- 產(chǎn)品描述
貓皰疹病毒IgG免疫熒光玻片
Feline Herpesvirus IgG IFA Substrate slide
廣州健侖生物科技有限公司
主要用途:用于檢測(cè)貓血清中貓皰疹病毒IgG抗體
產(chǎn)品規(guī)格:12 孔/張,10 張/盒
主要產(chǎn)品包括:包柔氏螺旋體菌、布魯氏菌、貝納特氏立克次體、土倫桿菌、鉤端螺旋體、新型立克次體、恙蟲病、立克次體、果氏巴貝西蟲、馬焦蟲、牛焦蟲、利什曼蟲、新包蟲、弓形蟲、貓流感病毒、貓冠狀病毒、貓皰疹病毒、犬瘟病毒、犬細(xì)小病毒等病原微生物的 IFA、MIF、ELISA試劑。
貓皰疹病毒IgG免疫熒光玻片
我司還提供其它進(jìn)口或國(guó)產(chǎn)試劑盒:登革熱、瘧疾、西尼羅河、立克次體、無形體、蜱蟲、恙蟲、利什曼原蟲、RK39、漢坦病毒、深林腦炎、流感、A鏈球菌、合胞病毒、腮病毒、乙腦、寨卡、黃熱病、基孔肯雅熱、克錐蟲病、違禁品濫用、肺炎球菌、軍團(tuán)菌、化妝品檢測(cè)、食品安全檢測(cè)等試劑盒以及日本生研細(xì)菌分型診斷血清、德國(guó)SiFin診斷血清、丹麥SSI診斷血清等產(chǎn)品。
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JL-FL54 | 牛雙芽巴貝西蟲免疫熒光玻片 | babesia bigemina IFA Substrate slide |
JL-FL55 | 牛雙芽巴貝西蟲免疫熒光試劑盒 | babesia bigemina IFA Kit |
JL-FL56 | 牛巴貝西蟲免疫熒光玻片 | babesia bovis IFA Substrate slide |
JL-FL57 | 牛巴貝西蟲免疫熒光試劑盒 | babesia bovis IFA Kit |
JL-FL58 | 駑巴貝西蟲免疫熒光玻片 | babesia caballi IFA Substrate slide |
JL-FL59 | 駑巴貝西蟲免疫熒光試劑盒 | babesia caballi IFA Kit |
JL-FL60 | 馬泰勒蟲免疫熒光玻片 | theileria equi IFA Substrate slide |
JL-FL61 | 馬泰勒蟲免疫熒光試劑盒 | theileria equi IFA Kit |
JL-FL62 | 利什曼蟲IgG免疫熒光試劑盒 | Leishmania IgG IFA Kit |
JL-FL63 | 新孢子蟲IgG免疫熒光試劑盒(檢測(cè)狗) | Neospora caninum IgG IFA Kit |
JL-FL64 | 新孢子蟲IgG免疫熒光試劑盒(檢測(cè)馬) | Neospora caninum IgG IFA Kit |
JL-FL65 | 貓杯狀病毒IgG免疫熒光玻片 | Feline Calicivirus IgG IFA Substrate slide |
JL-FL66 | 貓冠狀病毒IgG免疫熒光玻片 | Feline Coronavirus IgG IFA Substrate slide |
JL-FL67 | Feline Herpesvirus IgG IFA Substrate slide | |
JL-FL68 | 犬瘟病毒IgG免疫熒光玻片 | Canine Distemper IgG IFA Substrate slide |
JL-FL69 | 犬細(xì)小病毒IgG免疫熒光玻片 | Canine Parvovirus IgG IFA Substrate slide |
二維碼掃一掃
【公司名稱】 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
【企業(yè)文化】
例如,細(xì)胞通過將三個(gè)甲基附著到H3組蛋白的一個(gè)特異位點(diǎn)上就可以關(guān)閉一些基因。而將三個(gè)甲基附著到另一個(gè)H3位點(diǎn)上,這種稱之為H3K4me3的修飾則可對(duì)基因表達(dá)發(fā)揮正調(diào)控效應(yīng)。細(xì)胞通常將H3K4me3標(biāo)記添加到基因組小段區(qū)域的組蛋白上,然而現(xiàn)在研究人員注意到這種標(biāo)記有時(shí)可以遍布于更大的區(qū)域,修飾大量的組蛋白。
為了查明這些大H3K4me3標(biāo)記區(qū)域是否在組蛋白密碼中傳送了一種信息,斯坦福大學(xué)的分子遺傳學(xué)家Anne Brunet和同事們?cè)?0多種不同的細(xì)胞類型中追蹤了它們的存在。他們發(fā)現(xiàn)在不同的細(xì)胞類型中廣大的H3K4me3區(qū)域標(biāo)記了不同的基因。由此,研究人員認(rèn)識(shí)到根據(jù)廣大H3K4me3區(qū)域的染色質(zhì)定位,他們就可以將肝細(xì)胞與肌肉細(xì)胞或腎細(xì)胞區(qū)分開來。此外,他們還注意到這些H3K4me3區(qū)域往往標(biāo)記的是對(duì)細(xì)胞功能至關(guān)重要,或是幫助細(xì)胞確立*身份的一些基因。例如,在胚胎干細(xì)胞中它們出現(xiàn)在控制細(xì)胞特化能力的一些基因上。
