弓形虫IgG免疫荧光试剂盒（检测狗）

Toxoplasma IFA Canine IgG Kit

广州健仑生物科技有限公司

主要用途：用于检测狗血清中的弓形虫IgG抗体

产品规格：12 孔/张,10 张/盒

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弓形虫IgG免疫荧光试剂盒（检测狗）

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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】

此前研究人员已经发现了 5-LO 在炎性疾病比如哮喘症发病中的角色，研究者 Jessica Roos 教授表示，这项研究中我们发现，急性髓性白血病亚群中的白血病干细胞或许可以被5-LO抑制剂有效地选择性攻击，而且这种现象均可以在细胞培养基模型和白血病小鼠模型中观察到。
研究者表示，这项研究为开发新型的5-脂氧合酶抑制剂来抑制白血病的存货，从而为抑制并治疗急性髓性白血病提供了新的研究依据和线索。后期研究中研究人员还将通过深入研究来揭示5-脂氧合酶抑制剂在抑制白血病干细胞功能中的作用和机制。
科学家们早就知道，当细胞反复分裂时，就会发生染色体缺陷。随着时间的推移，这些缺陷就会导致癌症的发作。
现在，来自英国卡迪夫大学的邓肯·贝尔德教授和他的研究团队与来自明尼苏达大学的埃里克A·亨德里克森合作已经确定了，人类细胞为了生存所需的这些类型的缺陷的一个特定基因。
“我们发现，似乎是在进化过程中，可以驱动癌症的关键基因，” 卡迪夫大学的癌症与基因研究所的贝尔德教授说。“这是该基因的新作用，使其成为潜在的治疗靶点。”
随着细胞的分裂，它们的端粒——保护染色体末端免受损坏的DNA“帽”——缩短，使残余的染色体容易彼此粘在一起。
在正常细胞中，这种染色体的粘性是一个死亡的信号，该信号能够触发缺陷的细胞在清理过程中移动，并帮助清理它们的过程。
然而，恶性细胞，在某种程度上能够躲避这个清理过程。
发表于近期的《Cell Reports》杂志上的一项研究，确定一个允许衰老的细胞逃避死亡的重要组成部分。
使用*基因靶向技术使人类细胞中的特定基因失去活性，然后研究端粒融合的影响，研究人员发现，只有当连接酶3基因被激活时而不是它的作用，细胞才能逃过一死，这似乎更喜欢推动染色体内而不是不同的染色体之间的融合。
“在许多人类癌症中，已经确定端粒发生功能障碍，正如我们先前的研究显示，短端粒可以预测慢性淋巴细胞白血病患者的预后，可能也可用于很多其他类型的肿瘤，” 贝尔德教授说。“因此，这一过程需要连接酶3的发现是极其重要的。”
有趣的是，这项研究成为可能，是因为，在一次会议上卡迪夫大学的的贝尔德教授和明尼苏达大学的埃里克·亨德里克森教授的邂逅。
两人很快就发现，他们都期待连接酶3在癌症中的作用，于是，他们决定合作。
“此次合作得到了回报，因为我们发现了别人没有发现的东西，” 亨德里克森教授说。
重要的是，进一步的研究已经在进行中。特别是，细胞逃避死亡依赖于连接酶3，反过来，依赖另一个关键的DNA修复基因，p53基因的活性则可修复细胞。
“既然p53是人类肿瘤中zui常见的突变基因，现在我们理应认识到这两个基因的相互作用，看看我们是否能够利用这些信息来制定协同治疗方式，” 亨德里克森教授补充说。

Researchers have previously discovered the role of 5-LO in the pathogenesis of inflammatory diseases such as asthma. Researchers Professor Jessica Roos said that in this study, we found that leukemic stem cells in the acute myelogenous leukemia subgroup may be blocked by 5- LO inhibitors effectively selectively attack, and this phenomenon can be observed in both cell culture and leukemia mouse models.
The researchers said the study provides new research evidence and clues for the suppression and treatment of acute myeloid leukemia in order to develop new 5-lipoxygenase inhibitors to inhibit the stock of leukemia. In the latter part of the study, researchers will further study to reveal the role and mechanism of 5-lipoxygenase inhibitors in inhibiting leukemia stem cell function.
Scientists have long known that chromosomal defects occur when cells repeatedly divide. Over time, these shortcomings can lead to the onset of cancer.
Now that Professor Duncan Baird from Cardiff University in the UK and his research team have worked with Eric A. Hendrickson from the University of Minnesota, one of these types of defects that human cells need in order to survive Specific gene.
"We found it to be a key gene that can drive cancer in the evolutionary process," said Professor Baird, a professor of cancer and genetics at Cardiff University. "This is a new role for the gene, making it a potential therapeutic target."
As the cells divide, their omeres - protecting the chromosome ends from damaged DNA "caps" - shorten the residual chromosomes to stick together easily.
In normal cells, the stickiness of this chromosome is a signal of death that triggers defective cells to move during the cleaning process and help cleanse them.
However, malignant cells, to some extent, are able to evade this cleanup process.
A study published in the recent Cell Reports identified an important component that allows aging cells to escape death.
Using advanced gene targeting techniques to inactivate specific genes in human cells and then to study the effects of omere fusion, the researchers found that the cell can escape death only if it is activated rather than its effect Seems to prefer to promote the fusion between chromosomes rather than different chromosomes.
"In many human cancers, dysfunction of omeres has been identified and, as our previous study showed, short omeres predict the prognosis of patients with chronic lymphocytic leukemia and may also be used in many other types of tumors," said Professor Baird . "Therefore, the discovery that ligase 3 is required for this process is extremely important."
Interestingly, the study was made possible by encounters with Professor Baird at Cardiff University and Professor Eric Hendrickson at the University of Minnesota at an international conference.
They quickly discovered that they both looked for the role of ligase 3 in cancer, so they decided to work together.
"This cooperation paid off because we found something that others did not find," said Hendrickson.
Importantly, further research is already under way. In particular, cell death depends on Ligase 3, which, in turn, relies on another key DNA repair gene whose activity can repair cells.
"Since p53 is the most common mutation in human tumors, we should now recognize the interaction of these two genes and see if we can use that information to formulate a co-treatment approach," Professor Hendrickson added.