تمارس إجهادا إضافيا على شبكية العين 11،12. جميع الأمراض المذكورة تشترك في أن علم الأمراض المترجمة إلى ريتينوحده، وتشكل المجتمع بأمراض في العيون مع التحدي لايجاد سبل لحماية شبكية العين كنظام العصبي الحسي. في مخطط كهربية الشبكية (أرج) هو الطريقة المعيارية لتقييم وظيفة في الجسم الحي مستقبلة للضوء (أ-موجة) وظيفة من وظائف شبكية العين الداخلية (ب الموجة). يتم قياس أرج كل أقطاب الفضة التي أدخلت على القرنية ويتم تحفيز العينين عن طريق زيادة مستوى الضوء للكشف عن عيوب في قضبان أو الأقماع أو في شبكية العين الداخلية. يمكن الكشف عن عيوب مختلفة في شبكية العين بسبب التغيرات في السعة (قوة الاستجابة) أو الكمون (للاستجابة الفاصل الزمني إلى) من أرج. أرج البروتوكول وقياس أساليب مختلفة (نمط أرج، متعددة البؤر-ERG أو حقل مشرق أرج) تسمح بالمزيد من التمايز من العيوب. تم إدخال تقنية شبكية العين معزولة في الآونة الأخيرة، مما يجعل من الممكن لتقييم الآثار على شبكية العين دون تدخلات من مثل حيوان الدراسةردود الفعل العامة 13،14. وكان الغرض من هذه الدراسة لتقييم وتقديم نموذج الإجهاد محددة وموحدة لنقص الأكسجة والإجهاد الغلوتامات على شبكية العين معزولة superfused. وبالتالي، فإننا نأمل أن وضع الأسس للدراسات المستقبلية على آثار اعصاب من بعض وكلاء أو حلول الري داخل العين.

<table border="0" cellpadding="0" cellspacing="0" width="573">
	<tbody>
		<tr height="42">
			<td height="42" style="height:42px;width:216px;">Name of Material/ Equipment</td>
			<td style="width:71px;">Company</td>
			<td style="width:119px;">Catalog Number</td>
			<td style="width:167px;">Comments/Description</td>
		</tr>
		<tr height="63">
			<td height="63" style="height:63px;">120 mM NaCl&#160;</td>
			<td style="width:71px;">Merck Pharma, Germany</td>
			<td align="right" style="width:119px;">1,064,041,000</td>
			<td></td>
		</tr>
		<tr height="63">
			<td height="63" style="height:63px;width:216px;">2 mM KCl,&#160;&#160;</td>
			<td style="width:71px;">Merck Pharma, Germany</td>
			<td align="right" style="width:119px;">1,050,010,250</td>
			<td></td>
		</tr>
		<tr height="63">
			<td height="63" style="height:63px;width:216px;">0.1 mM MgCl2,&#160;</td>
			<td style="width:71px;">Merck Pharma, Germany</td>
			<td align="right" style="width:119px;">58,330,250</td>
			<td></td>
		</tr>
		<tr height="63">
			<td height="63" style="height:63px;width:216px;">0.15 mM CaCl2</td>
			<td style="width:71px;">Merck Pharma, Germany</td>
			<td style="width:119px;">111 TA106282</td>
			<td></td>
		</tr>
		<tr height="63">
			<td height="63" style="height:63px;width:216px;">1.5 mM NaH2PO4/13.5 mM Na2HPO4&#160;&#160;</td>
			<td style="width:71px;">Merck Pharma, Germany</td>
			<td align="right" style="width:119px;">1,065,860,500</td>
			<td></td>
		</tr>
		<tr height="63">
			<td height="63" style="height:63px;width:216px;">5 mM glucose</td>
			<td style="width:71px;">Merck Pharma, Germany</td>
			<td align="right" style="width:119px;">40,741,000</td>
			<td></td>
		</tr>
	</tbody>
</table>

glutamate and hypoxia as a stress model for the isolated perfused vertebrate retina

