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果氏巴貝西蟲IgG免疫熒光試劑盒
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- 已獲點(diǎn)擊：
- 2024年11月5日
- 2025年5月5日
- 廣東廣州市
- 美國
- 79次
【產(chǎn)品簡(jiǎn)介】
【詳細(xì)說明】
果氏巴貝西蟲IgG免疫熒光試劑盒
Babesia microti IgG IFA Kit
廣州健侖生物科技有限公司
主要用途：用于檢測(cè)人血清中的果氏巴貝西蟲IgG抗體
產(chǎn)品規(guī)格：12 孔/張,10 張/盒
主要產(chǎn)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(xì)小病毒等病原微生物的 IFA、MIF、ELISA試劑。
果氏巴貝西蟲IgG免疫熒光試劑盒
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| JL-FL38 | parkeri立克次體IgG ELISA | R. parkeri IgG ELISA Kit |
| JL-FL39 | montanensis立克次體IgG ELISA | R. montanensis IgG ELISA Kit |
| JL-FL40 | EB病毒衣殼IgG免疫熒光玻片試劑盒 | EBV Viral Capsid IgG IFA Kit |
| JL-FL41 | EB病毒衣殼IgM免疫熒光玻片試劑盒 | EBV Viral Capsid IgM IFA Kit |
| JL-FL42 | EB病毒早期抗原IgG免疫熒光玻片試劑盒 | EBV Early Antigens IgG IFA Kit |
| JL-FL43 | 鉤端螺旋體IgG免疫熒光試劑盒 | Leptospira IgG IFA Kit |
| JL-FL44 | 鉤端螺旋體IgM免疫熒光試劑盒 | Leptospira IgM IFA Kit |
| JL-FL45 | 果氏巴貝西蟲免疫熒光玻片 | Babesia microti IFA Substrate slide |
| JL-FL46 | Babesia microti IgG IFA Kit | |
| JL-FL47 | 果氏巴貝西蟲IgM免疫熒光試劑盒 | Babesia microti IgM IFA Kit |
| JL-FL48 | 埃立克體IgG微量免疫熒光試劑盒 | Ehrlichia canis Canine IFA IgG Kit |
| JL-FL49 | 包柔氏螺旋體菌IgG免疫熒光試劑盒 | Borrelia IgG IFA Kit |
| JL-FL50 | 布魯氏菌IgG免疫熒光試劑盒 | Brucella IgG IFA Kit |
| JL-FL51 | 里氏新立克次體IgG免疫熒光試劑盒 | Neorickettsia risticii IgG IFA Kit |
| JL-FL52 | 弓形蟲IgG免疫熒光試劑盒（檢測(cè)貓） | Toxoplasma IFA Feline IgG Kit |
| JL-FL53 | 弓形蟲IgG免疫熒光試劑盒（檢測(cè)狗） | Toxoplasma IFA Canine IgG Kit |
二維碼掃一掃
【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
【企業(yè)文化】
然而，加州大學(xué)圣地亞哥分校醫(yī)學(xué)院和穆爾斯癌癥中心的研究人員發(fā)現(xiàn)，調(diào)節(jié)抗原抗體期間的干細(xì)胞活化的信號(hào)被癌細(xì)胞劫持，用來生產(chǎn)快速增長，更具侵略性的腫瘤。相關(guān)文章發(fā)表于2014年8月11日的《Developmental Cell》雜志上。
Cell子刊:癌細(xì)胞劫持抗原抗體干細(xì)胞活化信號(hào)來增殖的機(jī)制
抗原抗體與抗原抗體癌之間的早已知道，但抗原抗體和抗原抗體癌風(fēng)險(xiǎn)之間的關(guān)系卻很復(fù)雜。雖然有一個(gè)孩子會(huì)降低婦女在以后生活中患抗原抗體癌的風(fēng)險(xiǎn)，但是，每次抗原抗體后都會(huì)有一個(gè)抗原抗體癌的高侵襲性形式發(fā)展的短期風(fēng)險(xiǎn)增加。目前的研究表明，懷孕期間，影響干細(xì)胞行為的重要分子可能促進(jìn)了這些與抗原抗體相關(guān)的更具侵襲性抗原抗體癌的發(fā)展，研究人員計(jì)劃進(jìn)一步研究這一種可能性。
作者們很快指出，他們的研究結(jié)果不應(yīng)該作為一個(gè)抗原抗體的理由。這個(gè)信號(hào)通路被癌細(xì)胞劫持并不能作為一個(gè)觸發(fā)抗原抗體癌的原因。相反，它可能惡化或加速由其他因素引發(fā)的癌癥，如潛在突變或遺傳傾向。
“我們的研究并沒有指出，觸發(fā)癌癥的真正原因，而是解釋了，一旦癌癥啟動(dòng)會(huì)發(fā)生什么，”病理學(xué)特聘教授和研發(fā)副主席David A. Cheresh博士說。“這里有一個(gè)比喻：得癌癥，你首先要開始激活一個(gè)致癌基因，一個(gè)攜帶突變并能夠啟動(dòng)癌癥的基因。這個(gè)致癌基因相當(dāng)于汽車的點(diǎn)火開關(guān)，而被癌細(xì)胞利用的信號(hào)通路就像汽油。有了它，汽車才能啟動(dòng)，這也意味著如果致癌基因還沒有開始激活，那么癌癥就不會(huì)發(fā)展。”
在本研究中，研究人員集中于一個(gè)被稱為整合素的細(xì)胞表面受體蛋白家族，它們充當(dāng)關(guān)鍵的通信渠道，zui終在這家稱為β-3整合的一個(gè)成員的作用歸零。也被稱為CD61，它已經(jīng)與轉(zhuǎn)移和抗腫瘤的藥物有關(guān)。
作者指出，CD61可以作為顯示參與懷孕和癌癥期間抗原抗體發(fā)育的信號(hào)通路的良好標(biāo)志。它很容易被檢測(cè)到，并可以用來診斷和治療乳房癌病例。
