西班牙Certest賈第鞭毛蟲抗體（克隆G18）

廣州健侖生物科技有限公司

廣州健侖長期供應各種生物原料，主要代理品牌：西班牙Certest。

主要產品包括各種生物單克隆抗原抗體、重組蛋白。

西班牙Certest賈第鞭毛蟲抗體（克隆G18）

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西班牙

肥胖是一種復雜性疾病，可導致糖尿病，心血管疾病，癌癥以及其他疾病發生概率增加，同時，肥胖正逐漸成為性難題。肥胖的發生主要是因為能量攝入過多或消耗較少而導致的白色脂肪過度生長，出現白色脂肪細胞肥大增生。根據研究顯示，白色脂肪組織的擴張和白色脂肪細胞的更新主要依賴于白色脂肪前體細胞(WAP)的增殖分化，但WAP對肥胖發生過程的必要性一直沒有得到很好的研究。
MG Kolonin小組在之前的研究中建立了一種利用多肽配體靶向結合細胞表面受體的方法。這種多肽能夠在體內轉運特定治療藥物到靶向細胞，該小組已經發現許多具有cell-homing結構域的稱為"hunter killer"的多肽能夠靶向結合細胞表面受體，介導細胞凋亡。zui近，他們發現一種多肽能夠靶向結合表達在CD34+PDGFRβ+CD31-CD45-WAP細胞表面而在其他器官的MSC細胞不表達的WAT7受體，因此，研究人員設計了一種叫做d WAT7- -KLAKLAK2(D-WAT)的雙峰多肽，靶向WAP并導致WAP發生細胞凋亡。之后發現，給與高脂誘導的肥胖小鼠D-WAT處理4周后，與對照組相比并沒有出現明顯體重差異，但通過Echo磁共振成像發現D-WAT處理小鼠脂肪含量明顯下降，而在停止處理8周后通過磁共振發現多肽處理小鼠脂肪積累明顯受到抑制。通過對小鼠進行代謝指標分析發現，WAP缺失小鼠除了導致高血糖癥的發生沒有出現其他血脂異常。研究人員同時發現，在缺失WAP后，D-WAT小鼠脂肪組織內米色脂肪細胞增加，并伴隨著能量消耗增加。MG Kolonin指出，在之前研究中發現米色脂肪前體細胞不同于WAP，其并不是從脂肪細胞轉分化而來，他們通過實驗證明，在WAP缺失后，一群具有PDGFRα+PDGFRβ?特征的基質層細胞被募集到脂肪組織部位分化為米色脂肪細胞。
綜上所述，該項研究發現在WAP缺失后，會導致高脂飲食小鼠抵抗肥胖，這種作用主要是因為WAP缺失后一群具有PDGFRα+PDGFRβ-特征的米色脂肪前體細胞被募集到脂肪組織部位增加了能量消耗而導致的。
由達特茅斯Norris癌癥研究中心Sentman實驗室開發的抗癌嵌合抗原受體(Chimeric antigen receptor，CAR)T細胞目前正在進行臨床I階段的試驗研究，研究者Charles Sentman教授表示，我們開發的CAR療法在很多不同的癌癥治療中都具有廣泛的應用價值，后期研究顯示，CAR療法不僅可以消除實驗動物機體中的腫瘤，而且有效抑制癌癥的復發。

西班牙

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【公司名稱】 廣州健侖生物科技有限公司
【市場部】    楊永漢

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【騰訊  】 2042552662
【公司地址】 廣州清華科技園創新基地番禺石樓鎮創啟路63號二期2幢101-103室

Obesity is a complex disease that can lead to an increased probability of diabetes, cardiovascular disease, cancer and other diseases, and obesity is becoming a global problem. Obesity occurs mainly because of excessive energy intake or less consumption of white fat caused by excessive growth, hypertrophy of white adipocytes. According to the study, the expansion of white adipose tissue and the renewal of white adipocytes mainly depend on the proliferation and differentiation of white adipose precursor cells (WAP), but the necessity of WAP for obesity has not been well studied.
In a previous study, MG Kolonin's group established a method for the targeted binding of cell surface receptors using polypeptide ligands. This polypeptide is capable of transporting specific therapeutic agents to target cells in vivo and the team has found that many polypeptides called "hunter killers" with cell-homing domains are able to target the binding of cell surface receptors to mediate apoptosis. Recently, they found that a polypeptide can target WAT7 receptors that do not express in MSC cells expressed on the surface of CD34 + PDGFRβ + CD31-CD45-WAP cells but not in other organs. Therefore, the researchers designed a peptide called d WAT7- -KLAKLAK2 (D-WAT), targets WAP and leads to apoptosis of WAPs. It was found that there was no significant difference in body weight between D-WAT treated with high-fat-induced obese mice and control group, but D-WAT-treated mice showed significantly decreased fat mass by Echo magnetic resonance imaging, On the other hand, the accumulation of fat in mice treated with peptide was found to be significantly inhibited by magnetic resonance imaging after 8 weeks of stopping treatment. Metabolic index analysis of mice found that WAP-deficient mice in addition to leading to the occurrence of hyperglycaemia did not appear other dyslipidemia. The researchers also found that in the absence of WAP, D-WAT mouse adipose tissue fat cells increased, accompanied by increased energy expenditure. MG Kolonin pointed out that in previous studies, it was found that beige adipose precursor cells are different from WAP and are not transdifferentiated from adipocytes. They have experimentally demonstrated that a group of stromal cells characterized by PDGFRα + PDGFRβ? Was recruited to adipose tissue differentiated into beige adipocytes.
Taken together, this study found that loss of WAP resulted in resistance to obesity in high-fat-diet mice mainly due to the recruitment of a group of beige adipose precursor cells characterized by PDGFRα + PDGFRβ- Tissue site increased energy consumption caused.
Chimeric antigen receptor (CAR) T cells developed by Sentman Laboratories, Norris Cancer Center, Dartmouth are currently undergoing Phase I clinical trial studies. Researcher Charles Sentman said that we developed CAR therapy has a wide range of applications in many different cancer treatments. Later studies showed that CAR therapy can not only eliminate tumors in experimental animals, but also effectively inhibit the recurrence of cancer.