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產(chǎn)品名稱	3D組織器官芯片模型, SynRAM 3D Inflammation Model ，SynRAM 3D炎癥模型–一次分析即可可視化滾動，粘附和遷移
品牌	synvivo
產(chǎn)品貨號	3D組織器官芯片模型, SynRAM 3D Inflammation Model ，SynRAM 3D炎癥模型–一次分析即可可視化滾動，粘附和遷移
產(chǎn)品價格	現(xiàn)貨詢價
聯(lián)系人	李先生
聯(lián)系電話	18618101725
產(chǎn)品說明 SynRAM 3D炎癥模型一次分析即可可視化滾動，粘附和遷移 SynVivo的SynRAM?3D炎癥模型是為研究動態(tài)環(huán)境中的整個炎癥途徑而開發(fā)的。 SynVivo平臺可提供生理上逼真的模型（包括流動和剪切），并能夠?qū)崟r跟蹤軋制，粘附和遷移過程。該模型重建具有內(nèi)皮細(xì)胞管腔的共培養(yǎng)組織和/或腫瘤細(xì)胞的組織切片。它已經(jīng)成功地針對體內(nèi)研究進(jìn)行了驗證，該研究顯示出與滾動速度，粘附模式和遷移過程具有ji好的相關(guān)性（Lamberti等，2014； Soroush等，2016）。 SynRAM 3D炎癥模型提供了一個現(xiàn)實的測試環(huán)境，其中包括：微血管環(huán)境中的生理切應(yīng)力具有wanquan封閉腔的體內(nèi)類血管形態(tài) 細(xì)胞間相互作用的共培養(yǎng)能力單個實驗的實時定量滾動，粘附和遷移數(shù)據(jù) synram遷移測定原理圖芯片上白細(xì)胞內(nèi)皮相互作用 SynRAM能夠在一個實驗中實時評估細(xì)胞相互作用，包括滾動，粘附和遷移通過多個細(xì)胞層，并代表與體內(nèi)結(jié)果密切相關(guān)的數(shù)據(jù)。 SynRAM的創(chuàng)新設(shè)計克服了流動室或基于Transwell室的測定法固有的當(dāng)前局限性。當(dāng)前的流動室設(shè)計過于簡單，缺乏微環(huán)境的規(guī)模和幾何形狀，并且wu法模擬遷移。同樣，Transwell腔室也不能解釋體內(nèi)觀察到的流體剪切力和大小/拓?fù)洹Ａ硗�，遷移的終點測量在Transwell腔室中wu法再現(xiàn)，并且不能提供實時可視化。 SynVivo的專有芯片設(shè)計范圍從復(fù)雜的體內(nèi)衍生的微血管網(wǎng)絡(luò)（從數(shù)字化圖像獲得）到簡化的里想化網(wǎng)絡(luò)。復(fù)雜的體內(nèi)網(wǎng)絡(luò)會產(chǎn)生逼真的細(xì)胞組成和血管形態(tài)，從而導(dǎo)致剪切和流動條件發(fā)生變化。簡化的里想化網(wǎng)絡(luò)旨在重現(xiàn)細(xì)胞組成，恒定剪切力和流動條件。在SynRAM器件中功能化的模型的示例 Synvivo Synram 實時可視化軋制，粘附，粘附和遷移實時跟蹤單細(xì)胞遷移實時跟蹤單細(xì)胞遷移白細(xì)胞內(nèi)皮相互作用白細(xì)胞內(nèi)皮相互作用 quan流明血管內(nèi)皮細(xì)胞芯片上的血管產(chǎn)品購買選項芯片：根據(jù)您的特定研究應(yīng)用，您可以從IMN2徑向SMN2微血管網(wǎng)絡(luò)芯片配置中進(jìn)行選擇。試劑盒：運(yùn)行SynRAM分析所需的基本組件都可以以試劑盒形式購買。提供兩種套件格式。入門套件：shou次購買時請選擇 10個SynRAM芯片（選擇IMN2放射狀或SMN2微血管網(wǎng)絡(luò)芯片）配件，包括油管，夾具，針頭和注射器氣動灌注裝置（灌注管路以除去空氣時需要）檢測試劑盒：如果您以前購買過氣動灌注設(shè)備，請選擇此試劑盒格式 10個SynRAM芯片（選擇IMN2徑向或SMN2微血管網(wǎng)絡(luò)芯片）配件，包括油管，夾具，針頭和注射器用于開發(fā)SynRAM炎癥模型的設(shè)備的示意圖。頂端室（外部通道）用于培養(yǎng)血管（內(nèi)皮細(xì)胞），而基底外側(cè)室（中心腔）用于組織細(xì)胞培養(yǎng)。多孔結(jié)構(gòu)使血管細(xì)胞與組織細(xì)胞之間可以進(jìn)行通訊。 Bioinspired Microfluidic Assay for In Vitro Modeling of Leukocyte–Endothelium Interactions Authors: G. Lamberti, B. Prabhakarpandian, C. Garson, A. Smith, K. Pant, B. Wang, and M.F. Kiani. Anal. Chem., 2014, 86 (16), pp 8344–8351 DOI:10.1021/ac5018716 SynRAM microfluidic chips comprising of realistic microvascular networks were used to understand the role of classical inhibitors of individual steps of the leukocyte adhesion cascade. Experimental results matched very well with in vivo data highlighting the unique ability of the platform for real-time analysis of these dynamic events in a morphologically realistic environment (Lamberti et al 2014). Rolling, adhesion, and migration of neutrophils in bMFA; migration of neutrophils (labeled with fluorescent dye) into the tissue compartment of bMFA after 120 min of continuous flow. (1 and 2) Solid arrows in the top right panels show a rolling neutrophil which (3) becomes adherent; dotted arrows in the top right panels show firmly adherent neutrophils. A neutrophil migrating from a vascular channel through the barrier into the tissue compartment over time (bottom right). Neutrophil rolling using SynRAM microfluidic chips is similar to leukocyte rolling in vivo; Box and whir plots summarizes the comparison of leukocytes