犬細(xì)小病毒IgG免疫熒光玻片

Canine Parvovirus 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)狗血清中犬細(xì)小病毒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。

犬細(xì)小病毒IgG免疫熒光玻片

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【公司名稱】 廣州健侖生物科技有限公司
【】    楊永漢 
【】 
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【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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Sejnowski說，這個(gè)行為結(jié)果只是冰山的一角。“該識(shí)別系統(tǒng)是非常重要的，”他補(bǔ)充說，它包括認(rèn)識(shí)到其他人，地點(diǎn)，事實(shí)，以及發(fā)生在過去的事情。有了這個(gè)新的發(fā)現(xiàn)，科學(xué)家們就可以開始更好地理解伽馬射線波的識(shí)別記憶的作用，他補(bǔ)充道。
在過去的幾年里，Whitehead研究所Susan Lindquist實(shí)驗(yàn)室的研究人員一直在探究，熱休克因子1(HSF1)在支持惡性腫瘤中所起的作用。在正常細(xì)胞中，包括熱、缺氧和毒素在內(nèi)的一些應(yīng)激情況會(huì)激活HSF1，HSF1發(fā)揮作用維持了蛋白質(zhì)穩(wěn)態(tài)，幫助細(xì)胞度過艱難的時(shí)期。癌細(xì)胞能夠劫持這一熱休克反應(yīng)來讓自身受益。兩年前，Lindquist實(shí)驗(yàn)室證實(shí)在癌細(xì)胞中HSF1激活了與熱休克過程中正常細(xì)胞內(nèi)上調(diào)的基因*不同的一組基因。
基于這一研究，該實(shí)驗(yàn)室現(xiàn)在發(fā)現(xiàn)HSF1不僅對(duì)腫瘤中的癌細(xì)胞起作用，還影響了稱之為間質(zhì)細(xì)胞的腫瘤微環(huán)境細(xì)胞。在這里HSF1驅(qū)動(dòng)了一種轉(zhuǎn)錄程序，其不同于在鄰近癌細(xì)胞中起作用的程序。HSF1在癌細(xì)胞和間質(zhì)細(xì)胞中激活，成為了一個(gè)強(qiáng)有力的、互補(bǔ)的組合推動(dòng)了惡性過程。
在一系列的實(shí)驗(yàn)中，Scherz-Shouval和同事們找到了確鑿的證據(jù)，證實(shí)HSF1在包括抗原抗體癌、肺癌、皮膚癌、食管癌、結(jié)腸癌和前列腺癌等各種人類腫瘤的癌相關(guān)成纖維細(xì)胞(CAFs)中激活。并且，他們發(fā)現(xiàn)在CAFs中HSF1激活不僅上調(diào)了一些支持惡性的基因，還抑制了周圍組織中通常觸發(fā)一種保護(hù)性、抗癌免疫反應(yīng)的一些基因。盡管這樣的協(xié)同動(dòng)態(tài)看似難以克服，其有可能為治療干預(yù)提供了一個(gè)真正的機(jī)會(huì)。
來自該研究另一個(gè)重要的發(fā)現(xiàn)是，可利用間質(zhì)HSF1激活作為一種診斷和預(yù)后生物標(biāo)記。分析來自抗原抗體癌患者的腫瘤樣本，科學(xué)家們發(fā)現(xiàn)間質(zhì)中HSF1激活與患者的不良預(yù)后有關(guān)，患者的無病生存率和總生存率降低。此外，研究還發(fā)現(xiàn)在來自早期非小細(xì)胞肺癌患者的樣本中間質(zhì)HSF1激活也與不良的預(yù)后有關(guān)。

Sejnowski said the result of this act is only the tip of the iceberg. "The identification system is very important," he added, including recognizing other people, places, facts, and what happened in the past. With this new discovery, scientists can begin to understand better the role of gamma-ray recognition memories, he added.
In the past few years, researchers at the Susan Lindquist Laboratory at the Whitehead Institute have been investigating the role of heat shock factor 1 (HSF1) in supporting malignant tumors. In normal cells, some stress conditions, including heat, hypoxia and toxins, activate HSF1, which acts to maintain protein homeostasis and help cells to pass tough times. Cancer cells can hijack this heat shock response to benefit themselves. Two years ago Lindquist Laboratories confirmed that HSF1 in cancer cells activates a compley different set of genes that are up-regulated in normal cells during heat shock.
Based on this study, the laboratory now found that HSF1 not only affects cancer cells in tumors but also affects tumor microenvironmental cells called stromal cells. Here HSF1 drives a transcription program that is distinct from the programs that play a role in neighboring cancer cells. HSF1 is activated in cancer cells and interstitial cells, becoming a powerful, complementary combination that drives the malignant process.
In a series of experiments, Scherz-Shouval and colleagues found conclusive evidence confirming that HSF1 is involved in the development of cancer-associated fibroblasts in a variety of human tumors including antigen-antibody, lung, skin, esophagus, colon and prostate Cells (CAFs) are activated. And, they found that HSF1 activation in CAFs not only up-regulates some of the genes that support malignancy, but also suppresses some of the genes in surrounding tissues that normally trigger a protective, anti-cancer immune response. While such synergistic dynamics may seem insurmountable, they may offer a real opportunity for therapeutic intervention.
Another important finding from this study is that stromal HSF1 activation can be exploited as a diagnostic and prognostic biomarker. Analyzing tumor samples from patients with antigen-antibody cancers, scientists found that HSF1 activation in the stroma was associated with poor prognosis in patients with a reduction in disease-free survival and overall survival. In addition, the study also found that stromal HSF1 activation in samples from patients with early non-small cell lung cancer is also associated with poor prognosis.