EIKEN軍團菌快速檢測試劑盒

廣州健侖生物科技有限公司

主要用途：用于檢測尿樣中嗜肺軍團菌血清型1抗原，以支持軍團菌感染的診斷。

產品規格：20T/盒

存儲條件：2-30℃

EIKEN軍團菌快速檢測試劑盒

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【產品介紹】

EIKEN

二維碼掃一掃

【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】 廣州清華科技園創新基地番禺石樓鎮創啟路63號二期2幢101-3室
【企業文化】

美國在肺癌治療上的花費超過120億美元。然而，肺癌的存活率不容樂觀，由于疾病極易轉移到整個身體，有80%的患者在診斷后5年之內死亡。
為了獲得轉移性，癌細胞會覆蓋一般保持細胞根植在它們各自位置的細胞器。癌癥可以迂回地打開和關閉細胞膜上突起的分子錨(稱為附著斑復合物)，為遷移準備細胞。這使得癌細胞開始經過血流遍歷體內，在新的器官駐留下來。
除了不同的癌癥能控制這些錨之外，大約五分之一的肺癌病例缺失一個抗癌基因，稱為LKB1(又名STK11)。缺失LKB1的癌癥通常是侵襲性的，可在體內迅速蔓延。然而，沒有知道LKB1和粘附斑之間是如何關聯的。
現在，索爾克研究小組發現了這個關聯，并發現了一個新的治療靶點：一個鮮為人知的基因，稱為DIXDC1。研究人員發現，DIXDC1接受來自LKB1的指令，轉到粘著斑，并改變它們的數量和大小。
當DIXDC1被“打開”，半打左右的粘著斑變大并具有粘性，將細胞錨定在它們的位置。當DIXDC1被阻斷或滅活時，粘著斑變小和量大，導致數百只小“手”向前拉動細胞，以響應細胞外的線索。轉移的傾向增加，有助于癌細胞從肺部逃跑，可讓腫瘤細胞存活下來，經過血液并停留在體內各處的器官。
本研究*作者、博士研究生Jonathan Goodwin稱：“LKB1和DIXDC1之間的交流可引起細胞內的一種‘鎖定(stay-put)’信號。人們了解較少的DIXDC1，在癌癥和轉移中原來是被抑制的。”
Shaw和同事在新的研究中發現，腫瘤有兩種方法來關閉這個“鎖定”信號。一是通過直接抑制DIXDC1。另一種方法是通過刪除LKB1，然后不再給DIXDC1發信號轉到粘著斑錨定細胞。鑒于此，科學家們想知道，是否復活DIXDC1就能停止癌癥的轉移。他們獲取了轉移細胞，這些細胞具有低水平的DIXDC1，并在細胞中過度表達這個基因。DIXDC1的加入，確實在體內和體外削弱了這些細胞的轉移能力。
Goodwin稱：“這非常非常的奇怪，這個基因會如此強大。在這項研究開始時，我們也不知道DIXDC1會參與轉移。LKB1會影響許多蛋白質;單*個基因控制如此多的表型，是我們沒有預料到的。”
現在，對具有LKB1或DIXDC1改變的癌癥，還沒有特定的治療方法，但是具有這些基因缺失的癌癥，可以通過靶定粘著斑的癌癥藥物得以治療。

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.