研究人員在成體神經(jīng)祖細(xì)胞中利用rnai技術(shù),進(jìn)一步證實(shí)這些標(biāo)記表明了細(xì)胞的身份。當(dāng)他們利用RNAi來下調(diào)攜帶大塊H3K4me3標(biāo)記的一些基因時(shí),發(fā)現(xiàn)損害了細(xì)胞增殖和生成神經(jīng)元的能力。而當(dāng)研究人員沉默只有短H3K4me3標(biāo)記區(qū)域或根本沒有H3K4me3區(qū)域的基因時(shí),祖細(xì)胞仍然正常分裂。換句話說,大H3K4me3標(biāo)記區(qū)域的存在有可能幫助了細(xì)胞終身維持身份。盡管細(xì)胞利用了幾種方法來確立它們的身份,“我們發(fā)現(xiàn)了一種新的標(biāo)記,”Brunet說。
凱斯西儲(chǔ)大學(xué)表觀基因組學(xué)家Peter Scacheri對(duì)這篇論文給予了高度的評(píng)價(jià):“我認(rèn)為它將震動(dòng)研究團(tuán)體。盡管許多其他的科學(xué)家們一直在研究H3K4me3標(biāo)記,認(rèn)為這一標(biāo)記可以區(qū)分所有的細(xì)胞類型這一觀點(diǎn)真是令人震驚。檢測(cè)這些標(biāo)記非常容易,因此這一研究發(fā)現(xiàn)使得人們能夠快速地鑒別一些細(xì)胞類型,在諸如癌癥診斷等情況下它將派上用場(chǎng)。”
當(dāng)你期待的東西——比如你在餐廳點(diǎn)餐——或者引發(fā)你興趣的東西,這時(shí)*的電節(jié)律就會(huì)席卷你的大腦。這些電波被稱為伽馬振蕩,它們反映了細(xì)胞的交響曲,即興奮性和抑制性相互協(xié)調(diào)。盡管γ波的作用一直有爭(zhēng)論,但其已與更高級(jí)別的腦功能相關(guān)聯(lián),以及它的干擾模式已與精神分裂癥,阿爾茨海默氏病,自閉癥,癲癇癥和其它疾病有關(guān)。
現(xiàn)在,索爾克研究所的新研究表明,小有名氣的被稱為星形膠質(zhì)細(xì)胞的大腦支持細(xì)胞,實(shí)際上可能是控制這些電波的主要參與者。相關(guān)文章發(fā)表于2014年7月28日的《PNAS》雜志上。
索爾克研究人員報(bào)告了新的,意想不到的策略(通過禁用星形膠質(zhì)細(xì)胞而不是神經(jīng)元)減小伽馬振蕩。在這個(gè)過程中,研究組表明,星形膠質(zhì)細(xì)胞有助于伽馬振蕩形成,這對(duì)于某些形式的記憶是至關(guān)重要的。
“這可以被稱為一個(gè)確鑿的證據(jù),”合作者Terrence Sejnowski說。他是索爾克生物科學(xué)研究所計(jì)算神經(jīng)生物學(xué)實(shí)驗(yàn)室的負(fù)責(zé)人和霍華德休斯醫(yī)學(xué)研究所的研究員。“有數(shù)百篇論文認(rèn)為伽馬振蕩和記憶力以及注意力有關(guān)。這是*,我們已經(jīng)能夠做一個(gè)因果的實(shí)驗(yàn)。通過選擇性地阻斷伽馬振蕩,研究表明,它對(duì)大腦與世界如何相互作用有一個(gè)非常具體的影響。”
索爾克研究所的Sejnowski教授,Inder Verma和斯蒂芬·海涅曼實(shí)驗(yàn)室合作, 在小鼠的大腦中,星形膠質(zhì)細(xì)胞鈣信號(hào)的活動(dòng)形式緊跟在伽馬振蕩之前。這表明,星形膠質(zhì)細(xì)胞,和神經(jīng)元一樣,使用許多相同的化學(xué)信號(hào)影響這些振蕩。
For example, cells can turn off some genes by attaching three methyls to a specific site on H3 histones. While attaching three methyls to another H3 site, this modification, called H3K4me3, can exert a positive regulatory effect on gene expression. Cells typically add the H3K4me3 marker to histones in small regions of the genome, but now researchers have noticed that such markers can sometimes modify large quantities of histones throughout a larger area.
