Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Permanent URI for this collectionhttps://hdl.handle.net/11147/7148
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Article Citation - WoS: 1Citation - Scopus: 1The Impact of Visual Thinking in Medical Education(Walter de Gruyter GmbH, 2022) Demir, Ayşe Banu; Okuyan, Zuhal; van Eck, Alexander; Mura, Gökhan; Gönlügür, Emre; Karaca, Can; Abacıoğlu, HakanBackground Considering medical humanities, medicine and art are two areas that resemble each other at several features. Clinical diagnosis involves the observation, description and interpretation of information of which visual ones take an important one. The skills described are important skills in the field of visual arts, as well. Underlying a good clinical practice; clinical examination and observation skills constitute an important place. Although in several studies, these skills are shown to be improved by analyzing visual art pieces, courses intended to improve visual thinking skills are not that much common in medical faculty curriculums. Materials and methods In this article, we share our opinion about the use of visual thinking in medical education by providing preliminary reflection results of learners from the second year of medical education about the visual thinking course that we have recently started to apply in Faculty of Medicine in collaboration with Faculty of Fine Arts in Izmir University of Economics in order to improve the observational skills of learners. Results Reflection results of the learners support the view that training art-viewing skill is helpful to improve observational and descriptive skills. Conclusions Increasing interdisciplinary programs on visual thinking in medical curriculums have the potential to overcome several professional development challenges in clinics.Article Citation - WoS: 10Citation - Scopus: 10High-Copy Overexpression Screening Reveals Pdr5 as the Main Doxorubicin Resistance Gene in Yeast(Public Library of Science, 2015) Demir, Ayşe Banu; Koç, AhmetDoxorubicin is one of the most potent anticancer drugs used in the treatment of various cancer types. The efficacy of doxorubicin is influenced by the drug resistance mechanisms and its cytotoxicity. In this study, we performed a high-copy screening analysis to find genes that play a role in doxorubicin resistance and found several genes (CUE5, AKL1, CAN1, YHR177W and PDR5) that provide resistance. Among these genes, overexpression of PDR5 provided a remarkable resistance, and deletion of it significantly rendered the tolerance level for the drug. Q-PCR analyses suggested that transcriptional regulation of these genes was not dependent on doxorubicin treatment. Additionally, we profiled the global expression pattern of cells in response to doxorubicin treatment and highlighted the genes and pathways that are important in doxorubicin tolerance/toxicity. Our results suggest that many efflux pumps and DNA metabolism genes are upregulated by the drug and required for doxorubicin tolerance.Article Citation - Scopus: 21Linking Peroxiredoxin and Vacuolar-Atpase Functions in Calorie Restriction-Mediated Life Span Extension(Hindawi Publishing Corporation, 2014) Molin, Mikael; Demir, Ayşe BanuCalorie restriction (CR) is an intervention extending the life spans of many organisms. The mechanisms underlying CR-dependent retardation of aging are still poorly understood. Despite mechanisms involving conserved nutrient signaling pathways proposed, few target processes that can account for CR-mediated longevity have so far been identified. Recently, both peroxiredoxins and vacuolar-ATPases were reported to control CR-mediated retardation of aging downstream of conserved nutrient signaling pathways. In this review, we focus on peroxiredoxin-mediated stress-defence and vacuolar-ATPase regulated acidification and pinpoint common denominators between the two mechanisms proposed for how CR extends life span. Both the activities of peroxiredoxins and vacuolar-ATPases are stimulated upon CR through reduced activities in conserved nutrient signaling pathways and both seem to stimulate cellular resistance to peroxide-stress. However, whereas vacuolar-ATPases have recently been suggested to control both Ras-cAMP-PKA- and TORC1-mediated nutrient signaling, neither the physiological benefits of a proposed role for peroxiredoxins in H 2O2-signaling nor downstream targets regulated are known. Both peroxiredoxins and vacuolar-ATPases do, however, impinge on mitochondrial iron-metabolism and further characterization of their impact on iron homeostasis and peroxide-resistance might therefore increase our understanding of the beneficial effects of CR on aging and age-related diseases. © 2014 Mikael Molin and Ayse Banu Demir.Article Citation - WoS: 12Citation - Scopus: 12Identification of Respiratory Chain Gene Mutations That Shorten Replicative Life Span in Yeast(Elsevier Ltd., 2012) Hacıoğlu, Elise; Demir, Ayşe Banu; Koç, AhmetAging is the progressive accumulation of alterations in cells that elevates the risk of death. The mitochondrial theory of aging postulates that free radicals produced by the mitochondrial respiratory system contribute to the aging process. However, the roles of individual electron transfer chain (ETC) components in cellular aging have not been elucidated. In this study, we analyzed the replicative life span of 73 yeast deletion mutants lacking the genes of the mitochondrial electron transfer chain system, and found that nine of these mutants (δ nde1, δ tcm62, δ rip1, δ cyt1, δ qrc8, δ pet117, δ cox11, δ atp11, δ fmc1) had significantly shorter life spans. These mutants had lower rates of respiration and were slightly sensitive to exogenous administration of hydrogen peroxide. However, only two of them, δ nde1 and δ fmc1, produced higher amounts of intrinsic superoxide radicals in the presence of glucose compared to that of wild type cells. Interestingly, there were no significant alterations in the mitochondrial membrane potentials of these mutants. We speculate that the shorter life spans of ETC mutants result from multiple mechanisms including the low respiration rate and low energy production rather than just a ROS-dependent path. © 2011 Elsevier Inc.Article Citation - WoS: 18Citation - Scopus: 19Assessment of Chronological Lifespan Dependent Molecular Damages in Yeast Lacking Mitochondrial Antioxidant Genes(Elsevier Ltd., 2010) Demir, Ayşe Banu; Koç, AhmetThe free radical theory of aging states that oxidative damage to biomolecules causes aging and that antioxidants neutralize free radicals and thus decelerate aging. Mitochondria produce most of the reactive oxygen species, but at the same time have many antioxidant enzymes providing protection from these oxidants. Expecting that cells without mitochondrial antioxidant genes would accumulate higher levels of oxidative damage and, therefore, will have a shorter lifespan, we analyzed oxidative damages to biomolecules in young and chronologically aged mutants lacking the mitochondrial antioxidant genes: G. RX2, CCP1, SOD1, GLO4, TRR2, TRX3, CCS1, SOD2, GRX5, and PRX1. Among these mutants, ccp1Δ, trx3Δ, grx5Δ, prx1Δ, mutants were sensitive to diamide, and ccs1Δ and sod2Δ were sensitive to both diamide and menadione. Most of the mutants were less viable in stationary phase. Chronologically aged cells produced higher amount of superoxide radical and accumulated higher levels of oxidative damages. Even though our results support the findings that old cells harbor higher amount of molecular damages, no significant difference was observed between wild type and mutant cells in terms of their damage content. © 2010 Elsevier Inc.