Araştırma Çıktıları | WoS | Scopus | TR-Dizin | PubMed
Permanent URI for this communityhttps://hdl.handle.net/20.500.14719/1741
Browse
224 results
Search Results
Publication Open Access Full analytical model for obtaining surface plasmon resonance modes of metal nanoparticle structures embedded in layered media(Optical Society of American (OSA) info@osa.org, 2010) Şimşek, Ergün; Ŝimŝek, Ergün, Department of Electrical and Electronic Engineering, Bahçeşehir Üniversitesi, Istanbul, TurkeyThis work addresses the need for a fully-retarded theoretical model for surface plasmons on metal nanoparticle chains and arrays embedded in a multilayered medium. The proposed method uses dyadic layered medium Green's functions not only to obtain the electric field created by an oscillating electric dipole but also to modify the polarizability of nanoparticles in a multilayered medium appropriately. Theoretically calculated resonance frequencies show a very good agreement with the experimental results found in the literature. Theoretical results suggest that surface plasmon propagation lengths of 1 μm are possible using silver or gold nanoparticles embedded in a multilayered medium. © 2010 Optical Society of America. © 2014 Elsevier B.V., All rights reserved.Publication Open Access An occlusion insensitive adaptive focus measurement method(Optical Society of American (OSA) info@osa.org, 2010) Aydın, Tarkan; Akgül, Yusuf Sinan; Aydin, Tarkan, Department of Computer Engineering, Gebze Teknik Üniversitesi, Gebze, Turkey, Department of Mathematics and Computer Science, Bahçeşehir Üniversitesi, Istanbul, Turkey; Akgül, Yusuf Sinan, Department of Computer Engineering, Gebze Teknik Üniversitesi, Gebze, TurkeyThis paper proposes a new focus measurement method for Depth From Focus to recover depth of scenes. The method employs an all-focused image of the scene to address the focus measure ambiguity problem of the existing focus measures in the presence of occlusions. Depth discontinuities are handled effectively by using adaptively shaped and weighted support windows. The size of the support window can be increased conveniently for more robust depth estimation without introducing any window size related Depth From Focus problems. The experiments on the real and synthetically refocused images show that the introduced focus measurement method works effectively and efficiently in real world applications. © 2010 Optical Society of America. © 2014 Elsevier B.V., All rights reserved.Publication Open Access Obtaining better quality final clustering by merging a collection of clusterings(2010) Mimaroglu, Selim N.; Erdil, Ertunç; Mimaroglu, Selim N., Department of Computer Engineering, Bahçeşehir Üniversitesi, Istanbul, Turkey; Erdil, Ertunç, Department of Computer Engineering, Bahçeşehir Üniversitesi, Istanbul, TurkeyMotivation: Clustering methods including k-means, SOM, UPGMA, DAA, CLICK, GENECLUSTER, CAST, DHC, PMETIS and KMETIS have been widely used in biological studies for gene expression, protein localization, sequence recognition and more. All these clustering methods have some benefits and drawbacks. We propose a novel graph-based clustering software called COMUSA for combining the benefits of a collection of clusterings into a final clustering having better overall quality. Results: COMUSA implementation is compared with PMETIS, KMETIS and k-means. Experimental results on artificial, real and biological datasets demonstrate the effectiveness of our method. COMUSA produces very good quality clusters in a short amount of time. © The Author 2010. Published by Oxford University Press. All rights reserved. © 2011 Elsevier B.V., All rights reserved.Publication Open Access Whole-exome sequencing identifies recessive WDR62 mutations in severe brain malformations(2010) Bilgüvar, Kaya; Öztürk, Ali Kemal; Louvi, Angeliki; Kwan, Kenneth Y.; Choi, Murim; Tatlí, Burak; Yalnizoǧlu, Dilek; Tüysüz, Beyhan; Caglayan, Ahmet Okay; Gökben, Sarenur; Bilgüvar, Kaya, Department of Neurosurgery, Yale School of Medicine, New Haven, United States, Department of Neurobiology, Yale School of Medicine, New Haven, United States, Department of Genetics, Yale School of Medicine, New Haven, United States; Öztürk, Ali Kemal, Department of Neurosurgery, Yale School of Medicine, New Haven, United States, Department of Neurobiology, Yale School