EIKEN嗜肺軍團(tuán)菌快速檢測(cè)卡

廣州健侖生物科技有限公司

主要用途：用于檢測(cè)尿樣中嗜肺軍團(tuán)菌血清型1抗原，以支持軍團(tuán)菌感染的診斷。

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存儲(chǔ)條件：2-30℃

EIKEN嗜肺軍團(tuán)菌快速檢測(cè)卡

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EIKEN

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【公司名稱(chēng)】 廣州健侖生物科技有限公司
【】    楊永漢 
【】 
【騰訊 】 2042552662
【公司地址】 廣州清華科技園創(chuàng)新基地番禺石樓鎮(zhèn)創(chuàng)啟路63號(hào)二期2幢101-3室
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大腦細(xì)胞的自我更新能力很差，細(xì)胞療法可使丟失腦細(xì)胞的得以更新，已成為中樞神經(jīng)系統(tǒng)損傷治療的潛力性方法。骨髓間充質(zhì)干細(xì)胞因其可分化為神經(jīng)元/神經(jīng)細(xì)胞，又可通過(guò)血腦屏障遷移至損傷神經(jīng)組織，還能分泌神經(jīng)營(yíng)養(yǎng)因子，營(yíng)造利于神經(jīng)再生的微環(huán)境，也被認(rèn)為是有希望的細(xì)胞治療項(xiàng)目。
伊朗Shahid Sadoughi 大學(xué)醫(yī)學(xué)院的Mohammad Ali Khalili教授所在研究團(tuán)隊(duì)，設(shè)計(jì)了給創(chuàng)傷性腦損傷模型大鼠尾靜脈注射3×106大鼠骨髓間充質(zhì)干細(xì)胞，靜脈移植后顯著促進(jìn)了創(chuàng)傷性損傷大腦皮質(zhì)神經(jīng)細(xì)胞的再生，作者認(rèn)為此方法可成為因損傷而丟失神經(jīng)細(xì)胞的有益補(bǔ)充。相關(guān)研究成果發(fā)表在《中國(guó)神經(jīng)再生研究(英文版)》雜志2014年5月第9期。
在人類(lèi)細(xì)胞中，位于制造能量的稱(chēng)為線粒體的結(jié)構(gòu)中的DNA 可能出現(xiàn)突變從而形成多個(gè)DNA變種。這種稱(chēng)為異質(zhì)性的情況是一批疾病的原因，但是健康人群的線粒體基因組中的致病異質(zhì)性的流行程度尚不清楚，這部分是由于樣本數(shù)量少或者此前研究的不充分的測(cè)序方法。
Zhenglong Gu及其同事分析了1000基因組項(xiàng)目的14個(gè)人群的1085個(gè)健康個(gè)體的整個(gè)線粒體基因組高質(zhì)量下一代測(cè)序數(shù)據(jù)。這些人的90%擁有至少一種異質(zhì)性，但是多數(shù)人的異質(zhì)性數(shù)量低。然而，所有這些人的19%攜帶了至少一種與疾病有關(guān)的異質(zhì)性。
這組作者說(shuō)，隨著時(shí)間的推移，健康個(gè)體的可能有害的線粒體DNA變種的數(shù)量可能在一些細(xì)胞中增加，zui終達(dá)到了一個(gè)可能致病的臨界極限值，這強(qiáng)調(diào)了管理異質(zhì)性從而防止疾病進(jìn)程的重要性。
美國(guó)Salk研究所Juan Carlos Izpisua Belmonte實(shí)驗(yàn)室、華大基因(BGI)李英睿團(tuán)隊(duì)和中科院生物物理研究所劉光慧研究組合作，*利用全基因組測(cè)序(WGS)明確了現(xiàn)有疾病基因組靶向矯正工具的安全可靠性，并創(chuàng)建了效率遠(yuǎn)高于目前基因組靶向編輯技術(shù)的新型人類(lèi)遺傳突變修復(fù)工具HDAdV，為開(kāi)展以干細(xì)胞為基礎(chǔ)的基因治療提供了重要的理論依據(jù)。 相關(guān)文章發(fā)表于2014年7月3日的《Cell Stem Cell》雜志上。
例子：血紅蛋白疾病(如鐮刀形細(xì)胞貧血癥和地中海貧血癥)的再生醫(yī)學(xué)治療策略
人誘導(dǎo)多能干細(xì)胞技術(shù)(iPSC)的出現(xiàn)，促進(jìn)了人類(lèi)疾病基因組靶向矯正技術(shù)的快速發(fā)展。目前可用于人類(lèi)疾病基因組靶向矯正的方法包括：核酶介導(dǎo)的DNA同源重組技術(shù)(如ZFN，TALEN及CRISPR/CAS9等)以及不依賴(lài)于核酶的大片段DNA同源重組技術(shù)(以第三代腺病毒載體HDAdV為代表)。經(jīng)遺傳修復(fù)的自體干細(xì)胞具有治療自身疾病的潛力，因此在個(gè)體醫(yī)學(xué)和再生醫(yī)學(xué)中具有廣闊的應(yīng)用前景。
劉光慧研究團(tuán)隊(duì)曾zui早利用HDAdV介導(dǎo)的基因組靶向編輯技術(shù)在兒童早衰癥患者iPSC中實(shí)現(xiàn)了對(duì)致病基因LMNA的靶向修復(fù)，從概念上證實(shí)了在病人細(xì)胞中原位矯正遺傳突變的可行性。他們繼而矯正了帕金森氏癥和范可尼貧血癥患者干細(xì)胞中的致病突變，為這些遺傳疾病的機(jī)理研究、藥物評(píng)價(jià)及個(gè)性化干細(xì)胞和基因治療奠定了基礎(chǔ)。

