军团菌快速检测试剂盒

EIKEN军团菌快速检测试剂盒

广州健仑生物科技有限公司

主要用途：用于检测尿样中嗜肺军团菌血清型1抗原，以支持军团菌感染的诊断。

产品规格：20T/盒

存储条件：2-30℃

EIKEN军团菌快速检测试剂盒

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【产品介绍】

EIKEN

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【公司名称】 广州健仑生物科技有限公司
【】    杨永汉 
【】 
【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101-3室
【企业文化】

美国在肺癌治疗上的花费超过120亿美元。然而，肺癌的存活率不容乐观，由于疾病极易转移到整个身体，有80%的患者在诊断后5年之内死亡。
为了获得转移性，癌细胞会覆盖一般保持细胞根植在它们各自位置的细胞器。癌症可以迂回地打开和关闭细胞膜上突起的分子锚(称为附着斑复合物)，为迁移准备细胞。这使得癌细胞开始经过血流遍历体内，在新的器官驻留下来。
除了不同的癌症能控制这些锚之外，大约五分之一的肺癌病例缺失一个抗癌基因，称为LKB1(又名STK11)。缺失LKB1的癌症通常是侵袭性的，可在体内迅速蔓延。然而，没有知道LKB1和粘附斑之间是如何关联的。
现在，索尔克研究小组发现了这个关联，并发现了一个新的治疗靶点：一个鲜为人知的基因，称为DIXDC1。研究人员发现，DIXDC1接受来自LKB1的指令，转到粘着斑，并改变它们的数量和大小。
当DIXDC1被“打开”，半打左右的粘着斑变大并具有粘性，将细胞锚定在它们的位置。当DIXDC1被阻断或灭活时，粘着斑变小和量大，导致数百只小“手”向前拉动细胞，以响应细胞外的线索。转移的倾向增加，有助于癌细胞从肺部逃跑，可让肿瘤细胞存活下来，经过血液并停留在体内各处的器官。
本研究*作者、博士研究生Jonathan Goodwin称：“LKB1和DIXDC1之间的交流可引起细胞内的一种‘锁定(stay-put)’信号。人们了解较少的DIXDC1，在癌症和转移中原来是被抑制的。”
Shaw和同事在新的研究中发现，肿瘤有两种方法来关闭这个“锁定”信号。一是通过直接抑制DIXDC1。另一种方法是通过删除LKB1，然后不再给DIXDC1发信号转到粘着斑锚定细胞。鉴于此，科学家们想知道，是否复活DIXDC1就能停止癌症的转移。他们获取了转移细胞，这些细胞具有低水平的DIXDC1，并在细胞中过度表达这个基因。DIXDC1的加入，确实在体内和体外削弱了这些细胞的转移能力。
Goodwin称：“这非常非常的奇怪，这个基因会如此强大。在这项研究开始时，我们也不知道DIXDC1会参与转移。LKB1会影响许多蛋白质;单*个基因控制如此多的表型，是我们没有预料到的。”
现在，对具有LKB1或DIXDC1改变的癌症，还没有特定的治疗方法，但是具有这些基因缺失的癌症，可以通过靶定粘着斑的癌症药物得以治疗。

The United States spends more than 12 billion U.S. dollars on lung cancer treatment. However, the survival rate of lung cancer is not optimistic, as the disease easily transferred to the entire body, 80% of patients died within 5 years after diagnosis.
In order to obtain metastaticity, cancer cells will cover organelles that generally keep the cells rooted in their respective locations. Cancers roundaboutly open and close protruding molecular anchors (called attachment plaque complexes) on the cell membrane, preparing cells for migration. This allows cancer cells to start traversing the bloodstream and residing in new organs.
In addition to the fact that different cancers can control these anchors, about one in five lung cancers lack an anti-cancer gene, called LKB1 (aka STK11). Cancers that lack LKB1 are usually aggressive and spread rapidly in the body. However, it is not known how LKB1 and adhesive spots are related.
Now, the Sork study found the link and found a new therapeutic target: a little-known gene called DIXDC1. The researchers found that DIXDC1 received instructions from LKB1, turned to sticky patches, and changed their number and size.
When DIXDC1 is "on", about half a dozen sticky patches become large and sticky, anchoring the cells in their place. When DIXDC1 is blocked or inactivated, the sticky patches become small and large, causing hundreds of small "hands" to pull the cells forward in response to extracellular cues. The increased tendency to metastasize helps the cancer cells escape from the lungs, allowing the tumor cells to survive, pass through the blood and remain in the organs throughout the body.
Jonathan Goodwin, Ph.D., lead author and lead author of the study, said: "The exchange between LKB1 and DIXDC1 causes a 'stay-put' signal in the cell.It has been known that less DIXDC1 is found in cancers and metastases Is suppressed. "
In a new study, Shaw and colleagues found that tumors have two ways to turn off this "lock" signal. First, by directly inhibiting DIXDC1. Another approach is by deleting LKB1 and then no longer signaling DIXDC1 to focal adhesion cells. In view of this, scientists wondered whether the resumption of DIXDC1 would halt the metastasis of cancer. They acquired metastatic cells that had low levels of DIXDC1 and over-expressed the gene in the cell. The addition of DIXDC1 does indeed weaken the metastatic capacity of these cells in vivo and in vitro.
"It's very, very strange, this gene is so powerful, and at the start of the study we did not know that DIXDC1 would be involved in the transfer, LKB1 affects many proteins, and controlling so many phenotypes by a single gene is what we Unexpectedly. "
There are no specific treatments for cancers with changes in LKB1 or DIXDC1, but cancers with these gene deletions can now be treated with cancer drugs that target focal adhesions.