EIKEN肺炎鏈球菌抗原檢測卡

廣州健侖生物科技有限公司

主要用途：用于檢測尿標(biāo)本中的肺炎鏈球菌抗原，以支持肺炎鏈球菌感染的診斷。

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EIKEN肺炎鏈球菌抗原檢測卡

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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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研究人員使用CD8 + T細(xì)胞沒有任何1型干擾素受體的小鼠探索工作機(jī)制是如何運作的，以及缺乏1型干擾素的CD8 + T細(xì)胞是如何耗盡NK細(xì)胞的。如果沒有自然殺手的存在，盡管缺乏干擾素檢測，但T細(xì)胞依然會增多，成熟和發(fā)育。此外，瑞士蘇黎世聯(lián)邦理工學(xué)院的免疫生物學(xué)家發(fā)現(xiàn)，這些無需傳感器的T細(xì)胞逐漸形成其表面的“識別標(biāo)簽”，一旦與NK細(xì)胞接觸，就會引發(fā)NK細(xì)胞的殺傷作用。因此，這些“應(yīng)激標(biāo)簽”的表達(dá)通過干擾素結(jié)合以及通過T細(xì)胞上的干擾素受體發(fā)出信號被抑制。如果由于受體的缺乏而阻止了信號的傳輸，那么細(xì)胞會大量表達(dá)這些應(yīng)激分子。
自身免疫性疾病的機(jī)制?
到目前為止，尚不清楚人類是否具有相同的機(jī)制。然而，人類免疫系統(tǒng)用來保護(hù)T細(xì)胞避免NK細(xì)胞攻擊的基本過程很可能是類似的。在一方面，研究人員現(xiàn)在揭示應(yīng)激T細(xì)胞需要保護(hù)自己免受NK細(xì)胞攻擊的機(jī)制。另一方面，這項發(fā)現(xiàn)形成了新的假設(shè)。例如，可以想到的是，缺乏干擾素受體的T細(xì)胞活化顯示出它們?yōu)?ldquo;應(yīng)激的”，并因此殺死了。自身免疫反應(yīng)性T細(xì)胞的活化過程中可能會出現(xiàn)這樣的情況，例如，它通常發(fā)生在不存在高濃度的1型干擾素。Oxenius和她的團(tuán)隊有很濃厚的興趣將在未來幾年內(nèi)測試這些令人興奮的假設(shè)。
加州大學(xué)圣地亞哥分校的生物學(xué)家發(fā)現(xiàn)能夠使動物細(xì)胞產(chǎn)生核糖體的化學(xué)系統(tǒng)中的‘未知環(huán)節(jié)’——每個細(xì)胞中含有數(shù)千蛋白‘工廠’加工所有建立組織和維持生命所必須的蛋白。他們的發(fā)現(xiàn)不僅強迫分子生物學(xué)基礎(chǔ)教科書的修訂，而且也為科學(xué)家提供較好的理解如何限制自由的細(xì)胞生長，如癌癥，也許通過控制核糖體的輸出來調(diào)節(jié)。這一研究發(fā)現(xiàn)發(fā)表在6月23日的《Genes & Development》期刊上。核糖體對于品種多樣蛋白的產(chǎn)生具有重要責(zé)任;包括酶;結(jié)構(gòu)分子如毛發(fā)、皮膚和骨骼;激素類如胰島素;以及我們免疫系統(tǒng)的組分如抗體。視為生命zui重要的分子機(jī)制，核糖體已被科學(xué)家廣泛研究(如，2009年的化學(xué)諾貝爾獎就頒發(fā)給核糖體結(jié)構(gòu)和功能的研究)。但是直到現(xiàn)在研究人員并沒有*了解用于組成核糖體的蛋白質(zhì)是如何自我產(chǎn)生的全部細(xì)節(jié)。
在多細(xì)胞動物中，如人類，核糖體由大約80種不同蛋白組成的(人類有79種，而其他動物有一些數(shù)量差異)與四種不同的RNA分子一樣。1969年，科學(xué)家們發(fā)現(xiàn)核糖體RNAs的合成是由專門的系統(tǒng)利用兩種酶：RNA聚合酶 I 和RNA聚合酶III執(zhí)行的。但是直到現(xiàn)在，科學(xué)家們?nèi)匀徊淮_定是否有一個互補系統(tǒng)也負(fù)責(zé)為裝配成核糖體的80種蛋白的生產(chǎn)。
“我們發(fā)現(xiàn)核糖體蛋白的合成經(jīng)過一種新奇的調(diào)節(jié)系統(tǒng)與RNA聚合酶II和一種稱為TRF2的因子，” Kadonaga 說。“對于多數(shù)蛋白質(zhì)的產(chǎn)生，RNA聚合酶II的功能與稱為TBP的因子，但對于核糖體蛋白質(zhì)的合成，它使用TRF2。”
美國芝加哥ICE/endO 2014大會發(fā)布的一項研究報告顯示，環(huán)境溫度能夠影響人體棕色脂肪的生成：涼爽環(huán)境會刺激生長，溫暖情況則起反作用。

