University of Iowa

About: University of Iowa is a education organization based out in Iowa City, Iowa, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 49229 authors who have published 109171 publications receiving 5021465 citations. The organization is also known as: UI & The University of Iowa.

The Effect of SOX Internal Control Deficiencies and Their Remediation on Accrual Quality

Abstract: This paper investigates the effect of internal control deficiencies and their remediation on accrual quality. We first document that firms reporting internal control deficiencies have lower quality accruals as measured by accrual noise and absolute abnormal accruals relative to firms not reporting internal control problems. Second, we find that firms that report internal control deficiencies have significantly larger positive and larger negative abnormal accruals relative to control firms. This finding suggests internal control weaknesses are more likely to lead to unintentional errors that add noise to accruals than intentional misstatements that bias earnings upward. Third, we doc- ument that firms whose auditors confirm remediation of previously reported internal control deficiencies exhibit an increase in accrual quality relative to firms that do not remediate their control problems. Finally, we find firms that receive different internal control audit opinions in successive years exhibit changes in accrual quality consistent with changes in internal control quality. Collectively, our cross-sectional and intertem- poral change tests provide strong evidence that the quality of internal control affects the quality of accruals.

Childhood risk factors for high adult blood pressure: the Muscatine Study.

Abstract: In adult populations, elevated blood pressure is related to the development of occlusive atherosclerosis, stroke, and renal disease The significance of blood pressure levels in childhood, unless extremely elevated, has not been related to disease outcomes In this study, the risk of high blood pressure in young adult life is evaluated based on the observations of blood pressure and other factors made during the school-aged years Subjects, 2445 in number, were first observed at ages 7 through 18 years and again between 20 and 30 years During childhood, measurements of blood pressure, height, and weight were made in alternate years At adult ages, the same measurements were again made and a health questionnaire was administered According to the data, adult blood pressure is correlated with childhood blood pressure, body size, and change in ponderosity from childhood to adult life Adult ponderosity is related to childhood ponderosity, and those who are most obese as adults show the greatest increase in weight for height from their childhood years These observations suggest that strategies to prevent the acquisition of excess ponderosity during adolescence may be useful in preventing adult hypertension

Creativity and mental illness: prevalence rates in writers and their first-degree relatives.

Abstract: Rates of mental illness were examined in 30 creative writers, 30 matched control subjects, and the first-degree relatives of both groups. The writers had a substantially higher rate of mental illness, predominantly affective disorder, with a tendency toward the bipolar subtype. There was also a higher prevalence of affective disorder and creativity in the writers' first-degree relatives, suggesting that these traits run together in families and could be genetically mediated. Both writers and control subjects had IQs in the superior range; the writers excelled only on the WAIS vocabulary subtest, confirming previous observations that intelligence and creativity are independent mental abilities.

Dopaminergic Neurons Protected from Degeneration by GDNF Gene Therapy

Abstract: Glial cell line-derived neurotrophic factor (GDNF) supports growth and survival of dopaminergic (DA) neurons. A replication-defective adenoviral (Ad) vector encoding human GDNF injected near the rat substantia nigra was found to protect DA neurons from the progressive degeneration induced by the neurotoxin 6-hydroxydopamine (6-OHDA) injected into the striatum. Ad GDNF gene therapy reduced loss of DA neurons approximately threefold 6 weeks after 6-OHDA lesion, as compared with no treatment or injection of Ad lacZ or Ad mGDNF (encoding a biologically inactive deletion mutant GDNF). These results suggest that Ad vector-mediated GDNF gene therapy may slow the DA neuronal cell loss in humans with Parkinson's disease.

The Pendred syndrome gene encodes a chloride-iodide transport protein.

Abstract: Pendred syndrome is the most common form of syndromic deafness and characterized by congenital sensorineural hearing loss and goitre. This disorder was mapped to chromosome 7 and the gene causing Pendred syndrome (PDS) was subsequently identified by positional cloning. PDS encodes a putative transmembrane protein designated pendrin. Pendrin is closely related to a family of sulfate transport proteins that includes the rat sulfate-anion transporter (encoded by Sat-1; 29% amino acid sequence identity), the human diastrophic dysplasia sulfate transporter (encoded by DTD; 32%) and the human sulfate transporter 'downregulated in adenoma' (encoded by DRA; 45%). On the basis of this homology and the presence of a slightly modified sulfate-transporter signature sequence comprising its putative second transmembrane domain, pendrin has been proposed to function as a sulfate transporter. We were unable to detect evidence of sulfate transport following the expression of pendrin in Xenopus laevis oocytes by microinjection of PDS cRNA or in Sf9 cells following infection with PDS-recombinant baculovirus. The rates of transport for iodide and chloride were significantly increased following the expression of pendrin in both cell systems. Our results demonstrate that pendrin functions as a transporter of chloride and iodide, but not sulfate, and may provide insight into thyroid physiology and the pathophysiology of Pendred syndrome.