世聯(lián)博研北京科技有限公司為美國(guó)flexcell bioflex拉伸培養(yǎng)板（皿）、FX-5000T細(xì)胞牽張拉伸應(yīng)力加載系統(tǒng)、FX-5000C細(xì)胞壓力加載系統(tǒng)、TissueTrain System細(xì)胞牽張加載系統(tǒng)以及radiology.vcu大學(xué)的液壓顱腦損傷儀(FPI),電子顱腦損傷儀(eCCI、細(xì)胞顱腦損傷儀(CIC)等全系列細(xì)胞組織牽張拉伸損傷產(chǎn)品在中國(guó)的**授權(quán)代理， 為廣大科研用戶提供flexcell全系列產(chǎn)品，詳情致電國(guó)內(nèi)免費(fèi)客服電話：400-650-8506咨詢索取資料.

創(chuàng)傷性腦損傷是神經(jīng)外科*常見(jiàn)的**，是導(dǎo)致創(chuàng)傷患者傷殘及死亡的主要原因。研究腦損傷后的神經(jīng)生化、神經(jīng)病理生理等方面的變化，可為探索行之有效的腦保護(hù)**提供幫助，將有助于提高顱腦損傷患者的生存率及生存質(zhì)量。故建立各種便于觀察和施加干預(yù)因素、控制性佳、可分級(jí)、可復(fù)制性好并符合人類腦創(chuàng)傷特點(diǎn)的創(chuàng)傷性腦損傷模型，是目前創(chuàng)傷性腦損傷的研究熱點(diǎn)。 
VCU動(dòng)物顱腦損傷儀可以分為:

• 液壓顱腦損傷儀(FPI),

• 電子顱腦損傷儀(eCCI)

• 細(xì)胞顱腦損傷儀(CIC)

這三種產(chǎn)品己廣泛應(yīng)用于世界范圍內(nèi)的顱腦創(chuàng)傷研究中心，是目前**的顱腦創(chuàng)傷模型制作的金標(biāo)準(zhǔn)。同時(shí),損傷儀還可應(yīng)用到眼科損傷模型，細(xì)胞損傷儀可以應(yīng)用到其它種類細(xì)胞損傷模型的制作。 
弗吉尼亞州立大學(xué)放射學(xué)系所有定制的設(shè)備都是由CDF（定制設(shè)計(jì)與制造）制作的。2000年的時(shí)候，CDF公司（定制設(shè)計(jì)與制造公司）建立了一個(gè)成本核算中心，以便拓展與其他需要定制設(shè)備的客戶的商業(yè)聯(lián)系。目前CDF公司提供了在機(jī)械和電子工程設(shè)備定制的**服務(wù)。除了網(wǎng)頁(yè)上面展示的產(chǎn)品外，我們還提供給用戶定制服務(wù)，希望您有想法告訴我們，我們幫您實(shí)現(xiàn)。 
液壓顱腦損傷儀(FPI)
 
液壓沖擊損傷儀（Fluid Percussion Injury）是由VCU大學(xué)所制作設(shè)計(jì)的，針對(duì)神經(jīng)創(chuàng)傷機(jī)制研究。成為全球研究神經(jīng)創(chuàng)傷廣泛使用的儀器，基本的組件是采取***的Power coating process技術(shù)，鋁制部分的組件都已經(jīng)電鍍以避免氧化且可以長(zhǎng)久使用。液壓沖擊腦損傷儀可以重復(fù)一致的產(chǎn)生液壓沖擊損傷(FPI)。 
系統(tǒng)優(yōu)點(diǎn)：

• 可方便的排除氣飽。

• 角度刻度可方便觀察撞擊角度。

• 集成壓基準(zhǔn)力輸出，方便校準(zhǔn)?？奢敵?*沖擊壓力。

• 配備高精度的壓力傳感

電子顱腦損傷儀(eCCI)
 