وكانت العصبية حقل قوي من التحقيق في الأبحاث لطب العيون في العقود الماضية، ويؤثر على أمراض مثل الزرق، وانسداد الأوعية الدموية في شبكية العين، انفصال الشبكية، واعتلال الشبكية السكري. وكان الهدف من هذه الدراسة إلى تقديم نموذج موحد لاختبار الإجهاد العلاجي قبل السريرية في المستقبل. تم إعداد شبكية العين الأبقار ومع perfused حل الأكسجين المشبعة المعيار، وتم تسجيل ERG. بعد تسجيل مستقرة ب-الأمواج، نقص الأكسجة (N النقي 2) أو الإجهاد الغلوتامات (250 ميكرون الغلوتامات) تم بذلها لمدة 45 دقيقة. للتحقيق في الآثار المترتبة على وظيفة مبصرة وحدها، أضيف 1 ملم اسبارتاتي للحصول على موجات. تم رصد أرج استرداد لمدة 75 دقيقة. لنقص الأكسجين، لوحظ وجود انخفاض في الموجة سعة 87.0٪ (P &lt;0.01) بعد وقت المعرض من 45 دقيقة (انخفاض بنسبة 36.5٪ بعد نهاية تبييض ع = 0.03). بالإضافة إلى ذلك، decr الأوليسهولة في سعة ب-موجة وسجلت 87.23٪، التي وصلت إلى دلالة إحصائية (P &lt;0.01، بانخفاض قدره 25.5٪ في نهاية الغسل، ص = 0.03). ل 250 ميكرون الغلوتامات، تخفيض 7.8٪ الأولي من سعة في الموجة (P&gt; 0.05)، يليه انخفاض قدرها 1.9٪ (P&gt; 0.05). والحد من 83.7٪ من سعة الموجة ب (P &lt;0.01) لوحظ. بعد فشل 75 دقيقة كان انخفاض 2.3٪ (ع = 0.62). في هذه الدراسة، يتم تقديم نموذج موحد الإجهاد التي قد تكون مفيدة لتحديد آثار اعصاب محتملة في المستقبل.

بعد 1 ساعة من نضح من الاستعدادات الشبكية مع المشبعة بالأكسجين حل القياسية (الشكل 1A و B) أظهرت ERG-سعة الاستقرار والتباين أقل من سعة بين القياسات واحدة. درجة الحموضة، والضغط الاسموزي، ودرجة الحرارة، وص 2 (باستثناء اختبار نقص الأكسجة) وظلت ثابتة لجميع الاختبا...

Watch this Scientific Journal Video about Glutamate and Hypoxia as a Stress Model for the Isolated Perfused Vertebrate Retina at JoVE.com

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

مع هذه الدراسة، ونحن نقدم نموذجا الإجهاد موحد لشبكية العين الأبقار superfused معزولة للاختبار العلاجي قبل السريرية في المستقبل. تم تقييم تأثير إما نقص الأكسجة (النقي N 2) أو الإجهاد الغلوتامات (250 ميكرومتر الغلوتامات) على وظيفة الشبكية التي يمثلها أ وسعة ب الموجة.

الغلوتامات ونقص الأكسجة نموذجا الإجهاد لمعزولة perfused لالفقارية الشبكية

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

glutamate-hypoxia-as-stress-model-for-isolated-perfused-vertebrate

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7.8K Views.  University Eye Hospital Tübingen.  مع هذه الدراسة، ونحن نقدم نموذجا الإجهاد موحد لشبكية العين الأبقار superfused معزولة للاختبار العلاجي قبل السريرية في المستقبل. تم تقييم تأثير إما نقص الأكسجة (النقي N 2) أو الإجهاد الغلوتامات (250 ميكرومتر الغلوتامات) على وظيفة الشبكية الت?...

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

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.

تطوير نموذج من جانب واحد lesioned الفأر 6 OHDA من مرض باركنسون

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

The Trier Social Stress Test Protocol for Inducing Psychological Stress

This article demonstrates a psychological stress protocol for use in a laboratory setting. Protocols that allow researchers to study the biological pathways of the stress response in health and disease are fundamental to the progress of research in stress and anxiety.1 Although numerous protocols exist for inducing stress response in the laboratory, many neglect to provide a naturalistic context or to incorporate aspects of social and psychological stress. Of psychological stress protocols, meta-analysis suggests that the Trier Social Stress Test (TSST) is the most useful and appropriate standardized protocol for studies of stress hormone reactivity.2 In the original description of the TSST, researchers sought to design and evaluate a procedure capable of inducing a reliable stress response in the majority of healthy volunteers.3 These researchers found elevations in heart rate, blood pressure and several endocrine stress markers in response to the TSST (a psychological stressor) compared to a saline injection (a physical stressor).3 Although the TSST has been modified to meet the needs of various research groups, it generally consists of a waiting period upon arrival, anticipatory speech preparation, speech performance, and verbal arithmetic performance periods, followed by one or more recovery periods. The TSST requires participants to prepare and deliver a speech, and verbally respond to a challenging arithmetic problem in the presence of a socially evaluative audience.3 Social evaluation and uncontrollability have been identified as key components of stress induction by the TSST.4 In use for over a decade, the goal of the TSST is to systematically induce a stress response in order to measure differences in reactivity, anxiety and activation of the hypothalamic-pituitary-adrenal (HPA) or sympathetic-adrenal-medullary (SAM) axis during the task.1 Researchers generally assess changes in self-reported anxiety, physiological measures (e.g. heart rate), and/or neuroendocrine indices (e.g. the stress hormone cortisol) in response to the TSST. Many investigators have adopted salivary sampling for stress markers such as cortisol and alpha-amylase (a marker of autonomic nervous system activation) as an alternative to blood sampling to reduce the confounding stress of blood-collection techniques. In addition to changes experienced by an individual completing the TSST, researchers can compare changes between different treatment groups (e.g. clinical versus healthy control samples) or the effectiveness of stress-reducing interventions.1

