In vitro preparation of biosurfactant based herbal-nano topical ointment from Tridax procumbens infused oil using gelatin stabilized silver nanoparticle and its efficacy on fibroblastic cell lines

Author(s):  
Lavanya Kubendiran ◽  
Sowmiya Theerthagiri ◽  
Naif Abdullah Al-Dhabi ◽  
Senthilkumar Palaninaicker ◽  
Shivakumar Muthugoundar Subramanian ◽  
...  
Blood ◽  
2000 ◽  
Vol 96 (13) ◽  
pp. 4267-4275
Author(s):  
Mami Fukuoka ◽  
Kenji Fukudome ◽  
Yoshio Yamashita ◽  
Miyoko Tokushima ◽  
Kensuke Miyake ◽  
...  

Conflicting findings regarding proadhesion and antiadhesion in cell-to-cell interactions were previously reported for CD43. We examined possible differences in the role of the 130-kd glycoform and the 115-kd glycoform of CD43 in cellular adhesion in vitro. We generated a monoclonal antibody (MFT3) that discriminates between helper and nonhelper murine T-cell clones. Characterization of MFT3 with use of biochemical analysis and complementary DNA (cDNA) transfection experiments showed that it is specific for the 130-kd glycoform of CD43. T-cell clones that expressed the 130-kd CD43 glycoform showed decreased homocytic aggregation and decreased adhesion to spleen cells, B-lymphoma cell lines, and fibroblastic cell lines compared with T-cell clones negative for the 130-kd glycoform. Expression of core 2 β-1, 6-N-acetylglucosaminyltransferase (C2GnT) cDNA together with CD43 cDNA resulted in expression of both the 130-kd CD43 glycoform and the 115-kd CD43 glycoform in fibroblastic cell lines. Using these cell lines, we showed that the 130-kd glycoform but not the 115-kd glycoform of CD43 has an antiadhesive function in cellular interactions. Our findings suggest that the antiadhesive function of CD43 is primarily carried out by the 130-kd glycoform.


2012 ◽  
Vol 26 (2) ◽  
pp. 238-251 ◽  
Author(s):  
Sanchali Gupta Mukherjee ◽  
Niall O’Claonadh ◽  
Alan Casey ◽  
Gordon Chambers

Blood ◽  
2000 ◽  
Vol 96 (13) ◽  
pp. 4267-4275 ◽  
Author(s):  
Mami Fukuoka ◽  
Kenji Fukudome ◽  
Yoshio Yamashita ◽  
Miyoko Tokushima ◽  
Kensuke Miyake ◽  
...  

Abstract Conflicting findings regarding proadhesion and antiadhesion in cell-to-cell interactions were previously reported for CD43. We examined possible differences in the role of the 130-kd glycoform and the 115-kd glycoform of CD43 in cellular adhesion in vitro. We generated a monoclonal antibody (MFT3) that discriminates between helper and nonhelper murine T-cell clones. Characterization of MFT3 with use of biochemical analysis and complementary DNA (cDNA) transfection experiments showed that it is specific for the 130-kd glycoform of CD43. T-cell clones that expressed the 130-kd CD43 glycoform showed decreased homocytic aggregation and decreased adhesion to spleen cells, B-lymphoma cell lines, and fibroblastic cell lines compared with T-cell clones negative for the 130-kd glycoform. Expression of core 2 β-1, 6-N-acetylglucosaminyltransferase (C2GnT) cDNA together with CD43 cDNA resulted in expression of both the 130-kd CD43 glycoform and the 115-kd CD43 glycoform in fibroblastic cell lines. Using these cell lines, we showed that the 130-kd glycoform but not the 115-kd glycoform of CD43 has an antiadhesive function in cellular interactions. Our findings suggest that the antiadhesive function of CD43 is primarily carried out by the 130-kd glycoform.


2020 ◽  
Author(s):  
Satsuki Murakami ◽  
Susumu Suzuki ◽  
Ichiro Hanamura ◽  
Kazuhiro Yoshikawa ◽  
Ryuzo Ueda ◽  
...  

2010 ◽  
Vol 49 (S 01) ◽  
pp. S64-S68
Author(s):  
E. Dikomey

SummaryIonising irradiation acts primarily via induction of DNA damage, among which doublestrand breaks are the most important lesions. These lesions may lead to lethal chromosome aberrations, which are the main reason for cell inactivation. Double-strand breaks can be repaired by several different mechanisms. The regulation of these mechanisms appears be fairly different for normal and tumour cells. Among different cell lines capacity of doublestrand break repair varies by only few percents and is known to be determined mostly by genetic factors. Knowledge about doublestrand break repair mechanisms and their regulation is important for the optimal application of ionising irradiation in medicine.


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