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Purpose Prior research has examined the impact of corporate governance mechanisms, including external auditing, on accounting restatements likelihood. However, little is known about auditor’s monitoring role in restatement disclosure practices. The purpose of this study is to address this gap by investigating the impact of auditor’s oversight on the timeliness of accounting restatement disclosures as measured by the length of the restatement dark period. Design/methodology/approach The study examines panel data from a sample of restating publicly traded US firms. Negative binomial regression is used to analyze the data because the dependent variable is a count variable and is over-dispersed. Findings The main study’s results indicate that longer auditor tenure and non-audit services provision improve restatement disclosure timeliness. Conversely, companies whose auditors exerted abnormally high levels of audit effort have longer restatement dark periods. Originality/value This study is the first archival research that focuses on auditor’s monitoring role and its impact on the timeliness of restatement disclosures. By doing so, this study contributes to the auditing academic research, professional practice and regulation by providing empirical evidence on an exasperating issue for all participants in the financial markets. In addition, it provides a better understanding of auditor’s monitoring role in the accounting restatement process and offers insights to policymakers, practitioners and investors interested in corporate financial transparency and corporate governance.

Prior research in agency theory views outside directors as being mostly extrinsically motivated by the potential for financial rewards, and as such stresses the value of using director stock options and equity to incentivize outside directors to pursue strategic risks. We draw on and extend agency-theory by arguing that outside directors are primarily intrinsically motivated, and therefore excessive emphasis on pecuniary rewards and punishments can ironically subvert a director's motives away from strategic risk-taking. In particular, we claim that more important than extrinsic rewards and government regulations is creating a secure environment for directors so that they may exercise their fiduciary duties without fear of litigation. We test our theory on a sample of 196 S&P 500 firms from 2005 to 2015 and find that the pressures imposed on the board through external regulations and controls can often backfire and result in outside directors signing off on less risky expenditure. A strong implication of these findings is no real substitute exists to creating a safe environment for directors, where they have the freedom to pursue the long-term interests of the principals, even if this goes against the short-termism of capital markets.

Agency theory views board independence, retaining a high fraction of outside directors, as a hallmark of effective corporate governance. As a result, many boards now remain so “independent” that ov...

This paper investigates the impact of earnings management on market return (by the proxies of discretionary accruals and earnings response coefficient/CAR regarded as accounting and market based earnings quality, respectively) along with a number of moderating (both governance and financial) variables in an emerging market context. Indonesia. Building on extant literature and using panel data approach, it examines 52 manufacturing firms listed on the Indonesia stock exchange during 2007 to 2010 periods. Applying Modified Jones Model to measure earnings management, our regression analysis reveals that earnings management has significant negative influence of market return. Of the moderating variables, board size, leverage and firm size are showing significant effects on market return, but not the institutional ownership. Again, observing the use of moderator effects on earnings management, our findings confirm that board size has more predictive power than institutional ownership in deterring earnings management and weaken the association between earnings management and market return. Similarly, leverage has strengthened the relation between earnings management and market return showing more exposure to earnings management while firm size showing a tendency to weakening earnings management, on the contrary. These results have enormous implications for Indonesian corporate sector and policy makers in adopting appropriate governance measures to constrain earnings management and improve quality of earnings

Does limiting the size of a large bank reduce its insolvency risk? This paper shows that the answer to this question depends on how exactly paring down of the bank size is done. In fact, the insolvency risk may go down or up depending on the composition of assets and liabilities of the bank relative to its pre-paring down composition. In addition, this study investigates mean-standard deviation efficiency of a typical Canadian large bank and its various possible paring down scenarios and finds both the original bank and its pared-down versions are inefficient. It then suggests mean-standard deviation efficient compositions of assets and liabilities, which do not depend on limiting the size of the bank. Therefore, the findings of this paper raise a serious doubt about the validity of the limit on size solution to the too-big-to-fail problem.

