EIKEN軍團菌檢測試劑盒

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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。

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EIKEN軍團菌檢測試劑盒

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【產(chǎn)品介紹】

EIKEN

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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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研究者Peter M. Glazer博士表示，長期以來我們一直知道含氧量低的腫瘤組織和較差的預后直接相關(guān)，但是含氧量低的腫瘤中往往也會發(fā)生某些特殊基因的沉默，這未必就是一件壞事;如今我們知道了缺氧狀態(tài)在誘發(fā)腫瘤惡化中的分子機制，下一步我們將通過更為深入的研究來解釋缺氧條件影響其它腫瘤抑制基因的分子機制。
白血病是一類造血干細胞惡性克隆性疾病，在兒科惡性腫瘤的發(fā)病率中居*位，它的死亡率在導致兒童及35歲以下成年人死亡的惡性腫瘤中排*。電離輻射是一個常見的致癌物，對白血病的發(fā)生非常關(guān)鍵。然而，其表觀學遺傳機制依然有很大一部分不為人知。
來自加拿大萊斯布里奇大學的研究團隊對小鼠胸腺中電離輻射(IR)引起的 micrornAome變化進行了研究，研究成果發(fā)布在6月刊的International Journal of Radiation Oncology*Biology*Physics上。
研究人員通過miRNA表達譜芯片分析(miRNA芯片項目由聯(lián)川生物承擔完成)鑒定小鼠胸腺中應(yīng)答輻射時差異表達的miRNAs，證實了在小鼠胸腺組織中IR能引起miR-27b差異表達，且呈劑量、時間和性別依賴的方式。在白血病細胞系CCL119和TIB152中，miR-27b表達被明顯抑制。有趣的是，ERα在上述兩個細胞系中過量表達，并與miR-27b表達呈負相關(guān)。
深入研究發(fā)現(xiàn)，β-雌二醇/ERα信號可能通過ERK1/2途徑，引起急性白血病細胞中miR-27b的表達下調(diào)，miR-27b可能通過結(jié)合細胞周期蛋白A2抑制細胞增殖，起到腫瘤抑制的作用。
此研究證實了IR能引起miR-27b差異表達，從而對白血病發(fā)生造成影響，為其表觀學遺傳機制提供了新見解，也為白血病的研究與治療提供了新思路。
美國懷俄明大學分子生物學系的副教授娜奧米·沃德，是zui近發(fā)表在美國國家科學院(PNAS)上的論文的資深作者。該研究探討了簡單的細菌細胞如何過渡到更為復雜的細胞，發(fā)展出植物，動物和人類。這項研究由美國國家科學基金會(NSF)資助。
Ekaterina Gottshall，分子和細胞生命科學博士計劃的研究生，這篇文章的*作者，實驗工作的主要貢獻者。其他的作者有分子生物學系副教授杰伊·加特林和沃德研究組的副研究員Corrine Seebart。

Dr. Peter M. Glazer, a researcher, said it has long been known that low oxygenated tumor tissues are directly linked to poor prognosis, but the silencing of specific genes often occurs in low oxygenated tumors, Is a bad thing; now we know the molecular mechanism of hypoxia in the induction of tumor progression, the next step we will be more in-depth study to explain the hypoxic conditions affect the molecular mechanisms of other tumor suppressor genes.
Leukemia, a hematopoietic malignant clonal disease of hematopoietic stem cells, ranks first in the incidence of pediatric malignancies and its mortality rate ranks first in malignancies leading to the death of children and adults under 35 years of age. Ionizing radiation is a common carcinogen that is crucial for the development of leukemia. However, a large part of its apparent genetic mechanism remains unknown.
A study team from the University of Lethbridge, Canada, studied the micrornAome changes induced by ionizing radiation (IR) in the mouse thymus, and the findings were published in the June issue of the International Journal of Radiation Oncology * Biology * Physics.
The researchers identified miRNAs that were differentially expressed during radiation response in the mouse thymus by miRNA profiling (miRNA microarray project was performed by UMC) and demonstrated that IR can cause differential expression of miR-27b in mouse thymus and that In a dose, time and gender-dependent manner. In the leukemia cell lines CCL119 and TIB152, miR-27b expression was significantly inhibited. Interestingly, ERα was overexpressed in both cell lines and negatively correlated with miR-27b expression.
In-depth study found that, β-estradiol / ERα signal may be through the ERK1 / 2 pathway, causing the expression of miR-27b in acute leukemia cells downregulation, miR-27b may inhibit cell proliferation by binding to cyclin A2, play a tumor suppressor effect.
This study confirmed that IR can cause the differential expression of miR-27b, which has an impact on the occurrence of leukemia, providing new insights into its apparent genetic mechanism, but also provides a new idea for the study and treatment of leukemia.
Naomi Ward, an associate professor of molecular biology at the University of Wyoming, is a senior author of recent papers published at the National Academy of Science (PNAS). The study explored how simple bacterial cells transition to more complex cells, developing plants, animals and humans. The study was funded by the National Science Foundation (NSF).
Ekaterina Gottshall, a graduate student in the Molecular and Cell Life Sciences Ph.D. program, is the lead author of this article and a major contributor to experimental work. Other authors include Jay Gatlin, associate professor of molecular biology and Corrine Seebart, associate research associate at Ward.