沙门氏菌（L)多价抗原血清学鉴定

广州健仑生物科技有限公司

我司长期供应尼古丁（可替宁）检测试剂盒，违禁品检测试剂盒，单卡检测，3联卡到12联卡，可以自由组合，根据您的需求自由组合，*，性价比高，产品质量很好。

保存要求：除了有特殊说明，免疫检测产品应保存在2-8°C

产品规格：2ml/瓶

保质期：2年

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

利用快速玻片凝集和对流免疫电泳(CIE)鉴定流感嗜血杆菌

沙门氏菌（L)多价抗原血清学鉴定

沙门氏菌（L)多价抗原血清学鉴定

【沙门氏知识点】

沙门氏等在霍乱流行时分离到猪霍乱沙门氏菌，故定名为沙门氏菌属。沙门氏菌属有的专对人类致病，有的只对动物致病，也有对人和动物都致病。沙门氏菌病是指由各种类型沙门氏菌所引起的对人类、家畜以及野生不同形式的总称。感染沙门氏菌的人或带菌者的粪便污染食品，可使人发生食物中毒。据统计在世界各国的种类细菌性食物中毒中，沙门氏菌引起的食物中毒常列。我国内陆地区也以沙门氏菌为*。
沙门氏菌病的病原体。属肠杆菌科，革兰氏阴性肠道杆菌。已发现的近一千种（或菌株）。按其抗原成分，可分为甲、乙、丙、丁、戊等基本菌组。其中与人体疾病有关的主要有甲组的副伤寒甲杆菌，乙组的副伤寒乙杆菌和鼠伤寒杆菌，丙组的副伤寒丙杆菌和猪霍乱杆菌，丁组的伤寒杆菌和肠炎杆菌等。除伤寒杆菌、副伤寒甲杆菌和副伤寒乙杆菌引起人类的疾病外，大多数仅能目引起家畜、鼠类和禽类等动物的疾病，但有时也可污染人类的食物而引起食物中毒。
沙门氏菌在水中不易繁殖，但可生存2-3周，冰箱中可生存3-4个月，在自然环境的粪便中可存活1-2个月。沙门氏菌zui适繁殖温度为37℃，在20℃以上即能大量繁殖，因此，低温储存食品是一项重要预防措施。
沙门氏菌是一种常见的食源性致病菌。沙门氏菌鉴定的传统方法主要是根据形态学特征、培养特征、生理生化特征、抗原特征、噬菌体特征等。

我司还有很多种血清学诊断血清、血液检测、免疫检测产品、毒素检测、凝集检测、酶免检测、层析检测、免疫荧光检测产品，。

（ MOB：杨永汉）

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。

想了解更多的产品及服务请扫描下方二维码：

【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

休克时机体细胞内溶酶体增多，体积增大，吞噬体显著增加。溶酶体内的酶向组织内外释放，多在肝和肠系膜等处，引起细胞和组织自溶。因此，在休克时，测定淋巴液和血液中溶酶体酶的含量高低，可作为细胞损伤轻重度的定量指标。通常以酸性磷酸酶、β-葡萄糖醛酸酶与组织蛋白酶为指标。关于休克时溶酶体释放的机理，有人提出是由于H降低和三羧酸循环受阻。休克时缺血缺氧，引起细胞H值的下降(约H)，酸性水解酶活化，水解溶酶体膜，zui终导致溶酶体膜裂解，溶酶体释放，使细胞、组织自溶。肿瘤溶酶体与肿瘤的关系日益引起人们的关注，一般有以下几种观点：()致癌物质引起细胞分裂调节机能的障阻及染色体畸变，可能与溶酶体释放水解酶的作用有关；()某些影响溶酶体膜通透性的物质，如巴豆油，某些去垢剂、高压氧等，是促进致癌作用的辅助因子，也能引发细胞的异常分裂；()在核膜残缺的情况下，核膜对核的保护丧失，溶酶体可以溶解染色质，而引起细胞突变；()溶酶体代谢过程中的某些产物是肿瘤细胞增殖的物质基础；()致癌物质进入细胞。
During shock, lysosomes increased, the volume increased, and phagosome increased significantly. Lysosomal enzymes are released inside and outside the tissues, mostly in the liver and mesenteries, causing autolysis of cells and tissues. Therefore, during shock, the levels of lysosomal enzymes in lymph and blood can be measured and used as quantitative indicators of the severity of cell damage. Acid phosphatase, β-glucuronidase, and cathepsin are commonly used as indicators. The mechanism of lysosomal release during shock has been suggested to be due to a decrease in H and a block in the tricarboxylic acid cycle. Ischemia and hypoxia during shock cause a decrease in the H value of cells (about H), activation of acid hydrolyzing enzymes, hydrolysis of lysosomal membranes, eventually leading to lysosomal membrane breakdown, release of lysosomes, and autolysis of cells and tissues. The relationship between tumor lysosomes and tumors has increasingly attracted people's attention. There are generally the following viewpoints: () carcinogens cause cell division and regulation of functional barriers and chromosomal aberrations, may be related to the role of lysosomes to release hydrolytic enzymes; ( ) Some substances that affect the permeability of lysosomal membranes, such as croton oil, certain detergents, hyperbaric oxygen, etc., are cofactors that promote carcinogenesis and can also trigger abnormal cell division; () in nuclear membrane insufficiency In the case of nuclear membranes, the protection of the nucleus is lost, and lysosomes can dissolve chromatin and cause cell mutations; () Some of the products of lysosome metabolism are the material basis for the proliferation of tumor cells; () The entry of carcinogens cell

