鼠型斑疹傷寒立克次體IgG免疫熒光玻片

Rickettsia typhi IgG IFA 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：12 孔/張,10 張/盒

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鼠型斑疹傷寒立克次體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 
【】 
【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】

在所附上的視頻上，顯微照片的時(shí)間序列顯示了，四桿狀酵母細(xì)胞收縮環(huán)的形成和收縮。一收縮環(huán)的蛋白質(zhì)顯示為白色。該蛋白質(zhì)簇環(huán)繞每個(gè)細(xì)胞的中間積累，然后冷凝成一個(gè)收縮環(huán)夾住細(xì)胞使之分為兩個(gè)。
近期的研究結(jié)果證實(shí)了，新的心肌細(xì)胞可以低速率生成，表明了心臟干細(xì)胞的存在。但人們對于這些細(xì)胞的起源卻并不清楚。
范德比爾特大學(xué)醫(yī)學(xué)、細(xì)胞與發(fā)育生物學(xué)副教授Antonis Hatzopoulos博士和同事們推測，排列于血管上內(nèi)皮細(xì)胞可能有潛力生成新的心肌細(xì)胞。他們知道，在發(fā)育過程中內(nèi)皮細(xì)胞可生成包括血細(xì)胞在內(nèi)的其他細(xì)胞類型。
現(xiàn)在，利用一些*技術(shù)在小鼠模型中“追蹤”細(xì)胞，他們證實(shí)冠狀動(dòng)脈中的內(nèi)皮細(xì)胞可以生成健康心臟中的新心肌細(xì)胞。他們發(fā)現(xiàn)在冠狀動(dòng)脈中有兩種心臟干細(xì)胞群：靜息的心臟干細(xì)胞群位于血管中膜層，增殖心臟干細(xì)胞群位于血管外膜層。
Hatzopoulos說，發(fā)現(xiàn)冠狀動(dòng)脈充當(dāng)了心臟干細(xì)胞的“微環(huán)境”具有有趣的含義。美國的1號(hào)殺手：冠狀動(dòng)脈病會(huì)影響這一微環(huán)境。他說：“我們的研究表明，冠狀動(dòng)脈病不僅可以阻斷動(dòng)脈，引起心臟病發(fā)作，還可通過影響心臟維持和再生的途經(jīng)來導(dǎo)致心力衰竭。”
在以往的研究中，Hatzopoulos和同事們證實(shí)心臟病發(fā)作后，內(nèi)皮細(xì)胞可生成一些產(chǎn)生瘢痕組織的成纖維細(xì)胞。“看起來相同的內(nèi)皮系統(tǒng)在穩(wěn)態(tài)過程中生成了肌細(xì)胞，并在心肌梗死后轉(zhuǎn)換生成了瘢痕組織。損傷之后，再生轉(zhuǎn)向了纖維化，”他說。

了解這種轉(zhuǎn)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(yùn)轉(zhuǎn)換的分子調(diào)控機(jī)制，或許我們就可以采用某種化合物或藥物來恢復(fù)再生，生成肌肉而不是瘢痕。我們認(rèn)為這是一次機(jī)會(huì)來改善我們對心肌梗死后來到診所的患者的治療方式。
近期的研究結(jié)果證實(shí)了，新的心肌細(xì)胞可以低速率生成，表明了心臟干細(xì)胞的存在。但人們對于這些細(xì)胞的起源卻并不清楚。
范德比爾特大學(xué)醫(yī)學(xué)、細(xì)胞與發(fā)育生物學(xué)副教授Antonis Hatzopoulos博士和同事們推測，排列于血管上內(nèi)皮細(xì)胞可能有潛力生成新的心肌細(xì)胞。他們知道，在發(fā)育過程中內(nèi)皮細(xì)胞可生成包括血細(xì)胞在內(nèi)的其他細(xì)胞類型。
現(xiàn)在，利用一些*技術(shù)在小鼠模型中“追蹤”細(xì)胞，他們證實(shí)冠狀動(dòng)脈中的內(nèi)皮細(xì)胞可以生成健康心臟中的新心肌細(xì)胞。他們發(fā)現(xiàn)在冠狀動(dòng)脈中有兩種心臟干細(xì)胞群：靜息的心臟干細(xì)胞群位于血管中膜層，增殖心臟干細(xì)胞群位于血管外膜層。
Hatzopoulos說，發(fā)現(xiàn)冠狀動(dòng)脈充當(dāng)了心臟干細(xì)胞的“微環(huán)境”具有有趣的含義。美國的1號(hào)殺手：冠狀動(dòng)脈病會(huì)影響這一微環(huán)境。他說：“我們的研究表明，冠狀動(dòng)脈病不僅可以阻斷動(dòng)脈，引起心臟病發(fā)作，還可通過影響心臟維持和再生的途經(jīng)來導(dǎo)致心力衰竭。”
在以往的研究中，Hatzopoulos和同事們證實(shí)心臟病發(fā)作后，內(nèi)皮細(xì)胞可生成一些產(chǎn)生瘢痕組織的成纖維細(xì)胞。“看起來相同的內(nèi)皮系統(tǒng)在穩(wěn)態(tài)過程中生成了肌細(xì)胞，并在心肌梗死后轉(zhuǎn)換生成了瘢痕組織。損傷之后，再生轉(zhuǎn)向了纖維化，”他說。

