Yazarlar Dan Firl, Chris Corbett ve Jesse Denson, doktora müteşekkiriz. Harçlar SR NIH NINDS R01 NS060765 tarafından sağlandı, LJ için P30 COBRE Pilot Programı ve New Mexico Üniversitesi&#39;nde LJ için Çocuk Sağlığı İmza Programı.

Kurumsal Bakım ve Kullanım Komiteleri hem Boston Çocuk Hastanesi&#39;nde ve New Mexico Sağlık Bilimleri Merkezi Üniversitesi, tüm deneysel prosedürleri onayladı. NOT: Ön işlem, mühür başlamadan, sterilize ve tüm cerrahi aletler ve cerrahi örtüler otoklav. Buna ek olarak,% 0.125 bipivucaine ve 0.1 mg / kg dahil olmak üzere, buprenorfin, steril şişeler içinde post-operatif ilaç hazırlanması. Ayrıca steril lipopolisakarit (LPS) bir çözelti hazırlamak: 0,04 mg / ml LPS (0111: B4) Evan mavisi seyreltik ihtiva eden steril tuzlu su içinde. 1. Anestezi <ol><li> % 3 izofluran dengeli bir% 70 azot ve% 30 oksijen karışımı ile embriyonik gün 18 (E18) hamile Sprague Dawley sıçan anestezi neden. </li><li> Indüksiyon odasından sıçan çıkarın ve 37 ° C&#39;de set dökümlü cerrahi dolaşan su battaniye sıçan sırtüstü yerleştirin. Burun konisi anestezi aktarın ve isoflura azaltmak% 2 ne düzeyde. </li><li> Yavaşça kornea kurumasını önlemek için her gözün oftalmik merhem uygulayın. İşlem sırasında sürekli sıcaklık, solunum hızı ve hayvan kalp atışlarının izlenmesi. Anne fizyolojisi prosedür boyunca sabit kalması gerekir. </li></ol> 2. Cerrahi Hazırlık ve Scrub <ol><li> Kullanımı küçük hayvan kesme alt karın bölgesindeki bütün tüylerden. Meme nicklemek veya canlı doğmuş yavruların gelecekteki hemşirelik için rahatsız edici olabilir jilet döküntü üreten önlemek için dikkatli bir dikdörtgen desen Tıraş. </li><li> Steril pamuklu çubukla povidon iyot ve% 70 etanol fırçalayın uygulama değiştirerek karın cildi hazırlayın. Povidon-iyot ve% 70 etanol her moda alternatif 3x uygulanan olacak şekilde fırçalayın tekrarlayın. Kurumaya bırakın. </li><li> Ayak-tutam refleksinin yokluğu yoluyla anestezi derinliği onaylayın. Ağrı refleksi uyaranların yokluğunda,% 1 izofluran seviyesini azaltır. </li><li> Steril cerrahi havlu kullanarak,hayvan asmak. Onlar rahim boynuzları kan akışını engellediği değil iken absorbe sulama sıvı miktarını maksimize şekilde uygun bir açıyla perdeler yerleştirmek için özen gösterin. </li></ol> 3. Abdominal Laparotomi <ol><li> Bir neşter kullanılarak hazırlanan karın derisinde 3 cm&#39;lik orta hat kesi yapmak. Açık açık makas ile karın fasya deri tabakasını incelemek. Forseps ve cerrahi makas kullanarak, karın fasya tabakası yükseltmek ve periton boşluğuna erişmek için avasküler linea alba bir kesi yapmak. </li><li> Kesi dış cerrahi gazlı bez yerleştirin ve steril tuzlu su ile nemlendirin. Karın künt forseps ve dış basınç kullanarak, yavaşça periton boşluğuna gelen rahim boynuzları kaldırmak ve nemlendirilmiş gazlı bez üzerine yerleştirin. </li><li> Dikkatle dolanması önlemek ve bağırsak ile temasa geçin. Fetusun bireysel amnion kesesi arasındaki tek kas dokusu ile temasa geçerek forseps kullanarak düzenleyin.Açığa ve künt diseksiyon ile 4 uterin arterler izole. NOT: Bakım rahim arterleri incelemek için alınmalıdır. Ortam doku ve damarları kendilerini son derece hassastır. Anne gemilere hasar kanamaya yol ve ciddi vakalarda, fetal ve maternal ölüm olabilir. </li></ol> Anevrizma Klipleri 4. Yerleştirme <ol><li> Her uterin arter üzerinde bir sıçan 30 G anevrizma klibi yerleştirin. Bireysel plasenta rahim dahil gemilerin proksimal ve distal bakliyat ve koyulaşması dahil kan akışının durması emin olun. Maruz boynuzları ve gazlı bez ile tüm cerrahi alanı kapsayacak ve steril tuzlu su ile yıkayın. Sulama yaklaşık her 10 dk ile nemli alan tutmaya özen gösterin. </li><li> 60 dakika sonra, gazlı bez kaldırmak ve alanını sulamak. Rahim boynuzları ve damarlar yeterince başarılı klip kaldırılması için ıslatılmış olduğundan emin olun. Yavaşça forseps kullanarak her anevrizma klibi kaldırın. Gemiye travma ve maint sebebiyet vermemek özen gösterinçıkarılması sırasında ain doku bütünlüğü. </li><li> İyice amnion kesesi gelen gazlı bez herhangi bir sokak Konuları kaldırmak için özen, rahim boynuzları ve alanını sulamak. </li></ol> Amniyon Sacs için Lipopolisakarit 5. Enjeksiyon <ol><li> Her amniyon kesesi dibinde, sadece plasental plaka ön amniyon sıvısına seyreltilmiş Evan mavi boya ile LPS (4 ug / kese) 100 ul enjekte edilir. Stabilize ve enjeksiyon için en uygun pozisyona her amniyotik kese döndürmek için künt forseps kullanın. Seyreltik Evan mavi boya uygun şırınga yerleştirme ve enjeksiyon teyit yararlı bir kontrast ajandır. NOT: intra-amniyotik enjeksiyonlar için ekli 8 mm 31 G iğne ile Yalnızca bir ultra-ince 0.3 ml insülin şırınga. Daha büyük göstergesi iğneler kullanılarak kronik amniyotik sıvı kaybı, fetal ölüm ve gebelik reabzorpsiyonunda neden olacaktır. Şırınga çıkartılması üzerine amniyotik sıvı sızıntı küçük miktarlarda mitig olabiliramniyon kesesi doğrudan basınç ile bir-. Bazı sıçan fetus oligohidramnios bir ölçüde tolere edebilir. Ancak, büyük göstergesi