Nasopharyngeal carcinoma (NPC) occurs with a striking geographic distribution, it is endemic in certain areas of Southeast Asia and North Africa. NPC is tightly linked to Epstein-Barr virus (EBV), however, only a small subset of EBV genes are expressed, among them the latent membrane protein 1 (LMP1). LMP1 is considered as the main EBV oncoprotein and its 30 bp deleted-variant has been reported to be more prevalent in biopsies of NPC. We have assessed the 30 bp deletion and the XhoI polymorphisms of the BNLF1 gene in 30 peripheral bloods of NPC patients and 62 nasopharyngeal biopsies, 42 being confirmed as undifferentiated nasopharyngeal carcinoma and 20 are normal nasopharyngeal epithelium cells. Our results show that 100% of individuals retained the XhoI restriction site. A rare NPC variant, having a 69 bp deletion in the C-terminus region of the BNLF1 gene, covering the 30 bp deletion, was found in two NPC biopsies. The deleted 30 and 69 bp deleted-variants are significantly (p = 0.006) more frequent in NPC (71.42%) than in control biopsies (52%). In peripheral blood of NPC patients, the deleted-variants (47%) are also lower than in tumor tissues (p = 0.0004), suggesting that the deletion could be associated with a risk of tumor genesis. Direct repeats, located at the extremities of the 30 and 69 bp deletions, should be involved in this process. We propose that other deletions could be found since another similar direct repeat is present at the vicinity of the former ones.

Hereditary non-syndromic deafness is extremely heterogeneous. Autosomal recessive forms account for approximately 80% of genetic cases. Autosomal recessive non-syndromic sensorineural deafness segregating in a large consanguineous Tunisian family was mapped to chromosome 6p21.2-22.3. A maximum lod score of 5.36 at Θ = 0 was obtained for the polymorphic microsatellite marker IR2/IR4. Haplotype analysis defined a 16.5-Mb critical region between microsatellite markers D6S1602 and D6S1665. The screening of 3 candidate genes, COL11A2, BAK1 and TMHS, did not reveal any disease causing mutation, suggesting that this is a novel deafness locus, which has been named DFNB66. A search in the Human Cochlear EST Library for ESTs located in this critical interval allowed us to identify several candidates. Further investigations on these candidates are needed in order to identify the deafness-causing gene in this Tunisian family.

Approximately 80% of the hereditary hearing loss is nonsyndromic. Isolated deafness is the most genetically heterogeneous trait. We have ascertained 10 individuals from a large consanguineous Tunisian family with congenital profound autosomal recessive deafness. All affected individuals are otherwise healthy. Genotype analysis excluded linkage to known recessive deafness loci in this family. Following a genome wide screening, a linkage was detected only with locus D1S206 on chromosome 1, thereby defining a novel deafness locus, DFNB32. In order to confirm linkage and for fine mapping the genetic interval, 12 individuals belonging to this family were added and 19 microsatellite markers were tested. A maximum two-point lodscore of 4.96 was obtained at a new polymorphic marker D1S21401. Haplotype analysis defined a 16 Mb critical region between D1S2868 and afmb014zb9. The interval of DFNB32 locus overlap with DFNA37 locus and the Marshall and Stickler syndromes locus. The entire coding region of COL11A1, responsible of the later syndromes, was screened and no mutation was observed. Towards the identification of the DFNB32 gene, a search on the Human Cochlear cDNA Library and EST Database was done. The genes corresponding to the ESTs found in the DFNB32 interval are being screened for deafness-causing mutations.

Despite the fact that most adult humans worldwide are latently infected by the Epstein-Barr virus (EBV), only a very small percentage of them will develop an EBV-associated malignancy. We do not know whether this situation reflects the existence of more sensitive individuals or of particularly tumorigenic EBV strains. We postulated that if highly tumorigenic EBV strains did exist, they would be preferentially found in consistently EBV-associated tumors, such as nasopharyngeal carcinoma (NPC), and differ significantly from the strains present in other, non-pathological sites of the same patients. To test this hypothesis, we compared the BNLF1 gene of the EBV strains present in tumors and in "reservoir lymphocytes" of 6 NPC-bearing patients from Tunisia. Our results show that all of these patients were infected by more than 1 (and up to 7) EBV strains. Moreover, lymphocytes and tumor cells from the same individual were systematically infected by different viral strains. The origin and biological significance of these multistrain infections are discussed.