On the attached video, the time series of photomicrographs shows the formation and contraction of the collapsible rings of four-rod yeast cells. A shrunken protein appears white. The protein cluster accumulates around the middle of each cell, then condenses into a constriction ring that clamps the cell and breaks it into two.
Recent findings confirm that new cardiomyocytes can be generated at low rates, indicating the presence of cardiac stem cells. But people do not know the origin of these cells.
Antonis Hatzopoulos, Ph.D., associate professor of medicine, cell and developmental biology at Vanderbilt University, and colleagues speculate that lining up vascular endothelial cells may have the potential to generate new cardiomyocytes. They know that endothelial cells can generate other cell types, including blood cells, during development.
Now, using advanced techniques to "track" cells in mouse models, they demonstrate that endothelial cells in the coronary arteries produce new cardiomyocytes in healthy hearts. They found that there are two groups of cardiac stem cells in the coronary arteries: the resting cardiac stem cell population is located in the vascular media layer, and the proliferating cardiac stem cell population is located in the outer vascular layer.
Hatzopoulos said it was interesting to find that the coronary arteries act as a "microenvironment" for heart stem cells. No. 1 killer in the United States: Coronary artery disease can affect this microenvironment. "Our research shows that coronary artery disease can not only block the arteries and cause heart attacks but can also lead to heart failure through pathways that affect heart maintenance and regeneration," he said.
In previous studies, Hatzopoulos and colleagues confirmed that after a heart attack, endothelial cells produce some scar tissue-producing fibroblasts. "The seemingly identical endothelium generates muscle cells during homeostasis and converts to scar tissue after myocardial infarction, and after the injury, the regenerative turns to fibrosis," he said.

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.
Recent findings confirm that new cardiomyocytes can be generated at low rates, indicating the presence of cardiac stem cells. But people do not know the origin of these cells.
Antonis Hatzopoulos, Ph.D., associate professor of medicine, cell and developmental biology at Vanderbilt University, and colleagues speculate that lining up vascular endothelial cells may have the potential to generate new cardiomyocytes. They know that endothelial cells can generate other cell types, including blood cells, during development.
Now, using advanced techniques to "track" cells in mouse models, they demonstrate that endothelial cells in the coronary arteries produce new cardiomyocytes in healthy hearts. They found that there are two groups of cardiac stem cells in the coronary arteries: the resting cardiac stem cell population is located in the vascular media layer, and the proliferating cardiac stem cell population is located in the outer vascular layer.
Hatzopoulos said it was interesting to find that the coronary arteries act as a "microenvironment" for heart stem cells. No. 1 killer in the United States: Coronary artery disease can affect this microenvironment. "Our research shows that coronary artery disease can not only block the arteries and cause heart attacks but can also lead to heart failure through pathways that affect heart maintenance and regeneration," he said.
In previous studies, Hatzopoulos and colleagues confirmed that after a heart attack, endothelial cells produce some scar tissue-producing fibroblasts. "The seemingly identical endothelium generates muscle cells during homeostasis and converts to scar tissue after myocardial infarction, and after the injury, the regenerative turns to fibrosis," he said.