The Institute of Philosophy of ASCR on November 26-27, 2012 hosted two lectures by Howard Hotson, professor of early modern intellectual history at the University of Oxford and steering committee chair of the Council for the Defence of British Universities. In his lecture Networking the Republic of Letters: an Introduction to Early Modern Letters Online Professor Hotson introduced his project on which he cooperates with scientists at the Institute of Philosophy of ASCR. In his lecture, Understanding the Global University Crisis: The Marketisation of English Higher Education in International Perspective, he criticizes the British government reforms of higher education. and Gabriela Adámková.
Tumour necrosis factor-stimulated gene 6 (TSG6) is a protective inflammatory reaction gene which is upregulated by inflammatory processes. Recent studies suggest that TSG-6 exhibits anti-scar-ring effects. However, the mechanism of TSG-6 action in the scar formation remains poorly understood. We investigated whether TSG-6 affects growth of the human hypertrophic scar fibroblasts (HSFs) via Fas/FasL signalling pathway. Cultured HSFs were transfected with a vector carrying the TSG6gene (pLVX-Puro-TSG-6) or with a vector not containing the TSG6 gene (pLVX-Puro). Untransfected HSFs served as a control group to both transfected HSFs. The expressions level of TSG-6 was up-regulated in the pLVX-Puro-TSG-6 group at the protein and mRNA level. MTT and flow cytometry were used to assess the effect of TSG-6 on the growth and apoptotic status of HSFs. Finally, qRT-PCR and western blot were used to measure the expression levels of Fas, FasL, FADD, caspase-3 and caspase-8 in each group. The apoptosis rate was significantly enhanced and the growth rate reduced in the HSFs transfected with the TSG6 gene vector. The expression levels of Fas, FasL, FADD, caspase-3 and caspase-8 were significantly raised in the TSG-6 overexpressing HSFs. It is concluded that increased expression of TSG-6 may induce apoptosis of human hypertrophic scar fibroblasts via activation of the Fas/FasL signalling pathway. and Corresponding author: Xiao-Jing Li