Relevancia de la información contable en el valor de las acciones de las entidades financieras que cotizan en el Mercado de Valores de Buenos Aires en el período 2012-2014

En la actualidad el Marco Conceptual de la Contabilidad Financiera determina que el objetivo de los informes financieros es “suministrar información útil al usuario”, ello es la causa fundamental del despertar y auge de la investigación empírica en contabilidad. De entenderse que el objetivo de los estados financieros era el de ejercer un control sobre el patrimonio en pos de su protección se pasó a otra concepción de la Contabilidad, de acuerdo a la cual ésta es considerada como un medio facilitador para que sus usuarios puedan tomar decisiones. (Casinelli, 2008, p.22). Según menciona Hendricksen (1974, p.67) esta nueva orientación comienza a gestarse a partir de la Gran Depresión. Actualmente, se cristaliza en la normativa internacional y también en la nacional, que adscriben al enfoque de la utilidad de la información para la toma de decisiones. A partir de este cambio de paradigma las investigaciones contables tratan de conocer y comprender cuáles son los modelos de decisión de los usuarios de los estados contables. Expresa Tua (1995) que es el usuario quién pasa a ser el determinante de la información a incluir en los estados financieros, cuyo contenido se establece a partir de los posibles requerimientos.Tema 3: Especialidad, Rama o Segmento Contable Económico Financiero.Facultad de Ciencias Económica

Relevancia de la información contable en el valor de las acciones de las entidades financieras que cotizan en el Mercado de Valores de Buenos Aires en el período 2012-2014

En la actualidad el Marco Conceptual de la Contabilidad Financiera determina que el objetivo de los informes financieros es “suministrar información útil al usuario”, ello es la causa fundamental del despertar y auge de la investigación empírica en contabilidad. De entenderse que el objetivo de los estados financieros era el de ejercer un control sobre el patrimonio en pos de su protección se pasó a otra concepción de la Contabilidad, de acuerdo a la cual ésta es considerada como un medio facilitador para que sus usuarios puedan tomar decisiones. (Casinelli, 2008, p.22). Según menciona Hendricksen (1974, p.67) esta nueva orientación comienza a gestarse a partir de la Gran Depresión. Actualmente, se cristaliza en la normativa internacional y también en la nacional, que adscriben al enfoque de la utilidad de la información para la toma de decisiones. A partir de este cambio de paradigma las investigaciones contables tratan de conocer y comprender cuáles son los modelos de decisión de los usuarios de los estados contables. Expresa Tua (1995) que es el usuario quién pasa a ser el determinante de la información a incluir en los estados financieros, cuyo contenido se establece a partir de los posibles requerimientos.Tema 3: Especialidad, Rama o Segmento Contable Económico Financiero.Facultad de Ciencias Económica

A Comprehensive Analysis of Gene Expression and Genomic Alterations in a Newly Formed Autotetraploid of \u3cem\u3ePaspalum Notatum\u3c/em\u3e

The proportion of angiosperms that have experienced one or more episodes of chromosome doubling is estimated to be of the order of 50-70%. This prominence of polyploidy probably implies some adaptive significance. The emergence of novel phenotypes could allow polyploids to enter new niches or enhance their chances of being selected for use in agriculture. Although the causes of novel variation in polyploids are not well understood, they could involve changes in gene expression through dosage-regulation, altered regulatory interactions and rapid genetic/epigenetic changes. The objective of this work was to carry out an extensive transcript profiling and genome analysis of a diploid genotype of the pasture grass Paspalum notatum and its tetraploid derivative obtained after colchicine treatment

Discovery and Functional Categorisation of Expressed Sequence Tags from Flowers of \u3cem\u3eEragrostis Curvula\u3c/em\u3e Genotypes Showing Different Ploidy Levels and Reproductive Modes

