Monkey see monkey do:\ud A cognitive model to loss of free will\ud

Free will (if any) may be lost because of fear and our dependence on others. In this paper, we develop cognitive models to support this argument. We do not describe what free will is but what free will is not. Our results indicate that moral responsibility is reversed and society is at fault. We argue that judgment (by society) is similar to pouring gasoline on fire, and forgiveness is the only way to regain free will if any

Türkiye Ermenileri ve Eçmiadzin Başpatrikliği

Taha Toros Arşivi, Dosya No: 77/A-Ermenilerİstanbul Kalkınma Ajansı (TR10/14/YEN/0033) İstanbul Development Agency (TR10/14/YEN/0033

An approch to the security problems in the TCP/IP protocol suite for a network security monitor design

Thesis (Master)--Izmir Institute of Technology, Computer Engineering, Izmir, 1999Includes bibliographical references (leaves: 99-102)Text in English; Abstract: Turkish and Englishxii, 102 leavesThere are a number of security problems in the TCP/IP protocol suite. In this thesis these problems will be analyzed in detail. The problems in several existing prevention methods will be analyzed as well in order to show that security policies based merely on preventive measures are not completely secure and convenient. Therefore, "network security moniJoring" will be proposed as an alternative and supplementary approach against Internet attacks

Dünyanın en büyük deniz ressamı Ayvazovski yeniden İstanbul'da

Taha Toros Arşivi, Dosya No: 4-AyvazovskiUnutma İstanbul projesi İstanbul Kalkınma Ajansı'nın 2016 yılı "Yenilikçi ve Yaratıcı İstanbul Mali Destek Programı" kapsamında desteklenmiştir. Proje No: TR10/16/YNY/010

Kitabımızla ilgili zihinlerde yaratılmak istenen sorular ve gerçekler

Taha Toros Arşivi, Dosya No: 3-B Harfi Gayrimüslimler (Blak Bey'ler, Balyanlar, Braune)İstanbul Kalkınma Ajansı (TR10/14/YEN/0033) İstanbul Development Agency (TR10/14/YEN/0033

Ünlüler oteli:Barons

Taha Toros Arşivi, Dosya Adı: Atatürk'ün Yaşadığı EvlerUnutma İstanbul projesi İstanbul Kalkınma Ajansı'nın 2016 yılı "Yenilikçi ve Yaratıcı İstanbul Mali Destek Programı" kapsamında desteklenmiştir. Proje No: TR10/16/YNY/010

Hoş geldin Vera!

Taha Toros Arşivi, Dosya Adı: Nazım Hikmetİstanbul Kalkınma Ajansı (TR10/14/YEN/0033) İstanbul Development Agency (TR10/14/YEN/0033

Characterization of a dand5 p.r152h control-derived ips cell line to be used as a tool for heart disease modeling

RESUMO: As doenças cardíacas congênitas (DCC) e os defeitos de lateralidade associados são uma das principais preocupações de saúde e 1,35 milhões de pessoas são diagnosticadas com DCC a cada ano em todo o mundo. A complexidade do desenvolvimento do coração e os obstáculos para investigar os fenótipos da doença tornam difícil identificar as causas subjacentes das DCC. O gene DAND5 é o homólogo humano do Cerl-2 de camundongo que codifica uma proteína envolvida na regulação da via de sinalização Nodal antagonizando a proteína Nodal no nódulo e inibindo a sinalização Nodal na mesoderme da placa lateral direita (RLPM). Em um estudo anterior, uma nova variante não-sinônima c.455G> A da DAND5 heterozigótica foi identificada e vinculada ao risco de doença em dois pacientes com DCC decorrentes de defeitos de lateralidade. Para modelar o fenótipo dos pacientes com a variante c.455G> A, uma linha iPSC humana foi previamente gerada e caracterizada (Cristo et al., 2017). Neste trabalho, caracterizamos uma linha iPSC de controle DAND5 de um doador do sexo masculino sadio (sem a variante) para servir de controle para a linha DAND5 c.455G>A. A caracterização foi baseada na detecção de marcadores de pluripotência a nível de genes e proteínas, e potencial diferencial in vitro. A análise de repetições curtas em tandem (STR) usou para provar a identidade genética das células ERE e das iPSCs reprogramadas. A cariotipagem das iPSCs após ≥ 20 passagens mostrou a estabilidade das iPSCs altamente proliferativas. Além disso, o teste de detecção de Mycoplasma mostrou a esterilidade da cultura de células. Esta linha celular de controlo será comparada com a linhagem celular c.455G> A da variante DAND5, para explorar ainda mais o nosso conhecimento sobre as consequências da variante nos fenótipos dos doentes (modelação da doença) e, mais precisamente, na proliferação de cardiomiócitos (terapia possível).ABSTRACT: Congenital heart diseases (CHDs) and associated laterality defects are a major health concern and 1,35 million people are diagnosed with CHDs each year worldwide. The complexity of heart development and the hurdles to investigate the disease phenotypes make it challenging to identify the underlying causes of CHDs. DAND5 is the human homologue of mouse Cerl-2 gene that codes for a protein involved in regulating the Nodal signalling pathway by antagonizing the Nodal protein in the node and inhibiting the Nodal signaling in the right lateral plate mesoderm (R-LPM). In a previous study, a new DAND5 heterozygous nonsynonymous variant c.455G>A was identified and linked to the risk of disease in two patients with CHDs arising from laterality defects. In order to model the phenotype of the patients with the variant c.455G>A, a human iPSC line was previously generated and characterized (Cristo et al., 2017). In this work, we characterized a DAND5-control iPSC line from a healthy male donor (without the variant) to serve as control for the DAND5 c.455G>A line. The characterization was based on the detection of pluripotency markers at gene- and protein level, and in vitro differential potential. Short tandem repeats (STR) analysis has used to prove the genetic identity of the ERE cells and the reprogrammed iPSCs. Karyotyping of the iPSCs after ≥20 passages has shown the stability of the highly proliferating iPSCs. Additionally, Mycoplasma detection test showed the sterility of the cell culture. This control cell line will be compared to the DAND5 variant c.455G>A cell line to further exploit our knowledge on the consequences of the variant in the phenotypes of the patients (disease modelling) and more precisely in the modulation of cardiomyocyte proliferation (possible therapy)