This article describes a protocol for inducing psychological stress in participants, which enables researchers to measure psychological, physiological and neuroendocrine responses to stress within single participants or between groups.

اختبار الإجهاد ترير الاجتماعي بروتوكول لإحداث الضغط النفسي

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

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.

المؤشرات الحيوية في نموذج حيواني لكشف الاقتران العصبية، الدموية، والسلوكية للPTSD

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

The In ovo CAM-assay as a Xenograft Model for Sarcoma

Sarcoma is a very rare disease that is heterogeneous in nature, all hampering the development of new therapies. Sarcoma patients are ideal candidates for personalized medicine after stratification, explaining the current interest in developing a reproducible and low-cost xenotransplant model for this disease. The chick chorioallantoic membrane is a natural immunodeficient host capable of sustaining grafted tissues and cells without species-specific restrictions. In addition, it is easily accessed, manipulated and imaged using optical and fluorescence stereomicroscopy. Histology further allows detailed analysis of heterotypic cellular interactions.
This protocol describes in detail the in ovo grafting of the chorioallantoic membrane with fresh sarcoma-derived tumor tissues, their single cell suspensions, and permanent and transient fluorescently labeled established sarcoma cell lines (Saos-2 and SW1353). The chick survival rates are up to 75%. The model is used to study graft- (viability, Ki67 proliferation index, necrosis, infiltration) and host (fibroblast infiltration, vascular ingrowth) behavior. For localized grafting of single cell suspensions, ECM gel provides significant advantages over inert containment materials. The Ki67 proliferation index is related to the distance of the cells from the surface of the CAM and the duration of application on the CAM, the latter determining a time frame for the addition of therapeutic products.

The In ovo CAM-assay as a Xenograft Model for Sarcoma

The in ovo chorioallantoic membrane (CAM) is grafted with fresh sarcoma-derived tumor tissues, their single cell suspensions, and permanent and transient fluorescently labeled established sarcoma cell lines. The model is used to study graft- (viability, Ki67 proliferation index, necrosis, infiltration) and host (fibroblast infiltration, vascular ingrowth) behavior.

ال<em&gt; في البيضة</em&gt; CAM-مقايسة باعتبارها Xenograftmodel عن الورم اللحمي

Sarcoma is a very rare disease that is heterogeneous in nature, all hampering the development of new therapies. Sarcoma patients are ideal candidates for ...

Retinal Detachment Model in Rodents by Subretinal Injection of Sodium Hyaluronate

Subretinal injection of sodium hyaluronate is a widely accepted method of inducing retinal detachment (RD). However, the height and duration of RD or the occurrence of subretinal hemorrhage can affect photoreceptor cell death in the detached retina. Hence, it is advantageous to create reproducible RDs without subretinal hemorrhage for evaluating photoreceptor cell death. We modified a previously reported method to create bullous and persistent RDs in a reproducible location with rare occurrence of subretinal hemorrhage. The critical step of this modified method is the creation of a self-sealing scleral incision, which can prevent leakage of sodium hyaluronate after injection into the subretinal space. To make the self-sealing scleral incision, a scleral tunnel is created, followed by scleral penetration into the choroid with a 30 G needle. Although choroidal hemorrhage may occur during this step, astriction with a surgical spear reduces the rate of choroidal hemorrhage. This method allows a more reproducible and reliable model of photoreceptor death in diseases that involve RD such as rhegmatogenous RD, retinopathy of prematurity, diabetic retinopathy, central serous chorioretinopathy, and age-related macular degeneration (AMD).

Creating experimental retinal detachments with a reproducible and sustained height of detachment, and without subretinal hemorrhage, is important for studying the pathophysiology of photoreceptor cell loss in retinal disease and evaluating potential therapeutic interventions. Here, we report such a method in detail.

