巴爾通體IgG免疫熒光玻片試劑盒

Bartonella henselae 120-test IgG IFA kit

廣州健侖生物科技有限公司

主要用途：用于檢測(cè)人血清中的巴爾通體 IgG 抗體

產(chǎn)品規(guī)格：12 孔/張,10 張/盒

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巴爾通體IgG免疫熒光玻片試劑盒

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【公司名稱(chēng)】 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
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與此同時(shí)，該細(xì)胞可有助于自身免疫性疾病的研究。“這項(xiàng)技術(shù)可能提供了一些方法來(lái)創(chuàng)建模型系統(tǒng)來(lái)研究糖尿病的遺傳基礎(chǔ)，或者發(fā)現(xiàn)新的提高現(xiàn)有β細(xì)胞的治療方法，，” 費(fèi)雷爾說(shuō)道。梅爾頓說(shuō)，他的實(shí)驗(yàn)室已經(jīng)有來(lái)自于糖尿病患者(1型和2型，并且β細(xì)胞沒(méi)有被破壞)和健康對(duì)照組的iPS細(xì)胞系。他們從那些細(xì)胞系中生成β細(xì)胞，去尋找可能解釋不同形式的糖尿病如何發(fā)展的差異。他們還將篩選出化學(xué)物質(zhì)，其可以阻止甚至逆轉(zhuǎn)糖尿病對(duì)β細(xì)胞的傷害。
梅爾頓說(shuō)，他的兒子和女兒——現(xiàn)在23和27歲，對(duì)他的研究小組取得的進(jìn)展感到很高興，但感到意外。扭轉(zhuǎn)了父子的角色,他們溫柔地嘮叨他“開(kāi)始著手解決[免疫排斥反應(yīng)]的問(wèn)題。”
得克薩斯大學(xué)西南醫(yī)學(xué)中心的研究人員在一個(gè)代謝途徑中發(fā)現(xiàn)一個(gè)“阿喀琉斯之踵”，其對(duì)于阻止肺癌細(xì)胞生長(zhǎng)有著至關(guān)重要作用。
在心臟中的這個(gè)通路位于PPARγ(過(guò)氧化物酶體增殖物激活受體γ)，是調(diào)節(jié)正常細(xì)胞的葡萄糖和脂質(zhì)代謝的一個(gè)蛋白。通過(guò)抗糖尿病藥物激活肺癌細(xì)胞的PPARγ，它們可以阻止這些腫瘤細(xì)胞的分裂。
“我們發(fā)現(xiàn)，激活PPARγ會(huì)導(dǎo)致癌細(xì)胞中的主要代謝發(fā)生變化，損害了它們處理氧化應(yīng)激的能力，” UT西南尤金·麥克德莫特人類(lèi)生長(zhǎng)和發(fā)育中心，藥理學(xué)系，哈羅德·西蒙斯C.癌癥中心和塞西爾H.和艾達(dá)綠色抗原抗體生物學(xué)科學(xué)中心的副教授Ralf Kittler博士說(shuō)。

At the same time, the cells can contribute to the study of autoimmune diseases. "This technique may offer ways to create a model system to study the genetic basis of diabetes or find new ways to improve existing beta-cells," Ferrer said. Melton said his lab already has iPS cell lines from patients with diabetes (type 1 and 2, with no destruction of beta cells) and healthy controls. They generated beta cells from those cell lines looking for differences that might explain how different forms of diabetes develop. They will also screen out chemicals that can prevent or even reverse the damage that beta-cells do in diabetes.
Melton said his son and daughter, now 23 and 27, are happy about the progress made by his team but were surprised. Reversing the role of father and son, they nagged gently that he "started to solve the problem of [immune rejection]."
Researchers at the University of Texas Southwestern Medical Center found a "Achilles heel" in a metabolic pathway that plays a crucial role in stopping the growth of lung cancer cells.
This pathway in the heart is located in PPARγ (Peroxisome Proliferator Activated Receptor γ) and is a protein that regulates glucose and lipid metabolism in normal cells. By anti-diabetic drugs activate lung cancer cells PPARγ, they can prevent the division of these tumor cells.
"We found that activation of PPARγ leads to changes in the major metabolism of cancer cells, impairing their ability to handle oxidative stress," UT Southwest Eugene McDermott Human Growth and Development Center, Department of Pharmacology, Harold "Said Ralf Kittler, Ph.D., Simons C. Cancer Center and Associate Professor at the Cecil H. and Ida Green Antigen Antibody Biology Science Center.