肺炎鏈球菌試劑盒

EIKEN肺炎鏈球菌試劑盒

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。

產(chǎn)品規(guī)格：20T/盒

存儲(chǔ)條件：2-30℃

EIKEN肺炎鏈球菌試劑盒

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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(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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為了解決測量問題，Ardehali和他的同事開創(chuàng)了稱為馬賽克分析雙標(biāo)記(或MADAM)的新穎遺傳方法，*次直接測量小鼠模型的心臟細(xì)胞分裂。他們發(fā)現(xiàn)心肌細(xì)胞分裂是有限的，終身對(duì)稱的，雖然小鼠中這種明顯的現(xiàn)象很少見，但在*個(gè)月的生活后顯著減小。研究人員說，并沒有任何的干細(xì)胞參與這一過程，以及心肌細(xì)胞的分裂每年僅限于不到1%。
研究人員說，子代的心肌細(xì)胞是這種罕見的細(xì)胞分裂的產(chǎn)品也能夠分裂，這很不平常(以前沒有研究發(fā)現(xiàn)過這種現(xiàn)象)?？茖W(xué)家發(fā)現(xiàn)，細(xì)胞分裂的速度并沒有隨著小鼠心肌梗塞誘導(dǎo)的一個(gè)修復(fù)反應(yīng)而提高。
“這是顯示心臟再生力量非常有限的zui有說服力的和直接的方式之一，” Ardehali說。 “這是一個(gè)非常令人興奮的發(fā)現(xiàn)，因?yàn)槲覀兿Ｍ眠@些知識(shí)zui終能夠使心臟組織再生。其目的是確定參與心肌細(xì)胞對(duì)稱分裂的分子途徑，以及在疾病或受傷后使用它們來誘導(dǎo)再生補(bǔ)充心臟肌肉組織。”
人類的免疫系統(tǒng)是非常復(fù)雜的，它有著大量不同的細(xì)胞具有各種各樣的功能，這確保侵入的微生物如病毒或細(xì)菌能夠迅速地使之無害并保持整個(gè)機(jī)體的健康。
免疫系統(tǒng)還包括自然殺傷細(xì)胞(NK細(xì)胞)，其識(shí)別并消除腫瘤或病毒感染的細(xì)胞。因此，NK細(xì)胞對(duì)抗人體自身的應(yīng)激細(xì)胞以防止它們成為一個(gè)潛在的危險(xiǎn)。然而，這種承擔(dān)是有風(fēng)險(xiǎn)性的。其他的免疫細(xì)胞——特異性殺傷細(xì)胞，也被稱為CD8 + T細(xì)胞，響應(yīng)于病毒感染時(shí)不斷地繁殖和變得成熟，也可以表現(xiàn)出應(yīng)激癥狀，從而可能終結(jié)在NK細(xì)胞的名單上。
免疫生物學(xué)教授Annette Oxenius的研究小組現(xiàn)在發(fā)現(xiàn)，是什么阻止nk細(xì)胞殺死免疫系統(tǒng)的“來自于其他部門的同事”：健康CD8 +T細(xì)胞能夠檢測免疫信使物質(zhì)1型干擾素，1型干擾素通過與這些免疫細(xì)胞的特定表面受體結(jié)合，從而隱藏它們的應(yīng)激。換句話說，1型干擾素作為一種偽裝斗篷使得免疫細(xì)胞不被NK細(xì)胞看見。如果T細(xì)胞缺乏1型干擾素的停泊位點(diǎn)，那么它們就會(huì)被NK細(xì)胞追殺直至滅絕。
使用感染兩種模型病毒的小鼠，研究人員發(fā)現(xiàn)，如果動(dòng)物的CD8 +t細(xì)胞缺乏這些干擾素的受體，不僅NK細(xì)胞消除感染病毒的細(xì)胞，而且免疫細(xì)胞也被認(rèn)為采取了行動(dòng)，從而削弱了抗病毒的免疫反應(yīng)。

In order to solve the measurement problem, Ardehali and his colleagues pioneered a novel genetic approach called mosaic analysis double labeling (or MADAM), the first direct measurement of cardiac cell division in mouse models. They found that cardiomyocyte division was limited and life-long symmetrical, although this notable phenomenon in mice was rare but significantly reduced after the first month of life. The researchers said that no stem cells involved in this process, and myocardial cell division is limited to less than 1% per year.
It is not uncommon for researchers to say that offspring of cardiomyocytes are the rare products of cell division that divide (this has not been done before). Scientists found that the rate of cell division did not increase with a repair response induced by myocardial infarction in mice.
"This is one of the most persuasive and direct ways to show that the power of heart regeneration is very limited," Ardehali said. "This is a very exciting finding because we hope to eventually use this knowledge to regenerate heart tissue and its purpose is to identify the molecular pathways involved in the symmetrical division of cardiomyocytes and their use in the event of illness or injury to induce regenerative heart replenishment Muscle tissue. "
The human immune system is very complex. It has a large number of different cells that have a variety of functions that ensure that invading microbes, such as viruses or bacteria, can quickly be rendered harmless and maintain the health of the entire body.
The immune system also includes natural killer cells (NK cells) that recognize and eliminate tumor or virus-infected cells. Therefore, NK cells fight the body's own stress cells to prevent them from becoming a potential danger. However, this commitment is risky. Other immune cell-specific killer cells, also known as CD8 + T cells, may also display stress symptoms in response to continued multiplication and maturation of the virus infection and may thus end up on the NK cell list .
Annette Oxenius' team of immunobiology professors now finds out what "colleagues from other departments" are preventing nk cells from killing the immune system: Healthy CD8 + T cells are able to detect immunocompetent substances Type 1 interferon, type 1 interferon By binding to specific surface receptors of these immune cells, their stress is hidden. In other words, type 1 interferons act as a camouflage cape so that immune cells are not seen by NK cells. If T cells lack type 1 interferon docking sites, they are killed by NK cells until they become extinct.
Using mice infected with both model viruses, the researchers found that if the animal's CD8 + T cells lacked these interferon receptors, not only did NK cells eliminate the virus-infected cells, but immune cells were also thought to have taken action that weakened Antiviral immune response.