شبكية العين مفرزة النموذجي في القوارض بواسطة حقن تحت الشبكية من هيالورونات الصوديوم

Subretinal injection of sodium hyaluronate is a widely accepted method of inducing retinal detachment (RD). However, the height and duration of RD or the ...

Excitotoxic Stimulation of Brain Microslices as an In vitro Model of Stroke

Examining molecular mechanisms involved in neuropathological conditions, such as ischemic stroke, can be difficult when using whole animal systems. As such, primary or &#39;neuronal-like&#39; cell culture systems are commonly utilized. While&#160;these systems are relatively easy to work with, and are useful model systems in which various functional outcomes (such as cell death) can be readily quantified, the examined outcomes and pathways in cultured immature neurons (such as excitotoxicity-mediated cell death pathways) are not necessarily the same as those observed in mature brain, or in intact tissue. Therefore, there is the need to develop models in which cellular mechanisms in mature neural tissue can be examined. We have developed an in vitro technique that can be used to investigate a variety of molecular pathways in intact nervous tissue. The technique described herein utilizes rat cortical tissue, but this technique can be adapted to use tissue from a variety of species (such as mouse, rabbit, guinea pig, and chicken) or brain regions (for example, hippocampus, striatum, etc.). Additionally, a variety of stimulations/treatments can be used (for example, excitotoxic, administration of inhibitors, etc.). In conclusion, the brain slice model described herein can be used to examine a variety of molecular mechanisms involved in excitotoxicity-mediated brain injury.

Excitotoxic Stimulation of Brain Microslices as an In vitro Model of Stroke

We have developed a brain slice model which can be used to examine molecular mechanisms involved in excitotoxicity-mediated brain injury.&#160;This technique generates viable mature brain tissue and reduces animal numbers required for experimentation, whilst keeping the neuronal circuitry, cellular interactions, and postsynaptic compartments partly intact.

excitotoxic المواد تحفيز الدماغ باعتبارها Microslices<em&gt; في المختبر</em&gt; نموذج من السكتة الدماغية

Examining molecular mechanisms involved in neuropathological conditions, such as ischemic stroke, can be difficult when using whole animal systems. As ...

Isolated Hepatic Perfusion as a Treatment for Liver Metastases of Uveal Melanoma

Isolated hepatic perfusion (IHP) is a procedure where the liver is surgically isolated and perfused with a high concentration of the chemotherapeutic agent melphalan. Briefly, the procedure starts with the setup of a percutaneous veno-venous bypass from the femoral vein to the external jugular vein. Via a laparotomy, catheters are then inserted into the proper hepatic artery and the caval vein. The portal vein and the caval vein, both supra- and infrahepatically, are then clamped. The arterial and venous catheters are connected to a heart lung machine and the liver is perfused with melphalan (1 mg/kg body weight) for 60 min. This way it is possible to locally perfuse the liver with a high dose of a chemotherapeutic agent, without leakage to the systemic circulation.
In previous studies including patients with isolated liver metastases of uveal melanoma, an overall response rate of 33-100% and a median survival between 9 and 13 months, have been reported. The aim of this protocol is to give a clear description of how to perform the procedure and to discuss IHP as a treatment option for liver metastases of uveal melanoma.

Here, we present a protocol how to perform an isolated liver perfusion (IHP) with melphalan and we also discuss IHP as a treatment option for liver metastases of uveal melanoma.

معزولة كبدي الإرواء كعلاج للالانبثاث الكبد من العنبية الميلانوما

Isolated hepatic perfusion (IHP) is a procedure where the liver is surgically isolated and perfused with a high concentration of the chemotherapeutic ...

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

Stroke research has endured many setbacks in translating neuroprotective therapies into clinical practice. In contrast, the real-world therapy (tPA thrombolysis) rarely produces benefits in mechanical occlusion-based experimental models, which dominate preclinical stroke research. This split between the bench and bedside suggests the need to employ tPA-responsive models in preclinical stroke research. To this end, a simple and tPA-reactive thrombotic stroke model is invented and described here. This model consists of transient occlusion of the unilateral common carotid artery and delivery of 7.5% oxygen through a face mask in adult mice for 30 min, while maintaining the animal rectal temperature at 37.5 &#177; 0.5 &#176;C. Although reversible ligation of the unilateral carotid artery or hypoxia each suppressed cerebral blood flow only transiently, the combination of both insults caused lasting reperfusion deficits, fibrin and platelet deposition, and large infarct in the middle cerebral artery-supplied territory. Importantly, tail-vein injection of recombinant tPA at 0.5, 1, or 4 hr post-tHI (10 mg/kg) provided time-dependent reduction of the mortality rate and infarct size. This new stroke model is simple and can be standardized across laboratories to compare experimental results. Further, it induces thrombosis without craniectomy or introducing pre-formed emboli. Given these unique merits, the tHI model is a useful addition to the repertoire of preclinical stroke research.

