Impairment losses: the impact of the first-time adoption of the accounting standardization system In Portugal

In 2010, Portuguese unlisted companies started to apply a new accounting frame of reference called Accounting Standardisation System (Sistema de Normalização Contabilística – SNC) based on IAS/IFRS. This paper seeks to analyse the impact of SNC first-time adoption regarding the accounting treatment of impairment losses. Portugal has been recognized as a Code-law country, with weak legal enforcement mechanisms, and conservative accounting practices. However, since 2005 Portuguese companies have been changing their financial reporting practices to a common-law institutional logic. Therefore, the present research setting might provide interesting insights to confirm if the differences found are due to management interests, rather than cultural issues. Differences found are neither due to cultural issues nor management interests. To mitigate political costs associated with their public visibility, larger companies present more credible financial statements that reflect their overall true financial and economic condition. This study is a valuable contribution to both the users of financial information and domestic standard-setters entities to help them understand and improve the impact of accounting standards. Consistent with Khalil and Simon (2014), it also contributes to the debate on the optimal flexibility permitted by International Financial Reporting Standards to improve reporting quality and reduce earnings management.info:eu-repo/semantics/acceptedVersio

X-exome sequencing of 405 unresolved families identifies seven novel intellectual disability genes

X-linked intellectual disability (XLID) is a clinically and genetically heterogeneous disorder. During the past two decades in excess of 100 X-chromosome ID genes have been identified. Yet, a large number of families mapping to the X-chromosome remained unresolved suggesting that more XLID genes or loci are yet to be identified. Here, we have investigated 405 unresolved families with XLID. We employed massively parallel sequencing of all X-chromosome exons in the index males. The majority of these males were previously tested negative for copy number variations and for mutations in a subset of known XLID genes by Sanger sequencing. In total, 745 X-chromosomal genes were screened. After stringent filtering, a total of 1297 non-recurrent exonic variants remained for prioritization. Co-segregation analysis of potential clinically relevant changes revealed that 80 families (20%) carried pathogenic variants in established XLID genes. In 19 families, we detected likely causative protein truncating and missense variants in 7 novel and validated XLID genes (CLCN4, CNKSR2, FRMPD4, KLHL15, LAS1L, RLIM and USP27X) and potentially deleterious variants in 2 novel candidate XLID genes (CDK16 and TAF1). We show that the CLCN4 and CNKSR2 variants impair protein functions as indicated by electrophysiological studies and altered differentiation of cultured primary neurons from Clcn4−/− mice or after mRNA knock-down. The newly identified and candidate XLID proteins belong to pathways and networks with established roles in cognitive function and intellectual disability in particular. We suggest that systematic sequencing of all X-chromosomal genes in a cohort of patients with genetic evidence for X-chromosome locus involvement may resolve up to 58% of Fragile X-negative cases