Pendred syndrome comprises congenital sensorineural hearing loss, thyroid goiter, and positive perchlorate discharge test. Recently, this autosomal recessive disorder was shown to be caused by mutations in the PDS gene, which encodes an anion transporter called pendrin. Molecular analysis of the PDS gene was performed in two consanguineous large families from Southern Tunisia comprising a total of 23 individuals affected with profound congenital deafness; the same missense mutation, L445W, was identified in all affected individuals. A widened vestibular aqueduct was found in all patients who underwent computed tomography (CT) scan exploration of the inner ear. In contrast, goiter was present in only 11 affected individuals, who interestingly had a normal result of the perchlorate discharge test whenever performed. The present results question the sensitivity of the perchlorate test for the diagnosis of Pendred syndrome and support the use of a molecular analysis of the PDS gene in the assessment of individuals with severe to profound congenital hearing loss associated with inner ear morphological anomaly even in the absence of a thyroid goiter.

Les deficits hereditaires de l'audition constituent l'atteinte sensorielle la plus frequente chez l'enfant. Certains sont associes a d'autres symptomes (surdites syndromiques). La plupart se presentent comme un deficit sensoriel isole. Ces derniers, souvent tres severes et congenitaux, compromettent l'acquisition du langage parle. Le terme de surdite isolee hereditaire recouvre un tres grand nombre d'atteintes monogeniques, pour l'essentiel autosomiques recessives. Ce n'est que tres recemment que ce domaine de la pathologie s'est ouvert a l'analyse genetique, qui devrait permettre d'etablir la definition clinique de ces diverses entites ainsi reconnues, et d'approcher leurs bases moleculaires et leur pathogenie.

Background and purpose Nasopharyngeal carcinoma (NPC) is generally responsive to radiation therapy. However therapeutic results after conventional radiotherapy remain relatively poor especially for patients with locoregional advanced NPC. The aim of this study was to evaluate the impact of a split course bifractionated radiotherapy regimen in a phase III randomised trial. Patients and methods From January 1997 to September 2003, 154 patients with M0 histologically proven NPC were treated in our institution. They were staged according to the American Joint Committee on Cancer – International Union Against Cancer (AJCC–UICC) 1986 TNM classification. Patients with locally advanced nodal disease (N2–N3) received induction chemotherapy. All patients were randomised to receive either conventional radiotherapy at 2 Gy/fraction/day, 5 days/week to 70 Gy/7 weeks or split course bifractionated radiotherapy at 1.6 Gy/fraction, twice daily, 5 days/week to 70.4 Gy/6 weeks. Response and toxicity were evaluated according to the WHO and RTOG criteria. Results Patients were well balanced between the two arms. The complete remission rate was 91% in conventional radiotherapy arm and 93% in bifractionated radiotherapy arm (p = 0.3). There was more grade II–III skin fibrosis in experimental arm with a 5 year actuarial probability of 66% vs 52% (p = 0.04). Locoregional and distant relapses occurred in 34% of cases in conventional arm and 38% in experimental arm (p = 0.28). With a median follow-up of 56 months, the 5 year overall survival and the disease free survival rates were, respectively (71% and 61%), in conventional arm and (62% and 60%) in bifractionated arm, the difference being statistically non significant. Comments The present trial comparing conventional radiotherapy to a split course bifractionated radiation therapy failed to demonstrate significant improvement in locoregional control and survival in experimental arm which was associated with more grade II–III skin fibrosis.