Thromboembolic stroke models are vital tools for optimizing the recanalization therapy. Here we report a murine thrombotic stroke model based on transient cerebral hypoxic-ischemic (tHI) insult, which triggers thrombosis and infarction, and responds favorably to tissue plasminogen activator (tPA)-mediated fibrinolysis in a therapeutic window similar to those in stroke patients.

A السكتة الدماغية نموذج الخثاري بناء على عابر الدماغي نقص الأكسجة-نقص التروية

Stroke research has endured many setbacks in translating neuroprotective therapies into clinical practice. In contrast, the real-world therapy (tPA ...

A Model to Simulate Clinically Relevant Hypoxia in Humans

In case of apnea, arterial partial pressure of oxygen (pO2) decreases, while partial pressure of carbon dioxide (pCO2) increases. To avoid damage to hypoxia sensitive organs such as the brain, compensatory circulatory mechanisms help to maintain an adequate oxygen supply. This is mainly achieved by increased cerebral blood flow. Intermittent hypoxia is a commonly seen phenomenon in patients with obstructive sleep apnea. Acute airway obstruction can also result in hypoxia and hypercapnia. Until now, no adequate model has been established to simulate these dynamics in humans. Previous investigations focusing on human hypoxia used inhaled hypoxic gas mixtures. However, the resulting hypoxia was combined with hyperventilation and is therefore more representative of high altitude environments than of apnea. Furthermore, the transferability of previously performed animal experiments to humans is limited and the pathophysiological background of apnea induced physiological changes is poorly understood. In this study, healthy human apneic divers were utilized to mimic clinically relevant hypoxia and hypercapnia during apnea. Additionally, pulse-oximetry and Near Infrared Spectroscopy (NIRS) were used to evaluate changes in cerebral and peripheral oxygen saturation before, during, and after apnea.

Hypoxia simulation in humans has usually been performed by inhaling hypoxic gas mixtures. For this study, apneic divers were used to simulate dynamic hypoxia in humans. Additionally, physiological changes in desaturation and re-saturation kinetics were evaluated with non-invasive tools such as Near-Infrared-Spectroscopy (NIRS) and peripheral oxygenation saturation (SpO2).

نموذج لمحاكاة نقص الأكسجة ذات الصلة سريريا في البشر

In case of apnea, arterial partial pressure of oxygen (pO2) decreases, while partial pressure of carbon dioxide (pCO2) increases. To avoid damage to ...

Isometric Contractility Measurement of the Mouse Mesenteric Artery Using Wire Myography

The wire myograph technique is used to assess the contractility of vascular smooth muscles in response to depolarization, GPCR agonists/inhibitors and drugs. It is widely used in many studies on the physiological functions of vascular smooth muscle, the pathogenesis of vascular diseases such as hypertension, and the development of smooth muscle relaxant drugs. The mouse is a widely used model animal with a large pool of disease models and genetically modified strains. We introduced this method to measure the isometric contraction of mouse mesenteric artery in detail. A 1.4-mm segment of mouse mesenteric resistance artery was isolated and mounted on a myograph chamber by passing two steel wires through its lumen. After equilibration and normalization steps, the vessel segment was potentiated by a high-K+ solution twice prior to the contraction assay. As an example of the application of this method in drug development, we measured the relaxant effect of a novel natural substance, neoliensinine, isolated from a Chinese herb, embryos of the lotus seed (Nelumbo nucifera Gaertn.) on mouse mesenteric arteries. The vessel segments mounted on the myograph chamber were stimulated with a high-K+ solution. When the force tension reached a stable sustained phase, cumulative doses of neoliensinine were added to the chamber. We found that neoliensinine had a dose-dependent relaxant effect on smooth muscle contraction, thus suggesting that it bears potential activity against hypertension. In addition, as the vessel segment can survive at least 4 hours after mounting and maintain contractility induced by the high-K+ solution for many times, we suggest that the wire myograph system may be used for the time-consuming process of drug screening.

The wire myograph technique is used to investigate vascular smooth muscle functions and screen new drugs. We report a detailed protocol for measuring the isometric contractility of the mouse mesenteric artery and for screening new relaxants of vascular smooth muscle.

متساوي القياس كونتراكتيليتي القياس الشريان المساريقي العلوي الماوس باستخدام أسلاك ميوجرافي

The wire myograph technique is used to assess the contractility of vascular smooth muscles in response to depolarization, GPCR agonists/inhibitors and ...