鼠型斑疹傷寒立克次體IgG ELISA試劑盒

R. typhi IgG ELISA Kit 

廣州健侖生物科技有限公司

主要用途：用于檢測人血清中的鼠型斑疹傷寒立克次體IgG抗體

產(chǎn)品規(guī)格：96T/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、犬細小病毒等病原微生物的 IFA、MIF、ELISA試劑。

鼠型斑疹傷寒立克次體IgG ELISA試劑盒

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【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號二期2幢101-3室
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了解這種轉換有可能促成一些新的策略，在心臟病發(fā)作后、衰老過程中或在諸如糖尿病及高血壓等疾病中再生和生成新的心肌。
Hatzopoulos說：“如果我們可以了解損傷后發(fā)生的這種命運轉換的分子調(diào)控機制，或許我們就可以采用某種化合物或藥物來恢復再生，生成肌肉而不是瘢痕。我們認為這是一次機會來改善我們對心肌梗死后來到診所的患者的治療方式。
綠膿桿菌在免疫系統(tǒng)較弱的人當中，可以引起嚴重的皮膚和肺部炎癥，特別是那些患有遺傳性疾病囊胞性纖維癥的人。當細菌進入人體細胞后，Gb3脂質(zhì)結合LecA蛋白并使細胞膜彎曲。荷蘭瓦格寧根大學的Christian Fleck教授在新研究中通過計算得出，這種結合足以將細菌包裹起來。
之前，研究人員只熟悉細菌侵染的方法，包括操控宿主細胞內(nèi)的信號。這項信號可控制肌動蛋白纖維——細胞的肌肉：這些纖維可使來自內(nèi)部的細胞被膜彎曲，并形成膜泡，細菌被吸收進其中。
為了證明沒有肌動蛋白該過程一樣能運行，德國佛萊堡大學BIOSS生物信號研究中心生物研究所II的Thorsten Eierhoff博士和Winfried R?mer教授帶領的一個研究小組，觀察了假單胞菌(Pseudomonas bacteria)對合成膜泡的影響。膜泡既不包含肌動蛋白，也不包含其他細胞組分，只有脂質(zhì)Gb3。當離體膜?？康奖砻嫔蠒r，就在細菌周圍折疊和關閉。然而，只有當細菌產(chǎn)生LecA蛋白時，才會發(fā)生這個包裝過程。實驗表明，假單胞菌使用這種脂質(zhì)拉鏈，使其自身進入細胞，而無需操控肌動蛋白。
研究人員證明，LecA和Gb3對于細菌到人類肺細胞的入侵也非常重要：當這一對分子消失時，透過細胞的細菌數(shù)量減少了70%。這些研究結果使R?mer的研究小組能夠發(fā)現(xiàn)一種潛在的藥物，來對抗綠膿桿菌。美國華盛頓州立大學的科學家已經(jīng)確定DNA修復的關鍵步驟，這有可能有助于開發(fā)遺傳性疾病的靶向基因治療法，如“月球來的孩子”和結腸癌的常見形式。
這種疾病是由錯誤的DNA修復系統(tǒng)引起的，該系統(tǒng)提高患癌癥和其它條件的風險。相關文章發(fā)表于2014年8月18日的《PNAS》雜志上。
董事教授Michael Smerdon和博士后研究員Peng Mao發(fā)現(xiàn)，當DNA被破壞時，一個特定的蛋白質(zhì)首先必須被“解開扣子”，以方便獲取DNA的“修理隊”。如果沒有蛋白解開這一過程，進入受損位點的這一過程會被染色質(zhì)的緊湊排列的基因和蛋白質(zhì)阻攔。

Understanding this transition may lead to new strategies to regenerate and generate new myocardium during a heart attack, during aging or in diseases such as diabetes and hypertension.
Hatzopoulos said: "If we can understand the molecular mechanisms of this fate shift that occur after a lesion, perhaps we could use a compound or drug to regain regeneration and produce muscle instead of scar, and we think this is an opportunity to improve us Treatment of patients who come to the clinic after myocardial infarction.
Pseudomonas aeruginosa can cause severe skin and lung inflammation in people with weakened immune systems, especially those with hereditary cystic fibrosis. When bacteria enter human cells, Gb3 lipids bind LecA protein and bend the cell membrane. Professor Christian Fleck from Wageningen University in the Netherlands calculated in a new study that this combination is enough to encapsulate the bacteria.
Previously, researchers were only familiar with methods of bacterial infection, including manipulating signals in host cells. This signal controls the actin fibers - the cells' muscles: these fibers bend the envelope of cells from inside and form vesicles, into which bacteria are absorbed.
To demonstrate that this process works without actin, a team led by Dr. Thorsten Eierhoff and Prof. Winfried Römer at the Institute of Biology II at the BIOSS Biosignal Research Center, University of Freiburg, Freiburg, Germany, observed that Pseudomonas bacteria on synthetic vesicles. The vesicles neither contain actin nor other cellular components, only lipid Gb3. When the detachment membrane stops on the surface, it folds and closes around the bacteria. However, this process of packaging occurs only when the bacteria produce LecA protein. Experiments have shown that Pseudomonas uses this lipid zipper to allow itself to enter cells without manipulating actin.
Researchers have demonstrated that LecA and Gb3 are also important for the invasion of bacteria into human lung cells: When the pair of molecules disappears, the number of bacteria that pass through the cells is reduced by 70%. These findings led R? Mer's team to discover a potential drug against Pseudomonas aeruginosa. Scientists at Washington State University have identified key steps in DNA repair that could potentially help target gene therapy for the development of genetic diseases such as the common form of "child from the moon" and colon cancer.
The disease is caused by a faulty DNA repair system that increases the risk of cancer and other conditions. The article was published in PNAS magazine on August 18, 2014.
Director Professor Michael Smerdon and postdoctoral fellow Peng Mao have found that a particular protein must first be "unbuttoned" to facilitate access to DNA's "repair team" when the DNA is destroyed. Without this process of protein unwinding, the process of getting into a damaged site is blocked by tightly packed genes and proteins in the chromatin.