凝集抗血清 A型、B型流感嗜血杆菌多群血清

A型、B型流感嗜血杆菌多群血清

广州健仑生物科技有限公司

本试剂盒主要用于对病菌细菌进行检测，利用快速玻片凝集检测技术，对大肠杆菌培养物进行血清学鉴定。本试剂盒仅供科研使用。

检测流感嗜血杆菌A型2ml诊断血清

检测流感嗜血杆菌A型2ml诊断血清

多型2ml流感嗜血杆菌检测血清价格

多型2ml流感嗜血杆菌检测血清价格

流感嗜血杆菌A/B型凝集抗血清Haemophilus

流感嗜血杆菌A/B型凝集抗血清Haemophilus

嗜血杆菌属血清群A型鉴定

嗜血杆菌属血清群A型鉴定

流感嗜血杆菌抗原试剂盒抗凝集血清

流感嗜血杆菌抗原试剂盒抗凝集血清

流感嗜血杆菌A/B/C型血清群

流感嗜血杆菌A/B/C型血清群

流感嗜血杆菌A/B/C3型凝集抗血清

流感嗜血杆菌A/B/C3型凝集抗血清

a型流感嗜血杆菌诊断血清

a型流感嗜血杆菌诊断血清

玻片凝集法鉴定流感嗜血杆菌

玻片凝集法鉴定流感嗜血杆菌

b型2ml流感嗜血杆菌快速玻片法检测血清

b型2ml流感嗜血杆菌快速玻片法检测血清

A型、B型流感嗜血杆菌多群血清

我司还提供其它进口或国产试剂盒：登革热、疟疾、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。

（ MOB：杨永汉） 

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【公司名称】 广州健仑生物科技有限公司
【市场部】    杨永汉

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【腾讯  】 
【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101-103

  免疫复合物型肾小球炎是由链球 菌可溶性抗原与抗体结合，沉积于肾小球基底膜，激活补体，吸 引中性粒细胞，释放各种酶类损伤肾小球所致。风湿免疫疾病是 由类风湿因子/抗“O”过高与免疫球蛋白IgG结合形成过剩的免疫 复合物，随着血液循环，沉积于关节骨膜、皮下组织等处引起风 湿、类风湿关节炎等，所以只有清除过剩的免疫复合物才是ZL 风湿免疫病的关键点。由于本病病人皮肤和肝脏中都能检测到IgA 沉积，提示为系统性疾病。由于在肾小球系膜区和毛细血管均可 有颗粒状IgA和C3沉积，提示其免疫复合物性发病机理。现时的研 究围绕着抗原通过粘膜的能力、粘膜屏障是否存在缺陷；IgA结构 是否有缺陷和免疫调节功能是否有缺陷等方面展开。早年的研究 曾提示本病所沉积的IgA可能是粘膜源性的。然而近年的研究使用 了高度专一性的技术，证实本病所沉积的是IgA1，主要是系统源 性的，主要由和淋巴系统所产生；粘膜源性的IgA2则主要见 于性肾小球硬化症中的IgA沉积中。在本病病人循环中也可见 到总IgA1和含IgA1的免疫复合物ZG，中产生IgA1的浆细胞 增多并形成多聚体为主。在本病的肾组织中可发现存在J链，故提 示沉积的IgA是多聚体；而分泌块则十分罕见。尽管如此，现有资 料尚不能Z终确定本病的IgA沉积物的来源。众多的抗原，包括多 种病毒和多种食物的抗原可在本病病人的系膜区中被检出，并常 常伴有IgA1沉积。这些抗原的抗体也属IgA1。由于这些抗体也可 存在于正常人的循环中，上述抗原并无专一性或特征性。
Immune complex type glomerulitis is caused by the binding of soluble antigens of Streptomyces with antibodies, deposition on the glomerular basement membrane, activation of complement, absorption of neutrophils, and release of various enzyme-damaged glomeruli. Rheumatism immune disease is caused by excess rheumatoid factor/anti-"O" combined with immunoglobulin IgG to form excess immune complexes. As the blood circulates, it accumulates in the joint periosteum, subcutaneous tissue, etc. causing rheumatism, rheumatoid arthritis, etc. Therefore, only the removal of excess immune complexes is the key point in the treatment of rheumatic immune diseases. Because of the detection of IgA deposition in the skin and liver of patients with this disease, it is indicated as a systemic disease. Because of the deposition of granular IgA and C3 in both the mesangial area and the capillaries, the pathogenesis of immune complexes is suggested. The current research centers on the ability of antigens to pass through the mucous membranes, whether there is a defect in the mucosal barrier, whether the IgA structure is defective and whether there is a defect in the immune regulatory function. Early studies have suggested that IgA deposited in this disease may be of mucosal origin. However, recent studies have used highly specific techniques to confirm that the disease is deposited in IgA1, mainly systemically, mainly produced by the bone marrow and lymphatic system; mucosally derived IgA2 is mainly found in liver-derived kidneys. IgA deposition in myosclerosis. In patients with this disease, the total IgA1 and immune complexes containing IgA1 are also seen to increase, and the plasma cells that produce IgA1 in the bone marrow increase and form multimers. The presence of the J chain in the renal tissue of this disease suggests that the deposited IgA is a multimer; secretory blocks are rare. Despite this, existing data cannot yet determine the source of the IgA sediments of this disease. Numerous antigens, including multiple viruses and multiple food antigens, can be detected in the mesangial area of ​​patients with this disease and are often accompanied by IgA1 deposition. Antibodies against these antigens also belong to IgA1. Since these antibodies can also exist in the circulation of normal people, the above antigens are not specific or characteristic.