iğne veya kronik sıvı sızıntısı ile sonuçlanan kazayla ponksiyonu, fetal kayıp ve ciddi vakalarda sonuçları, komşu gebelik kaybı ile delinerek akut amniyotik sıvı kaybı. </li><li> Boynuzları steril serum fizyolojik ile 3x uterus yıkayın. </li></ol> 6. laparotomi Kapanış <ol><li> Forseps kullanarak, dikkatli periton boşluğuna rahim boynuzları geri dönün. Amnion kesesi ve orta hat kesi arasında yeterli boşluk sağlanması, çalışan 3-0 ipek sütür kullanılarak muskulofasyal katman kenarlarını yeniden yaklaşmaktadır. Kas kesi kapatırken amnion kesesi yerleştirme farkında olun. Içine veya kese ile sütür için değil dikkatli olun. </li><li> Cilt katmanı kapatarak, bir çalışan 3-0 ipek sütür kullanılarak, cilt tabakası yeniden yaklaşmaktadır. NOT: laparotomi izin devamlı sütür iki kat kapalı olmalıdırCilt ve gebelik artan kas genişleme. Sürekli dikişler eşit olarak dağıtılmış yara gerginliği için izin verir. Birden knot rahatsız edici ve kolayca anestezi kurtarma üzerine sıçan tarafından çiğnenmiş edilebilir Kesilen sütür az arzu edilir. Cerrahi zımba arzu edilmez. Cerrahi knot kuyrukları çok kısa (&lt;3 mm) kesilmelidir. </li><li> Bir 26 G iğne kullanılarak% 0.125 bupivakain deri altından yaklaşık yara kenarlarının 1 ml enjekte edilir. Ense de kg buprenorfin subkutan 0.1 mg tek doz / yönetmek. </li><li> Izofluran ve havlu kuru sıçan gerekirse kapatın. Temiz ev kafeste yerleştirin ve anestezi ayilmanizi. Hipotermik hale gelmez sıçan olun. </li></ol> 7. Ameliyat Sonrası Kurtarma ve Bakım <ol><li> Yavrular (yaklaşık E22 veya E23) doğarlar kadar günlük sonra 72 saat boyunca siçana her 8-12 saat Monitör ve. Buprenorfın q8-12 saat / 72 saat ek doz yönetmek veya IACUC tarafından belirlenen prn. </li><li> Ağrı, rahatsızlık, vajinal kanama ya da cerrahi sitesinden kanama belirtileri için sıçanları izleyin. Sütürler ve kesi kontrol edin ve sıçan çiğneme veya erken kendi sütür kaldırarak görmediğinden emin olmak için özen gösterin. Derece nadir olmasına rağmen, onların sütürler tehlikeye sıçanlar yara açılma riski altındadır. NOT: Bazen sıçanlar yatak ya da gıda dışı maddelerin aşırı miktarda yemek olabilir, buprenorfın yönetiminin bir yan etkisi olarak, pika denir. Çok nadir olmakla birlikte, sıçanlar pika ve potansiyel sonraki barsak tıkanıklığı için izlenmesi gerekir. </li></ol> 8. Doku İşleme ve Cryosectioning <ol><li> , Hematoksilen (H &amp; E) doğum sonrası beyin boyanması için hazırlık doğum sonrası gün 2 (P2) üzerine evlerine kafes yavrular kaldırmak için. Cerrahi makas hafifçe sıçan yavrular başını kesmek ve kullanma kafatası beyin kaldırmak. </li><li> Fosfat tamponlu tuzlu su içinde% 4 paraformaldehit 7 ml içeren 15 ml konik bir tüp içinde düzeltme beyin bırakın(PBS). 4 ° C &#39;de beyin yerleştirin ve 72 saat boyunca sabitlemek. </li><li> 72 saat sonra,% 30 sukroz ihtiva eden bir steril PBS çözeltisi beyinleri transferi (w / v) ve 4 ° C &#39;geri dönün. NOT: beyinleri sukroz çözeltisi damla kez onlar bir kriyostat üzerinde kesitli hazırdır. </li><li> Hızla beynini dondurma ve dondurulmuş koronal kesitlerin edinimi için kriyostat tokmak monte. 20 mikron dondurulmuş koronal bölümleri kesmek ve slaytlar monte. Emin olun bölümler seri toplanır. </li><li> Slaytlar gece boyunca oda sıcaklığında kurumaya bırakın. -20 ° C&#39;de de kayar. </li></ol> 9. Hematoksilen &amp; Eosin Boyama <ol><li> Oda sıcaklığına slayt monte donmuş bölümleri ve sıcak atın. NOT: Tüm çözümler taze hazırlayın. </li><li> 2 saat boyunca 50 ° C&#39;ye kadar bir slayt sıcak grubu yerleştirin kayar. </li><li> Transfer boyama raf kayar. Dip (GKD 2 O) çifte damıtılmış deiyonize su içinde 10x slaytlar. </li><li> 5 dakika boyunca% 100 hematoksilin slaytlar inkübe edin. Tihematoksilin beni mor boyama derecesine bağlı olarak optimize edilebilir. </li><li> Dip slaytlar musluk H 2 O 4x ve 1 dakika süreyle 2 O temiz musluk H bekletilir. </li><li> Dip (250 mi,% 70 etanol + 1 mi konsantre hidroklorik asit) asidi alkol içinde 15x kayar. </li><li> Dip slaytlar musluk H 2 O 4x ve 1 dakika süreyle 2 O temiz musluk H bekletilir. </li><li> 2 dakika için% 1 lityum karbonat inkübe edin. </li><li> Dip slaytlar musluk H 2 O 4x ve 1 dakika süreyle 2 O temiz musluk H bekletilir. </li><li> 1 dakika boyunca% 95 etanol içinde inkübe edin. </li><li> Dip slaytlar% 100 Eosin içinde 7x. Eosin batırma sayısı pembe boyama derecesine bağlı olarak modifiye edilebilir. </li><li> Dip slaytlar% 95 etanol içinde 5 kata. </li><li> % 95 etanol taze değişiklik Lamı 5x. </li><li> 1 dakika boyunca% 100 etanol içinde slaytlar inkübe edin. </li><li> 1 dakika boyunca% 100 etanol içinde taze değişiklik slaytlar inkübe edin. </li><li> 15 dakika% 100 ksilen slaytlar inkübe edin. NOT: Ksilen adımlar veBir çeker ocak içinde gerçekleşmelidir coverslipping. </li><li> 15 dakika boyunca ksilen taze değişiklikler slaytlar kuluçkaya yatmaktadır. </li><li> Permount ile lamel ve davlumbaz kurumaya bırakın. </li><li> Görüntü bir ışık mikroskobu ile kayar. </li></ol>