Two novel genotypes of weeping lovegrass (Eragrostis curvula) - a dihaploid strain obtained in vitro from an apomictic cultivar and a tetraploid plant derived from the dihaploid after chromosome duplication – have recently been developed. These materials represent an excellent system for the identification, through transcriptional profiling, of genes involved in diplospory and/or ploidy level gene regulation. The aim of this work was the discovery and functional classification of expressed sequence tags (ESTs) from immature inflorescences of the apomictic E. curvula cultivar Tanganyika (2n=4x=40), a dihaploid sexual strain derived from it (2n=2x=20) and a tetraploid sexual strain (2n=4x=40) obtained by colchicine duplication of the dihaploid

The intrahepatic signalling niche of hedgehog is defined by primary cilia positive cells during chronic liver injury

Background & Aims: In vertebrates, canonical Hedgehog (Hh) pathway activation requires Smoothened (SMO) translocation to the primary cilium (Pc), followed by a GLI-mediated transcriptional response. In addition, a similar gene regulation occurs in response to growth factors/cytokines, although independently of SMO signalling. The Hh pathway plays a critical role in liver fibrosis/regeneration; however, the mechanism of activation in chronic liver injury is poorly understood. This study aimed to characterise Hh pathway activation upon thioacetamide (TAA)- induced chronic liver injury in vivo by defining Hh-responsive cells, namely cells harbouring Pc and Pc-localised SMO. Methods: C57BL/6 mice (wild-type or Ptc1+/_) were TAA-treated. Liver injury and Hh ligand/pathway mRNA and protein expression were assessed in vivo. SMO/GLI manipulation and SMO dependent/ independent activation of GLI-mediated transcriptional response in Pc-positive (Pc+) cells were studied in vitro. Results: In vivo, Hh activation was progressively induced following TAA. At the epithelial-mesenchymal interface, injured hepatocytes produced Hh ligands. Progenitors, myofibroblasts, leukocytes and hepatocytes were GLI2+. Pc+ cells increased following TAA, but only EpCAM+/GLI2+ progenitors were Pc+/SMO+. In vitro, SMO knockdown/hGli3-R overexpression reduced proliferation/viability in Pc+ progenitors, whilst increased proliferation occurred with hGli1 overexpression. HGF induced GLI transcriptional activity independently of Pc/SMO. Ptc1+/_ mice exhibited increased progenitor, myofibroblast and fibrosis responses. Conclusions: In chronic liver injury, Pc+ progenitors receive Hh ligand signals and process it through Pc/SMO-dependent activation of GLI-mediated transcriptional response. Pc/SMO-independent GLI activation likely occurs in Pc_/GLI2+ cells. Increased fibrosis in Hh gain-of-function mice likely occurs by primary progenitor expansion/proliferation and secondary fibrotic myofibroblast expansion, in close contact with progenitors

A P53-Independent DNA Damage Response Suppresses Oncogenic Proliferation and Genome Instability

The Mre11-Rad50-Nbs1 complex is a DNA double-strand break sensor that mediates a tumor-suppressive DNA damage response (DDR) in cells undergoing oncogenic stress, yet the mechanisms underlying this effect are poorly understood. Using a genetically inducible primary mammary epithelial cell model, we demonstrate that Mre11 suppresses proliferation and DNA damage induced by diverse oncogenic drivers through a p53-independent mechanism. Breast tumorigenesis models engineered to express a hypomorphic Mre11 allele exhibit increased levels of oncogene-induced DNA damage, R-loop accumulation, and chromosomal instability with a characteristic copy number loss phenotype. Mre11 complex dysfunction is identified in a subset of human triple-negative breast cancers and is associated with increased sensitivity to DNA-damaging therapy and inhibitors of ataxia telangiectasia and Rad3 related (ATR) and poly (ADP-ribose) polymerase (PARP). Thus, deficiencies in the Mre11-dependent DDR drive proliferation and genome instability patterns in p53-deficient breast cancers and represent an opportunity for therapeutic exploitation

Paraspeckle subnuclear bodies depend on dynamic heterodimerisation of DBHS RNA-binding proteins via their structured domains

