鼠型斑疹傷寒立克次體IgM ELISA試劑盒

R. typhi IgG ELISA Kit 

廣州健侖生物科技有限公司

主要用途：用于檢測(cè)人血清中的鼠型斑疹傷寒立克次體IgM抗體

產(chǎn)品規(guī)格：96T/盒

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鼠型斑疹傷寒立克次體IgM ELISA試劑盒

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【公司名稱】 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】

Smerdon和Mao的發(fā)現(xiàn)是*記錄了修復(fù)過(guò)程在染色質(zhì)上是如何發(fā)生的細(xì)節(jié)之一。
DNA修復(fù)日常需求
Smerdon說(shuō)，每個(gè)人體細(xì)胞都會(huì)遭受各種各樣的攻擊，每天zui多可以創(chuàng)建100,000 個(gè)DNA損傷。細(xì)胞必須不斷的修復(fù)這些損傷，以及迅速產(chǎn)生可替代的DNA和蛋白質(zhì)。
RNA聚合酶就像一個(gè)小火車頭，不斷來(lái)回地進(jìn)行DNA的復(fù)制遺傳信息。當(dāng)它達(dá)到蛋白質(zhì)是細(xì)胞所需的一個(gè)基因時(shí)，它就會(huì)停止，并解開雙鏈DNA，然后復(fù)制一條鏈，并將這條鏈發(fā)送到機(jī)器中生產(chǎn)新的蛋白質(zhì)。
但是，Smerdon說(shuō)，當(dāng)DNA遭到紫外線輻射或有害物質(zhì)損壞時(shí)，它就會(huì)形成一個(gè)堅(jiān)不可摧的塊狀，使得RNA聚合酶停止。就像鐵軌上的巨石，毫無(wú)生命的腫塊阻斷了該基因生產(chǎn)所有的蛋白質(zhì)。除非很快就能夠進(jìn)行修復(fù)，否則細(xì)胞就會(huì)死亡。
在健康的人群中，酶的維修人員與RNA聚合酶一同移動(dòng)，并立即沖進(jìn)去切除損傷和消除痕跡。這就是所謂的轉(zhuǎn)錄偶聯(lián)修復(fù)，或TCT，四個(gè)已知的DNA修復(fù)系統(tǒng)之一的一個(gè)方面。Smerdon說(shuō)，在任何修復(fù)系統(tǒng)中，甚至只有局部缺陷都有可能導(dǎo)致危及生命的病癥。
月球來(lái)的孩子
Smerdon的實(shí)驗(yàn)室研究了修復(fù)缺陷疾病，如著色性干皮病或XP，在1874年*發(fā)現(xiàn)作為一個(gè)可能的遺傳疾病。被稱為月球來(lái)的孩子，XP患者缺乏切除受損DNA的酶，并對(duì)紫外線照射非常敏感，甚至在熒光燈下，皮膚都能夠起泡。
他們的皮膚癌發(fā)病率比沒(méi)有異常的人們高出2000倍。他們只有在黑暗中才能夠安全。
Smerdon和他的同事還研究科凱恩綜合征，一種TCR缺陷疾病，可導(dǎo)致的陽(yáng)光敏感，神經(jīng)系統(tǒng)退化和過(guò)早老化。
其他的DNA修復(fù)缺陷也可導(dǎo)致各種各樣的疾病，如白血病，抗原抗體癌和遺傳性非息肉性大腸癌(導(dǎo)致西方國(guó)家大腸癌的一種常見原因)。

The discovery by Smerdon and Mao was one of the first to document how the repair process took place on the chromatin.
DNA repair daily needs
Smerdon says each human cell suffers from a variety of attacks that create up to 100,000 DNA damage per day. Cells must constantly repair these lesions and rapidly produce alternative DNA and protein.
RNA polymerase is like a small locomotive, DNA replication genetic information back and forth. When it reaches the protein, which is a gene your cell needs, it stops and unlocks double-stranded DNA, then duplicates a strand and sends it to the machine to make new proteins.
However, Smerdon said that when DNA is damaged by UV radiation or harmful substances, it forms an indestructible block that stops RNA polymerase. Like boulders on rails, inanimate lumps block the production of all the proteins in the gene. Unless repaired soon enough, or the cell will die.
In a healthy population, enzyme maintainers move with the RNA polymerase and immediay rush in to remove the lesion and remove traces. This is one aspect of one of the four known DNA repair systems called TCT, or TCT. Smerdon said that even in the case of any repair system, only partial defects can lead to life-threatening conditions.
Children from the moon
Smerdon's lab studied repair of defective diseases such as xeroderma pigmentosum or XP, first discovered in 1874 as a possible genetic disorder. Known as the child from the moon, XP patients lack the enzyme to remove damaged DNA and are very sensitive to UV light, even under fluorescent lighting.
Their skin cancer rates are 2000 times higher than those without abnormalities. They can be safe only in the darkness.
Smerdon and his colleagues also studied Cockney's syndrome, a TCR-deficient disease that can cause extreme sun sensitivity, nervous system degeneration and premature aging.
Other defects in DNA repair can also lead to a variety of diseases such as leukemia, antigen-antibody and hereditary non-polypost colorectal cancers (a common cause of colorectal cancer in Western countries).