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美国Alfa 盐酸克伦特罗、莱克多巴胺、沙丁胺醇（尿检）快速检测三联卡
广州健仑生物科技有限公司
我司长期供应瘦肉精三联检测卡，本产品用于快速检测动物尿样、组织和饲料中盐酸克伦特罗、莱克多巴胺、沙丁胺醇残留，整个检测过程只需要3-5分钟左右，具有操作简单，方便快捷，灵敏度高特异性强等特点。
瘦肉精检测试剂进口品牌：美国Alfa、美国US
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。
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瘦肉精检测试剂盒、瘦肉精检测试剂、瘦肉精检测卡、瘦肉精检测试纸、瘦肉精快速检测卡、瘦肉精三联检测卡、盐酸克伦特罗检测卡、莱克多巴胺检测卡、沙丁胺醇检测卡
【瘦肉精的危害】
“瘦肉精”进入动物体内后主要分布于肝脏。肌肉中含量较肝脏低很多。人摄入后在体内存留时间较长，其不良反应主要有：可引起心率加速，特别是原有心律失常的病例更易发生心脏反应，可见心室早搏、ST段与T波幅压低，还会发出肌肉震颤，引发四肢、面颈部骨骼肌震颤，尤其是交感神经功能亢进的病例更易发生。此外，还可引起代谢紊乱、血钾降低，引起心慌、肌肉震颤、头痛以及脸部潮红等。对心率失常、高血压、青光眼、糖尿病、甲状腺机能亢进等疾病的患者有较大危害。
美国Alfa 盐酸克伦特罗、莱克多巴胺、沙丁胺醇（尿检）快速检测三联卡
【产品简介】
本产品为克伦特罗-莱克多巴胺-沙丁胺醇三合一胶体金快速检测卡，用于定性检测猪、牛、羊尿液、组织和饲料中的瘦肉精残留，整个检测过程只需要3-5分钟左右。
【检测限】
克伦特罗3ng/ml（3ppb），莱克多巴胺3ng/ml（3ppb），沙丁胺醇3ng/ml（3ppb）
【产品组成】
克伦特罗-莱克多巴胺-沙丁胺醇三合一胶体金快速检测卡（40T/盒）
滴管（1个/袋）、干燥剂（1片/袋）
【样品处理】
用干燥、洁净的离心管或适当容器采集50ml左右尿液。如果不立即检测，待检样本在2-8℃存放，可保存24小时，注意避免腐坏造成失效或污染。出现阳性结果应按法定程序分瓶封装样品用于确证法检测。
【使用步骤】
1、测试前先完整阅读说明书，使用前将检测卡和待检样本溶液恢复至室温4～30℃。
2、从原包装袋中取出检测卡，打开后请在一个小时内尽快地使用。
3、将检测卡平放，用滴管吸取待检样品溶液，缓慢垂直滴加2-3滴于加样孔中，加样后开始计时。
4、结果应在3-5分钟时读取，其他时间判读无效，根据示意图判定结果。
【结果判断】
【注意事项】
1、检测卡请在保质期内一次性使用；
2、检测时避免阳光直射和电风扇直吹；
3、尽量不要触摸检测卡中央的白色膜面；
4、采样滴管不可混用，以免交叉污染；
5、如果待检样本出现沉淀或浑浊物，请离心后再检测；
6、试验遇到的任何问题，请与供应商。
【储存及有效期】
原包装应储存于4～40℃，阴凉避光干燥处，切勿冷冻；有效期24个月。有效期及批号见外包装。
美国Alfa
ε毒素是由B和D型产气荚膜梭菌所产生的致死性毒素，其可被小肠内的胰凝乳蛋白酶和胰蛋白酶充分激活，激活后的ε毒素毒性可增加至少1000倍。据报道，ε毒素是除破伤风毒素和肉毒毒素外，毒性违禁品的毒素。近年来，有报道指出D型产气荚膜梭菌曾被ETX（生物违禁品主义）列为可能使用的生物化学武器，也被美国疾病预防和控制中心列为B类生物制剂。
ε毒素是D型产气荚膜梭菌致病机理中zui重要的毒素，其易在畜禽中传播，多数患肠毒血症的经济动物均由该毒素所导致，患病动物病程极短，多数都来不及治疗而死亡，从而给养殖户带来经济损失。
ε毒素可感染所有年龄段的羊（羔羊和青年羊zui常感染），发病率为10%，但死亡率为100%。体内无该抗体的羔羊发生该病后通常2h内死亡，个别也会在12h内死亡，多数羔羊死亡时只有几分钟的抽搐，或甚至无症状。患该病幸存的羊可能出现角弓反张、里急后重、流涎、过敏等临床症状。
动物的大肠、小肠是D型产气荚膜梭菌和其毒素主要的繁殖和产生场所，各个肠段皆可吸收ε毒素，结肠是吸收ε毒素zui主要的部位。此外，高浓度葡萄糖、氯化钠和强酸性的肠道环境可能是反刍动物肠道吸收毒素的重要原因，其环境也可导致反刍动物肠毒血症的发生。
虽然ε毒素能引起肠道病变导致器官功能性病变和毒素的吸收，但临床上由D型产气荚膜梭菌引起的肠毒血症的这些病变并不经常发生。研究表明，ε毒素通过破坏紧密连接的粘膜、扩张细胞间隙、固有层退行性变化，致使体液积聚，肠道通透性增加。粘膜破坏，固有层退化影响了流体平衡，能通过旁细胞途径，因此，水，电解质和大分子被释放进入肠道，这也是肠毒血症发生后动物腹泻或肠道内水样的原因。目前对ε毒素与肠上皮细胞的结合机理尚不明确，毒素与黏膜其他部位的相互作用也是未知的。
有人曾将啮齿类动物应用于ε毒素对神经病理性损害模型的建立。小鼠经ε毒素攻毒后，其临床表现为脑水肿、肺水肿及急性肾小管坏死等症状。有人曾将该毒素用生里盐水稀释后注入小鼠的胃和结扎的肠段中，经比较后发现小肠和大肠均能很好的吸收该毒素，但在胃内的吸收不*；此研究还发现，小肠吸收该毒素的致死率要远低于结肠吸收该毒素的致死率。相关动物试验证实，ε毒素可使患病动物的肾脏、大脑及小肠的血管通透性升高，许多组织器官发生充血及水肿。
美国Alfa
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、食品安全、化妆品检测、药物滥用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
【】
【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室
The epsilon toxin, a lethal toxin produced by Clostridium perfringens types B and D, is fully activated by chymotrypsin and trypsin in the small intestine and increases the ε-toxin toxicity after activation by at least 1000-fold. It is reported that ε toxins are toxins of toxic contraband except tetanus toxin and botulinum toxin. In recent years, it has been reported that Clostridium perfringens type D has been listed as a possible biochemical weapon by ETX (Biological Contrabandism) and also as a Category B biological agent by the Centers for Disease Control and Prevention.
