- 产品描述
EIKEN肺炎链球菌快速检测试剂盒
广州健仑生物科技有限公司
主要用途:用于检测尿标本中的肺炎链球菌抗原,以支持肺炎链球菌感染的诊断。
产品规格:20T/盒
存储条件:2-30℃
EIKEN肺炎链球菌快速检测试剂盒
我司还提供其它进口或国产试剂盒:登革热、疟疾、西尼罗河、立克次体、无形体、蜱虫、恙虫、利什曼原虫、RK39、汉坦病毒、深林脑炎、流感、A链球菌、合胞病毒、腮病毒、乙脑、寨卡、黄热病、基孔肯雅热、克锥虫病、违禁品滥用、肺炎球菌、军团菌、化妆品检测、食品安全检测等试剂盒以及日本生研细菌分型诊断血清、德国SiFin诊断血清、丹麦SSI诊断血清等产品。
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【产品介绍】
货号 | 产品名称 | 产品描述 | 产品规格 | 保存条件 |
JL-ET01 | 免疫捕获诺如病毒检测试剂盒 | 用于检测粪便标本中的诺如病毒抗原,以支持诺如病毒感染的诊断。 | 20T/盒 | 2-30℃ |
JL-ET02 | 免疫捕获军团菌检测试剂盒 | 用于检测尿样中嗜肺军团菌血清型1抗原,以支持军团菌感染的诊断。 | 20T/盒 | 2-30℃ |
JL-ET03 | 免疫捕获肺炎链球菌检测试剂盒 | 用于检测尿标本中的肺炎链球菌抗原,以支持肺炎链球菌感染的诊断。 | 20T/盒 | 2-30℃ |
EIKEN
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【公司名称】 广州健仑生物科技有限公司
【】 杨永汉
【】
【腾讯 】 2042552662
【公司地址】 广州清华科技园创新基地番禺石楼镇创启路63号二期2幢101-3室
【企业文化】
几个主要的癌症相关的Rb突变和功能失调,以及细胞周期蛋白D一直被描述为促进癌症的一个致癌基因,因为它被认为是通过一种叫做磷酸化的过程,使Rb的抑癌功能失活。
道迪和他的同事们精心计算细胞周期进程期间的磷酸盐添加到Rb的数量。这多达14个,但科学家发现,细胞周期蛋白D只增加了一个单磷酸,且只有细胞周期进程的早期G1期的14个位点中的一个,基本上有14个不同亚型的Rb。单磷酸盐的作用是激活RB,不使它失活,这个认知已超过了20年。
研究人员说,这项研究从根本上改变了对G1期细胞周期调控和许多癌症相关的分子起源的理解。非常重要的是要明白一个基因通路的实际功能和中断它的后果,尤其是细胞周期蛋白D的多种药物抑制剂用于抗原抗体癌的临床试验测试这种情况下。
据认为,当器官一旦*形成,肾细胞就不能够繁殖了。但新的研究表明,肾脏在人类的整个生命中能够进行再生和自我修复。
美国斯坦福大学干细胞生物学和再生医学研究所,以及以色列赛克勒医学院的研究人员展示了,肾脏如何不断增长以及自我更新的惊人能力,这项发现抗原抗体了数十年来认为肾脏不能够再生的*理论,它也打开了通向修复肾脏甚至增长的新方法。
“这些基本理论对肾脏疾病和肾脏再生有直接的影响,”论文的主要作者Yuval Rinkevich博士说。这项研究发表于2014年5月15日的《Cell Reports》杂志上。
Cell Reports:肾脏的再生能力贯穿人的一生
长期以来,人们一直认为,肾细胞在器官一旦*形成的时候就丧失了再生的能力。这项新的研究表明,肾脏在人类的整个生命中都能够进行再生和自我修复。
“这项研究告诉我们,肾脏决不是一个静态的器官,” 本文的高级作者、赛克勒医学院的儿科系副教授本杰明·德克尔博士说。“令人难以置信,肾脏可以自己恢复活力,并继续生成专门的肾细胞。”
本文的另一个高级作者是病理学和发育生物学的教授和斯坦福研究所的主任欧文·韦斯曼博士。
Several major cancer-associated Rb mutations and dysfunctions, as well as cyclin D, have long been described as an oncogene that promotes cancer as it is thought to cause the tumor suppressor function of Rb through a process called phosphorylation live.
Dodi and his colleagues carefully calculated the amount of phosphate added to the Rb during the cell cycle progression. This is up to 14, but scientists have found that cyclin D only adds one monophosphate and that only one of 14 sites in the early G1 phase of the cell cycle process has essentially 14 different subtypes of Rb. The role of monophosphates is to activate RB without inactivating it, a fact that has been recognized for more than 20 years.
The researchers said the study radically changed the understanding of the molecular origins of G1-phase cell cycle regulation and many cancers. It is very important to understand the actual function of a gene pathway and to disrupt its consequences, especially in the case of a clinical trial of multiple drug inhibitors of cyclin D for antigen-antibody cancer.
It is believed that when the organ is fully formed, the kidney cells can not reproduce. But new research shows that the kidneys are able to regenerate and repair themselves throughout human life.
Researchers at the Stem Cell Biology and Regenerative Medicine Institute at Stanford University in the United States and at the Scythian Institute of Medicine in Israel demonstrated how the kidneys are constantly growing and the amazing ability to self-renew, the antigenic antibody that for decades has not been able to regenerate the kidneys The accepted theory, it also opened up new ways to repair the kidneys and even growth.
"These basic theories have a direct impact on kidney disease and kidney regeneration," said lead author Yuval Rinkevich, PhD. The study was published in Cell Reports on May 15, 2014.
Cell Reports: The ability of the kidneys to regenerate throughout one's entire life
It has long been believed that kidney cells lose their ability to regenerate once the organ is fully formed. This new study shows that the kidneys are able to regenerate and repair themselves throughout human life.
"This study ls us that the kidney is by no means a static organ," said Benjamin Dinkel, a senior author of the article and associate professor of pediatrics at Seckler School of Medicine. "It's incredible that the kidneys can regain their own vitality and continue to produce specialized kidney cells."
Another top author of this article is a professor of pathology and developmental biology and Dr. Irving Weissman, director of the Stanford Institute.