Brain cells are poor at self-renewal and cell therapies that allow for the loss of brain cells have been renewed and have become a potential method of treatment for CNS injury. Bone marrow-derived mesenchymal stem cells are also considered promising because of their ability to differentiate into neurons / neurons, migration to damaged nerve tissue through the blood-brain barrier, secretion of neurotrophic factors, and creation of a microenvironment conducive to nerve regeneration Cell Therapy Project.
Professor Mohammad Ali Khalili, a professor at the Shahid Sadoughi University School of Medicine in Iran, designed a rat model of traumatic brain injury to inject 3 × 10 6 rat bone marrow mesenchymal stem cells into the tail vein of the traumatic brain injury model and significantly promote traumatic injury to the cerebral cortex Regeneration of nerve cells, the authors believe that this method can become a beneficial supplement due to injury and loss of nerve cells. Relevant research results published in the "Chinese Journal of Nervous Regeneration Research (English Edition)" magazine in May 2014 No. 9.
In human cells, DNA located in the structure called mitochondria that make energy can mutate to form multiple DNA variants. This condition, known as heterogeneity, is responsible for a number of diseases, but the prevalence of pathogenic heterogeneity in the mitochondrial genome of healthy populations is unclear, partly due to the small sample size or inadequay studied Sequencing method.
Zhenglong Gu and colleagues analyzed high-quality, next-generation sequencing data from the entire mitochondrial genome of 1085 healthy individuals in 14 global populations of 1000 genome projects. 90% of these people have at least one heterogeneity, but most people have low levels of heterogeneity. However, 19% of all these people carry at least one disease-related heterogeneity.
Over time, the authors say, the number of potentially harmful mitochondrial DNA variants in healthy individuals may increase in some cells, culminating in a potentially pathogenic threshold, emphasizing the management of heterogeneity and thus preventing The importance of the disease process.
The team of Juan Carlos Izpisua Belmonte, Salk Institute of USA, BGL Li Ying-Rui team and Liu Guang-hui Research Group, Institute of Biophysics, Chinese Academy of Sciences, for the first time made use of whole genome sequencing (WGS) to clarify the safety of existing disease genomic targeted remediation tools Reliability and create HDAdV, a novel human genetic mutation repair tool far more efficient than current genomic targeted editing techniques, providing an important theoretical basis for stem cell-based gene therapy. The article appeared in the July 3, 2014 issue of Cell Stem Cell.
Examples: Regenerative medical treatment strategies for hemoglobin diseases such as sickle cell anemia and thalassemia
The advent of human induced pluripotent stem cell technology (iPSC) has led to the rapid development of targeted therapies for human disease genomes. Currently available methods for target-directed genomic remediation of human diseases include ribozyme-mediated DNA homologous recombination techniques (eg, ZFN, TALEN and CRISPR / CAS9, etc.) and large fragment DNA-independent recombination techniques independent of ribozyme Third generation adenovirus vector HDAdV is representative). Genetically repaired autologous stem cells have the potential to treat their own diseases and therefore have broad applications in both individual medicine and regenerative medicine.
Liu Guanghui's team first used the HDAdV-mediated genome-targeted editing technique to target the pathogenic gene LMNA in the iPSC of patients with APA, and conceptually confirmed the feasibility of in situ correction of genetic mutations in patient cells . They then corrected pathogenic mutations in stem cells in patients with Parkinson's and Fanconi anemia and laid the foundation for mechanistic studies of these genetic diseases, drug evaluation, and personalized stem cell and gene therapy.