EIKEN军团菌快速检测卡

广州健仑生物科技有限公司

主要用途：用于检测尿样中嗜肺军团菌血清型1抗原，以支持军团菌感染的诊断。

产品规格：20T/盒

存储条件：2-30℃

EIKEN军团菌快速检测卡

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【产品介绍】

EIKEN

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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】

Shaw说：“好消息是，这一发现可预测，缺失任一基因的患者，应该会对靶定粘着斑酶的新疗法发生反应，当前这种疗法症处于早期临床试验的检测当中。”
Goodwin补充说：“通过识别某些肿瘤中DIXDC1和LKB1之间这种意想不到的关联，我们已经扩大了潜在的患者群体，他们可能是这些疗法的优秀候选人。”
老年群体抗原抗体益增多痴呆患者的现象对现行的医疗体系是个巨大的考验。阿尔茨海默病(AD)、帕金森综合症(PD)，以及额颞区痴呆(Frontotemporal dementia)患者的脑部病灶都存有异常的大量不溶蛋白质，会导致神经元的大量丢失。为了减少这些不溶蛋白质造成的长期损伤，凋亡的细胞和聚集的蛋白质必须被有效地降解或清除，这正是被称为小神经胶质细胞(Microglia)这种特殊的吞噬细胞的作用所在。小神经胶质细胞仅存于中央神经系统，属于先天性免疫体系的一部分，它就像大脑的卫生检查员，确保垃圾被及时清除，以免这些垃圾威胁到周边正常细胞。
该研究发现，TREM2 基因能调节小神经胶质细胞的吞噬效率。正常情况下，TREM2嵌入小神经胶质细胞的外膜，膜以外的功能域能识别死亡细胞留下的碎片。然而，TREM2基因的特定突变会干扰蛋白质合成过程中蛋白链的正常折叠，使之在运送到小神经胶质细胞外膜之前就被降解了，导致小神经胶质细胞处理细胞碎片的效率降低，继而那些有毒的不溶蛋白质以及凋亡的细胞在大脑聚集，并触发炎症反应，导致神经元受损。
研究人员表示，这项新发现明确了多种不同脑部疾病的共同机理，并为延缓那些已经表征痴呆症状的患者的治疗指明了道路。
老年群体抗原抗体益增多痴呆患者的现象对现行的医疗体系是个巨大的考验。阿尔茨海默病(AD)、帕金森综合症(PD)，以及额颞区痴呆(Frontotemporal dementia)患者的脑部病灶都存有异常的大量不溶蛋白质，会导致神经元的大量丢失。为了减少这些不溶蛋白质造成的长期损伤，凋亡的细胞和聚集的蛋白质必须被有效地降解或清除，这正是被称为小神经胶质细胞(Microglia)这种特殊的吞噬细胞的作用所在。小神经胶质细胞仅存于中央神经系统，属于先天性免疫体系的一部分，它就像大脑的卫生检查员，确保垃圾被及时清除，以免这些垃圾威胁到周边正常细胞。
该研究发现，TREM2 基因能调节小神经胶质细胞的吞噬效率。正常情况下，TREM2嵌入小神经胶质细胞的外膜，膜以外的功能域能识别死亡细胞留下的碎片。然而，TREM2基因的特定突变会干扰蛋白质合成过程中蛋白链的正常折叠，使之在运送到小神经胶质细胞外膜之前就被降解了，导致小神经胶质细胞处理细胞碎片的效率降低，继而那些有毒的不溶蛋白质以及凋亡的细胞在大脑聚集，并触发炎症反应，导致神经元受损。

The good news is, "The good news is that the finding predicts that patients who lack either gene should respond to new therapies targeting the focal adhesion enzyme, which is currently being tested in early clinical trials."
Goodwin added: "By identifying this unexpected association between DIXDC1 and LKB1 in some tumors, we have expanded the potential patient population, who may be excellent candidates for these therapies."
Antibiotics in the elderly population increases the number of patients with dementia on the current medical system is a huge test. Alzheimer's disease (AD), Parkinson's disease (PD), and brain lesions in patients with frontotemporal dementia have abnormally large amounts of insoluble proteins that result in substantial neuronal loss. In order to reduce the long-term damage caused by these insoluble proteins, apoptotic cells and aggregated proteins must be effectively degraded or cleared, which is what is known as the special phagocyte called microglia. Microglia, which reside only in the central nervous system and are part of the innate immune system, acts like a brain health inspector to ensure that rubbish is removed in time to prevent the rubbish from threatening the surrounding normal cells.
The study found that, TREM2 gene can regulate the phagocytic efficiency of microglia. Under normal circumstances, TREM2 embedded in the outer membrane of microglial cells, the membrane outside the domain can identify the debris left by dead cells. However, certain mutations in the TREM2 gene interfere with the normal folding of protein chains during protein synthesis, degrading them before they are delivered to the outer microglia, resulting in a reduction in the efficiency of microglial cells handling cell debris, Then those toxic insoluble proteins and apoptotic cells accumulate in the brain and trigger an inflammatory response, leading to neuronal damage.
The researchers said the new findings pinpoint common causes of many different brain diseases and point the way to delaying the treatment of those who already have symptoms of dementia.
Antibiotics in the elderly population increases the number of patients with dementia on the current medical system is a huge test. Alzheimer's disease (AD), Parkinson's disease (PD), and brain lesions in patients with frontotemporal dementia have abnormally large amounts of insoluble proteins that result in substantial neuronal loss. In order to reduce the long-term damage caused by these insoluble proteins, apoptotic cells and aggregated proteins must be effectively degraded or cleared, which is what is known as the special phagocyte called microglia. Microglia, which reside only in the central nervous system and are part of the innate immune system, acts like a brain health inspector to ensure that rubbish is removed in time to prevent the rubbish from threatening the surrounding normal cells.
The study found that, TREM2 gene can regulate the phagocytic efficiency of microglia. Under normal circumstances, TREM2 embedded in the outer membrane of microglial cells, the membrane outside the domain can identify the debris left by dead cells. However, certain mutations in the TREM2 gene interfere with the normal folding of protein chains during protein synthesis, degrading them before they are delivered to the outer microglia, resulting in a reduction in the efficiency of microglial cells handling cell debris, Then those toxic insoluble proteins and apoptotic cells accumulate in the brain and trigger an inflammatory response, leading to neuronal damage.