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L. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Modeling+transformations+of+neurodevelopmental+sequences+across+mammalian+species.">Modeling transformations of neurodevelopmental sequences across mammalian species.</a> J Neurosci. 33, 7368-7383 (2013).</li><li>Herlenius, E., Lagercrantz, H. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Development+of+neurotransmitter+systems+during+critical+periods.">Development of neurotransmitter systems during critical periods.</a> Exper Neurol. 190, S8-S21 (2004).</li><li>Kelsom, C., Lu, W. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Development+and+specification+of+GABAergic+cortical+interneurons.">Development and specification of GABAergic cortical interneurons.</a> Cell Biosci. 3, 19 (2013).</li><li>Kinney, H., Back, S. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Human+oligodendroglial+development+Relationship+to+periventricualr+leukomalacia.">Human oligodendroglial development Relationship to periventricualr leukomalacia.</a> Semin Pediatr Neuro. 5, 180-189 (1998).</li><li>Robinson, S., Li, Q., DeChant, A., Cohen, M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Neonatal+loss+of+gamma+amino+butyric+acid+pathway+expression+after+human+perinatal+brain+injury.">Neonatal loss of gamma amino butyric acid pathway expression after human perinatal brain injury.</a> J Neurosurg Peds. 104, 396-408 (2006).</li><li>Xu, G., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Late+development+of+the+GABAergic+system+in+the+human+cerebral+cortex+and+white+matter.">Late development of the GABAergic system in the human cerebral cortex and white matter.</a> J Neuropathol Exp Neurol. 70, 841-858 (2011).</li><li>Segovia, K. N., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Arrested+oligodendrocyte+lineage+maturation+in+chronic+perinatal+white+matter+injury.">Arrested oligodendrocyte lineage maturation in chronic perinatal white matter injury.</a> Ann Neurol. 63, 520-530 (2008).</li><li>Robinson, S., Li, Q., Dechant, A., Cohen, M. L. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Neonatal+loss+of+gamma+aminobutyric+acid+pathway+expression+after+human+perinatal+brain+injury.">Neonatal loss of gamma aminobutyric acid pathway expression after human perinatal brain injury.</a> J Neurosurg. 104, 396-408 (2006).</li><li>Boksa, P. <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+prenatal+infection+on+brain+development+and+behavior+a+review+of+findings+from+animal+models.">Effects of prenatal infection on brain development and behavior a review of findings from animal models.</a> Brain Behav Immun. 24, 881-897 (2010).</li><li>Burd, I., Brown, A., Gonzalez, J. M., Chai, J., Elovitz, M. A. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=A+mouse+model+of+term+chorioamnionitis+unraveling+causes+of+adverse+neurological+outcomes.">A mouse model of term chorioamnionitis unraveling causes of adverse neurological outcomes.</a> Repro Sci. 18, 900-907 (2011).</li><li>Bergeron, J. D., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=White+matter+injury+and+autistic+like+behavior+predominantly+affecting+male+rat+offspring+exposed+to+group+B+streptococcal+maternal+inflammation.">White matter injury and autistic like behavior predominantly affecting male rat offspring exposed to group B streptococcal maternal inflammation.</a> Devel Neurosci. 35, 504-515 (2013).</li><li>Uchida, K., et al. <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+Ureaplasma+parvum+lipoprotein+multiple+banded+antigen+on+pregnancy+outcome+in+mice.">Effects of Ureaplasma parvum lipoprotein multiple banded antigen on pregnancy outcome in mice.</a> J Reprod Immunol. 100, 118-127 .</li></ol>

Yazarlar ifşa hiçbir şey yok.

Prematüre Ensefalopati nedeniyle yaralanma mekanizmaları örtüşen etiyolojiler, nörogelişimsel zamanla, insan beyin ağ oluşumu karışıklık, karmaşık etkileşim hayvanlarda modellenmesi zordur ve MSS farklı fenotipleri insan erken doğmuş bebeklerde tezahür hakaretler. EOP hücre tipine özel güvenlik ile ilişkilidir (örneğin, olgunlaşmamış oligodendrositler) 21, hem de çok çeşitli gelişimsel olarak düzenlenmiş yolları (örneğin, Plaka yapısı, membran taşıy?...

