恙蟲(chóng)病IgG微量免疫熒光試劑盒

Francisella tularensis IgM IFA Kit

廣州健侖生物科技有限公司

主要用途：用于檢測(cè)人血清中的恙蟲(chóng)病 IgG 抗體

產(chǎn)品規(guī)格：12 孔/張,10 張/盒

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恙蟲(chóng)病IgG微量免疫熒光試劑盒

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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
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在人體內(nèi)，新分裂的細(xì)胞不斷補(bǔ)充著肺、皮膚、肝臟及其他器官。但大多數(shù)人體細(xì)胞不能無(wú)限期地分裂下去——每一次分裂后，染色體末端的細(xì)胞計(jì)時(shí)器就會(huì)縮短。當(dāng)這種名為端粒的計(jì)時(shí)器變得極短時(shí)，細(xì)胞就不再分裂，導(dǎo)致器官和組織退化，這種現(xiàn)象經(jīng)常發(fā)生在衰老階段。但存在一種繞過(guò)這種倒計(jì)時(shí)現(xiàn)象的方法：一些細(xì)胞會(huì)產(chǎn)生一種端粒酶，這種酶可以修復(fù)端粒，并讓細(xì)胞無(wú)限期地分裂下去。
索爾克生物研究所科研人員9月19日在《基因與發(fā)育》雜志上發(fā)表研究報(bào)告稱(chēng)，他們發(fā)現(xiàn)端粒酶可以被關(guān)閉。
該研究報(bào)告資深作者維基·倫德布拉德教授說(shuō)：“早前的研究認(rèn)為端粒酶一旦聚合，在需要時(shí)可隨時(shí)利用。我們意外地發(fā)現(xiàn)端粒酶有一個(gè)‘關(guān)閉’開(kāi)關(guān)，這個(gè)開(kāi)關(guān)可以讓它分解。”
理解如何操縱這一“關(guān)閉”開(kāi)關(guān)——進(jìn)而延緩端粒變短的過(guò)程，可以為治療衰老性疾病帶來(lái)新方法，比如，在生命晚期再造重要的人體器官。
倫德布拉德與報(bào)告*作者、研究生蒂莫西·圖西對(duì)釀酒酵母展開(kāi)了研究。早前，倫德布拉德的團(tuán)隊(duì)利用這種簡(jiǎn)單的單細(xì)胞生物體揭示了端粒酶的大量信息，并為在人體細(xì)胞中尋找類(lèi)似結(jié)果奠定基礎(chǔ)。
圖西說(shuō)：“我們本希望能夠研究端粒酶復(fù)合體的每一種成分，但事實(shí)上這并不是一項(xiàng)簡(jiǎn)單的任務(wù)。”圖西制定了一套方法，可以讓他以*的分辨率觀察處于細(xì)胞生長(zhǎng)和分裂期的每一種成分。
每當(dāng)細(xì)胞分裂時(shí)，細(xì)胞的整個(gè)基因組就會(huì)被復(fù)制。當(dāng)基因組進(jìn)行復(fù)制時(shí)，圖西發(fā)現(xiàn)端粒酶在準(zhǔn)備組合成一個(gè)復(fù)合體時(shí)，會(huì)缺失一個(gè)重要的分子亞基。但在基因組全部復(fù)制后，這個(gè)缺失的亞基會(huì)加入它的同伴中，形成一個(gè)完整的、充分活躍的端粒酶復(fù)合體。在此基礎(chǔ)上，端粒酶可以補(bǔ)充不斷磨損的染色體末端，并確保健康的細(xì)胞分裂。

In the body, newly dividing cells are constantly replenished with lungs, skin, liver and other organs. But most human somatic cells do not divide indefiniy - the cell timer at the end of the chromosome will be shortened after each division. When this timer called omere becomes extremely short, the cells no longer divide, resulting in the degeneration of organs and tissues, a phenomenon that often occurs during the aging phase. But there is a way to get around this countdown: Some cells produce a omerase that repairs omeres and allows cells to divide indefiniy.
Researchers at the Salk Institute for Biological Research published a study in the journal Gene and Development on September 19th saying they found that omerase can be turned off.
Professor Velen Lundbrand, senior author of the study, said: "Earlier studies suggested that omerase, once polymerized, may be readily available when needed, and we have unexpectedly found that omerase has a 'switch-off' switch It can be broken down. "
Understanding how to manipulate this "switch-off" switch, which in turn slows omere shortening, can bring new ways of treating aging diseases, such as rebuilding vital human organs in later life.
Lund Brad and the report's first author, graduate student Timothy Tucci studied Saccharomyces cerevisiae. Earlier, Lund Brad's team used this simple single-cell organism to reveal a wealth of information on omerase and laid the groundwork for finding similar results in human cells.
Tucci said: "We would have liked to study each of the components of the omerase complex, but in fact it is not a simple task." Tucci has developed a methodology that allows him to distinguish Rate observed in the cell growth and division of each component.
Every time a cell divides, the entire genome of the cell is copied. When the genome was replicating, Tucci found that omerase was missing an important molecular subunit in preparation for its assembly into a complex. But after the genome is fully replicated, this missing subunit joins its companion to form a complete and fully active omerase complex. On this basis, omerase can replenish the end of worn chromosomes and ensure healthy cell division.