美國Seracare血清線性盤（Linearity Panels）

廣州健侖生物科技有限公司

SeraCare Life Sciences公司主要在美國、歐洲和亞洲提供促進(jìn)人類和動物診斷和治療學(xué)的探索、開發(fā)和生產(chǎn)的產(chǎn)品和服務(wù)。其業(yè)務(wù)分為兩個部分：診斷和生物制藥產(chǎn)品和生物服務(wù)。診斷和生物制藥產(chǎn)品部門生產(chǎn)和銷售診斷和控制面板產(chǎn)品，用于測試傳染性疾病的臨床實驗室及員工培訓(xùn)和能力測試。生物服務(wù)部門提供生物銀行、來樣加工和測試服務(wù)。

美國SeraCare收購BBI公司，即原BBI血清盤已經(jīng)改名為SeraCare血清盤。

其產(chǎn)品包括有：傳染病陽性質(zhì)控品、疾病標(biāo)準(zhǔn)品、細(xì)菌陽性質(zhì)控品、人血清白蛋白、人伽馬球蛋白、牛血清白蛋白、血清盤、人血漿、人血清。

SeraCare的血清盤包括：HIV-1轉(zhuǎn)化盤、HIV性能盤、HBV轉(zhuǎn)化盤、HBV性能盤、HCV轉(zhuǎn)化盤、HCV性能盤、弓形蟲性能盤、線性盤和質(zhì)控盤等等。

我司還提供其它進(jìn)口或國產(chǎn)試劑盒：登革熱、瘧疾、流感、A鏈球菌、合胞病毒、腮病毒、乙腦、寨卡、黃熱病、基孔肯雅熱、克錐蟲病、違禁品濫用、肺炎球菌、軍團(tuán)菌、化妝品檢測、食品安全檢測等試劑盒以及日本生研細(xì)菌分型診斷血清、德國SiFin診斷血清、丹麥SSI診斷血清等產(chǎn)品。

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美國Seracare血清線性盤（Linearity Panels）

美國

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【公司名稱】 廣州健侖生物科技有限公司

【市 場 部】    楊永漢

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【騰訊Q Q】 2042552662

【公司地址】 廣州清華科技園創(chuàng)新基地番禺石樓鎮(zhèn)創(chuàng)啟路63號二期2幢101-103室

研究人員發(fā)現(xiàn)用來源于細(xì)菌細(xì)胞壁的脂多糖(LPS)刺激小鼠巨噬細(xì)胞能夠上調(diào)表達(dá)tRNA的相關(guān)基因的轉(zhuǎn)錄。nf-kb是介導(dǎo)炎癥信號的一個關(guān)鍵轉(zhuǎn)錄因子,LPS處理能夠會增強(qiáng)NF-kB的p65亞基與tRNA基因的作用。除此之外，研究人員還發(fā)現(xiàn)p65能夠直接與RNA聚合酶III復(fù)合物中的轉(zhuǎn)錄因子TFIIIB相互作用，并且p65過表達(dá)會誘導(dǎo)pol III依賴性的轉(zhuǎn)錄過程。抑制巨噬細(xì)胞內(nèi)的pol III活性能夠阻止巨噬細(xì)胞分泌細(xì)胞因子并抑制其吞噬作用，這也是巨噬細(xì)胞的兩個關(guān)鍵功能特征。
這項研究揭示了RNA聚合酶III對巨噬細(xì)胞功能的重要調(diào)控作用，證明RNA聚合酶III可能對于惡性腫瘤細(xì)胞相關(guān)的免疫反應(yīng)具有重要影響。
效應(yīng)T細(xì)胞遷移進(jìn)入炎癥組織會加重組織損傷并會導(dǎo)致炎癥性疾病惡化。來自賓夕法尼亞大學(xué)的科研人員發(fā)現(xiàn)缺少接頭蛋白CRK和CRK-like的T細(xì)胞會出現(xiàn)黏附性，趨化性下降等特征，并通過實驗證明CRK蛋白家族能夠選擇性調(diào)控t細(xì)胞黏附性及向效應(yīng)位點遷移的能力，并提出針對CRK蛋白家族或可開發(fā)針對移植物抗宿主病(GVHD)的治療方法。zui近，這一研究成果在著名臨床雜志JCI在線發(fā)表。
研究人員利用條件敲除小鼠發(fā)現(xiàn)，在缺少CRK和CRK-like蛋白后，T細(xì)胞的黏附性，趨化性均出現(xiàn)下降，并且發(fā)現(xiàn)CRK和CRK-like這兩種蛋白存在大量功能冗余，過表達(dá)兩者中任一個都能導(dǎo)致兩者缺失導(dǎo)致的T細(xì)胞功能缺陷得到恢復(fù)。研究人員通過對機(jī)制研究發(fā)現(xiàn)，CRK能夠與RAP鳥嘌呤核苷酸交換因子C3G和黏附駐留分子CASL協(xié)同作用激活整合素調(diào)節(jié)性GTPase RAP1。CRK蛋白對效應(yīng)T細(xì)胞向炎癥部位遷移至關(guān)重要，但不影響效應(yīng)T細(xì)胞向淋巴器官遷移。

The researchers found that stimulation of mouse macrophages with lipopolysaccharide (LPS) derived from the bacterial cell wall upregulates the transcription of related genes that express tRNA. Nf-kb is a key transcription factor that mediates inflammation. LPS treatment can enhance the role of NF-kB p65 subunit and tRNA gene. In addition, the researchers also found that p65 interacts directly with the transcription factor TFIIIB in the RNA polymerase III complex, and that overexpression of p65 induces pol III-dependent transcription. Inhibition of pol III activity in macrophages can prevent macrophages from secreting cytokines and inhibit their phagocytosis, which is also a key feature of macrophages.
This study revealed an important regulatory role of RNA polymerase III in macrophage function, demonstrating that RNA polymerase III may have an important influence on the immune response associated with malignant cells.
The migration of effector T cells into inflammatory tissue can exacerbate tissue damage and lead to the deterioration of inflammatory diseases. Researchers from the University of Pennsylvania found that the lack of the adaptor proteins CRK and CRK-like T cells exhibited features such as adhesion, decreased chemotaxis, and experiments demonstrated that the CRK protein family can selectively regulate t cell adhesion and effector sites. The ability to migrate and propose treatments for the CRK protein family or can be developed for graft-versus-host disease (GVHD). Recently, this research result was published on the well-known clinical journal JCI Online.
Using conditional knockout mice, the researchers found that in the absence of CRK and CRK-like proteins, T cell adhesion and chemotaxis both decreased, and CRK and CRK-like proteins were found to have a lot of functional redundancy. Overexpression of either of them can lead to the restoration of T cell function defects resulting from the loss of both. Through the study of mechanism, the researchers found that CRK can cooperate with RAP guanine nucleotide exchange factor C3G and adhesion resident molecule CASL to activate integrin-regulated GTPase RAP1. The CRK protein is essential for the migration of effector T cells to the site of inflammation but does not affect the migration of effector T cells to the lymphoid organs.