37 hafta tahmini gebelik yaşı 1 önce Amerika Birleşik Devletleri&#39;nde doğan bebeklerin% 12&#39;nin üzerinde olan, prematürite perinatal beyin hasarı (PBI) kalıcı sakatlık önemli bir nedenidir. PBI prematürite, prematüre olarak da adlandırılır ensefalopati (EOP), tüm merkezi sinir sistemi (CNS) etkilemektedir. MSS yaralanması genellikle in utero başlar ve koriyoamniyonit ve hipoksi ve sepsis gibi doğum sonrası komplikasyonlar da dahil olmak üzere doğum öncesi süreçler tarafından şiddetlenir. Sistemik hakaret gelen PBI nöro-gelişimsel sürecini değiştirir ve duygusal regülasyonu, bellek ve yürütücü işlev 1,2 etkileyen serebral palsi, epilepsi, bilişsel gecikme ve çok sayıda nöropsikiyatrik bozukluklara yol açar. Çok ilerleme kaydedilmiş olmasına rağmen, sınırlı bir anlayış erken doğumdan itibaren MSS yaralanma hücresel ve moleküler sonuçları preterm doğan çocuklarda nörolojik sekel çokluk çevirmek nasıl kalır. Bilgi hind bu eksikliğiGerçek zamanlı MSS yaralanma şiddetinin tanı ve gelişmekte olan müdahalelerin haberdar dozaj ers. Ayrıca, bu savunmasız hasta popülasyonu için yaşa uygun tedavi stratejileri zor kalır. Rahim içi iltihabı, aşırı prematüre çok yaygın olan ve 3 karmaşık bir fetal-maternal-plasental inflamatuar dizisini içerir. Intrauterin enfeksiyon genellikle subklinik olduğunu. Akut inflamasyon veya histolojik koryoamniyonit ile uyumlu Belirli plasental bulgular, fetal enflamatuar yanıtın önemli belirleyicileri ve erken doğum 3-5 ile ilişkili beyin hasarı ile tesadüf. Nitekim, fetal inflamatuvar yanıt erken doğumdan itibaren uzun vadeli sonuçları için farklı klinik etkileri vardır. Gebelik yaşı (SGA) ya da kim enfeksiyon deneyim için küçük bebekler nörolojik defisit 3,4 ile son derece açıktır. Koryoamniyonit tipik patolojik tanı takip erken doğum olduğunu <sup&gt; 6,7 ve histolojik inceleme çok erken 4 doğan bebeklerin gelen plasenta% 70 iltihabın belirtileri ortaya koymaktadır. Dahası, korioamnionit iki yıl 8&#39;de bilişsel bozukluğu ile ilişkilidir. Son derece erken doğan bebeklerin plasentada maternal vasküler underperfusion kanıtı da çocukluk 9 serebral palsi ile ilişkilidir. Korioamnionit ve plasental perfüzyon defektlerinin sinerjik etkisi de yaş 10,11 iki yıl bu hasta popülasyonunda anormal nörolojik sonuçların oldukça yüksek risk gösterilmiştir. Patojen kaynaklı inflamasyon ile ilişkili insan sistemik plasental perfüzyon defektleri ve koryoamniyonit taklit etmek, sıçanlarda içi amniyotik lipopolisakarit (LPS) ile kombine prenatal geçici sistemik hipoksi-iskemi (TSHI) bir model geliştirdi. Amacımız, intrauterin iltihabı dahil yalnız sıçanlarda 12-16 TSHI bizim modeli adapte olduerken doğum ile ilgili CNS yaralanma preklinik modelleme kolaylaştırmak için. TSHI başına oligodendroglial soyu hücreleri, kortikal nöronlar kalıcı zarar ortaya koymuştur, prenatal beyin hasarı 16 ile uyumlu bir yaralanma kademeli kalıp giden aşamalı iskemik aralıklı, hücre ölümü artışı ve pro-enflamatuar sitokin seviyelerinin yüksek. Onlar 17-19 yaş olarak bu modelin iskemik bileşenlerine değişiklikler de sıçanlarda hafıza kodlama, kısa ve uzun süreli hafıza ve hafif kas-iskelet değişiklikler eksiklikler göstermiştir. Gerçekten de, daha önce TSHI + LPS kombinasyonu oligodendrosit ve nöronal kaybın, aksonal yaralanma, enflamasyon ve fonksiyonel hücre anormallikleri dahil olmak üzere, 20 EOP patofizyolojik işaretlerinden, tekrarlar olduğunu göstermiştir.