of Medicine, New Haven, United States, Department of Genetics, Yale School of Medicine, New Haven, United States; Louvi, Angeliki, Department of Neurosurgery, Yale School of Medicine, New Haven, United States, Department of Neurobiology, Yale School of Medicine, New Haven, United States, Department of Genetics, Yale School of Medicine, New Haven, United States; Kwan, Kenneth Y., Department of Neurobiology, Yale School of Medicine, New Haven, United States, Kavli Institute for Neuroscience, Yale School of Medicine, New Haven, United States; Choi, Murim, Department of Genetics, Yale School of Medicine, New Haven, United States; Tatlí, Burak, Department of Pediatrics, İstanbul Tıp Fakültesi, Istanbul, Turkey; Yalnizoǧlu, Dilek, Department of Pediatrics, Hacettepe Üniversitesi, Ankara, Turkey; Tüysüz, Beyhan, Department of Pediatrics, İstanbul University-Cerrahpaşa Cerrahpaşa Faculty of Medicine, Istanbul, Turkey; Caglayan, Ahmet Okay,; Gökben, Sarenur, Department of Pediatrics, Ege University Medical School, Izmir, TurkeyThe development of the human cerebral cortex is an orchestrated process involving the generation of neural progenitors in the periventricular germinal zones, cell proliferation characterized by symmetric and asymmetric mitoses, followed by migration of post-mitotic neurons to their final destinations in six highly ordered, functionally specialized layers1,2. An understanding of the molecular mechanisms guiding these intricate processes is in its infancy, substantially driven by the discovery of rare mutations that cause malformations of cortical development3-6. Mapping of disease loci in putative Mendelian forms of malformations of cortical development has been hindered by marked locus heterogeneity, small kindred sizes and diagnostic classifications that may not reflect molecular pathogenesis. Here we demonstrate the use of whole-exome sequencing to overcome these obstacles by identifying recessive mutations in WD repeat domain 62 (WDR62) as the cause of a wide spectrum of severe cerebral cortical malformations including microcephaly, pachygyria with cortical thickening as well as hypoplasia of the corpus callosum. Some patients with mutations in WDR62 had evidence of additional abnormalities including lissencephaly, schizencephaly, polymicrogyria and, in one instance, cerebellar hypoplasia, all traits traditionally regarded as distinct entities. In mice and humans, WDR62 transcripts and protein are enriched in neural progenitors within the ventricular and subventricular zones. Expression of WDR62 in the neocortex is transient, spanning the period of embryonic neurogenesis. Unlike other known microcephaly genes, WDR62 does not apparently associate with centrosomes and is predominantly nuclear in localization. These findings unify previously disparate aspects of cerebral cortical development and highlight the use of whole-exome sequencing to identify disease loci in settings in which traditional methods have proved challenging. © 2010 Macmillan Publishers Limited. All rights reserved. © 2012 Elsevier B.V., All rights reserved., MEDLINE® is the source for the MeSH terms of this document.Publication Open Access Recessive LAMC3 mutations cause malformations of occipital cortical development(2011) Barak, Tanyeri; Kwan, Kenneth Y.; Louvi, Angeliki; Demirbilek, Veysi; Sütçü Saygı, Serap; Tüysüz, Beyhan; Choi, Murim; Boyacı, Hüseyin; Doerschner, Katja; Zhu, Ying; Barak, Tanyeri, Department of Neurosurgery, Yale School of Medicine, New Haven, United States, Department of Neurobiology, Yale School of Medicine, New Haven, United States, Department of Genetics, Yale School of Medicine, New Haven, United States; Kwan, Kenneth Y., Department of Neurobiology, Yale School of Medicine, New Haven, United States, Kavli Institute for Neuroscience, Yale School of Medicine, New Haven, United States; Louvi, Angeliki, Department of Neurosurgery, Yale School of Medicine, New Haven, United States, Department of Neurobiology, Yale School of Medicine, New Haven, United States; Demirbilek, Veysi, Department of Neurology, Istanbul University-Cerrahpasa, Istanbul, Turkey; Saygı, Serap Sütçü, Department of Neurology, Hacettepe Üniversitesi, Ankara, Turkey; Tüysüz, Beyhan, Department of Pediatrics, Istanbul University-Cerrahpasa, Istanbul, Turkey; Choi, Murim, Department of Genetics, Yale School of