Seracare志贺氏菌属阳性对照

美国Seracare志贺氏菌属阳性对照

广州健仑生物科技有限公司

广州健仑长期供应各种生物原料，主要代理品牌：美国Seracare、西班牙Certest、美国Fuller等等。

主要产品包括各种标准品、阳性对照品、阳性质控品、单克隆抗原抗体。

其中常见的有：弓形虫病、西尼罗河病毒、类风湿因子、疟疾、麻疹、莱姆病、百日咳杆菌、大肠杆菌、鼠伤寒沙门氏菌、李斯特菌等阳性对照品。

美国Seracare志贺氏菌属阳性对照

我司还提供其它进口或国产试剂盒：登革热、疟疾、流感、A链球菌、合胞病毒、腮病毒、乙脑、寨卡、黄热病、基孔肯雅热、克锥虫病、违禁品滥用、肺炎球菌、军团菌、化妆品检测、食品安全检测等试剂盒以及日本生研细菌分型诊断血清、德国SiFin诊断血清、丹麦SSI诊断血清等产品。

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研究发现两个细胞动力，之前认为它们之间是相互竞争的，其实可以一起工作帮助细胞挤压穿过拥挤的细胞群。
源于细胞膜的一种细胞动力，柔韧的外膜包围所有细胞，通过形成所谓的伪突起鼓出。“在此情况下，细胞移动是由机能蛋白支架的局部生长从内部抵抗细胞膜驱使的。细胞利用复杂的调节，连接环境传感，制造伪突起高精度控制装置，虽然只有有限的能力。”Dr Tyson说。
第二种动力更快速继承，细胞泡形成中压力驱动突出。这些提供更高的力量，像破城槌打开缺口为细胞挤压进入到其他紧密连接细胞之间。“像一块肌肉，一个细胞能够使自己收缩，增加其内压力并且使细胞膜从细胞支架的下面局部撕开。然后压力向外吹强迫旁边其他细胞或创建立足点作为牵引就像攀爬着的岩石，”Dr Tyson说。与伪突起相比，泡出现在较低精确控制之下在它们形成的细胞表面，制造印迹。
zui近剑桥大学的Evgeny Zatulovskiy 和 Rob Kay揭示网柱菌属细胞，是研究细胞移动的通俗模式生物，能够同时利用这两种动力，提升它们也许相互干扰的问题。
为了解决这一问题，沃威克大学的Richard Tyson 和Till Bretschneider 开发了一项新计算机算法能够追踪大量的两种泡和网柱菌属细胞的显微镜电影中的伪突起。在目前的研究中，泡和伪突起在趋化作用期间如何合作，他们证明细胞形状的影响怎样影响这些动力相互作用。当缓慢的伪突起延伸它们的变形细胞膜创造一种内部弯曲区域。
在健康细胞中，TRAP-1是代谢的重要调节蛋白，并且已显示出在调节线粒体能量生产中发挥的重要作用。在肿瘤细胞的线粒体中，TRAP-1是过量的。
Wistar研究所科学家创造了TRAP-1基因敲除小鼠，利用其来进行药物Gamitrinib(其可靶定肿瘤细胞线粒体中的蛋白质)的研究。TRAP-1是热休克90(HSP90)蛋白家族的一成员，肿瘤利用HSP90蛋白如TRAP-1，以帮助在治疗下生存。
在肿瘤中，TRAP-1的缺失是有重大后果的，会触发包括代谢问题的灾难性缺陷，zui终导致肿瘤细胞死亡。然而，一开始就缺少TRAP-1的小鼠在子宫内有三周时间来补偿此蛋白质的缺失。
研究人员发现，在他们的基因敲除小鼠中，TRAP-1的缺失会导致线粒体蛋白错误折叠，然后触发代偿性反应，导致细胞消耗更多的氧气和代谢更多的糖。这将导致基因敲除小鼠线粒体产生失调水平的ATP。

美国

我司还提供其它进口或国产试剂盒：登革热、疟疾、流感、A链球菌、合胞病毒、腮病毒、乙脑、寨卡、黄热病、基孔肯雅热、克锥虫病、违禁品滥用、肺炎球菌、军团菌、食品安全、化妆品检测、药物滥用检测等试剂盒以及日本生研细菌分型诊断血清、德国SiFin诊断血清、丹麦SSI诊断血清等产品。

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【公司名称】 广州健仑生物科技有限公司
【市场部】    杨永汉

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【腾讯  】 2042552662
【公司地址】 广州清华科技园创新基地番禺石楼镇创启路63号二期2幢101-103室

The study found that two cell motives, previously thought to be competing with each other, actually work together to help cells squeeze through crowded cell populations.
A cell-powered, cell-permeable, flexible outer membrane that surrounds all cells and forms a so-called pseudo-bulge. "In this case, cell movement is driven internally by the local growth of a functional protein scaffold against cell membranes." Cells use complex accommodation and environmental sensing to create highly accurate control of false protrusions, albeit with limited capabilities. "Dr Tyson said.
The second power is inherited more quickly, with stress-driven prominences in the formation of cell foam. These provide higher power, breaking the gap like broken hammers to squeeze cells into other tightly-connected cells. "Like a muscle, a cell can contract itself, increase its internal pressure and partially tear the cell membrane from underneath the cell holder. Then the pressure blows outwards to force other cells alongside or create a foothold as a pulling-like rock , "Dr Tyson said. Blotting occurs with less precise control on the cell surface on which they form than the dummy protrusions, making a blot.
Recently, Evgeny Zatulovskiy and Rob Kay of Cambridge University revealed that the cells of the genus Mycena, a popular model organism for studying the movement of cells, could exploit both of these motivations to enhance their mutual interference.
To tackle this problem, Richard Tyson and Till Bretschneider of Warwick University have developed a new computer algorithm that can track artifacts in a large number of microscopic films of both Bubble and Mycena cells. In the present study, how bubbles and pseudopromas work together during chemotaxis demonstrate how the effects of cell shape affect these kinetic interactions. When slow pseudoprojections extend their deformable cell membranes creating an inner curved area.
In healthy cells, TRAP-1 is an important regulatory protein of metabolism and has been shown to play an important role in the regulation of mitochondrial energy production. TRAP-1 is excessive in tumor cell mitochondria.
Wistar Institute scientists have created TRAP-1 knockout mice that allow them to study the drug Gamitrinib, which targets proteins in tumor cell mitochondria. TRAP-1 is a member of the heat shock 90 (HSP90) protein family that utilizes HSP90 proteins such as TRAP-1 to help survive the treatment.
In tumors, the absence of TRAP-1 has major consequences, triggering catastrophic defects that include metabolic problems that eventually lead to the death of tumor cells. However, mice lacking TRAP-1 initially had three weeks in the uterus to compensate for the protein loss.
The researchers found that in their knockout mice, the absence of TRAP-1 causes misfolding of mitochondrial proteins and triggers compensatory reactions that cause cells to consume more oxygen and metabolize more sugar. This will result in knockout of mitochondrial ATP levels in mice.