The Convergence Of Multinational Standards And Practices In International Financial Reporting

The International Financial Reporting Standards (IFRS) is pending a move to incorporate a single set of accounting standards across International borders. The definitive decision for uniting the standards appears to be stalemated. The pending move by the United States to adopt financial reporting practices set forth by the IFRS to encompass a single set of reporting standards bears both advantages and disadvantages for multinational corporations. This paper examines some of the difficulties that can arise by using a single set of standards and addresses two significant studies regarding converging reporting standards. The paper concludes by discussing issues that could potentially arise if the standards are adopted in their entirety by the United States and the political issues that could emerge resultant of their adoption. The significance of international investment opportunities in foreign equity securities by investors in the United States and the significant number of foreign corporations registered on various securities exchanges around the world make the adoption and establishment of international reporting standards a challenge to many accounting professionals

The Impact Of Switching To International Financial Reporting Standards On United States Businesses

There has been controversy brewing among accounting professionals regarding the impact of switching to International Financial Reporting Standards (IFRS) on United States corporations as deemed to converge in the near future (Deming, 2005). The viewpoint presented in this paper is that the United States should conform to the international standards primarily because a single set of standards creates uniformity and comparability for stakeholders regardless of their geographic location. This paper addresses the potential advantages and disadvantages of moving to a global set of standards as well as how the Financial Accounting Standards Board (FASB) will need to work with the International Accounting Standards Board (IASB) to align the current United States Generally Accepted Accounting Principles (GAAP) with the newly proposed international accounting standards. If adopted, a wide range of issues relating to the operations within a business will need consideration in the future. One of these issues include effects of taxes as businesses will need to become keenly aware of how a country’s tax law and auditing practices affect their operations. The paper presents the repercussions United States corporations will face as a result of the convergence and how future accounting professionals, investors, financial institutions and students of accountancy. They will need to continue to stay abreast of changes in this area as these changes can ultimately change the way accounting standards are practiced, credentialed and taught over the next decade

DNAH6 and Its Interactions with PCD Genes in Heterotaxy and Primary Ciliary Dyskinesia.

Heterotaxy, a birth defect involving left-right patterning defects, and primary ciliary dyskinesia (PCD), a sinopulmonary disease with dyskinetic/immotile cilia in the airway are seemingly disparate diseases. However, they have an overlapping genetic etiology involving mutations in cilia genes, a reflection of the common requirement for motile cilia in left-right patterning and airway clearance. While PCD is a monogenic recessive disorder, heterotaxy has a more complex, largely non-monogenic etiology. In this study, we show mutations in the novel dynein gene DNAH6 can cause heterotaxy and ciliary dysfunction similar to PCD. We provide the first evidence that trans-heterozygous interactions between DNAH6 and other PCD genes potentially can cause heterotaxy. DNAH6 was initially identified as a candidate heterotaxy/PCD gene by filtering exome-sequencing data from 25 heterotaxy patients stratified by whether they have airway motile cilia defects. dnah6 morpholino knockdown in zebrafish disrupted motile cilia in Kupffer\u27s vesicle required for left-right patterning and caused heterotaxy with abnormal cardiac/gut looping. Similarly DNAH6 shRNA knockdown disrupted motile cilia in human and mouse respiratory epithelia. Notably a heterotaxy patient harboring heterozygous DNAH6 mutation was identified to also carry a rare heterozygous PCD-causing DNAI1 mutation, suggesting a DNAH6/DNAI1 trans-heterozygous interaction. Furthermore, sequencing of 149 additional heterotaxy patients showed 5 of 6 patients with heterozygous DNAH6 mutations also had heterozygous mutations in DNAH5 or other PCD genes. We functionally assayed for DNAH6/DNAH5 and DNAH6/DNAI1 trans-heterozygous interactions using subthreshold double-morpholino knockdown in zebrafish and showed this caused heterotaxy. Similarly, subthreshold siRNA knockdown of Dnah6 in heterozygous Dnah5 or Dnai1 mutant mouse respiratory epithelia disrupted motile cilia function. Together, these findings support an oligogenic disease model with broad relevance for further interrogating the genetic etiology of human ciliopathies

High Prevalence of Respiratory Ciliary Dysfunction in Congenital Heart Disease Patients With Heterotaxy

Patients with congenital heart disease (CHD) and heterotaxy show high postsurgical morbidity/mortality, with some developing respiratory complications. Although this finding is often attributed to the CHD, airway clearance and left-right patterning both require motile cilia function. Thus, airway ciliary dysfunction (CD) similar to that of primary ciliary dyskinesia (PCD) may contribute to increased respiratory complications in heterotaxy patients

The ubiquitin ligase HECTD1 promotes retinoic acid signaling required for development of the aortic arch

The development of the aortic arch is a complex process that involves remodeling of the bilaterally symmetrical pharyngeal arch arteries (PAAs) into the mature asymmetric aortic arch. Retinoic acid signaling is a key regulator of this process by directing patterning of the second heart field (SHF), formation of the caudal PAAs and subsequent remodeling of the PAAs to form the aortic arch. Here, we identify the HECTD1 ubiquitin ligase as a novel modulator of retinoic acid signaling during this process. Hectd1opm/opm homozygous mutant embryos show a spectrum of aortic arch abnormalities that occur following loss of 4th PAAs and increased SHF marker expression. This sequence of defects is similar to phenotypes observed in mutant mouse models with reduced retinoic acid signaling. Importantly, HECTD1 binds to and influences ubiquitination of the retinoic acid receptor, alpha (RARA). Furthermore, reduced activation of a retinoic acid response element (RARE) reporter is detected in Hectd1 mutant cells and embryos. Interestingly, Hectd1opm/+ heterozygous embryos exhibit reduced retinoic acid signaling, along with intermediate increased expression of SHF markers; however, heterozygotes show normal development of the aortic arch. Decreasing retinoic acid synthesis by reducing Raldh2 (also known as Aldh1a2) gene dosage in Hectd1opm/+ heterozygous embryos reveals a genetic interaction. Double heterozygous embryos show hypoplasia of the 4th PAA and increased incidence of a benign aortic arch variant, in which the transverse arch between the brachiocephalic and left common carotid arteries is shortened. Together, our data establish that HECTD1 is a novel regulator of retinoic acid signaling required for proper aortic arch development