rolling velocity measured in vivo and in SynRAM chips and shows no significant difference (p=0.758; Mann-Whitney Rank Sum Test). The “+” marked in the box indicates the mean. Neutrophil adhesion in SynRAM microfluidic chips is similar to leukocyte adhesion in vivo; Distribution of the number of adhered leukocytes and neutrophils as a function of distance from the nearest bifurcation in vivo in mouse cremaster muscle model and in vitro in microfluidic chips, respectively. Both histograms are wed to the left indicating that leukocytes and neutrophils preferentially adhere near bifurcations with the peak occurring at one vessel or channel diameter from the nearest bifurcation. Investigation of the Effect of Blocking of Specific Steps of the Inflammation Pathway using Monoclonal Antibodies Antibody blocking of specific steps in the adhesion/migration cascade downregulates other steps of the cascade; Monoclonal antibodies against E-selectin (aE-selectin), ICAM-1(aICAM-1), and PI3K (wortmannin) significantly reduced the number of rolling, adhering, and migrating neutrophils in SynRAM microfluidic devices. Antibody blocking of specific steps in the adhesion/migration cascade downregulates other steps of the cascade; monoclonal antibodies against E-selectin (aE-selectin), ICAM-1(aICAM-1), and PI3K (wortmannin) significantly reduced the number of rolling, adhering, and migrating neutrophils in bMFA. The numbers represent the percentage of activity after treating cells with the respective blockers in comparison to their corresponding control values (mean ± SEM; N = 3). Elucidation of the Mechanism of Protein Kinase C delta (PKCδ) in Sepsis Related Inflammation Response A Novel Microfluidic Assay Reveals a Key Role for Protein Kinase C δ in Regulating Human Neutrophil-Endothelium Interaction Authors: Soroush F, Zhang T, King DJ, Tang Y, Deosarkar S, Prabhakarpandian B, Kilpatrick LE, Kiani MF. J Leukoc Biol November 2016 100:1027–1035. The SynRAM model was used to identify the underlying mechanism of Protein Kinase C delta (PKCδ) dependent neutrophil-endothelium interactions. These interactions have been found to play a significant role in the inflammatory response. They found that PKC? was a critical regulator of human neutrophil adhesion and migration through human endothelial cells during inflammation. This was validated by testing physiological fluid flow conditions of the entire inflammation process comprised of rolling, adhesion, and migration in real-time. PKCδ inhibitor significantly reduces migration of neutrophils from the vascular channels, across the inflammed endothelium (treated with TNF-α for 4 or 24 hour), into the tissue compartment in response to fMLP mediated signaling compared to untreated controls. Immunohistochemical detection of myeloperoxidase (MPO) in representative lung tissue sections from 24 h post surgery. Few MPO-positive cells in Sham surgery. Sepsis induces the infiltration of numerous MPO-positive cells throughout the lung parenchyma. PKCδ-TAT Inhibitor significantly reduces sepsis-induced, MPO-positive cell numbers in the lung indicating decreased neutrophil migration.

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