Yazar "Aydin, F." seçeneğine göre listele

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    A Novel Method for GDC Recovery During Solid Oxide Fuel Cell Manufacturing
    (WILEY-V C H VERLAG GMBH, 2012) Demir, I.; Aydin, F.
    There have been a tremendous research affects in recent years for alternative routes of electricity generation using some maximum yield technologies, increased reliability, and minimum pollution. From this point of view, the solid oxide fuel cells (SOFCs) are considered as the cleanest technologies for obtaining electrical energy generation. However, an important fraction of production is wasted during the manufacturing steps. From both economical and environmental point of view, recovery of waste GDC (Gd0.1Ce0.9O3) materials is deemed important. Hence, it is the main purpose of the present study to develop a novel method to recover waste GDC materials and afterwards to produce a new SOFC (solid oxide fuel cell) from the recovered materials. The results showed that recovered GDC cell worked as efficient as the fresh materials, revealing the success of the recovery process proposed.
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    Comprehensive Mutation Analysis of the RAS/RAF/MEK/ERK Pathway in Paediatric Leukaemia and Significant Inferences
    (Medcom Ltd, 2021) Akin-Bali, D. F.; Aktas, S. H.; Ozcan, A.; Yilmaz, E.; Aydin, F.; Gok, V; Unal, E.
    Objectives: Leukaemia is the most common cancer among paediatric population accounting for about 30% of paediatric cancer. As it's known, germ line mutations increase the risk of development of haematopoietic malignancy in childhood and deregulation of the Rat Sarcoma Viral Proto-Oncogene/Raf-1 Proto-Oncogene/Mitogen-Activated Protein Kinases/Extracellular Regulated Kinases (RAS/RAF/MEK/ERK) pathway is often caused by somatic mutations in the genes coding proteins of KRAS, NRAS, FLT3, PTPN11 and BRAF. However, mutations in this pathway in paediatric Acute Lymphoblastic Leukaemia (ALL) have not been thoroughly investigated, yet. Methods: Specific exons of 7 significant genes which were frequently mutated in the RAS/RAF/MEK/ERK pathway were determined inclusively by DNA sequence analysis in 27 children with leukaemia. PolyPhen-2 and SNAP tools were used to verify and estimate the determined changes. Also, evolutionary conservation analysis was performed. Results: Seven changes out of 22 changes were identified for the first time in this study. ERK2 p.P319S (18.5%) mutation and KRAS splice site mutation (3.7%) were predicted to be pathogenic. ERK2 p.P319S mutations was found to be pathogenic and at the critical point on the aminoacid which is evalutionary conserved. Although the frequency of mutations in ERK2 is very low in cancers (0.88%), the frequency of ERK2 p.P319S missense change was detected in our study at a significant rate such as 18.5%. Conclusion: There is limited knowledge about ERK inhibitors in leukaemia. The low frequency of ERK gene compared to KRAS and NRAS genes does not make ERK mutations less important. Our findings indicate the importance of this pathway mutations in paediatric ALL and associated with high risk leukaemia group characteristics. Hence, it can be evaluated as a signalisation pathway to target pharmacologically.