Conflict affected peoples’ access to education: IDP pupils in Georgia

This work seeks to understand what kind of impact educational policies have had on the secondary school students among internally displaced persons (IDPs) and their identity reconstruction in Georgia. The study offers a snapshot of the current situation based on desk study and interviews conducted among a sample of secondary school IDP pupils. In the final chapter, the findings will be reflected against the broader political context in Georgia and beyond. The study is interdisciplinary and its methodology is based on social identity theory. I shall compare two groups of IDPs who were displaced as a result of two separate conflicts. The IDPs displaced as a result of conflict in Abkhazia in 1992–1994 are named as old caseload IDPs. The second group of IDPs were displaced after a conflict in South Ossetia in 2008. Additionally, I shall touch upon the situation of the pupils among the returnees, a group of Georgian old caseload IDPs, who have spontaneously returned to de facto Abkhazia. According to the interviews, the secondary school student IDPs identify themselves strongly with the Georgian state, but their group identities are less prevailing. Particularly the old case load IDP students are fully integrated in local communities. Moreover, there seems not to be any tangible bond between the old and new caseload IDP students. The schools have neither tried nor managed to preserve IDP identities which would, for instance, make political mobilisation likely along these lines. Right to education is a human right enshrined in a number of international conventions to which the IDPs are also entitled. Access to education or its denial has a deep impact on individual and societal development. Furthermore, education has a major role in (re)constructing personal as well as national identity.

Epigenetic signature in persons with Down Syndrome

Persons affected by Down Syndrome show a heterogeneous phenotype that includes developmental defects and cognitive and haematological disorders. Premature accelerated aging and the consequent development of age associated diseases like Alzheimer Disease (AD) seem to be the cause of higher mortality late in life of DS persons. Down Syndrome is caused by the complete or partial trisomy of chromosome 21, but it is not clear if the molecular alterations of the disease are triggered by the specific functions of a limited number of genes on chromosome 21 or by the disruption of genetic homeostasis due the presence of a trisomic chromosome. As epigenomic studies can help to shed light on this issue, here we used the Infinium HumanMethilation450 BeadChip to analyse blood DNA methylation patterns of 29 persons affected by Down syndrome (DSP), using their healthy siblings (DSS) and mothers (DSM) as controls. In this way we obtained a family-based model that allowed us to monitor possible confounding effects on DNA methylation patterns deriving from genetic and environmental factors. We showed that defects in DNA methylation map in genes involved in developmental, neurological and haematological pathways. These genes are enriched on chromosome 21 but localize also in the rest of the genome, suggesting that the trisomy of specific genes on chromosome 21 induces a cascade of events that engages many genes on other chromosomes and results in a global alteration of genomic function. We also analysed the methylation status of three target regions localized at the promoter (Ribo) and at the 5’ sequences of 18S and 28S regions of the rDNA, identifying differently methylated CpG sites. In conclusion, we identified an epigenetic signature of Down Syndrome in blood cells that sustains a link between developmental defects and disease phenotype, including segmental premature aging.