落基山斑疹傷寒立克次體IgG ELISA試劑盒

Rickettsia rickettsii IgG ELISA Kit

廣州健侖生物科技有限公司

主要用途：用于檢測人血清中的落基山斑疹傷寒立克次體IgG抗體

產品規(guī)格：96人份/盒

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落基山斑疹傷寒立克次體IgG 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號二期2幢101-3室
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人體的另一個謎題已經被科學家解開了，科學家已經確定了一個在人類發(fā)育工作中*的分子馬達。他們還正確的指出，與該馬達相關的基因突變?yōu)槭裁磿l(fā)各種各樣的人類疾病。
英國布里斯托爾大學的研究人員已經確定了人類版本的分子馬達組成，它被稱為“胞質動力蛋白-2”，這對于正常的人類發(fā)育有著至關重要的作用。動力蛋白2指引分子進入纖毛以及控制其沿著纖毛運動。
纖毛是一種細長突起，幾乎充當了所有人體細胞的觸須，它們在傳感信號指導細胞功能中具有很重要的作用。已知，纖毛功能失調會引發(fā)長期癱瘓和有時甚至危及生命的遺傳病。這會對多個系統(tǒng)產生影響，導致失明，耳聾，慢性呼吸道感染，腎疾病，心臟疾病，抗原抗體，肥胖和糖尿病。
這些人類疾病統(tǒng)稱為ciliopathies，其中許多這種疾病，包括年輕綜合征(Jeune Syndrome)，都與兒童的發(fā)育有關。在英國，每10萬個嬰兒中就有一個在出生時患有年輕綜合征——這是一種罕見的遺傳疾病，會影響孩子的軟骨和骨骼發(fā)育。
這項新的研究是由醫(yī)學研究委員會資助，并且發(fā)表于2014年9月9日的《Journal of Cell science》雜志上，*精確的解釋人類胞質動力蛋白-2馬達是如何工作的。這項新的成果可能有助于診斷，并且科學家希望他們能夠改變缺陷馬達的功能，有益于治療。
來自布里斯托爾大學的生物化學學院的戴維·斯蒂芬斯教授了這項研究。他說：“這個馬達新組分的發(fā)現(xiàn)，給我們提供了一個很好地機會，去了解缺乏動力蛋白-2是如何引發(fā)疾病的。”
在簡單的模型生物體(如綠藻)上完成工作，研究還表明，與年輕綜合征相關的兩個基因(WDR34和WDR60)是人類版本中這種馬達的必要組成部分。

Another mystery of the human body has been solved by scientists, who have identified a molecular motor that is indispensable in the work of human development. They also rightly pointed out why genetic mutations associated with the motor can trigger a wide range of human diseases.
Researchers at the University of Bristol in the United Kingdom have identified a human version of the molecular motor composition called "cytoplasmic dynein-2," which plays a crucial role in normal human development. Motokin 2 directs molecules into the cilia and controls their movement along the cilia.
Cilia is a slender process that acts almost as a whisker of all human cells and plays an important role in sensing signaling functions of cells. It is known that cilia dysfunction can cause long-term paralysis and sometimes life-threatening genetic diseases. This can affect multiple systems, resulting in blindness, deafness, chronic respiratory infections, kidney disease, heart disease, antigen-antibody, obesity and diabetes.
These human diseases are collectively referred to as ciliopathies, and many of these diseases, including the Jeune Syndrome, are related to children's development. In the UK, one out of every 100,000 infants is born with a young syndrome - a rare genetic disorder that affects the child's cartilage and bone development.
The new study, funded by the Medical Research Council and published in the September 9, 2014 issue of the Journal of Cell Sciences, for the first time accuray explains how the human cytoplasmic dynein-2 motor works. The new results may help diagnose, and scientists hope they will be able to change the function of the defective motor, beneficial treatment.
Professor David Stephens from the University of Bristol's School of Biochemistry led the study. "The discovery of new components in this motor provides us with a good opportunity to understand how the lack of dynamin-2 can trigger disease," he said.
Working on a simple model organism, such as green algae, studies have also shown that two genes associated with young syndromes (WDR34 and WDR60) are essential components of this motor in the human version.