<table border="0" cellpadding="0" cellspacing="0" >
	<tbody>
		<tr >
			<td >Saline Solution, 0.9%</td>
			<td >Sigma</td>
			<td >S8776</td>
			<td ></td>
		</tr>
		<tr >
			<td >LPS 011B4</td>
			<td>Sigma</td>
			<td>L2630</td>
			<td></td>
		</tr>
		<tr >
			<td >Evan&#39;s Blue Dye</td>
			<td>Sigma</td>
			<td>E2129</td>
			<td></td>
		</tr>
		<tr >
			<td >Surgical gloves</td>
			<td>Biogel</td>
			<td>40870</td>
			<td></td>
		</tr>
		<tr >
			<td >OR Towels</td>
			<td>Cardinal Health</td>
			<td>287000-008</td>
			<td>Sterile</td>
		</tr>
		<tr >
			<td >PDI Alcohol Prep Pads</td>
			<td>Fisherbrand</td>
			<td>06-669-62</td>
			<td></td>
		</tr>
		<tr >
			<td >Mini Arco Rechargeable Clippers</td>
			<td>Kent Scientific Corp.</td>
			<td>CL8787</td>
			<td></td>
		</tr>
		<tr >
			<td >Betadine surgical scrub</td>
			<td>Purdue Products L.P.</td>
			<td>67618-151-17</td>
			<td></td>
		</tr>
		<tr >
			<td >Eye Lubricant</td>
			<td>Refresh Lacri Lube</td>
			<td>00023-0312</td>
			<td></td>
		</tr>
		<tr >
			<td >Blunt Forceps</td>
			<td>Roboz</td>
			<td>RS-8100</td>
			<td></td>
		</tr>
		<tr >
			<td >Scissors</td>
			<td>Roboz</td>
			<td>RS-6808</td>
			<td></td>
		</tr>
		<tr >
			<td >Surgical Scissors</td>
			<td>Roboz</td>
			<td>RS-5880</td>
			<td></td>
		</tr>
		<tr >
			<td >Surgical Scissors</td>
			<td>F.S.T.</td>
			<td>14002-16</td>
			<td></td>
		</tr>
		<tr >
			<td >Syringe</td>
			<td>BD</td>
			<td>309628</td>
			<td>1 ml</td>
		</tr>
		<tr >
			<td >Needle</td>
			<td>BD</td>
			<td>305122</td>
			<td>25G 5/8</td>
		</tr>
		<tr >
			<td >Needle</td>
			<td>BD</td>
			<td>305128</td>
			<td>30G 1</td>
		</tr>
		<tr >
			<td >Cotton-tipped Applicators</td>
			<td>Fisherbrand</td>
			<td>23-400-114</td>
			<td>Small, 6 inch sterile</td>
		</tr>
		<tr >
			<td >Cotton Gauze Sponge</td>
			<td>Fisherbrand</td>
			<td>22-362-178</td>
			<td></td>
		</tr>
		<tr >
			<td >Needle Holders</td>
			<td>Kent Scientific Corp.</td>
			<td>INS600109</td>
			<td>12.5 CM STR</td>
		</tr>
		<tr >
			<td >Vessel Clips</td>
			<td>Kent Scientific Corp.</td>
			<td>INS600120</td>
			<td>30G Pressure</td>
		</tr>
		<tr >
			<td >3-0 Perma Hand Silk Sutures</td>
			<td>Ethicon</td>
			<td>1684G</td>
			<td>Black braided, 3-0 (2 metric), 18&#34;, non-absorbable,&#160; PS-1 24mm needle, 3/8 circle</td>
		</tr>
		<tr >
			<td >Insulin Syringes</td>
			<td>BD</td>
			<td>328438</td>
			<td>0.3cc 3mm 31G</td>
		</tr>
		<tr >
			<td >Pentobarbital</td>
			<td></td>
			<td></td>
			<td></td>
		</tr>
		<tr >
			<td >Buprenorphine</td>
			<td></td>
			<td></td>
			<td></td>
		</tr>
		<tr >
			<td >Bupivacaine</td>
			<td></td>
			<td></td>
			<td></td>
		</tr>
		<tr >
			<td >Isoflurane</td>
			<td></td>
			<td></td>
			<td></td>
		</tr>
		<tr >
			<td >Lithium Carbonate</td>
			<td>Acros Chemicals</td>
			<td>554-13-2</td>
			<td></td>
		</tr>
		<tr >
			<td >Superfrost Plus Microscope Slides</td>
			<td>VWR</td>
			<td>48311-703</td>
			<td></td>
		</tr>
		<tr >
			<td >Hematoxylin</td>
			<td>Leica</td>
			<td>3801521</td>
			<td>Surgipath Gill II Hematoxylin</td>
		</tr>
		<tr >
			<td >Eosin</td>
			<td>Leica</td>
			<td>3801601</td>
			<td>Surgipath Eosin</td>
		</tr>
		<tr >
			<td >Xylenes</td>
			<td>Fisherbrand</td>
			<td>X3S-4</td>
			<td>Histological Grade</td>
		</tr>
		<tr >
			<td >Permount</td>
			<td>Fisherbrand</td>
			<td>SP15-100</td>
			<td></td>
		</tr>
		<tr >
			<td >Coverglass</td>
			<td>Fisherbrand</td>
			<td>12-548-5P</td>
			<td>Fisher Finest Premium Coverglass</td>
		</tr>
	</tbody>
</table>

modeling encephalopathy of prematurity using prenatal hypoxia-ischemia with intra-amniotic lipopolysaccharide in rats

Prematüre Ensefalopati (EOP) en ileri öteleme hedefleri belirleyin. Erken doğum ile ilişkili anormallikleri merkezi sinir sistemini (MSS) kapsayan bir terimdir ve erken doğum ile ilişkili beyin hasarı için yeni tedavi stratejileri ortaya çıkarmak, ÇOP&#39;un preklinik modelleri benzer mekanizmalar içermelidir Prenatal küresel yaralanma insanlarda görülen ve anne-plasental-fetal sistemin birden fazla bileşen içerir. İdeal olarak, modeller, olgun hayvan fonksiyonel açıklarının benzer spektrumunu üretmek ve patofizyoloji birden yönlerini özetlemek gerekir. Erken erken doğum patojen kaynaklı iltihap ile bağlantılı insan plasental perfüzyon sistemik bozuklukları, plasental underperfusion ve / veya koryoamniyonit taklit etmek için, içi amniyotik lipopolisakarit (LPS) ile bir araya prenatal geçici sistemik hipoksi, iskemi (TSHI) içindeki bir model geliştirmiştir. Hamile Sprague Dawley sıçanlarda, TSHI uterin arter tıkanıklığı o yoluylan embriyonik gün 18 (E18) fetusta MSS hasarı artan ilişkili bir kademeli plasental underperfusion kusur neden olur. Intra-amniyotik LPS enjeksiyonu ile kombine edildiğinde, plasental inflamasyon artar ve MSS hasar ilişkili beyaz cevher, yürüme ve manyetik rezonans görüntüleme bulguları ile karmaşıklaşır. Prenatal TSHI ve TSHI + LPS prenatal hakaret nöronlar, oligodendrositler ve akson, Plaka yapısı kaybı ve son derece doğan çocuklarda gözlenen taklit yetişkin hayvanlarda fonksiyonel açıklarının kaybına neden intrauterin hakaret recapitulating içeren bir ÇOP&#39;un modeli kriterlerine çeşitli karşılamak erken. Ayrıca, bu model farklı yaralanma türlerine neden olduğu inflamasyonun diseksiyon sağlar.

E18 de TSHI + LPS&#39;yi ardından, hematoksilen ve eozin boyama önemli histopatolojik plasenta hem anormallikler (Şekil 1) ve beyinde (Şekil 2) ortaya koymaktadır. E19 ve E21 üzerine incelenen plasenta desidua ve labirent boyunca mikro kanama ve nekroz ile fena halde ödemli bulunmaktadır. Önemli inflamatuar infiltrasyon ve artan damarlanma da görülmektedir. P2 incelenen beyinleri ventrikülomegali ortaya yanı sıra beyaz cevher ve Plaka yapısı nöron kaybı Shams göre. Da...