Medicine, New Haven, United States; Boyaci, Huseyin, Department of Psychology, Bilkent Üniversitesi, Ankara, Turkey, National Magnetic Resonance Research Center, Bilkent Üniversitesi, Ankara, Turkey; Doerschner, Katja, Department of Psychology, Bilkent Üniversitesi, Ankara, Turkey, National Magnetic Resonance Research Center, Bilkent Üniversitesi, Ankara, Turkey; Zhu, Ying, Department of Neurobiology, Yale School of Medicine, New Haven, United States, Kavli Institute for Neuroscience, Yale School of Medicine, New Haven, United StatesThe biological basis for regional and inter-species differences in cerebral cortical morphology is poorly understood. We focused on consanguineous Turkish families with a single affected member with complex bilateral occipital cortical gyration abnormalities. By using whole-exome sequencing, we initially identified a homozygous 2-bp deletion in LAMC3, the laminin 33 gene, leading to an immediate premature termination codon. In two other affected individuals with nearly identical phenotypes, we identified a homozygous nonsense mutation and a compound heterozygous mutation. In human but not mouse fetal brain, LAMC3 is enriched in postmitotic cortical plate neurons, localizing primarily to the somatodendritic compartment. LAMC3 expression peaks between late gestation and late infancy, paralleling the expression of molecules that are important in dendritogenesis and synapse formation. The discovery of the molecular basis of this unusual occipital malformation furthers our understanding of the complex biology underlying the formation of cortical gyrations. © 2011 Nature America, Inc. All rights reserved. © 2011 Elsevier B.V., All rights reserved., MEDLINE® is the source for the MeSH terms of this document.Publication Open Access Efficient reverse-engineering of a developmental gene regulatory network(Public Library of Science, 2012) Crombach, Anton; Wotton, Karl R.; Cicin-Sain, Damjan; Ashyraliyev, Maksat; Jaeger, Johannes; Crombach, Anton, EMBL/CRG Research Unit in Systems Biology, Universitat Pompeu Fabra Barcelona, Barcelona, Spain; Wotton, Karl R., EMBL/CRG Research Unit in Systems Biology, Universitat Pompeu Fabra Barcelona, Barcelona, Spain; Cicin-Sain, Damjan, EMBL/CRG Research Unit in Systems Biology, Universitat Pompeu Fabra Barcelona, Barcelona, Spain; Ashyraliyev, Maksat, Department of Mathematics and Computer Science, Bahçeşehir Üniversitesi, Istanbul, Turkey; Jaeger, Johannes, EMBL/CRG Research Unit in Systems Biology, Universitat Pompeu Fabra Barcelona, Barcelona, SpainUnderstanding the complex regulatory networks underlying development and evolution of multi-cellular organisms is a major problem in biology. Computational models can be used as tools to extract the regulatory structure and dynamics of such networks from gene expression data. This approach is called reverse engineering. It has been successfully applied to many gene networks in various biological systems. However, to reconstitute the structure and non-linear dynamics of a developmental gene network in its spatial context remains a considerable challenge. Here, we address this challenge using a case study: the gap gene network involved in segment determination during early development of Drosophila melanogaster. A major problem for reverse-engineering pattern-forming networks is the significant amount of time and effort required to acquire and quantify spatial gene expression data. We have developed a simplified data processing pipeline that considerably increases the throughput of the method, but results in data of reduced accuracy compared to those previously used for gap gene network inference. We demonstrate that we can infer the correct network structure using our reduced data set, and investigate minimal data requirements for successful reverse engineering. Our results show that timing and position of expression domain boundaries are the crucial features for determining regulatory network structure from data, while it is less important to precisely measure expression levels. Based on this, we define minimal data requirements for gap gene network inference. Our results demonstrate the feasibility of reverse-engineering with much reduced experimental effort. This enables more widespread use of the method in different developmental contexts and organisms. Such systematic application