Hereditary non-syndromic profound deafness affects about 1 in 2000 children prior to language acquisition. In 80% of the cases, the mode of transmission is autosomal recessive. The number of genes involved in these recessive forms of isolated deafness (DFNB genes) has been estimated to between 30 and 100. So far, ten DFNB genes have been mapped to human chromosomes, one of which has been isolated2. By linkage analysis of a single family whose members were affected with profound deafness, some of them presenting with vestibular dysfunction, DFNB2 has been mapped to chromosome 11q13 (ref. 3). The gene responsible for a form of Usher syndrome type I, USH1B, has been assigned to the same chromosomal region4. Usher syndrome associates profound congenital deafness and vestibular dysfunction with retinitis pigmentosa. In the homologous murine region are located the shaker-1 mutations responsible for deafness and vestibular dysfunction. It has been demonstrated that the murine shaker-1 and human USH1B phenotypes result from mutations in the gene encoding myosin-VIIA5,6. Based on mapping data as well as on the similarities between the phenotypes of DFNB2-affected patients and shaker-1 mouse mutants, we have proposed that a defective myosin-VIIA may also be responsible for DFNB2 (ref. 1). Sequence analysis of each of the coding exons of the myosin-VIIA gene (MYO7A) was thus undertaken in the DFNB2-affected family. In the last nucleotide of exon 15, a G to A transition was detected, a type of mutation that is known to decrease the efficiency of splicing7‐14. Accordingly, this result shows that different mutations in MYO7A result in either an isolated or a syndromic form of deafness.

We explored the mitochondrial 12S rRNA and the tRNASer(UCN) genes in 100 Tunisian families affected with NSHL and in 100 control individuals. We identified the mitochondrial A1555G mutation in one out of these 100 families and not in the 100 control individuals. Members of this family harbouring the A1555G mutation showed phenotypic heterogeneity which could be explained by an eventual nuclear-mitochondrial interaction. So, we have screened three nuclear genes: GJB2, GJB3, and GJB6 but we have not found correlation between the phenotypic heterogeneity and variants detected in these genes. We explored also the entire mitochondrial 12S rRNA and the tRNASer(UCN) genes. We detected five novel polymorphisms: T742C, T794A, A813G, C868T, and C954T, and 12 known polymorphisms in the mitochondrial 12S rRNA gene. None of the 100 families or the 100 controls were found to carry mutations in the tRNASer(UCN) gene. We report here the first mutational screening of the mitochondrial 12S rRNA and the tRNASer(UCN) genes in the Tunisian population which describes the second family harbouring the A1555G mutation in Africa and reveals novel polymorphisms in the mitochondrial 12S rRNA gene.

Hereditary non-syndromic deafness is extremely heterogeneous. Autosomal recessive forms account for approximately 80% of genetic cases. Autosomal recessive non-syndromic sensorineural deafness segregating in a large consanguineous Tunisian family was mapped to chromosome 6p21.2-22.3. A maximum lod score of 5.36 at theta=0 was obtained for the polymorphic microsatellite marker IR2/IR4. Haplotype analysis defined a 16.5-Mb critical region between microsatellite markers D6S1602 and D6S1665. The screening of 3 candidate genes, COL11A2, BAK1 and TMHS, did not reveal any disease causing mutation, suggesting that this is a novel deafness locus, which has been named DFNB66. A search in the Human Cochlear EST Library for ESTs located in this critical interval allowed us to identify several candidates. Further investigations on these candidates are needed in order to identify the deafness-causing gene in this Tunisian family.

Usher syndrome (USH) is an autosomal recessive disorder characterised by hearing impairment and retinitis pigmentosa (RP). The prevalence of USH varies from one population to another, for example, 3-4.4 per 100 000 in Scandinavian and North American populations1,2 and 6.2-10 per 100 000 in the city of Birmingham, UK.3 This syndrome is clinically heterogeneous and three clinical forms have been described4: (1) USH type I (USH1) is characterised by severe to profound congenital deafness, constant vestibular dysfunction, and prepubertal onset of RP; (2) USH type II (USH2) is characterised by congenital moderate to severe deafness, absence of vestibular dysfunction, and onset of RP usually in the late second to early third decade; (3) USH type III (USH3) is characterised by postlingual progressive deafness, occasional vestibular dysfunction, and progressive RP with a variable age of onset (see also http://www.ncbi.nlm.nih.gov/omim). Usher syndrome is also genetically heterogeneous; at least six distinct loci are responsible for USH1 (USH1A-F), three for USH2 (USH2A-C), and one for USH35 (Hereditary hearing loss homepage at URL, http://dnalab.www.uia.ac.be/dnalab/hhh). Usher syndrome type II (USH2) appears to be the commonest clinical form of the disorder in the American population, accounting for more than 50% of all USH cases.3,6 This clinical form tends to be rare in other populations.7 In the Tunisian population, only two USH2 families, Us8 and Z (this work), have been identified so far. These families were ascertained from villages from the south and the north of Tunisia, respectively, where endogamous marriage is relatively common for social and cultural reasons. Of all the USH2 subtypes, USH2A seems to be the most frequent. According to a study performed in various ethnic populations, USH2A is responsible for more than 85% of USH2 cases.9 This genetic form showed considerable phenotypic …