休克时机体细胞内溶酶体增多，体积增大，吞噬体显著增加。溶酶体内的酶向组织内外释放，多在肝和肠系膜等处，引起细胞和组织自溶。因此，在休克时，测定淋巴液和血液中溶酶体酶的含量高低，可作为细胞损伤轻重度的定量指标。通常以酸性磷酸酶、β-葡萄糖醛酸酶与组织蛋白酶为指标。关于休克时溶酶体释放的机理，有人提出是由于H降低和三羧酸循环受阻。休克时缺血缺氧，引起细胞H值的下降(约H)，酸性水解酶活化，水解溶酶体膜，zui终导致溶酶体膜裂解，溶酶体释放，使细胞、组织自溶。肿瘤溶酶体与肿瘤的关系日益引起人们的关注，一般有以下几种观点：()致癌物质引起细胞分裂调节机能的障阻及染色体畸变，可能与溶酶体释放水解酶的作用有关；()某些影响溶酶体膜通透性的物质，如巴豆油，某些去垢剂、高压氧等，是促进致癌作用的辅助因子，也能引发细胞的异常分裂；()在核膜残缺的情况下，核膜对核的保护丧失，溶酶体可以溶解染色质，而引起细胞突变；()溶酶体代谢过程中的某些产物是肿瘤细胞增殖的物质基础；()致癌物质进入细胞。
During shock, lysosomes increased, the volume increased, and phagosome increased significantly. Lysosomal enzymes are released inside and outside the tissues, mostly in the liver and mesenteries, causing autolysis of cells and tissues. Therefore, during shock, the levels of lysosomal enzymes in lymph and blood can be measured and used as quantitative indicators of the severity of cell damage. Acid phosphatase, β-glucuronidase, and cathepsin are commonly used as indicators. The mechanism of lysosomal release during shock has been suggested to be due to a decrease in H and a block in the tricarboxylic acid cycle. Ischemia and hypoxia during shock cause a decrease in the H value of cells (about H), activation of acid hydrolyzing enzymes, hydrolysis of lysosomal membranes, eventually leading to lysosomal membrane breakdown, release of lysosomes, and autolysis of cells and tissues. The relationship between tumor lysosomes and tumors has increasingly attracted people's attention. There are generally the following viewpoints: () carcinogens cause cell division and regulation of functional barriers and chromosomal aberrations, may be related to the role of lysosomes to release hydrolytic enzymes; ( ) Some substances that affect the permeability of lysosomal membranes, such as croton oil, certain detergents, hyperbaric oxygen, etc., are cofactors that promote carcinogenesis and can also trigger abnormal cell division; () in nuclear membrane insufficiency In the case of nuclear membranes, the protection of the nucleus is lost, and lysosomes can dissolve chromatin and cause cell mutations; () Some of the products of lysosome metabolism are the material basis for the proliferation of tumor cells; () The entry of carcinogens cell