ε toxin is the most important toxin in the pathogenesis of Clostridium perfringens type D, which is easily transmitted in livestock and poultry. Most of the economically infected animals with enterotoxemia are caused by the toxin, and the disease duration of the sick animals is very short , Most of them are dead before treatment and thus bring economic losses to farmers.
The epsilon toxin can infect sheep of all ages (the most common infection in lambs and young sheep), with a 10% incidence but a 100% mortality rate. Lambs that do not have the antibody in vivo usually die within 2 hours after the onset of the disease, individually within 12 hours of death, and most lambs have only a few minutes of convulsions or even asymptomatic death. Sheep suffering from the disease may appear angle arch anti-Zhang, tenesmus, salivation, allergies and other clinical symptoms.
Animals of the large intestine, small intestine is Clostridium perfringens type D and its toxins the main breeding and production sites, each segment of the intestine can absorb ε toxins, the colon is to absorb the most important sites of ε toxins. In addition, high concentrations of glucose, sodium chloride and a strongly acidic enteric environment may be important contributors to the intestinal absorption of toxins in ruminants and may also contribute to the development of ruminant enterotoxemia.
Although ε toxin can cause intestinal lesions leading to organ dysfunction and toxin absorption, these lesions, which are clinically induced by Clostridium perfringens type D, do not occur frequently. Studies have shown that ε toxins destroy the tightly connected mucosa, dilate the interstitial space, and degenerative changes of the lamina propria, resulting in the accumulation of body fluids and the increase of intestinal permeability. Mucosal destruction, degradation of the lamina propria affects fluid balance and can bypass paracellular pathways. As a result, water, electrolytes, and macromolecules are released into the intestine, which is why animal diarrhea or intestinal water after enterotoxemia occurs. At present, the binding mechanism between ε toxin and intestinal epithelial cells is not yet clear, and the interaction between toxins and other parts of the mucosa is unknown.
Rodents have been used in the establishment of a model of neuropathic damage by ε-toxin. After mice were challenged with ε toxin, their clinical manifestations were cerebral edema, pulmonary edema and acute tubular necrosis. Some people once diluted with saline into the stomach of mice and ligation of the bowel, after comparison found that the small intestine and the large intestine can absorb the toxins, but not compley absorbed in the stomach; this study It has also been found that the lethality of the small intestine to absorb the toxin is much lower than the lethality of the colon to absorb the toxin. Relevant animal experiments confirmed that ε toxin can make the affected animal's kidneys, brain and small intestine vascular permeability increased, many tissues and organs of congestion and edema.