Usher type II syndrome is defined by the association of retinitis pigmentosa, appearing in the late second to early third decade of life, with congenital moderate to severe non-progressive hearing loss. This double sensory impairment is not accompanied by vestibular dysfunction. To date, only one Usher type II locus, USH2A, at chromosome band 1q41, has been defined. Here, we demonstrate by linkage analysis, that the gene responsible for Usher type II syndrome in a Tunisian consanguineous family maps to chromosome 3 at position p23-24.2, thus providing definitive evidence for the genetic heterogeneity of the syndrome. A maximum lod score of 4.3 was obtained with the polymorphic microsatellite markers corresponding to loci D3S1578, D3S3647 and D3S3658. This maps the gene underlying USH2B to a chromosomal region which overlaps the interval defined for the non-syndromic sensorineural recessive deafness DFNB6, raising the possibility that a single gene underlies both defects. However, the audiometric features in the patients affected by USH2B and DFNB6 are very different.

Approximately 80% of hereditary hearing loss is non-syndromic. Non-syndromic deafness is the most genetically heterogeneous trait. The most common and severe form of hereditary hearing impairment is autosomal recessive non-syndromic hearing loss (ARNSHL), accounting for approximately 80% of cases of genetic deafness. To date, 22 genes implicated in ARNSHL have been identified. Recently a gene, DFNB31/WHRN, which encodes a putative PDZ scaffold protein called whirlin, was found to be responsible for the ARNSHL DFNB31. We found evidence for linkage to the DFNB31 locus in a consanguineous Tunisian family segregating congenital profound ARNSHL. Mutation screening of DFNB31/WHRN revealed four nonpathogenic sequence variants and a novel frameshift mutation [c.2423delG] + [c.2423delG] that changed the reading frame and induced a novel stop codon at amino acid 818 ([p.Gly808AspfsX11] + [p.Gly808AspfsX11]). To determine the contribution of the DFNB31 locus in the childhood deafness, we performed linkage analysis in 62 unrelated informative families affected with ARNSHL. No linkage was found to this locus. From this study, we concluded that DFNB31/WHRN is most likely to be a rare cause of ARNSHL in the Tunisian population. © 2005 Wiley-Liss, Inc.

Editor—Congenital deafness occurs in approximately 1 in 1000 live births and at least 50% of these cases are hereditary.1 Among the prelingual genetic forms of deafness, the autosomal recessive forms ( DFNB ) are frequent (80% of the cases) and in most cases are sensorineural and severe.1 Twenty eight loci that cause autosomal recessive non-syndromic hearing loss (ARNSHL) have been identified (http://dnalab-www.uia.ac.be./dnalab/hhh/index.html). The first locus defined for recessive deafness ( DFNB1 ) is linked to chromosome 13q12-13 and was identified by homozygosity mapping in two large consanguineous families from Tunisia.2 This initial report was followed by the identification of other consanguineous families of different ethnic origins which were linked to the DFNB1 locus and of several non-consanguineous white families in which the ARNSHL phenotype cosegregated with markers from chromosome 13q12-13.3-6Mutations in connexin26 ( Cx26 ), a gene that encodes gap junction protein beta-2 (GJB-2), have been shown to result in autosomal recessive ( DFNB1 ) and dominant ( DFNA3 ) non-syndromic sensorineural deafness.7 Mutations in the Cx26 gene have been found to be the most common cause of autosomal recessive deafness and the most frequently observed mutation is 35delG.8-12 The high prevalence of Cx26 mutations and their importance as a cause of ARNSHL have prompted the development of several different mutation detection assays to screen the single Cx26 coding exon.13-16 A rapid method to detect mutations in the GJB2 …