- 產品描述
斑點熱立克次體IgG ELISA檢測試劑盒
Spotted fever group 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斑點熱立克次體IgG抗體
產品規(guī)格:96T/盒
主要產品包括:包柔氏螺旋體菌、布魯氏菌、貝納特氏立克次體、土倫桿菌、鉤端螺旋體、新型立克次體、恙蟲病、立克次體、果氏巴貝西蟲、馬焦蟲、牛焦蟲、利什曼蟲、新包蟲、弓形蟲、貓流感病毒、貓冠狀病毒、貓皰疹病毒、犬瘟病毒、犬細小病毒等病原微生物的 IFA、MIF、ELISA試劑。
斑點熱立克次體IgG ELISA檢測試劑盒
我司還提供其它進口或國產試劑盒:登革熱、瘧疾、西尼羅河、立克次體、無形體、蜱蟲、恙蟲、利什曼原蟲、RK39、漢坦病毒、深林腦炎、流感、A鏈球菌、合胞病毒、腮病毒、乙腦、寨卡、黃熱病、基孔肯雅熱、克錐蟲病、違禁品濫用、肺炎球菌、軍團菌、化妝品檢測、食品安全檢測等試劑盒以及日本生研細菌分型診斷血清、德國SiFin診斷血清、丹麥SSI診斷血清等產品。
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JL-FL41 | EB病毒衣殼IgM免疫熒光玻片試劑盒 | EBV Viral Capsid IgM IFA Kit | 用于檢測人血清中的EB病毒衣殼IgM抗體 |
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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
【企業(yè)文化】
研究人員構建了脂肪細胞缺乏ALK7,但是其他細胞都能夠正常產生ALK7的小鼠。研究人員發(fā)現(xiàn),缺乏ALK7受體的脂肪細胞對腎上腺素和去甲腎上腺素信號更加敏感,這一發(fā)現(xiàn)解釋了,為何這些小鼠積累的脂肪更少,即使這些小鼠被喂食高脂肪飲食。腎上腺素和去甲腎上腺素是新陳代謝的關鍵因子。這些激素引發(fā)能量爆發(fā),并加快心臟速率以及血壓升高,這些都是對“戰(zhàn)或逃”激素的必需應答。
這些激素通常刺激脂肪的分解,但是當營養(yǎng)物質很豐富時,脂肪細胞就會對這個信號產生抗性,從而儲存脂肪。這一機制在食物供應豐富時轉變?yōu)橛欣谀芰績Υ妫瑥亩岣唣囸I時的生存率。在工業(yè)化國家,食物經常供應不斷,這種阻力可能會導致體內脂肪不健康的增加,進而導致肥胖癥。
然后,研究人員研究了,阻止ALK7是否能夠防止肥胖。目前,還沒有已知的ALK7抑制劑,但研究人員利用小鼠生成ALK7的一個特殊突變體,使得它通過化學物質來抑制敏感,從而解決了上述的問題。這有可能實現(xiàn)作者能夠在任何時間阻斷其它正常成年動物的受體。
“使用這種方法,我們可以通過化學物質的簡單調控,使得高脂肪飲食小鼠變瘦。這表明,ALK7受體的急性抑制可預防成年動物的肥胖,”神經科學系和這項研究的*作者 Tingqing Guo說。
研究人員還發(fā)現(xiàn),ALK7受體在人類的脂肪細胞中的工作方式與小鼠類似。
“總的來說,這些結果表明,ALK7受體阻滯劑可能代表了一種防止人類肥胖的策略,” 神經科學系和這項研究的主要作者卡洛斯·伊瓦涅斯說。
細胞突破正常組織界限進入其他組織和器官,這是許多正常生理過程的重要一步,包括胚胎發(fā)育、傷口復原和新血管的形成。但是有時這個過程會出錯。例如在轉移性癌癥中,指的是癌細胞從它們的源頭那里開始無限擴散,并在身體的其他部位形成腫瘤。
杜克大學的生物學副教授大衛(wèi)·舍伍德的一個團隊采用1毫米長的秀麗隱桿線蟲(C. elegans.),研究正常發(fā)育及癌癥中的調控細胞侵襲的分子機制。
The researchers constructed mice that lacked ALK7 in their fat cells, but all other cells were able to produce ALK7 normally. The researchers found that adipocytes lacking the ALK7 receptor are more sensitive to epinephrine and norepinephrine signaling, a finding that explains why these mice accumulate less fat, even though these mice are fed a high-fat diet. Epinephrine and norepinephrine are the key metabolic factors. These hormones trigger an energy burst and speed up the heart rate and blood pressure, which are all necessary responses to "war or escape" hormones.
These hormones usually stimulate the breakdown of fat, but when the nutrients are plentiful, fat cells resist the signal and store fat. This mechanism transforms into beneficial energy storage when food supplies are abundant, thereby increasing survival rates in the event of hunger. In industrialized countries, where food is regularly supplied, this resistance can lead to an unhealthy increase in body fat which can lead to obesity.
Then, the researchers studied whether preventing ALK7 could prevent obesity. There are no known inhibitors of ALK7, but researchers have used mice to generate a special mutant of ALK7 that makes it immune to chemicals by chemicals that solve the problem. This makes it possible for the author to block the receptors of other normal adult animals at any time.
"By using this method, we can make mice with high-fat diet thin by simple chemical regulation, suggesting that acute inhibition of ALK7 receptors may prevent obesity in adult animals," the Department of Neuroscience and the One author, Tingqing Guo said.
The researchers also found that ALK7 receptors work similarly in mice as fat cells in humans.
"Overall, these results suggest that ALK7 blockers may represent a strategy to prevent human obesity," said Carlos Ibanez, lead author of the Department of Neuroscience and the study.
Cells that break through normal tissue boundaries into other tissues and organs are a significant step in many normal physiological processes, including embryonic development, wound healing and neovascularization. But sometimes this process goes wrong. In metastatic cancers, for example, cancer cells start to proliferate infiniy from their source and form tumors in other parts of the body.
A team led by David Sherwood, an associate professor of biology at Duke University, used the 1-millimeter C. elegans to study the molecular mechanisms that regulate cell invasion in normal development and cancer.