Watch this Scientific Journal Video about Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats at JoVE.com

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Encephalopathy of prematurity encompasses the central nervous system abnormalities associated with injury from preterm birth. This report describes a clinically relevant rat model of in utero transient systemic hypoxia-ischemia and intra-amniotic lipopolysaccharide administration (LPS) that mimics chorioamnionitis, and the related impact of infectious stimuli and placental underperfusion on CNS development.

Prematüre Modelleme Ensefalopati Sıçanlarda İçi amniyotik Lipopolisakkarid ile Prenatal Hipoksi-iskemi kullanma

Encephalopathy of prematurity (EoP) is a term that encompasses the central nervous system (CNS) abnormalities associated with preterm birth. To best ...

modeling-encephalopathy-prematurity-using-prenatal-hypoxia-ischemia

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11.2K Görüntüleme.  University of New Mexico. Encephalopathy of prematurity encompasses the central nervous system abnormalities associated with injury from preterm birth. This report describes a clinically relevant rat model of in utero transient systemic hypoxia-ischemia and intra-amniotic lipopolysaccharide administration (LPS) that mimics chorioamnionitis, and the related impact of infectious stimuli and placental underperfusion on CNS development.

Video: Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Modeling Stroke in Mice - Middle Cerebral Artery Occlusion with the Filament Model

Stroke is among the most frequent causes of death and adult disability, especially in highly developed countries. However, treatment options to date are very limited. To meet the need for novel therapeutic approaches, experimental stroke research frequently employs rodent models of focal cerebral ischaemia. Most researchers use permanent or transient occlusion of the middle cerebral artery (MCA) in mice or rats.
Proximal occlusion of the middle cerebral artery (MCA) via the intraluminal suture technique (so called filament or suture model) is probably the most frequently used model in experimental stroke research. The intraluminal MCAO model offers the advantage of inducing reproducible transient or permanent ischaemia of the MCA territory in a relatively non-invasive manner. Intraluminal approaches interrupt the blood flow of the entire territory of this artery. Filament occlusion thus arrests flow proximal to the lenticulo-striate arteries, which supply the basal ganglia. Filament occlusion of the MCA results in reproducible lesions in the cortex and striatum and can be either permanent or transient. In contrast, models inducing distal (to the branching of the lenticulo-striate arteries) MCA occlusion typically spare the striatum and primarily involve the neocortex. In addition these models do require craniectomy. In the model demonstrated in this article, a silicon coated filament is introduced into the common carotid artery and advanced along the internal carotid artery into the Circle of Willis, where it blocks the origin of the middle cerebral artery. In patients, occlusions of the middle cerebral artery are among the most common causes of ischaemic stroke. Since varying ischemic intervals can be chosen freely in this model depending on the time point of reperfusion, ischaemic lesions with varying degrees of severity can be produced. Reperfusion by removal of the occluding filament at least partially models the restoration of blood flow after spontaneous or therapeutic (tPA) lysis of a thromboembolic clot in humans.
In this video we will present the basic technique as well as the major pitfalls and confounders which may limit the predictive value of this model.

Filamentous occlusion of the Middle cerebral artery is a common model for studying ischemic stroke in mice.

Fare Modelleme İnme - Filament Model Orta Serebral Arter Tıkanıklığı

Stroke is among the most frequent causes of death and adult disability, especially in highly developed countries. However, treatment options to date are ...

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Non-invasive Imaging and Analysis of Cerebral Ischemia in Living Rats Using Positron Emission Tomography with 18F-FDG

Stroke is the third leading cause of death among Americans 65 years of age or older1. The quality of life for patients who suffer from a stroke fails to return to normal in a large majority of patients2, which is mainly due to current lack of clinical treatment for acute stroke. This necessitates understanding the physiological effects of cerebral ischemia on brain tissue over time and is a major area of active research. Towards this end, experimental progress has been made using rats as a preclinical model for stroke, particularly, using non-invasive methods such as 18F-fluorodeoxyglucose (FDG) coupled with Positron Emission Tomography (PET) imaging3,10,17. Here we present a strategy for inducing cerebral ischemia in rats by middle cerebral artery occlusion (MCAO) that mimics focal cerebral ischemia in humans, and imaging its effects over 24 hr using FDG-PET coupled with X-ray computed tomography (CT) with an Albira PET-CT instrument. A VOI template atlas was subsequently fused to the cerebral rat data to enable a unbiased analysis of the brain and its sub-regions4. In addition, a method for 3D visualization of the FDG-PET-CT time course is presented. In summary, we present a detailed protocol for initiating, quantifying, and visualizing an induced ischemic stroke event in a living Sprague-Dawley rat in three dimensions using FDG-PET.

Non-invasive Imaging and Analysis of Cerebral Ischemia in Living Rats Using Positron Emission Tomography with 18F-FDG

Brain damage resulting from cerebral ischemia may be non-invasively imaged and studied in rats using pre-clinical positron emission tomography coupled with the injectable radioactive probe, 18F-fluorodeoxyglucose. Further, the use of modern software tools that include volume of interest (VOI) brain templates dramatically increase the quantitative information gleaned from these studies.

Pozitron Emisyon Tomografi ile kullanma Non-invaziv Görüntüleme ve Serebral iskemi Analizi Yaşam Sıçanlarda<sup&gt; 18</sup&gt; F-FDG

Stroke is the third leading cause of death among Americans 65 years of age or older1. The quality of life for patients who suffer from a stroke fails to ...