由VCU大學(xué)所制作設(shè)計(jì)的電子大腦皮質(zhì)挫傷撞擊儀（electric Cortical Contusion Impactor），主要針對(duì)腦皮質(zhì)挫傷模型。是神經(jīng)損傷研究機(jī)構(gòu)*受歡迎的損傷模型制作工具。電子大腦皮質(zhì)挫傷撞擊儀（eCCI）的組件有： 堅(jiān)固的鋁架，動(dòng)物平臺(tái)，撞擊控制器和撞擊頭。動(dòng)物平臺(tái)可以和各種立體定位儀搭配使用。eCCI電子大腦皮質(zhì)挫傷撞擊儀使用**的線性馬達(dá)驅(qū)動(dòng)撞擊頭，并由控制器來(lái)控制撞擊參數(shù)，實(shí)現(xiàn)不同程度的損傷。撞擊頭的組件部分有含感應(yīng)器，可以確定速率、撞擊深度及撞擊停留。這些撞擊參數(shù)完全可以重復(fù)實(shí)現(xiàn)。
與傳統(tǒng)Feeney’s自由落體硬膜外撞擊方法相比有以下優(yōu)點(diǎn)： 
可**連續(xù)的控制撞擊速度，并獲得實(shí)際撞擊深度和停留時(shí)間等參數(shù)。而非重量差異很大的撞擊。由于可**控制撞擊速度和獲得實(shí)際撞擊結(jié)果參數(shù)，eCCI電子大腦皮質(zhì)挫傷撞擊儀可以**重復(fù)制作挫傷損傷模型。減少動(dòng)物死亡。使實(shí)驗(yàn)過(guò)程更加直觀，可控。 
細(xì)胞顱腦損傷儀(CIC)
 
細(xì)胞損傷控制儀（Cell Injury Controller II）采取電子式控制，采取電子式控制，適合腦源性細(xì)胞培養(yǎng)樣品，或其它離體培養(yǎng)細(xì)胞的牽張性損傷模型制作。損傷后可進(jìn)行神經(jīng)生化、形態(tài)學(xué)、生理學(xué)，**干預(yù)等方面的研究。 
細(xì)胞損傷控制儀使用Flexcell公司的Tissue Train ? 三維細(xì)胞組織應(yīng)力加載系統(tǒng)。 
細(xì)胞損傷控制儀平均把壓縮氣體送到每個(gè)培養(yǎng)室，以造成培養(yǎng)組織牽張性的損傷，損傷的嚴(yán)重程度是依靠控制進(jìn)出密閉培養(yǎng)室的氣體量。養(yǎng)室的峰值壓力同時(shí)被記錄下來(lái)，這個(gè)數(shù)值可以用來(lái)**地表明引起牽張性細(xì)胞損傷的氣壓值。細(xì)胞損傷控制儀（CIC II）可以搭配Flex I29.45cm2 柔性基底培養(yǎng) I (針對(duì)VCU早期的細(xì)胞損傷控制儀)或BioFlex? 57.75cm2 柔性基底培養(yǎng)板。因?yàn)楦鶕?jù)所采用的細(xì)胞種類、損傷的程度、培養(yǎng)的狀況，受損后的細(xì)胞或許會(huì)因?yàn)樯鲜鲆蛩厮劳龌蛐迯?fù)，所以VCU的細(xì)胞損傷控制儀(CIC II)很適合應(yīng)用在下列損傷反應(yīng)研究：細(xì)胞受損、修護(hù)，死亡，**介入。

*Note that the CIC Model 94A Flex I deformation data is the measured distension of a dry reference well. The corresponding peak pressure values are based on the anticipated injury deformation with the addition of 1 ml of fluid media. The presence of 1 ml of fluid increases the deformation approximately 5 percent over the reference well measurement.
美國(guó)Flexcellint國(guó)際公司，成立于1987年，該公司專注于細(xì)胞力學(xué)培養(yǎng)產(chǎn)品的設(shè)計(jì)和制造。以提供獨(dú)特的體外細(xì)胞拉應(yīng)力、壓應(yīng)力和流體剪切應(yīng)力加載刺激系統(tǒng)以及配套的培養(yǎng)板、硅膠膜載片等耗材聞名于世。 
世聯(lián)博研北京科技有限公司是Flexcell細(xì)胞力學(xué)設(shè)備與耗材在中國(guó)大陸、香港、澳門、馬來(lái)西亞、新加波區(qū)域總授權(quán)代理商， 為廣大科研用戶提供flexcell全系列產(chǎn)品，詳情致電國(guó)內(nèi)免費(fèi)客服電話：400-650-8506咨詢索取資料.

