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瘦肉精β类胶体金检测卡(尿卡)

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产品型号美国Alfa

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美国Alfa 瘦肉精β类胶体金检测卡(尿卡)

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 瘦肉精β类胶体金检测卡(尿卡)

【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】

 

  1. 阴性(-):两条紫红色条带出现。表示样品中不含有瘦肉精或其浓度低于检测限。
  2. 阳性(+):检测T线无显色,则表示样品中瘦肉精浓度高于检测限。
  1. 无效:未出现质控C线,表明操作过程不正确或检测卡已失效。

【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 瘦肉精β类胶体金检测卡(尿卡)

ε毒素还可穿过血脑屏障在脑组织内蓄积,从而使脑组织中的血管通透性升高,由此造成外周血管水肿。所以,患肠毒血症的动物在病程末期通常表现出惊厥、角弓反张、濒死期挣扎等神经症状。目前虽有报道证实,A型和C型产气荚膜梭菌均可感染人类,并使人患肠道疾病,但这两个型的产气荚膜梭菌均不生产ε毒素,且至今仍未发现ε毒素使人和灵长类动物患病的病例。有人曾利用小动物的致死性试验得出该毒素对人的致死剂量约为100 ng/kg(静脉注射)。该毒素以口服或气溶胶方式对人的致死剂量主要受人体胃肠道、呼吸道与毒素的相互作用,而这方面的研究至今未见报道。
β毒素是B型和C型产气荚膜梭菌(Clostridium perfringens)所产生的重要的致病毒素,人们误食被该菌感染的食物后可导致食物中毒,导致胃和肠道炎症的发生,病情严重者甚至会出现创伤性气性坏疽。其临床表现为:腹痛、腹泻、违禁品及呕吐等,严重者可导致死亡(多为抵抗力弱的老年人和幼儿感染者)。
感染β毒素的动物主要为猪、牛、山羊、绵羊、兔、鸡等畜禽,肠毒血症和坏死性肠炎是被该毒素感染后的主要症状。此外,也有一些野生动物(如狐狸、貂等)感染产气荚膜梭菌β毒素的报道。虽然B型和C型产气荚膜梭菌的基因组上同时也携带转录其他毒素的基因,如α毒素和产气荚膜梭菌裂解素等,然而研究表明,β毒素是B型和C型菌株的主要致死性。
β毒素是一种致死性毒素,是一种成孔毒素,能裂解细胞,致死动物,可引起人和动物的坏死性肠炎,但其介导的损伤过程的分子机制目前尚未研究透彻。有人研究β毒素对小鼠的zui小致死量,通过不同剂量免疫小鼠发现,β毒素对豚鼠和小鼠的zui小致死量为2ng,半数致死量大约为1.9μg /kg。皮内注射zui小致死量的β毒素能造成豚鼠皮肤坏死等典型症状。毒素作用于小鼠皮肤能导致渗出和水肿,实验发现苯海拉明能抑制毒素对小鼠的渗出作用。
β毒素的感染发病还和机体在营养不良的状态下或食入含有胰蛋白酶抑制剂的食物时更容易受产气荚膜梭菌β毒素的侵袭。其原因是胰蛋白酶抑制剂会降阻碍蛋白酶对β毒素的降解作用,进而为坏死性肠炎的发生提共了有利条件。
此外,就该病的发病率而言,新生动物要高于成年动物。这是由于新生动物所摄取的初乳中含有抑制胰蛋白酶特性的成分,所以新生动物更容易感染该病。
在β毒素侵袭的病变部位中:空肠是其主要的病变场所,其病理变化主要表现为肠粘膜出血坏死、肠壁变薄,从而使得肠壁更容易破裂或穿孔;十二指肠基本不受其影响,这可能是由于十二指肠内的胰蛋白酶含量高,抑制了β毒素的活性。在发病肠段的微细血管中常发现有血栓的形成,镜检可见有出血、水肿及淋巴细胞浸润等病理变化。

美国Alfa 瘦肉精β类胶体金检测卡(尿卡)

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 also accumulates in the brain tissue through the blood-brain barrier, thereby increasing vascular permeability in brain tissue, thereby causing peripheral vascular edema. Therefore, animals with enterotoxemia often exhibit neurological symptoms such as convulsions, cornering bow reversed, and dying struggles at the end of the course of the disease. Although it has been reported that both Clostridium perfringens type A and C can infect humans and cause intestinal diseases, neither of these two types of Clostridium perfringens produce ε-toxin and so far There are still no cases of human toxins and primate diseases. Some people have used the lethal test of small animals to find that the lethal dose of this toxin to humans is about 100 ng / kg (iv). The lethal dose of the toxin to humans by oral or aerosol is mainly affected by the gastrointestinal tract, respiratory tract and toxins in the human body. However, studies on this toxin have not been reported so far.
β toxins are important toxins produced by Clostridium perfringens type B and C. People who ingest food contaminated with the bacteria can cause food poisoning that can lead to stomach and intestinal inflammation In severe cases, there may even be traumatic gas gangrene. The clinical manifestations are: abdominal pain, diarrhea, contraband and vomiting, severe cases can lead to death (mostly vulnerable elderly and young children infected).
Infected with β toxins mainly for pigs, cattle, goats, sheep, rabbits, chickens and other livestock and poultry, enterotoxemia and necrotic enteritis is the main symptoms after the toxin infection. In addition, some wild animals (such as foxes, minks, etc.) have also been reported to infect C. perfringens beta toxin. Although the genomes of Clostridium perfringens type B and C also carry genes that transcribe other toxins, such as alpha toxins and Clostridium perfringens, studies have shown that beta toxins are both type B and C The main lethal strain.
β toxin is a lethal toxin, which is a pore-forming toxin that can lyse cells and cause death in animals. It can cause necrotizing enterocolitis in humans and animals. However, the molecular mechanism of β-thaliana is not yet thoroughly studied. Some people to study the minimum lethal dose of β toxin in mice, mice were immunized by different doses of β toxin found in guinea pigs and mice the minimum lethal dose of 2ng, median lethal dose of about 1.9μg / kg. Intradermal injection of the smallest lethal dose of toxin can cause typical symptoms such as skin necrosis in guinea pigs. Toxins can cause exudation and edema on mouse skin. Diphenhydramine was found to inhibit the exudation of toxins in mice.
Infection with [beta] toxins is also more likely to be affected by C. perfringens beta toxin in the body as well as in the body under conditions of malnutrition or when fed in foods containing trypsin inhibitors. The reason is that trypsin inhibitor will reduce the protease degradation of β-toxin, which in turn provides a favorable condition for the occurrence of necrotic enteritis.
In addition, as far as the incidence of the disease is concerned, newborn animals are higher than adult animals. This is because neonatal animals intake of colostrum contains trypsin-inhibiting ingredients, so new animals are more susceptible to the disease.
In the invasion site of beta toxin: jejunum is its main lesion, the pathological changes are mainly manifested as intestinal mucosal hemorrhage and necrosis, thinning of the intestinal wall, making the wall easier to rupture or perforation of the duodenum basically not The effect, which may be due to the high content of trypsin in the duodenum, inhibited the activity of beta toxin. The incidence of intestinal segments of the tiny blood vessels often found in the formation of thrombus, microscopic examination showed bleeding, edema and lymphocyte infiltration and other pathological changes.

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