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日本生研甲乙型流感快檢試劑盒

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【公司名稱】 廣州健侖生物科技有限公司
【市場部】    楊永漢

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【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號二期2幢101-103室

“隨著其它基因變化一起，失活的Pax5驅(qū)動正常血細(xì)胞變成白血病細(xì)胞，之前已經(jīng)報(bào)道過，”劉女士說。“然而我們*揭示重新復(fù)活Pax5能夠使細(xì)胞重新開始其正常發(fā)育并丟失那些類似癌癥的特性，有效地治療白血病。吸引我們的是只是回復(fù)Pax5就足夠使這些癌細(xì)胞恢復(fù)常態(tài)化，盡管其它基因是改變的。”
白血病中，未成熟白血細(xì)胞復(fù)制異常并在骨髓中累積，干擾正常血細(xì)胞的產(chǎn)生。
劉女士說在兒童B-ALL中Pax5常常是一個‘消失’的基因。“Pax5對于一種白血細(xì)胞——b細(xì)胞正常發(fā)育*的，”她說。“當(dāng)Pax5功能缺乏抵抗力時，發(fā)育中的B細(xì)胞陷入一種不成熟狀態(tài)并且變成癌性的。我們證明恢復(fù)Pax5功能，即使是在已經(jīng)發(fā)生癌病的細(xì)胞中，移除這個‘阻塞’，使得細(xì)胞發(fā)育成正常白血細(xì)胞。”
Dickins博士說這項(xiàng)研究揭示了Pax5的功能，是約100種已知‘抑制’人類腫瘤的基因之一。“當(dāng)這些腫瘤抑制基因通過改變DNA而被失活時，腫瘤開始發(fā)育，”Dickins博士說。
“這項(xiàng)工作揭示如何鈍化腫瘤抑制基因Pax5促成B-ALL 發(fā)育以及白血病細(xì)胞如何變成‘熱愛’低Pax5水平以繼續(xù)激增?？v使B-ALL 細(xì)胞有多種基因突變，只是簡單的復(fù)活Pax5引起腫瘤細(xì)胞恢復(fù)正常發(fā)育并失去它們的癌變性質(zhì)。”

"As other genetic changes, inactivated Pax5 drives normal blood cells to become leukemic cells, as previously reported," Ms. Liu said. "However, for the first time, we have shown that resuscitation of Pax5 allows cells to restart their normal development and lose those cancers-like properties that effectively treat leukemias, and it is enough to appeal to Pax5 that these cells are restored to normalization, although other genes are changed."
In leukemia, immature white blood cells replicate abnormally and accumulate in the bone marrow, interfering with the production of normal blood cells.
Ms. Liu said Pax5 is often a 'vanishing' gene in children with B-ALL. "Pax5 is essential for the normal development of a white blood cell-b cell," she said. "When Pax5 function lacks resistance, developing B cells plunge into an immature state and become cancerous.We show that restoring Pax5 function, even in cells where cancer has already occurred, removes this 'obstruction' , Making the cells develop into normal white blood cells. "
Dr. Dickins said the study revealed the function of Pax5 and is one of about 100 genes known to 'suppress' human tumors. "Tumors begin to develop when these tumor suppressor genes are inactivated by changing DNA," says Dr. Dickins.
"This work revealed how to passivate the tumor suppressor gene Pax5 to promote B-ALL development and how leukemic cells turn into 'loving' low Pax5 levels to continue the surge even though B-ALL cells have multiple genetic mutations that simply cause Pax5 to resuscitate Tumor cells resume normal development and lose their cancerous properties. "