Flexcell公司的FX-5000TT型號(hào)的Tissue Train 三維細(xì)胞組織應(yīng)力加載系統(tǒng)

對(duì)生長(zhǎng)在三維狀態(tài)下的細(xì)胞進(jìn)行靜態(tài)的或者周期性的應(yīng)力刺激。 
使用三維組織培養(yǎng)模具和三維細(xì)胞培養(yǎng)板可以進(jìn)行三維細(xì)胞培養(yǎng) 
通過(guò)Flexcell應(yīng)力加載系統(tǒng)和弧矩形加載平臺(tái)對(duì)生長(zhǎng)在三維環(huán)境下的細(xì)胞進(jìn)行單軸向或者雙軸向的靜態(tài)或者周期性的應(yīng)力加載實(shí)驗(yàn)。 
使用Flexcell程序，可建立特制的各種模擬實(shí)驗(yàn)：心率模擬實(shí)驗(yàn)，步行模擬實(shí)驗(yàn)，跑動(dòng)模擬實(shí)驗(yàn)和其他動(dòng)力模擬實(shí)驗(yàn)。 
構(gòu)建長(zhǎng)度達(dá)35mm的生物人工組織 
使用標(biāo)準(zhǔn)正立式顯微鏡實(shí)時(shí)觀察細(xì)胞在三維狀態(tài)下的反應(yīng) 
FX-5000T細(xì)胞牽張拉伸應(yīng)力加載系統(tǒng)(Flexcell FX5000 Tension system) 

系統(tǒng)基本原理（負(fù)氣壓交換模式）： 
橡膠密封墊在細(xì)胞培養(yǎng)板基底膜與基板之間形成封閉腔，把此密封腔的進(jìn)、出氣管插入二氧化碳培養(yǎng)箱里，把此密封腔放入二氧化碳培養(yǎng)箱， 利用封閉腔抽真空產(chǎn)生的負(fù)壓使彈性基底膜（拉動(dòng)三維支架）發(fā)生形變，通過(guò)計(jì)算機(jī)控制系統(tǒng)調(diào)節(jié)氣體的壓力來(lái)改變基底膜的形變量,進(jìn)而使貼壁生長(zhǎng)的細(xì)胞受到牽拉加載刺激。 
亮點(diǎn)： 
1）該系統(tǒng)對(duì)二維、三維細(xì)胞和組織各種培養(yǎng)物提供軸向和圓周應(yīng)力加載；不但具有雙軸向拉伸力加載，還具備單軸向加力功能 
2）計(jì)算機(jī)控制的應(yīng)力加載系統(tǒng)，為體外培育的細(xì)胞提供**的、可控制的、可重復(fù)的、靜態(tài)的或者周期性的應(yīng)力變化。 
3）使用真空泵，抻拉培養(yǎng)板底部的彈性硅膠模，細(xì)胞培養(yǎng)板底部*高伸展度可達(dá)到33%，通過(guò)氣體裝置可以自動(dòng)調(diào)節(jié)和控制應(yīng)力。 
4）基于柔性膜基底變形、受力均勻;
5）可實(shí)時(shí)觀察細(xì)胞、組織在應(yīng)力作用下的反應(yīng);
6）獨(dú)具的flexstop隔離閥可使同一塊培養(yǎng)板力的一部分培養(yǎng)孔的細(xì)胞受力，一部分培養(yǎng)孔的細(xì)胞不受力，方便對(duì)比實(shí)驗(yàn); 
7）與壓力傳導(dǎo)儀整合，同時(shí)兼?zhèn)涠嗤ǖ兰?xì)胞壓力加載功能;
8）與Flex Flow平行板流室配套，可在牽拉細(xì)胞的同時(shí)施加流體切應(yīng)力;
9）多達(dá)4通道，可4個(gè)不同程序同時(shí)運(yùn)行，進(jìn)行多個(gè)不同拉伸形變率對(duì)比實(shí)驗(yàn)； 
10）同一程序中可以運(yùn)行多種頻率，多種振幅和多種波形； 
11）加載模擬波形種類豐富：靜態(tài)波形、正旋波形、心動(dòng)波形、三角波形、矩形以及各種特制波形；
12）更好地控制在超低或超高應(yīng)力下的波形； 
13)電腦系統(tǒng)對(duì)牽張拉伸力加載周期、大小、頻率、持續(xù)時(shí)間**智能調(diào)控
14)加載分析各種細(xì)胞在牽張拉應(yīng)力刺激下的生物化學(xué)反應(yīng)
15)伸展度范圍廣：0-33%
16)牽拉頻率范圍廣：0.01-5Hz 
BioFLEX?雙向應(yīng)力細(xì)胞培養(yǎng)板(BioFLEX?CULTURE PLATES) 

• BioFlex細(xì)胞培養(yǎng)板和FX-5000T應(yīng)力加載系統(tǒng)配套使用，為細(xì)胞提供應(yīng)力加載。

• 孔板底部是由彈性硅膠模制作而成，柔韌性好，透明度高。

• 6孔圓形，總生長(zhǎng)面積57.75 cm2(9.62 cm2/孔).