RNA-binding proteins of the DBHS (Drosophila Behavior Human Splicing) family, NONO, SFPQ, and PSPC1 have numerous roles in genome stability and transcriptional and posttranscriptional regulation. Critical to DBHS activity is their recruitment to distinct subnuclear locations, for example, paraspeckle condensates, where DBHS proteins bind to the long noncoding RNA NEAT1 in the first essential step in paraspeckle formation. To carry out their diverse roles, DBHS proteins form homodimers and heterodimers, but how this dimerization influences DBHS localization and function is unknown. Here, we present an inducible GFP-NONO stable cell line and use it for live-cell 3D-structured illumination microscopy, revealing paraspeckles with dynamic, twisted elongated structures. Using siRNA knockdowns, we show these labeled paraspeckles consist of GFP-NONO/endogenous SFPQ dimers and that GFP-NONO localization to paraspeckles depends on endogenous SFPQ. Using purified proteins, we confirm that partner swapping between NONO and SFPQ occurs readily in vitro. Crystallographic analysis of the NONOSFPQ heterodimer reveals conformational differences to the other DBHS dimer structures, which may contribute to partner preference, RNA specificity, and subnuclear localization. Thus overall, our study suggests heterodimer partner availability is crucial for NONO subnuclear distribution and helps explain the complexity of both DBHS protein and paraspeckle dynamics through imaging and structural approaches.Pei Wen Lee, Andrew C. Marshall, Gavin J. Knott, Simon Kobelke, Luciano Martelotto, Ellie Cho, Paul J. McMillan, Mihwa Lee, Charles S. Bond, and Archa H. Fo

Renal epithelial cells retain primary cilia during human acute renal allograft rejection injury

OBJECTIVES: Primary cilia are sensory organelles which co-ordinate several developmental/repair pathways including hedgehog signalling. Studies of human renal allografts suffering acute tubular necrosis have shown that length of primary cilia borne by epithelial cells doubles throughout the nephron and collecting duct, and then normalises as renal function returns. Conversely the loss of primary cilia has been reported in chronic allograft rejection and linked to defective hedgehog signalling. We investigated the fate of primary cilia in renal allografts suffering acute rejection. RESULTS: Here we observed that in renal allografts undergoing acute rejection, primary cilia were retained, with their length increasing 1 week after transplantation and remaining elevated. We used a mouse model of acute renal injury to demonstrate that elongated renal primary cilia in the injured renal tubule show evidence of smoothened accumulation, a biomarker for activation of hedgehog signalling. We conclude that primary cilium-mediated activation of hedgehog signalling is still possible during the acute phase of renal allograft rejection

MYBL1 rearrangements and MYB amplification in breast adenoid cystic carcinomas lacking the MYB–NFIB fusion gene

Breast adenoid cystic carcinoma (AdCC), a rare type of triple-negative breast cancer, has been shown to be driven by MYB pathway activation, most often underpinned by the MYB–NFIB fusion gene. Alternative genetic mechanisms, such as MYBL1 rearrangements, have been reported in MYB–NFIB-negative salivary gland AdCCs. Here we report on the molecular characterization by massively parallel sequencing of four breast AdCCs lacking the MYB–NFIB fusion gene. In two cases, we identified MYBL1 rearrangements (MYBL1–ACTN1 and MYBL1–NFIB), which were associated with MYBL1 overexpression. A third AdCC harboured a high-level MYB amplification, which resulted in MYB overexpression at the mRNA and protein levels. RNA-sequencing and whole-genome sequencing revealed no definite alternative driver in the fourth AdCC studied, despite high levels of MYB expression and the activation of pathways similar to those activated in MYB–NFIB-positive AdCCs. In this case, a deletion encompassing the last intron and part of exon 15 of MYB, including the binding site of ERG-1, a transcription factor that may downregulate MYB, and the exon 15 splice site, was detected. In conclusion, we demonstrate that MYBL1 rearrangements and MYB amplification probably constitute alternative genetic drivers of breast AdCCs, functioning through MYBL1 or MYB overexpression. These observations emphasize that breast AdCCs probably constitute a convergent phenotype, whereby activation of MYB and MYBL1 and their downstream targets can be driven by the MYB–NFIB fusion gene, MYBL1 rearrangements, MYB amplification, or other yet to be identified mechanisms. Copyright © 2017 Pathological Society of Great Britain and Ireland