of data-driven models to real-world networks has enormous potential. Only the quantitative investigation of a large number of developmental gene regulatory networks will allow us to discover whether there are rules or regularities governing development and evolution of complex multi-cellular organisms. © 2012 Crombach et al. © 2022 Elsevier B.V., All rights reserved.Publication Open Access A reference finding rarely seen in primary hyperparathyroidism: Brown tumor(Hindawi Limited, 2012) Mantar, Ferhan; Gündüz, Şeyda Gülenay; Gündüz, Umut Rıza; Mantar, Ferhan, Department of Endocrinology, Bahçeşehir Üniversitesi, Istanbul, Turkey; Gündüz, Şeyda Gulenay, Department of Medical Oncology, Akdeniz Üniversitesi, Antalya, Turkey; Gündüz, Umut Riza, Department of Surgery, Antalya Education and Research Hospital, Antakya, TurkeyPrimary hyperparathyroidism is an endocrinopathy which is characterized with the hypersecretion of parathormone. During the progress of the disease bone loss takes place due to resorption on the subperiosteal and endosteal surfaces. Brown tumor is a localized form of osteitis fibrosa cystica, being part of the hyperparathyroid bone disease. It is rarely the first symptom of hyperparathyroidism. Nowadays, the diagnosis is made at an asymptomatic or minimally symptomatic stage. We present a male patient presented with a massive painless swelling in the left maxilla as the first manifestation of primary hyperparathyroidism due to a parathyroid adenoma. Parathyroidectomy was performed, and there was a regression of the bone lesion, without the need of performing other local surgical procedures. © 2012 F. Mantar et al. © 2017 Elsevier B.V., All rights reserved.Publication Open Access The effects of zinc treatment on the blood-brain barrier permeability and brain element levels during convulsions(2013) Yorulmaz, Hatice; Şeker, Fatma Burcu; Demir, Göksel; Yalçın, İbrahim Ertuǧrul; Öztaş, Baria; Yorulmaz, Hatice, Haliç Üniversitesi, Istanbul, Turkey; Şeker, Fatma Burcu, Faculty of Medicine, Yeditepe University, Istanbul, Turkey; Demir, Goksel, Environmental Engineering Department, Bahçeşehir Üniversitesi, Istanbul, Turkey; Ertugrul Yalcin, Ibrahim Ertuǧrul, Environmental Engineering Department, Bahçeşehir Üniversitesi, Istanbul, Turkey; Öztaş, Baria, İstanbul Tıp Fakültesi, Istanbul, TurkeyWe evaluated the effect of zinc treatment on the blood-brain barrier (BBB) permeability and the levels of zinc (Zn), natrium (Na), magnesium (Mg), and copper (Cu) in the brain tissue during epileptic seizures. The Wistar albino rats were divided into four groups, each as follows: (1) control group, (2) pentylenetetrazole (PTZ) group: rats treated with PTZ to induce seizures, (3) Zn group: rats treated with ZnCl2 added to drinking water for 2 months, and (4) Zn + PTZ group. The brains were divided into left, right hemispheres, and cerebellum + brain stem regions. Evans blue was used as BBB tracer. Element concentrations were analyzed by inductively coupled plasma optical emission spectroscopy. The BBB permeability has been found to be increased in all experimental groups (p < 0.05). Zn concentrations in all brain regions in Zn-supplemented groups (p < 0.05) showed an increase. BBB permeability and Zn level in cerebellum + brain stem region were significantly high compared to cerebral hemispheres (p < 0.05). In all experimental groups, Cu concentration decreased, whereas Na concentrations showed an increase (p < 0.05). Mg content in all the brain regions decreased in the Zn group and Zn + PTZ groups compared to other groups (p < 0.001). We also found that all elements' levels showed hemispheric differences in all groups. During convulsions, Zn treatment did not show any protective effect on BBB permeability. Chronic Zn treatment decreased Mg and Cu concentration and increased Na levels in the brain tissue. Our results indicated that Zn treatment showed proconvulsant activity and increased BBB permeability, possibly changing prooxidant/antioxidant balance and neuronal excitability during seizures. © 2012 The Author(s). © 2013 Elsevier B.V., All rights reserved.Publication Open Access The Identification of Pathway Markers in Intracranial Aneurysm Using Genome-Wide Association Data from Two Different Populations(2013) Bakir Güngör, Burcu; Sezerman, Osman Uğur; Bakir-Güngör, Burcu, Department of