• 孔板底部的硅膠模超薄，厚度僅為0.020",(0.0508cm)可以使用標(biāo)準(zhǔn)正立式顯微鏡/倒立顯微鏡觀察細(xì)胞。

• 五種不同包被的培養(yǎng)表面：Amino, Collagen (Type I or IV), Elastin, ProNectin (R GD), Laminin (YIGSR).
  Covalently bound matrix surfaces: Amino, Collagen (Type I or IV), Elastin, Pronectin?(RGD), and Laminin (YIGSR).（包被材料選擇參考）

• 光學(xué)性能佳，自身熒光低。

• 當(dāng)與圓柱形加載平臺(tái)共同使用時(shí)，可以對(duì)細(xì)胞進(jìn)行均勻的徑向和圓周應(yīng)力加載。

Flexcell 牽張拉伸損傷文獻(xiàn) 
美國(guó)Fexcell?研制的體外細(xì)胞組織拉應(yīng)力、壓應(yīng)力、和流體剪切力加載仿真模擬模型系統(tǒng)智能、精準(zhǔn)誘導(dǎo)來(lái)自各種細(xì)胞、組織在拉力、壓力和流體切應(yīng)力等體外機(jī)械力刺激作用下發(fā)生的生化生理變化，專業(yè)、細(xì)膩的闡釋了體外細(xì)胞、組織機(jī)械力刺激加載、力學(xué)信號(hào)感受和響應(yīng)機(jī)制。國(guó)內(nèi)外有近3000篇成功應(yīng)用文獻(xiàn)案例，詳見(jiàn)應(yīng)用案例文獻(xiàn)庫(kù),是細(xì)胞組織力學(xué)研究者的優(yōu)選。 
Halachmi S, Aitken KJ, Szybowska M, Sabha N, Dessouki S, Lorenzo A, Tse D, Bagli DJ. Role of signal transducer and activator of transcription 3 (STAT3) in stretch injury to bladder smooth muscle cells.
Cell Tissue Res 326(1):149-158, 2006.

Upadhyay J, Aitken KJ, Damdar C, Bolduc S, Bagli DJ. Integrins expressed with bladder extracellular matrix after stretch injury in vivo mediate bladder smooth muscle cell growth in vitro. J Urol 169(2):750-755, 2003.

Birukova AA, Tian Y, Meliton A, Leff A, Wu T, Birukov KG. Stimulation of Rho signaling by pathologic mechanical stretch is a "second hit" to Rho-independent lung injury induced by IL-6. Am J Physiol Lung Cell Mol Physiol302(9):L965-75, 2012. doi: 10.1152/ajplung.00292.2011. Epub 2012 Feb 17.

Meltzer KR, Cao TV, Schad JF, King H, Stoll ST, Standley PR. In vitro modeling of repetitive motion injury and myofascial release. J Bodyw Mov Ther 14(2):162-171, 2010. Epub 2010 Jan 29.

Frank JA, Wray CM, McAuley DF, Schwendener R, Matthay MA. Alveolar macrophages contribute to alveolar barrier dysfunction in vent
Birukova AA, Fu P, Xing J, Cokic I, Birukov KG. Lung endothelial barrier protection by iloprost in the 2-hit models of ventilator-induced lung injury (VILI) involves inhibition of Rho signaling. Transl Res 155(1):44-54, 2010.

Birukova AA, Tian Y, Meliton A, Leff A, Wu T, Birukov KG. Stimulation of Rho signaling by pathologic mechanical stretch is a "second hit" to Rho-independent lung injury induced by IL-6. Am J Physiol Lung Cell Mol Physiol302(9):L965-75, 2012. doi: 10.1152/ajplung.00292.2011. Epub 2012 Feb 17.

25. Dubrovskyi O, Birukova AA, Birukov KG. Measurement of local permeability at subcellular level in cell models of agonist- and ventilator-induced lung injury. Lab Invest 93(2):254-63, 2013. doi: 10.1038/labinvest.2012.159. Epub 2012 Nov 19.