休克时机体细胞内溶酶体增多，体积增大，吞噬体显著增加。溶酶体内的酶向组织内外释放，多在肝和肠系膜等处，引起细胞和组织自溶。因此，在休克时，测定淋巴液和血液中溶酶体酶的含量高低，可作为细胞损伤轻重度的定量指标。通常以酸性磷酸酶、β-葡萄糖醛酸酶与组织蛋白酶为指标。关于休克时溶酶体释放的机理，有人提出是由于H降低和三羧酸循环受阻。休克时缺血缺氧，引起细胞H值的下降(约H)，酸性水解酶活化，水解溶酶体膜，zui终导致溶酶体膜裂解，溶酶体释放，使细胞、组织自溶。肿瘤溶酶体与肿瘤的关系日益引起人们的关注，一般有以下几种观点：()致癌物质引起细胞分裂调节机能的障阻及染色体畸变，可能与溶酶体释放水解酶的作用有关；()某些影响溶酶体膜通透性的物质，如巴豆油，某些去垢剂、高压氧等，是促进致癌作用的辅助因子，也能引发细胞的异常分裂；()在核膜残缺的情况下，核膜对核的保护丧失，溶酶体可以溶解染色质，而引起细胞突变；()溶酶体代谢过程中的某些产物是肿瘤细胞增殖的物质基础；()致癌物质进入细胞。
During shock, lysosomes increased, the volume increased, and phagosome increased significantly. Lysosomal enzymes are released inside and outside the tissues, mostly in the liver and mesenteries, causing autolysis of cells and tissues. Therefore, during shock, the levels of lysosomal enzymes in lymph and blood can be measured and used as quantitative indicators of the severity of cell damage. Acid phosphatase, β-glucuronidase, and cathepsin are commonly used as indicators. The mechanism of lysosomal release during shock has been suggested to be due to a decrease in H and a block in the tricarboxylic acid cycle. Ischemia and hypoxia during shock cause a decrease in the H value of cells (about H), activation of acid hydrolyzing enzymes, hydrolysis of lysosomal membranes, eventually leading to lysosomal membrane breakdown, release of lysosomes, and autolysis of cells and tissues. The relationship between tumor lysosomes and tumors has increasingly attracted people's attention. There are generally the following viewpoints: () carcinogens cause cell division and regulation of functional barriers and chromosomal aberrations, may be related to the role of lysosomes to release hydrolytic enzymes; ( ) Some substances that affect the permeability of lysosomal membranes, such as croton oil, certain detergents, hyperbaric oxygen, etc., are cofactors that promote carcinogenesis and can also trigger abnormal cell division; () in nuclear membrane insufficiency In the case of nuclear membranes, the protection of the nucleus is lost, and lysosomes can dissolve chromatin and cause cell mutations; () Some of the products of lysosome metabolism are the material basis for the proliferation of tumor cells; () The entry of carcinogens cell

休克时机体细胞内溶酶体增多，体积增大，吞噬体显著增加。溶酶体内的酶向组织内外释放，多在肝和肠系膜等处，引起细胞和组织自溶。因此，在休克时，测定淋巴液和血液中溶酶体酶的含量高低，可作为细胞损伤轻重度的定量指标。通常以酸性磷酸酶、β-葡萄糖醛酸酶与组织蛋白酶为指标。关于休克时溶酶体释放的机理，有人提出是由于H降低和三羧酸循环受阻。休克时缺血缺氧，引起细胞H值的下降(约H)，酸性水解酶活化，水解溶酶体膜，zui终导致溶酶体膜裂解，溶酶体释放，使细胞、组织自溶。肿瘤溶酶体与肿瘤的关系日益引起人们的关注，一般有以下几种观点：()致癌物质引起细胞分裂调节机能的障阻及染色体畸变，可能与溶酶体释放水解酶的作用有关；()某些影响溶酶体膜通透性的物质，如巴豆油，某些去垢剂、高压氧等，是促进致癌作用的辅助因子，也能引发细胞的异常分裂；()在核膜残缺的情况下，核膜对核的保护丧失，溶酶体可以溶解染色质，而引起细胞突变；()溶酶体代谢过程中的某些产物是肿瘤细胞增殖的物质基础；()致癌物质进入细胞。
During shock, lysosomes increased, the volume increased, and phagosome increased significantly. Lysosomal enzymes are released inside and outside the tissues, mostly in the liver and mesenteries, causing autolysis of cells and tissues. Therefore, during shock, the levels of lysosomal enzymes in lymph and blood can be measured and used as quantitative indicators of the severity of cell damage. Acid phosphatase, β-glucuronidase, and cathepsin are commonly used as indicators. The mechanism of lysosomal release during shock has been suggested to be due to a decrease in H and a block in the tricarboxylic acid cycle. Ischemia and hypoxia during shock cause a decrease in the H value of cells (about H), activation of acid hydrolyzing enzymes, hydrolysis of lysosomal membranes, eventually leading to lysosomal membrane breakdown, release of lysosomes, and autolysis of cells and tissues. The relationship between tumor lysosomes and tumors has increasingly attracted people's attention. There are generally the following viewpoints: () carcinogens cause cell division and regulation of functional barriers and chromosomal aberrations, may be related to the role of lysosomes to release hydrolytic enzymes; ( ) Some substances that affect the permeability of lysosomal membranes, such as croton oil, certain detergents, hyperbaric oxygen, etc., are cofactors that promote carcinogenesis and can also trigger abnormal cell division; () in nuclear membrane insufficiency In the case of nuclear membranes, the protection of the nucleus is lost, and lysosomes can dissolve chromatin and cause cell mutations; () Some of the products of lysosome metabolism are the material basis for the proliferation of tumor cells; () The entry of carcinogens cell