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肺炎链球菌试剂盒

肺炎链球菌试剂盒

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EIKEN肺炎链球菌试剂盒 肺炎链球菌 需要了解更多产品可以咨询我们,本产品由广州健仑生物科技有限公司提供

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EIKEN肺炎链球菌试剂盒

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肺炎链球菌试剂盒

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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】

为了解决测量问题,Ardehali和他的同事开创了称为马赛克分析双标记(或MADAM)的新颖遗传方法,*次直接测量小鼠模型的心脏细胞分裂。他们发现心肌细胞分裂是有限的,终身对称的,虽然小鼠中这种明显的现象很少见,但在*个月的生活后显著减小。研究人员说,并没有任何的干细胞参与这一过程,以及心肌细胞的分裂每年仅限于不到1%。
研究人员说,子代的心肌细胞是这种罕见的细胞分裂的产品也能够分裂,这很不平常(以前没有研究发现过这种现象)。科学家发现,细胞分裂的速度并没有随着小鼠心肌梗塞诱导的一个修复反应而提高。
“这是显示心脏再生力量非常有限的zui有说服力的和直接的方式之一,” Ardehali说。 “这是一个非常令人兴奋的发现,因为我们希望利用这些知识zui终能够使心脏组织再生。其目的是确定参与心肌细胞对称分裂的分子途径,以及在疾病或受伤后使用它们来诱导再生补充心脏肌肉组织。”
人类的免疫系统是非常复杂的,它有着大量不同的细胞具有各种各样的功能,这确保侵入的微生物如病毒或细菌能够迅速地使之无害并保持整个机体的健康。
免疫系统还包括自然杀伤细胞(NK细胞),其识别并消除肿瘤或病毒感染的细胞。因此,NK细胞对抗人体自身的应激细胞以防止它们成为一个潜在的危险。然而,这种承担是有风险性的。其他的免疫细胞——特异性杀伤细胞,也被称为CD8 + T细胞,响应于病毒感染时不断地繁殖和变得成熟,也可以表现出应激症状,从而可能终结在NK细胞的名单上。
免疫生物学教授Annette Oxenius的研究小组现在发现,是什么阻止nk细胞杀死免疫系统的“来自于其他部门的同事”:健康CD8 +T细胞能够检测免疫信使物质1型干扰素,1型干扰素通过与这些免疫细胞的特定表面受体结合,从而隐藏它们的应激。换句话说,1型干扰素作为一种伪装斗篷使得免疫细胞不被NK细胞看见。如果T细胞缺乏1型干扰素的停泊位点,那么它们就会被NK细胞追杀直至灭绝。
使用感染两种模型病毒的小鼠,研究人员发现,如果动物的CD8 +t细胞缺乏这些干扰素的受体,不仅NK细胞消除感染病毒的细胞,而且免疫细胞也被认为采取了行动,从而削弱了抗病毒的免疫反应。

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.

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