Eckle T, Brodsky K, Bonney M, Packard T, Han J, Borchers CH, Mariani TJ, Kominsky DJ, Mittelbronn M, Eltzschig HK. HIF1A reduces acute lung injury by optimizing carbohydrate metabolism in the alveolar epithelium.PLoS Biol 11(9):e1001665, 2013. doi: 10.1371/journal.pbio.1001665. Epub 2013 Sep 24.

Eckle T, Fullbier L, Wehrmann M, Khoury J, Mittelbronn M, Ibla J, Rosenberger P, Eltzschig HK. Identification of ectonucleotidases CD39 and CD73 in innate protection during acute lung injury. The Journal of Immunology 178:8127-8137, 2007.

Frank JA, Wray CM, McAuley DF, Schwendener R, Matthay MA. Alveolar macrophages contribute to alveolar barrier dysfunction in ven

Lee HS, Wang Y, Maciejewski BS, Esho K, Fulton C, Sharma S, Sanchez-Esteban J.Interleukin-10 protects cultured fetal rat type II epithelial cells from injury induced by mechanical stretch. Am J Physiol Lung Cell Mol Physiol 294:L225–L232, 2008.

Makena PS, Luellen CL, Balazs L, Ghosh MC, Parthasarathi K, Waters CM, Sinclair SE. Preexposure to hyperoxia causes increased lung injury and epithelial apoptosis in mice ventilated with high tidal volumes. Am J Physiol Lung Cell Mol Physiol299(5):L711-L719, 2010. Epub 2010 Sep 10.

Arundine M, Chopra GK, Wrong A, Lei S, Aarts MM, MacDonald JF, Tymianski M. Enhanced vulnerability to NMDA toxicity in sublethal traumatic neuronal injury in vitro.Journal of Neurotrauma 20(12):1377-1395, 2003.

Gladman SJ, Huang W, Lim SN, Dyall SC, Boddy S, Kang JX, Knight MM, Priestley JV, Michael-Titus AT.Improved outcome after peripheral nerve injury in mice with increased levels of endogenous ω-3 polyunsaturated fatty acids. J Neurosci 32(2):563-571, 2012.

Lau A, Arundine M, Sun HS, Jones M, Tymianski M. Inhibition of caspase-mediated apoptosis by peroxynitrite in traumatic brain injury. J Neurosci 26(45):11540-11553, 2006.

Ebihara S, Hussain SN, Danialou G, Cho WK, Gottfried SB, Petrof BJ. Mechanical ventilation protects against diaphragm injury in sepsis: interaction of oxidative and mechanical stresses. Am J Respir Crit Care Med165(2):221-228, 2002.

Tsivitse SK, Mylona E, Peterson JM, Gunning WT, Pizza FX. Mechanical loading and injury induce human myotubes to release neutrophil chemoattractants. Am J Physiol Cell Physiol 288(3):C721-C729, 2005.

Ni J, Waldman A, Khachigian LM. c-Jun regulates shear- and injury-inducible Egr-1 expression, vein graft stenosis after autologous end-to-side transplantation in rabbits, and intimal hyperplasia in human saphenous veins. J Biol Chem 285(6):4038-4048, 2010. Epub 2009 Nov 23.

Ahmed SM, Rzigalinski BA, Willoughby KA, Sitterding HA, Ellis EF. Stretch-induced injury alters mitochondrial membrane potential and cellular ATP in cultured astrocytes and neurons. J Neurochem 74(5):1951-1960, 2000.
2. Ahmed SM, Weber JT, Liang S, Willoughby

Ellis EF, Willoughby KA, Sparks SA, Chen T. S100B protein is released from rat neonatal neurons, astrocytes, and microglia by in vitro trauma and anti-S100 increases trauma-induced delayed neuronal injury and negates the protective effect of exogenous S100B on neurons. J Neurochem 101(6):1463-1470, 2007. Epub 2007 Apr 2

Floyd CL, Gorin FA, Lyeth BG. Mechanical strain injury increases intracellular sodium and reverses Na+/Ca2+ exchange in cortical astrocytes. Glia 51(1):35-46, 2005.

Floyd CL, Rzigalinski BA, Weber JT, Sitterding HA, Willoughby KA, Ellis EF.Traumatic injury of cultured astrocytes alters inositol (1,4,5)-trisphosphate-mediated signaling. Glia 33(1):12-23, 2001.

Goforth PB, Ellis EF, Satin LS. Enhancement of AMPA-mediated current after traumatic injury in cortical neurons. J Neurosci 19(17):7367-7374, 1999.