A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy

Birth asphyxia, which causes hypoxic-ischemic encephalopathy (HIE), accounts for 0.66 million deaths worldwide each year, about a quarter of the world&#8217;s 2.9 million neonatal deaths. Animal models of HIE have contributed to the understanding of the pathophysiology in HIE, and have highlighted the dynamic process that occur in brain injury due to perinatal asphyxia. Thus, animal studies have suggested a time-window for post-insult treatment strategies. Hypothermia has been tested as a treatment for HIE in pdiglet models and subsequently proven effective in clinical trials. Variations of the model have been applied in the study of adjunctive neuroprotective methods and piglet studies of xenon and melatonin have led to clinical phase I and II trials1,2. The piglet HIE model is further used for neonatal resuscitation- and hemodynamic studies as well as in investigations of cerebral hypoxia on a cellular level. However, it is a technically challenging model and variations in the protocol may result in either too mild or too severe brain injury. In this article, we demonstrate the technical procedures necessary for establishing a stable piglet model of neonatal HIE. First, the newborn piglet (&#60; 24 hr old, median weight 1500 g) is anesthetized, intubated, and monitored in a setup comparable to that found in a neonatal intensive care unit. Global hypoxia-ischemia is induced by lowering the inspiratory oxygen fraction to achieve global hypoxia, ischemia through hypotension and a flat trace amplitude integrated EEG (aEEG) indicative of cerebral hypoxia. Survival is promoted by adjusting oxygenation according to the aEEG response and blood pressure. Brain injury is quantified by histopathology and magnetic resonance imaging after 72 hr.

Hypoxic-ischemic encephalopathy following perinatal asphyxia can be studied using animal models. We demonstrate the procedures necessary for establishing a piglet model of neonatal hypoxic-ischemic encephalopathy.

Yenidoğan Hipoksik-İskemik Ensefalopati A Piglet Modeli

Birth asphyxia, which causes hypoxic-ischemic encephalopathy (HIE), accounts for 0.66 million deaths worldwide each year, about a quarter of the ...

Assessing Transmissible Spongiform Encephalopathy Species Barriers with an In Vitro Prion Protein Conversion Assay

Studies to understanding interspecies transmission of transmissible spongiform encephalopathies (TSEs, prion diseases) are challenging in that they typically rely upon lengthy and costly in vivo animal challenge studies. A number of in vitro assays have been developed to aid in measuring prion species barriers, thereby reducing animal use and providing quicker results than animal bioassays. Here, we present the protocol for a rapid in vitro prion conversion assay called the conversion efficiency ratio (CER) assay. In this assay cellular prion protein (PrPC) from an uninfected host brain is denatured at both pH 7.4 and 3.5 to produce two substrates. When the pH 7.4 substrate is incubated with TSE agent, the amount of PrPC that converts to a proteinase K (PK)-resistant state is modulated by the original host&#8217;s species barrier to the TSE agent. In contrast, PrPC in the pH 3.5 substrate is misfolded by any TSE agent. By comparing the amount of PK-resistant prion protein in the two substrates, an assessment of the host&#8217;s species barrier can be made. We show that the CER assay correctly predicts known prion species barriers of laboratory mice and, as an example, show some preliminary results suggesting that bobcats (Lynx rufus) may be susceptible to white-tailed deer (Odocoileus virginianus) chronic wasting disease agent.

Assessing Transmissible Spongiform Encephalopathy Species Barriers with an In Vitro Prion Protein Conversion Assay

Measuring the barrier to the interspecies transmission of prion diseases is challenging and typically involves animal challenges or biochemical assays. Here, we present an in vitro prion protein conversion assay with the ability to predict species barriers.

Bir ile Bulaşıcı Süngerimsi Ensefalopati Türler Engelleri değerlendirilmesi<em&gt; İn Vitro</em&gt; Prion Proteini Dönüştürme Deneyi

Studies to understanding interspecies transmission of transmissible spongiform encephalopathies (TSEs, prion diseases) are challenging in that they ...

Simultaneous PET/MRI Imaging During Mouse Cerebral Hypoxia-ischemia

Dynamic changes in tissue water diffusion and glucose metabolism occur during and after hypoxia in cerebral hypoxia-ischemia reflecting a bioenergetics disturbance in affected cells. Diffusion weighted magnetic resonance imaging (MRI) identifies regions that are damaged, potentially irreversibly, by hypoxia-ischemia. Alterations in glucose utilization in the affected tissue may be detectable by positron emission tomography (PET) imaging of 2-deoxy-2-(18F)fluoro-&#7429;-glucose ([18F]FDG) uptake. Due to the rapid and variable nature of injury in this animal model, acquisition of both modes of data must be performed simultaneously in order to meaningfully correlate PET and MRI data. In addition, inter-animal variability in the hypoxic-ischemic injury due to vascular differences limits the ability to analyze multi-modal data and observe changes to a group-wise approach if data is not acquired simultaneously in individual subjects. The method presented here allows one to acquire both diffusion-weighted MRI and [18F]FDG uptake data in the same animal before, during, and after the hypoxic challenge in order to interrogate immediate physiological changes.

The method presented here uses simultaneous positron emission tomography and magnetic resonance imaging. In the cerebral hypoxia-ischemia model, dynamic changes in diffusion and glucose metabolism occur during and after injury. The evolving and irreproducible damage in this model necessitates simultaneous acquisition if meaningful multi-modal imaging data are to be acquired.

Fare Serebral Hipoksi-iskemi sırasında Eşzamanlı PET / MR Görüntüleme

Dynamic changes in tissue water diffusion and glucose metabolism occur during and after hypoxia in cerebral hypoxia-ischemia reflecting a bioenergetics ...

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.

Geçici Serebral Hipoksi-iskemi Dayalı Bir Trombotik İnme Modeli

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

Circumscribed Capsular Infarct Modeling Using a Photothrombotic Technique

Recent increase in the prevalence rate of white matter stroke demands specific research in the field. However, the lack of a pertinent animal model for white matter stroke has hampered research investigations. Here, we describe a novel method for creating a circumscribed capsular infarct that minimizes damage to neighboring gray matter structures. We used pre-surgery neural tracing with adeno-associated virus-green fluorescent protein (AAV-GFP) to identify somatotopic organization of the forelimb area within the internal capsule. The adjustment of light intensity based on different optical properties of gray and white matter contributes to selective destruction of white matter with relative preservation of gray matter. Accurate positioning of optical-neural interface enables destruction of entire forelimb area in the internal capsule, which leads to a marked and persistent motor deficit. Thus, this technique produces highly replicable capsular infarct lesions with a persistent motor deficit. The model will be helpful not only to study white matter stroke (WMS) at the behavioral, circuit, and cellular levels, but also to assess its usefulness for development of new therapeutic and rehabilitative interventions.