Genetics and Bioinformatics, Bahçeşehir Üniversitesi, Istanbul, Turkey, Advanced Genomics and Bioinformatics Research Center, UEKAE, Kocaeli, Turkey; Sezerman, Osman Uğur, Biological Sciences and Bioengineering Program, Sabancı Üniversitesi, Tuzla, TurkeyThe identification of significant individual factors causing complex diseases is challenging in genome-wide association studies (GWAS) since each factor has only a modest effect on the disease development mechanism. In this study, we hypothesize that the biological pathways that are targeted by these individual factors show higher conservation within and across populations. To test this hypothesis, we searched for the disease related pathways on two intracranial aneurysm GWAS in European and Japanese case-control cohorts. Even though there were a few significantly conserved SNPs within and between populations, seven of the top ten affected pathways were found significant in both populations. The probability of random occurrence of such an event is 2.44E-36. We therefore claim that even though each individual has a unique combination of factors involved in the mechanism of disease development, most targeted pathways that need to be altered by these factors are, for the most part, the same. These pathways can serve as disease markers. Individuals, for example, can be scanned for factors affecting the genes in marker pathways. Hence, individual factors of disease development can be determined, and this knowledge can be exploited for drug development and personalized therapeutic applications. Here, we discuss the potential avenues of pathway markers in medicine and their translation to preventive and individualized health care. © 2013 Bakir-Gungor, Sezerman. © 2013 Elsevier B.V., All rights reserved., MEDLINE® is the source for the MeSH terms of this document.Publication Open Access Mutations in LAMB1 cause cobblestone brain malformation without muscular or ocular abnormalities(2013) Radmanesh, Farid; Çağlayan, Ahmet Okay; Silhavy, Jennifer L.; Yılmaz, Cahide; Cantagrel, Vincent; Omar, Tarek E.I.; Rosti, Başak; Kaymakçalan, Hande; Gabriel, Stacey Bolk; Li, Mingfeng; Radmanesh, Farid, Department of Neurosciences, La Jolla, United States, Howard Hughes Medical Institute, Chevy Chase, United States; Caglayan, Ahmet Okay, Department of Neurosurgery, Yale School of Medicine, New Haven, United States; Silhavy, Jennifer L., Department of Neurosciences, La Jolla, United States, Howard Hughes Medical Institute, Chevy Chase, United States; Yilmaz, Cahide, Department of Pediatrics, Mustafa Kemal Üniversitesi, Antakya, Turkey; Cantagrel, Vincent, Department of Neurosciences, La Jolla, United States, Howard Hughes Medical Institute, Chevy Chase, United States; Omar, Tarek E.I., Department of Pediatric Neurology, Faculty of Medicine, Alexandria, Egypt; Rosti, Başak, Department of Neurosciences, La Jolla, United States, Howard Hughes Medical Institute, Chevy Chase, United States; Kaymakçalan, Hande, Department of Genetics and Bioinformatics, Bahçeşehir Üniversitesi, Istanbul, Turkey; Gabriel, Stacey Bolk, Massachusetts Institute of Technology, Cambridge, United States; Li, Mingfeng, Department of Neurobiology, Yale School of Medicine, New Haven, United StatesCobblestone brain malformation (COB) is a neuronal migration disorder characterized by protrusions of neurons beyond the first cortical layer at the pial surface of the brain. It is usually seen in association with dystroglycanopathy types of congenital muscular dystrophies (CMDs) and ocular abnormalities termed muscle-eye-brain disease. Here we report homozygous deleterious mutations in LAMB1, encoding laminin subunit beta-1, in two families with autosomal-recessive COB. Affected individuals displayed a constellation of brain malformations including cortical gyral and white-matter signal abnormalities, severe cerebellar dysplasia, brainstem hypoplasia, and occipital encephalocele, but they had less apparent ocular or muscular abnormalities than are typically observed in COB. LAMB1 is localized to the pial basement membrane, suggesting that defective connection between radial glial cells and the pial surface mediated by LAMB1 leads to this malformation. © 2013 The American Society of Human Genetics. © 2013 Elsevier B.V., All rights reserved., MEDLINE® is the source for the MeSH terms of this document.