Goforth PB, Ellis EF, Satin LS. Mechanical injury modulates AMPA receptor kinetics via an NMDA receptor-dependent pathway. Journal of Neurotrauma 21(6):719-732, 2004.

Kao CQ, Goforth PB, Ellis EF, Satin LS. Potentiation of GABA(A) currents after mechanical injury of cortical neurons. Journal of Neurotrauma 21(3):259-270, 2004.

Lapanantasin S, Chongthammakun S, Floyd CL, Berman RF. Effects of 17β-estradiol on intracellular calcium changes and neuronal survival after mechanical strain injury in neuronal-glial cultures. Synapse 60(5):406-410, 2006.

McKinney JS, Willoughby KA, Liang S, Ellis EF. Stretch-induced injury of cultured neuronal, glial, and endothelial cells. Effect of polyethylene glycol-conjugated superoxide dismutase. Stroke 27(5):934-940, 1996.

Neary JT, Kang Y, Tran M, Feld J. Traumatic injury activates protein kinase B/Akt in cultured astrocytes: role of extracellular ATP and P2 purinergic receptors. Journal of Neurotrauma 22(4):491-500, 2005.

Neary JT, Kang Y, Willoughby KA, Ellis EF. Activation of extracellular signal-regulated kinase by stretch-induced injury in astrocytes involves extracellular ATP and P2 purinergic receptors. J Neurosci 23(6):2348-2356, 2003

Rzigalinski BA, Liang S, McKinney JS, Willoughby KA, Ellis EF. Effect of Ca2+ on in vitro astrocyte injury. J Neurochem 68(1):289-296, 1997. 
McKinney JS, Willoughby KA, Liang S, Ellis EF. Stretch-induced injury of cultured neuronal, glial, and endothelial cells. Effect of polyethylene glycol-conjugated superoxide dismutase. Stroke 27(5):934-940, 1996.

Neary JT, Kang Y, Tran M, Feld J. Traumatic injury activates protein kinase B/Akt in cultured astrocytes: role of extracellular ATP and P2 purinergic receptors. Journal of Neurotrauma 22(4):491-500, 2005.

Neary JT, Kang Y, Willoughby KA, Ellis EF. Activation of extracellular signal-regulated kinase by stretch-induced injury in astrocytes involves extracellular ATP and P2 purinergic receptors. J Neurosci 23(6):2348-2356, 2003.

Slemmer JE, Matser EJ, De Zeeuw CI, Weber JT. Repeated mild injury causes cumulative damage to hippocampal cells. Brain 125(Pt 12):2699-2709, 2002.

Slemmer JE, Zhu C, Landshamer S, Trabold R, Grohm J, Ardeshiri A, Wagner E, Sweeney MI, Blomgren K, Culmsee C, Weber JT, Plesnila N. Causal role of apoptosis-inducing factor for neuronal cell death following traumatic brain injury. Am J Pathol 173(6):1795-1805, 2008. Epub 2008 Nov 6.

Tavalin SJ, Ellis EF, Satin LS. Inhibition of the electrogenic Na pump underlies delayed depolarization of cortical neurons after mechanical injury or glutamate. J Neurophysiol 77:632-638, 1997.

Weber JT, Rzigalinski BA, Ellis EF. Traumatic injury of cortical neurons causes changes in intracellular calcium stores and capacitative calcium influx. J Biol Chem276(3):1800-1807, 2001.

Weber JT, Rzigalinski BA, Willoughby KA, Moore SF, Ellis EF. Alterations in calcium-mediated signal transduction after traumatic injury of cortical neurons. Cell Calcium 26(6):289-299, 1999.

Willoughby KA, Kleindienst A, Muller C, Chen T, Muir JK, Ellis EF. S100B protein is released by in vitro trauma and reduces delayed neuronal injury. J Neurochem91(6):1284-1291, 2004.

Tymianski M. Method of screening peptides useful in treating traumatic injury to the brain or spinal cord. Issued March 31, 2009. Patent No. 7,510,824. 
索取多更應(yīng)用案例文獻(xiàn)請(qǐng)致電010-67529703，或QQ：736597338

產(chǎn)品留言

標(biāo)題

聯(lián)系人

聯(lián)系電話

內(nèi)容

驗(yàn)證碼

點(diǎn)擊換一張

注：1.可以使用快捷鍵Alt+S或Ctrl+Enter發(fā)送信息!
2.如有必要,請(qǐng)您留下您的詳細(xì)聯(lián)系方式!