This manuscript describes a modeling technique of capsular infarct. Here we utilized a modified photothrombotic technique with low intensity of light after pre-surgery target mapping. Using this technique, we created a circumscribed capsular infarct model with persistent motor impairment.

Bir FOTOTROMBOTİK Tekniği sınırlı Kapsül Enfarktüs Modelleme

Recent increase in the prevalence rate of white matter stroke demands specific research in the field. However, the lack of a pertinent animal model for ...

Preparation of Decellularized Kidney Scaffolds in Rats

Tissue engineering is a cutting-edge discipline in biomedicine. Cell culture techniques can be applied for regeneration of functional tissues and organs to replace diseased or damaged organs. Scaffolds are needed to facilitate the generation of three-dimensional organs or tissues using differentiated stem cells in vivo. In this report, we describe a novel method for developing vascularized scaffolds using decellularized rat kidneys. Eight-week-old Sprague-Dawley rats were used in this study, and heparin was injected into the heart to facilitate flow into the renal vessels, allowing heparin to perfuse into the renal vessels. The abdominal cavity was opened, and the left kidney was collected. The collected kidneys were perfused for 9 h using detergents, such as Triton X-100 and sodium dodecyl sulfate, to decellularize the tissue. Decellularized kidney scaffolds were then gently washed with 1% penicillin/streptomycin and heparin to remove cellular debris and chemical residues. Transplantation of stem cells with the decellularized vascular scaffolds is expected to facilitate the generation of new organs. Thus, the vascularized scaffolds may provide a foundation for tissue engineering of organ grafts in the future.

This protocol introduces a method to develop a scaffold using decellularized rat kidneys. The protocol includes decellularization and recellularization processes to confirm bioavailability. Decellularization is performed using Triton X-100 and sodium dodecyl sulfate.

Sıçanlarda Hücreden Sönmemiş Böbrek İskelelerinin Hazırlanması

Tissue engineering is a cutting-edge discipline in biomedicine. Cell culture techniques can be applied for regeneration of functional tissues and organs ...

Analysis of Raw and Processed Cyperi Rhizoma Samples Using Liquid Chromatography-Tandem Mass Spectrometry in Rats with Primary Dysmenorrhea

Cyperi rhizoma (CR) is widely used in gynecology and is a general medicine for treating women's diseases in China. Since the analgesic effect of CR is enhanced after processing with vinegar, CR processed with vinegar (CRV) is generally used clinically. However, the mechanism by which the analgesic effect is enhanced by vinegar processing is unclear. In this study, the ultra-high pressure liquid chromatographytandem mass spectrometry (UPLC-MS/MS) technique was used to examine changes in the blood levels of the exogenous constituents and metabolites between CR-treated and CRV-treated rats with dysmenorrhea. The results revealed differing levels of 15 constituents and two metabolites in the blood of these rats. Among them, the levels of (-)-myrtenol and [(1R,2S,3R,4R)-3-hydroxy-1,4,7,7-tetramethylbicyclo[2.2.1]hept-2-yl]acetic acid in the CRV group were considerably higher than in the CR group. CRV reduced the level of 2-series prostanoids and 4-series leukotrienes with proinflammatory, platelet aggregation, and vasoconstriction activities and provided analgesic effects by modulating arachidonic acid and linoleic acid metabolism and the biosynthesis of unsaturated fatty acids. This study revealed that vinegar processing enhances the analgesic effect of CR and contributes to our understanding of the mechanism of action of CRV.

Here, a comparative analysis of raw and processed Cyperi rhizoma (CR) samples is presented using ultra-high performance liquid chromatography-high-resolution tandem mass spectrometry (UPLC-MS/MS) in rats with primary dysmenorrhea. The changes in blood levels of the metabolites and the sample constituents were examined between rats treated with CR and CR processed with vinegar (CRV).

Primer Dismenore Olan Sıçanlarda Sıvı Kromatografi-Tandem Kütle Spektrometrisi Kullanılarak Ham ve İşlenmiş Siperi Rizom Örneklerinin Analizi

Cyperi rhizoma (CR) is widely used in gynecology and is a general medicine for treating women's diseases in China. Since the analgesic effect of CR is ...

Sıçanlarda Diz Osteoartriti için Standardize Tuina Manipülasyonu

Tuina Manipulation to Reduce Inflammation and Cartilage Loss in Knee Osteoarthritis Rats

Clinical trials suggest that Tuina manipulation is effective in treating knee osteoarthritis (KOA), while further studies are required to discover its mechanism. Therefore, the manipulation of animal models of knee osteoarthritis is critical. This protocol provides a standard process for Tuina manipulation on KOA rats and a preliminary exploration of the mechanism of Tuina for KOA. The press and kneading manipulation method (a kind of Tuina manipulation that refers to pressing and kneading the specific area of the body surface) is applied on 5 acupoints around the knee joint of rats. The force and frequency of the manipulation were standardized by finger pressure recordings, and the position of the rat during manipulation is described in detail in the protocol. The effect of manipulation can be measured by pain behavior tests and microscopic findings in synovial and cartilage. KOA rats showed significant improvement in pain behavior. The synovial tissue inflammatory infiltration was reduced in the Tuina group, and the expression of tumor necrosis factor (TNF)-&#945; was significantly lower. Compared to the control group, chondrocyte apoptosis was less in the Tuina group. This study provides a standardized protocol for Tuina manipulation on KOA rats and preliminary proof that the therapeutic effects of Tuina may be related to reducing synovial inflammation and delayed chondrocyte apoptosis.

Yazar Spotlight: Sıçanlarda Tuina Manipülasyon Mekanizmasını Anlamak 

We present a protocol for Tuina manipulation performed on plaster-immobilized-induced knee osteoarthritis rats. Based on the preliminary results, it suggested that the efficacy of the method relied on the reduction of inflammation and cartilage loss.

Diz Osteoartritli Sıçanlarda Enflamasyonu ve Kıkırdak Kaybını Azaltmak için Tuina Manipülasyonu

Clinical trials suggest that Tuina manipulation is effective in treating knee osteoarthritis (KOA), while further studies are required to discover its ...