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人類皰疹病毒6 IgG免疫熒光玻片試劑盒
Human Herpesvirus-6 IgG IFA 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人類皰疹病毒 6 IgG 抗體
產品規格：12 孔/張,10 張/盒
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人類皰疹病毒6 IgG免疫熒光玻片試劑盒
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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】 廣州清華科技園創新基地番禺石樓鎮創啟路63號二期2幢101-3室
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“氧化應激的增加zui終抑制了腫瘤的生長。我們發現，PPARγ的激活能夠殺死生長在培養皿中的癌細胞和小鼠的腫瘤。在此我們幾乎完整觀察了腫瘤生長抑制過程，” Kittler博士說。
發表于《細胞代謝》(Cell metabolism)的這項研究，建立在一個大機構的工作表明，當與正常細胞相比時，癌細胞中的代謝被改變了。代謝的改變可使癌細胞更容易受到治療藥物的攻擊，這使得這些藥物更好地靶向癌癥治療。這項研究還擴展了Steven Kliewer博士的早期觀察，他是一名分子生物學和藥理學教授，*發現噻唑烷二酮靶向PPARγ。
Kittler博士和他的團隊確定了激活PPARγ能夠引發葡萄糖和脂質代謝中的變化，導致活性氧(ROS)的水平升高。ROS是高反應性的含氧分子，當以高水平存在會損害細胞，這種現象被稱為氧化應激。ROS的增加zui終阻止癌細胞的分裂。
“腫瘤細胞的代謝異常往往會導致氧化應激增加，并且任何進一步的增加都能夠把癌細胞‘推’到懸崖上，” Kittler博士說。
研究結果表明，靶向PPARγ可能是肺癌和潛在的其他癌癥的有前途的、新的治療方法。研究人員看到，激活PPARγ可引起抗原抗體癌細胞中的相似分子變化。
“這是一個重要的發現，因為激活PPARγ的藥物包括FDA批準的抗糖尿病藥物，相對于化療來說，副作用沒有那么大。了解它們的作用機制，為我們提供了線索，用于挑選適合這種治療的腫瘤，結合這些藥物和抗癌藥物使得治療更加有效，以及指標來衡量腫瘤在患者中對這些藥物的反應，” Kittler說。
"Increased oxidative stress ultimay inhibits tumor growth and we found that activation of PPARγ killed tumors in both cancer cells and mice grown in Petri dishes and we have almost compley observed the tumor growth inhibition process here," Kittler Said the doctor.
The study, published in Cell metabolism, builds on the work of a large organization that shows that the metabolism in cancer cells is altered when compared to normal cells. Metabolic changes make cancer cells more susceptible to attack by therapeutic agents, which makes them better targeted to cancer therapy. The study also extends the early observation by Dr. Steven Kliewer, a professor of molecular biology and pharmacology, that for the first time, thiazolidinedione targets PPARγ.
Dr. Kittler and his team determined that activating PPARγ triggers changes in glucose and lipid metabolism, resulting in elevated levels of reactive oxygen species (ROS). ROS is a highly reactive oxygen-containing molecule that, when present at high levels, can damage cells, a phenomenon known as oxidative stress. The increase of ROS ultimay prevents the division of cancer cells.
"Metabolic abnormalities in tumor cells often result in increased oxidative stress and any further increase can push cancer cells to the cliff," says Dr. Kittler.
The results suggest that targeting PPARγ may be a promising new therapeutic approach for lung cancer and potentially other cancers. The researchers saw that activating PPARγ causes similar molecular changes in antigen-antibody cancer cells.
"This is an important finding as the drugs that activate PPARγ include FDA-approved antidiabetic drugs with less side effects than chemotherapy, and understanding their mechanism of action provides us with a clue to pick for this The treatment of the tumor, the combination of these and the anticancer drug make the treatment more effective, and the designation of a measure of how the tumor responds to the drug in the patient, "Kittler said.