英國進口沙門氏G多價血清鑒定H抗原

廣州健侖生物科技有限公司

我司長期供應尼古?。商鎸帲z測試劑盒，違禁品檢測試劑盒，單卡檢測，3聯(lián)卡到12聯(lián)卡，可以自由組合，根據(jù)您的需求自由組合，*，性價比高，產品質量很好。

保存要求：除了有特殊說明，免疫檢測產品應保存在2-8°C

產品規(guī)格：2ml/瓶

保質期：2年

本試劑盒主要用于對病菌細菌進行檢測，利用快速玻片凝集檢測技術

利用快速玻片凝集和對流免疫電泳(CIE)鑒定流感嗜血桿菌

英國進口沙門氏G多價血清鑒定H抗原

2ml沙門氏菌H抗原(E)多價eh,enx,enzl5血清

沙門氏菌診斷血清H抗原 G（O多價O單價）

沙門氏菌診斷血清H抗原 G（O多價O單價）

【沙門氏知識點】

沙門氏等在霍亂流行時分離到豬霍亂沙門氏菌，故定名為沙門氏菌屬。沙門氏菌屬有的專對人類致病，有的只對動物致病，也有對人和動物都致病。沙門氏菌病是指由各種類型沙門氏菌所引起的對人類、家畜以及野生不同形式的總稱。感染沙門氏菌的人或帶菌者的糞便污染食品，可使人發(fā)生食物中毒。據(jù)統(tǒng)計在世界各國的種類細菌性食物中毒中，沙門氏菌引起的食物中毒常列。我國內陸地區(qū)也以沙門氏菌為*。
沙門氏菌病的病原體。屬腸桿菌科，革蘭氏陰性腸道桿菌。已發(fā)現(xiàn)的近一千種（或菌株）。按其抗原成分，可分為甲、乙、丙、丁、戊等基本菌組。其中與人體疾病有關的主要有甲組的副傷寒甲桿菌，乙組的副傷寒乙桿菌和鼠傷寒桿菌，丙組的副傷寒丙桿菌和豬霍亂桿菌，丁組的傷寒桿菌和腸炎桿菌等。除傷寒桿菌、副傷寒甲桿菌和副傷寒乙桿菌引起人類的疾病外，大多數(shù)僅能目引起家畜、鼠類和禽類等動物的疾病，但有時也可污染人類的食物而引起食物中毒。
沙門氏菌在水中不易繁殖，但可生存2-3周，冰箱中可生存3-4個月，在自然環(huán)境的糞便中可存活1-2個月。沙門氏菌zui適繁殖溫度為37℃，在20℃以上即能大量繁殖，因此，低溫儲存食品是一項重要預防措施。
沙門氏菌是一種常見的食源性致病菌。沙門氏菌鑒定的傳統(tǒng)方法主要是根據(jù)形態(tài)學特征、培養(yǎng)特征、生理生化特征、抗原特征、噬菌體特征等。

我司還有很多種血清學診斷血清、血液檢測、免疫檢測產品、毒素檢測、凝集檢測、酶免檢測、層析檢測、免疫熒光檢測產品，。

（ MOB：楊永漢）

我司還提供其它進口或國產試劑盒：登革熱、瘧疾、流感、A鏈球菌、合胞病毒、腮病毒、乙腦、寨卡、黃熱病、基孔肯雅熱、克錐蟲病、違禁品濫用、肺炎球菌、軍團菌、化妝品檢測、食品安全檢測等試劑盒以及日本生研細菌分型診斷血清、德國SiFin診斷血清、丹麥SSI診斷血清等產品。

想了解更多的產品及服務請掃描下方二維碼：

【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號二期2幢101-103

Due to gene defects, the body can lack a certain hydrolase in lysosomes, resulting in the degradation of the corresponding substances and accumulation in the lysosomes, resulting in cell metabolism barriers and the formation of lysosomal storage diseases. The main pathological manifestations are lysosomal overload in organs (liver, kidney, myocardium, skeletal muscles), ie excessive intake of cells or indigestible substances, or decreased activity of lysosomal enzymes, and the age of the organism. Growth, resulting in a large number of lysosomal accumulation in the cell caused by overload. At present, there are known more than one such disease, and there are many kinds of detectable diseases in the country (see entry: lysosomal storage disease). Among them, type II glycogen storage disease was first discovered. Due to a gene defect in the autosomal hepatocyte, the lack of α-glucosidase in the lysosome leads to the inability of glycogen to degrade to glucose, resulting in a large accumulation of glycogen in the liver and muscle. The disease mostly occurs in infants. Clinical manifestations of muscle weakness, heart enlargement, progressive heart failure, more than two years before death, it is also known as heart-type glycogen deposition disease. The cause of rheumatoid arthritis in rheumatoid arthritis is unclear, but the inflammatory changes in the joint periosteal tissue shown by this disease and the erosion of articular chondrocytes are thought to be due to the local release of lysosomes in cells. The reason may be due to a rheumatoid factor, such as anti-IgG, phagocytosed by macrophages, neutrophils, etc., to promote lysosomes escape. Some of these enzymes, such as collagenase, can erode cartilage and produce localized joint damage, while cartilage-digested metabolites, such as chondroitin sulfate, can also contribute to the production of kinins and participate in joint inflammation. During the shock process, the body's microcirculation is disordered, and tissue ischemia and hypoxia affect the energy supply system, making the membrane unstable, causing leakage of lysosomal enzymes, and causing cell and body damage.