Researchers using mice that did not have any Type 1 interferon receptor on CD8 + T cells explored how the working mechanism works and how NK cells are depleted by CD8 + T cells lacking type 1 interferon. Without the existence of a natural killer, T-cells will continue to proliferate, mature, and develop despite the lack of interferon testing. In addition, immune biologists at the Federal Institute of Technology in Zurich, Switzerland, found that these sensorless T cells evolved to form "labels" on their surface that, when contacted with NK cells, elicited NK cell killing. Thus, the expression of these "stress tags" is inhibited by interferon binding as well as signaling by interferon receptors on T cells. If signaling is blocked because of lack of receptors, the cells express large quantities of these stressors.
Mechanisms of autoimmune diseases?
So far, it is unclear whether human beings have the same mechanism. However, the basic process that the human immune system uses to protect T cells from NK cell challenge is likely to be similar. On the one hand, researchers now reveal that stressed T cells need a mechanism to protect themselves from attack by NK cells. On the other hand, this finding has led to new assumptions. For example, it is conceivable that T cell activation, which lacks interferon receptors, shows that they are "stressed" and therefore killed. This may occur during the activation of autoimmune reactive T cells, for example, it typically occurs in the absence of high concentrations of type 1 interferons. Oxenius and her team are very interested in testing these exciting assumptions in the coming years.
Biologists at the University of California, San Diego discovered the 'unknown' part of the chemical system that produces ribosomes in animal cells - thousands of proteins in each cell. The 'factory' processes all the proteins necessary to build and sustain life. Their findings not only force the revision of basic textbooks in molecular biology, but also provide scientists with a better understanding of how to limit free cell growth, such as cancer, perhaps by controlling ribosomal output. The study was published in the June 23 issue of Genes & Development. Ribosomes have an important responsibility for the production of a diverse range of proteins; enzymes; structural molecules such as hair, skin and bone; hormones such as insulin; and components of our immune system such as antibodies. Considered the most important molecular mechanism of life, ribosomes have been extensively studied by scientists (eg, the 2009 Nobel Prize in Chemistry for the study of ribosomal structure and function). But until now researchers did not fully understand all the details of how the proteins used to make ribosomes are produced by themselves.
In multicellular animals, such as humans, the ribosome consists of about 80 different proteins (79 in humans and some in other animals), like the four different RNA molecules. In 1969, scientists found that the synthesis of ribosomal RNAs was performed by specialized systems using two enzymes, RNA polymerase I and RNA polymerase III. But until now, scientists are still not sure if there is a complementary system that is responsible for the production of 80 proteins assembled into ribosomes.
"We found that the synthesis of ribosomal proteins goes through a novel regulatory system with RNA polymerase II and a factor called TRF2," Kadonaga said. "For most protein production, RNA polymerase II functions with a factor called TBP, but for ribosomal protein synthesis, it uses TRF2."
A study released by ICE / endO 2014 in Chicago shows that ambient temperature can affect the body's production of brown fat: cool environment stimulates growth and warm conditions are counter-productive.