However, researchers at the University of California San Diego School of Medicine and the Moores Cancer Center found that signals that regulate stem cell activation during antigen-antibody abstraction were hijacked by cancer cells to produce rapidly-growing, more aggressive tumors. Related article was published in Developmental Cell magazine on August 11, 2014.
Cell Subcategory: Mechanisms of Proliferation of Cancer Cells Hijacking Antigen-derived Antibody Stem Cells
The link between antigen and antigen-antibody cancers has long been known, but the relationship between antigen-antibody and antigen-antibody cancer risk is complex. Although having one child reduces the risk of developing anti-cancer antibodies in later life, there is an increased short-term risk of development of a highly aggressive form of antigen-antibody cancer after each antigen-antibody. Current research shows that important molecules that influence stem cell behavior during pregnancy may contribute to the development of more aggressive antigen-antibody cancers associated with antigen antibodies, and the researchers plan to investigate this possibility further.
The authors quickly pointed out that their findings should not be used as a reason for antigen-antibody. This signal pathway is hijacked by cancer cells and does not serve as a trigger for antigen-antibody cancer. On the contrary, it may exacerbate or accelerate cancer caused by other factors, such as potential mutations or genetic predisposition.
"Our research did not point out the real cause of triggering cancer but explained what would happen once the cancer started," said David A. Cheresh, Ph.D., professor of pathology and vice chairman of R & D. Here's a metaphor: In cancer, you first have to start activating an oncogene, a gene that carries the mutation and activates the cancer, an oncogene that's equivalent to a car's ignition switch, and the signaling pathways used by cancer cells are like petrol. With it, the car can start, which means that if the oncogenes have not yet started to activate, then the cancer will not develop. "
In this study, researchers focused on a family of cell-surface receptor proteins called integrins that served as key communication channels and eventually zeroed in the role of a member of the family called beta-3 integration. Also known as CD61, it has been associated with metastatic and anti-tumor drugs.
The authors note that CD61 can serve as a good indicator of the signaling pathways involved in antigen and antibody development during pregnancy and cancer. It is easily detectable and can be used to diagnose and treat cases of breast cancer.