- 产品描述
马泰勒虫免疫荧光试剂盒
theileria equi IFA Kit
广州健仑生物科技有限公司
主要用途:用于检测马血清中的马泰勒虫IgG/IgM抗体
产品规格:12 孔/张,10 张/盒
主要产品包括:包柔氏螺旋体菌、布鲁氏菌、贝纳特氏立克次体、土伦杆菌、钩端螺旋体、新型立克次体、恙虫病、立克次体、果氏巴贝西虫、马焦虫、牛焦虫、利什曼虫、新包虫、弓形虫、猫流感病毒、猫冠状病毒、猫疱疹病毒、犬瘟病毒、犬细小病毒等病原微生物的 IFA、MIF、ELISA试剂。
马泰勒虫免疫荧光试剂盒
我司还提供其它进口或国产试剂盒:登革热、疟疾、西尼罗河、立克次体、无形体、蜱虫、恙虫、利什曼原虫、RK39、汉坦病毒、深林脑炎、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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JL-FL54 | 牛双芽巴贝西虫免疫荧光玻片 | babesia bigemina IFA Substrate slide |
JL-FL55 | 牛双芽巴贝西虫免疫荧光试剂盒 | babesia bigemina IFA Kit |
JL-FL56 | 牛巴贝西虫免疫荧光玻片 | babesia bovis IFA Substrate slide |
JL-FL57 | 牛巴贝西虫免疫荧光试剂盒 | babesia bovis IFA Kit |
JL-FL58 | 驽巴贝西虫免疫荧光玻片 | babesia caballi IFA Substrate slide |
JL-FL59 | 驽巴贝西虫免疫荧光试剂盒 | babesia caballi IFA Kit |
JL-FL60 | 马泰勒虫免疫荧光玻片 | theileria equi IFA Substrate slide |
JL-FL61 | theileria equi IFA Kit | |
JL-FL62 | 利什曼虫IgG免疫荧光试剂盒 | Leishmania IgG IFA Kit |
JL-FL63 | 新孢子虫IgG免疫荧光试剂盒(检测狗) | Neospora caninum IgG IFA Kit |
JL-FL64 | 新孢子虫IgG免疫荧光试剂盒(检测马) | Neospora caninum IgG IFA Kit |
JL-FL65 | 猫杯状病毒IgG免疫荧光玻片 | Feline Calicivirus IgG IFA Substrate slide |
JL-FL66 | 猫冠状病毒IgG免疫荧光玻片 | Feline Coronavirus IgG IFA Substrate slide |
JL-FL67 | 猫疱疹病毒IgG免疫荧光玻片 | Feline Herpesvirus IgG IFA Substrate slide |
JL-FL68 | 犬瘟病毒IgG免疫荧光玻片 | Canine Distemper IgG IFA Substrate slide |
JL-FL69 | 犬细小病毒IgG免疫荧光玻片 | Canine Parvovirus IgG IFA Substrate slide |
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【公司名称】 广州健仑生物科技有限公司
【】 杨永汉
【】
【腾讯 】 2042552662
【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101-3室
【企业文化】
在胰腺β细胞内葡萄糖的代谢对于胰岛素基因表达和胞外分泌的贺尔蒙来说是很关键的一环,但是有越来越多的证据显示,葡萄糖代谢途径同时对于β-细胞发育和维持成年人的β细胞质量非常重要。在小鼠β细胞中针对葡萄糖激酶剃除后不仅防止了葡萄糖所刺激的胰岛素分泌,而且也抑制了β细胞的增殖,并与细胞凋亡的增加有关联。在组织培养中,直接操纵胚胎胰脏的葡萄糖可用性实验则显示了转录调控因子神经元素3(Neurog3)和NEUROD对于α和β细胞的发育是很必要的存在。
针对此主题,帕特尔等人的论文提到丙酮酸脱氢酶α组件是丙酮酸脱氢酶复合物调控丙酮酸代谢的速率决定酵素;在老鼠实验模式中剔除了β细胞的丙酮酸脱氢酶α组件之后,如同预期的会引起胰岛素可用性降低以及葡萄糖敏感性释放,但是却也同时观察到新生老鼠β细胞数目减少以及Neurog3,NEUROD和的Pdx1的表达。有趣的是,同时也在胰岛素免疫阳性,特胰岛的内分泌小细胞簇中看到数目的减少,意味着也减少了新生β-细胞的来源。这个新发现强调了β-细胞中控制葡萄糖代谢的途径对于维持β-细胞质量以及贺尔蒙和生长因子,例如胰高血糖素样多肽1(GLP1)是同等重要的。
此研究主题刊登于2014年8月的《实验生物及医学》,证明了丙酮酸脱氢酶复合体不仅对于胰岛素基因表达和葡萄糖刺激的胰岛素分泌非常必要,同时还直接影响β-细胞的生长和成熟,更阐明了葡萄糖代谢会直接调控β细胞质量和可塑性。
纽约州立大学水牛城分校生物化学、医学和生物医学科学学院的特聘教授,同时也是资深作者的莫成?帕特尔博士说道:“这些发现显示了葡萄糖代谢是调控β细胞质量的主要调控因子,很可能是独立的讯息传递路径,例如可能不同于胰岛素受体作用物2讯息传递路径。”
Glucose metabolism in pancreatic beta cells is a crucial link to hormonal gene expression and extracellular secretion of hormones, but there is growing evidence that glucose metabolism contributes both to beta-cell development and maintenance of adulthood Human β-cell mass is very important. Shaved for glucokinase in mouse beta cells not only prevents glucose-stimulated insulin secretion but also inhibits beta cell proliferation and correlates with increased apoptosis. Glucose availability experiments directly manipulating embryonic pancreas in tissue culture showed that the transcriptional regulators Neurog3 and NEUROD are essential for the development of alpha and beta cells.
In response to this topic, Pa et al.'s paper mentions that the pyruvate dehydrogenase alpha component is a pyruvate dehydrogenase complex that regulates the rate at which pyruvate is metabolized; removing pyruvate from beta cells in experimental models of rats After the hydrogenase α-component, as expected, a decrease in insulin availability and glucose-sensitive release was caused, however, a decrease in the number of β-cells in neonatal mice and the expression of Neurog3, NEUROD and Pdx1 were also observed. Interestingly, a decrease in the number seen also in insulin-immunoreactive, insulinotropic endocrine small cell clusters means that the source of nascent β-cells is also reduced. This new finding emphasizes that the pathways that control glucose metabolism in β-cells are equally important for maintaining β-cell mass and for hormones and growth factors such as glucagon-like polypeptide 1 (GLP1).
The subject of the study, published in August 2014, "Experimental Biology and Medicine," demonstrates that pyruvate dehydrogenase complexes are essential not only for insulin gene expression and glucose-stimulated insulin secretion, but also for β-cell growth and Mature, but also shows that glucose metabolism will directly regulate β-cell quality and plasticity.
Dr. Moblie Pa, Distinguished Professor of Biochemistry, Medical and Biomedical Sciences at the State University of New York at Buffalo, said: "These findings show that glucose metabolism is a major regulator of beta-cell mass, Probably an independent messaging pathway, for example, may differ from the insulin receptor 2 signaling pathway.