To see if these large H3K4me3 marker regions send a message in histone codes, Anne Brunet, a molecular geneticist at Stanford University, and colleagues track their presence in more than 20 different cell types. They found that a wide range of H3K4me3 regions marked different genes in different cell types. As a result, the researchers realized that based on the chromatin localization of the vast H3K4me3 region, they could distinguish hepatocytes from muscle cells or kidney cells. In addition, they also noted that these H3K4me3 regions often tagged genes that are crucial to cellular function or help cells establish unique identities. For example, in embryonic stem cells they appear on a few genes that control the cell's specialized ability.
Using rnai technology in adult neural progenitors, the researchers further confirmed that these markers indicate cellular identity. When they used RNAi to down-regulate a few genes that carry large H3K4me3 markers, they were found to impair the ability of cells to proliferate and produce neurons. When researchers silenced only the short H3K4me3-tagged region or no H3K4me3 region, the progenitor cells normally split. In other words, the presence of a large H3K4me3 tagged region may have helped the cell stay alive for life. Although the cells utilize several ways to establish their identity, "we found a new marker," Brunet said.
Peter Scacheri, an epigenomologist at Case Western Reserve University, commented highly on the paper: "I think it will shake the research community, and while many other scientists have been studying the H3K4me3 marker, they think the marker distinguishes all Of the cell types are so alarming.The detection of these markers is so easy that the study found that it enabled people to quickly identify a few cell types that would be useful in cases such as cancer diagnosis.
When you look for something - such as when you order at a restaurant - or something that interests you, the unique rhythm rolls over your brain. These waves are called gamma oscillations, and they reflect the symphony of the cell, the excitatory and inhibitory coordination of each other. Although the role of gamma-wave has been debated, it has been associated with higher levels of brain function and its mode of interference has been associated with schizophrenia, Alzheimer's disease, autism, epilepsy and other diseases .
Now, new studies at the Salk Institute show that the little-known brain-supporting cells, called astrocytes, could actually be the main players in controlling these waves. The article was published in the July 28, 2014 PNAS magazine.
Sork researchers reported new and unexpected strategies to reduce gamma oscillations by disabling astrocytes instead of neurons. In the process, the team showed that astrocytes help form gamma oscillations, which are crucial for some forms of memory.
"This can be called a conclusive evidence," said collaborator Terrence Sejnowski. He is the head of the computational neurobiology lab at the Salk Institute for Biological Sciences and a researcher at the Howard Hughes Medical Institute. "Hundreds of papers have argued that gamma oscillations are associated with memory and attention, and for the first time, we have been able to do a causal experiment, and by selectively blocking gamma oscillations, research shows how it interacts with the world and the brain The role has a very specific impact. "
In collaboration with Professor Sejnowski at the Salk Institute, Inder Verma, and Stephen Heinemann Laboratories, the astroglial calcium signaling activity follows the gamma oscillations in the brains of mice. This suggests that astrocytes, like neurons, affect many of these oscillations using many of the same chemical signals.