布魯氏菌IgG免疫熒光試劑盒

Brucella IgG IFA Kit

廣州健侖生物科技有限公司

主要用途：用于檢測(cè)狗血清中的布魯氏菌IgG抗體

產(chǎn)品規(guī)格：12 孔/張,10 張/盒

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布魯氏菌IgG免疫熒光試劑盒

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【公司名稱(chēng)】 廣州健侖生物科技有限公司
【】    楊永漢 
【】 
【騰訊 】 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(hào)二期2幢101-3室
【企業(yè)文化】

zui近劍橋大學(xué)的Evgeny Zatulovskiy 和 Rob Kay揭示網(wǎng)柱菌屬細(xì)胞，是研究細(xì)胞移動(dòng)的通俗模式生物，能夠同時(shí)利用這兩種動(dòng)力，提升它們也許相互干擾的問(wèn)題。
為了解決這一問(wèn)題，沃威克大學(xué)的Richard Tyson 和Till Bretschneider 開(kāi)發(fā)了一項(xiàng)新計(jì)算機(jī)算法能夠追蹤大量的兩種泡和網(wǎng)柱菌屬細(xì)胞的顯微鏡電影中的偽突起。在目前的研究中，泡和偽突起在趨化作用期間如何合作，他們證明細(xì)胞形狀的影響怎樣影響這些動(dòng)力相互作用。當(dāng)緩慢的偽突起延伸它們的變形細(xì)胞膜創(chuàng)造一種內(nèi)部彎曲區(qū)域。
在健康細(xì)胞中，TRAP-1是代謝的重要調(diào)節(jié)蛋白，并且已顯示出在調(diào)節(jié)線(xiàn)粒體能量生產(chǎn)中發(fā)揮的重要作用。在腫瘤細(xì)胞的線(xiàn)粒體中，TRAP-1是過(guò)量的。
Wistar研究所科學(xué)家創(chuàng)造了TRAP-1基因敲除小鼠，利用其來(lái)進(jìn)行藥物Gamitrinib(其可靶定腫瘤細(xì)胞線(xiàn)粒體中的蛋白質(zhì))的研究。TRAP-1是熱休克90(HSP90)蛋白家族的一成員，腫瘤利用HSP90蛋白如TRAP-1，以幫助在治療下生存。
在腫瘤中，TRAP-1的缺失是有重大后果的，會(huì)觸發(fā)包括代謝問(wèn)題的災(zāi)難性缺陷，zui終導(dǎo)致腫瘤細(xì)胞死亡。然而，一開(kāi)始就缺少TRAP-1的小鼠在子宮內(nèi)有三周時(shí)間來(lái)補(bǔ)償此蛋白質(zhì)的缺失。
研究人員發(fā)現(xiàn)，在他們的基因敲除小鼠中，TRAP-1的缺失會(huì)導(dǎo)致線(xiàn)粒體蛋白錯(cuò)誤折疊，然后觸發(fā)代償性反應(yīng)，導(dǎo)致細(xì)胞消耗更多的氧氣和代謝更多的糖。這將導(dǎo)致基因敲除小鼠線(xiàn)粒體產(chǎn)生失調(diào)水平的ATP。
線(xiàn)粒體活性的增加實(shí)際上會(huì)適度刺激氧化應(yīng)激(自由基損傷)和相關(guān)的DNA損傷。雖然DNA損傷似乎不利于長(zhǎng)壽養(yǎng)生，但低程度DNA損傷實(shí)際上減少了細(xì)胞的增殖，減慢生長(zhǎng)速度，使細(xì)胞的自然修復(fù)機(jī)制生效。

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.
Increased mitochondrial activity can actually moderay stimulate oxidative stress (free radical damage) and related DNA damage. Although DNA damage seems to be detrimental to longevity, low levels of DNA damage actually reduce cell proliferation, slow the rate of growth and allow the cell's natural repair mechanism to work.