斑點(diǎn)熱立克次體IgG ELISA檢測(cè)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(cè)人血清中的斑點(diǎn)熱立克次體IgG抗體

產(chǎn)品規(guī)格：96T/盒

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斑點(diǎn)熱立克次體IgG ELISA檢測(cè)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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研究人員構(gòu)建了脂肪細(xì)胞缺乏ALK7，但是其他細(xì)胞都能夠正常產(chǎn)生ALK7的小鼠。研究人員發(fā)現(xiàn)，缺乏ALK7受體的脂肪細(xì)胞對(duì)腎上腺素和去甲腎上腺素信號(hào)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(guān)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(duì)“戰(zhàn)或逃”激素的必需應(yīng)答。
這些激素通常刺激脂肪的分解，但是當(dāng)營(yíng)養(yǎng)物質(zhì)很豐富時(shí)，脂肪細(xì)胞就會(huì)對(duì)這個(gè)信號(hào)產(chǎn)生抗性，從而儲(chǔ)存脂肪。這一機(jī)制在食物供應(yīng)豐富時(shí)轉(zhuǎn)變?yōu)橛欣谀芰績(jī)?chǔ)存，從而提高饑餓時(shí)的生存率。在工業(yè)化國(guó)家，食物經(jīng)常供應(yīng)不斷，這種阻力可能會(huì)導(dǎo)致體內(nèi)脂肪不健康的增加，進(jìn)而導(dǎo)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(méi)有已知的ALK7抑制劑，但研究人員利用小鼠生成ALK7的一個(gè)特殊突變體，使得它通過(guò)化學(xué)物質(zhì)來(lái)抑制敏感，從而解決了上述的問(wèn)題。這有可能實(shí)現(xiàn)作者能夠在任何時(shí)間阻斷其它正常成年動(dòng)物的受體。
“使用這種方法，我們可以通過(guò)化學(xué)物質(zhì)的簡(jiǎn)單調(diào)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(yù)防成年動(dòng)物的肥胖，”神經(jīng)科學(xué)系和這項(xiàng)研究的*作者 Tingqing Guo說(shuō)。
研究人員還發(fā)現(xiàn)，ALK7受體在人類(lèi)的脂肪細(xì)胞中的工作方式與小鼠類(lèi)似。
“總的來(lái)說(shuō)，這些結(jié)果表明，ALK7受體阻滯劑可能代表了一種防止人類(lèi)肥胖的策略，” 神經(jīng)科學(xué)系和這項(xiàng)研究的主要作者卡洛斯·伊瓦涅斯說(shuō)。
細(xì)胞突破正常組織界限進(jìn)入其他組織和器官，這是許多正常生理過(guò)程的重要一步，包括胚胎發(fā)育、傷口復(fù)原和新血管的形成。但是有時(shí)這個(gè)過(guò)程會(huì)出錯(cuò)。例如在轉(zhuǎn)移性癌癥中，指的是癌細(xì)胞從它們的源頭那里開(kāi)始無(wú)限擴(kuò)散，并在身體的其他部位形成腫瘤。
杜克大學(xué)的生物學(xué)副教授大衛(wèi)·舍伍德的一個(gè)團(tuán)隊(duì)采用1毫米長(zhǎng)的秀麗隱桿線蟲(chóng)(C. elegans.)，研究正常發(fā)育及癌癥中的調(diào)控細(xì)胞侵襲的分子機(jī)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.