A型,、B型流感嗜血桿菌多群血清

廣州健侖生物科技有限公司

本試劑盒主要用于對病菌細(xì)菌進(jìn)行檢測,，利用快速玻片凝集檢測技術(shù)，對大腸桿菌培養(yǎng)物進(jìn)行血清學(xué)鑒定,。本試劑盒僅供科研使用,。

檢測流感嗜血桿菌A型2ml診斷血清

檢測流感嗜血桿菌A型2ml診斷血清

多型2ml流感嗜血桿菌檢測血清價(jià)格

多型2ml流感嗜血桿菌檢測血清價(jià)格

流感嗜血桿菌A/B型凝集抗血清Haemophilus

流感嗜血桿菌A/B型凝集抗血清Haemophilus

嗜血桿菌屬血清群A型鑒定

嗜血桿菌屬血清群A型鑒定

流感嗜血桿菌抗原試劑盒抗凝集血清

流感嗜血桿菌抗原試劑盒抗凝集血清

流感嗜血桿菌A/B/C型血清群

流感嗜血桿菌A/B/C型血清群

流感嗜血桿菌A/B/C3型凝集抗血清

流感嗜血桿菌A/B/C3型凝集抗血清

a型流感嗜血桿菌診斷血清

a型流感嗜血桿菌診斷血清

玻片凝集法鑒定流感嗜血桿菌

玻片凝集法鑒定流感嗜血桿菌

b型2ml流感嗜血桿菌快速玻片法檢測血清

b型2ml流感嗜血桿菌快速玻片法檢測血清

A型、B型流感嗜血桿菌多群血清

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（ MOB：楊永漢） 

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【公司名稱】 廣州健侖生物科技有限公司
【市場部】    楊永漢

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【騰訊  】 
【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101-103

  免疫復(fù)合物型腎小球炎是由鏈球 菌可溶性抗原與抗體結(jié)合,，沉積于腎小球基底膜,，激活補(bǔ)體，吸 引中性粒細(xì)胞,，釋放各種酶類損傷腎小球所致,。風(fēng)濕免疫疾病是 由類風(fēng)濕因子/抗“O”過高與免疫球蛋白IgG結(jié)合形成過剩的免疫 復(fù)合物，隨著血液循環(huán),，沉積于關(guān)節(jié)骨膜,、皮下組織等處引起風(fēng) 濕,、類風(fēng)濕關(guān)節(jié)炎等，所以只有清除過剩的免疫復(fù)合物才是治療 風(fēng)濕免疫病的關(guān)鍵點(diǎn),。由于本病病人皮膚和肝臟中都能檢測到IgA 沉積，提示為系統(tǒng)性疾病,。由于在腎小球系膜區(qū)和毛細(xì)血管均可 有顆粒狀I(lǐng)gA和C3沉積,，提示其免疫復(fù)合物性發(fā)病機(jī)理。現(xiàn)時(shí)的研 究圍繞著抗原通過粘膜的能力,、粘膜屏障是否存在缺陷,；IgA結(jié)構(gòu) 是否有缺陷和免疫調(diào)節(jié)功能是否有缺陷等方面展開。早年的研究 曾提示本病所沉積的IgA可能是粘膜源性的,。然而近年的研究使用 了高度專一性的技術(shù),，證實(shí)本病所沉積的是IgA1，主要是系統(tǒng)源 性的,，主要由骨髓和淋巴系統(tǒng)所產(chǎn)生,；粘膜源性的IgA2則主要見 于肝源性腎小球硬化癥中的IgA沉積中。在本病病人循環(huán)中也可見 到總IgA1和含IgA1的免疫復(fù)合物增高,，骨髓中產(chǎn)生IgA1的漿細(xì)胞 增多并形成多聚體為主,。在本病的腎組織中可發(fā)現(xiàn)存在J鏈，故提 示沉積的IgA是多聚體,；而分泌塊則十分罕見,。盡管如此，現(xiàn)有資 料尚不能zui終確定本病的IgA沉積物的來源,。眾多的抗原,，包括多 種病毒和多種食物的抗原可在本病病人的系膜區(qū)中被檢出，并常 常伴有IgA1沉積,。這些抗原的抗體也屬IgA1,。由于這些抗體也可 存在于正常人的循環(huán)中，上述抗原并無專一性或特征性,。
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.