36 research outputs found
Trends in book-tax income and balance sheet differences.
Conference paperWe use Compustat and tax return data to describe trends from 1991-1998 in differences
between book and tax measures of income and balance sheet amounts. Our primary findings
confirm that book-tax income differences are growing throughout the 1990s. Extending prior
work, we partition the sample to describe the differences by industry, global character and
profitability. Secondly, we compare Compustat financial statement assets and liabilities to the
book balance sheet reported on the tax return and find that the tax return amounts exceed the
financial statement amounts in the aggregate. We plan to investigate suggested explanations for
this excess, including differences in book versus tax consolidation reporting and off-balance
sheet activity
Vancomycin-induced gut microbial dysbiosis alters enteric neuron-macrophage interactions during a critical period of postnatal development
Vancomycin is a broad-spectrum antibiotic widely used in cases of suspected sepsis in premature neonates. While appropriate and potentially lifesaving in this setting, early-life antibiotic exposure alters the developing microbiome and is associated with an increased risk of deadly complications, including late-onset sepsis (LOS) and necrotizing enterocolitis (NEC). Recent studies show that neonatal vancomycin treatment disrupts postnatal enteric nervous system (ENS) development in mouse pups, which is in part dependent upon neuroimmune interactions. This suggests that early-life antibiotic exposure could disrupt these interactions in the neonatal gut. Notably, a subset of tissue-resident intestinal macrophages, muscularis macrophages, has been identified as important contributors to the development of postnatal ENS. We hypothesized that vancomycin-induced neonatal dysbiosis impacts postnatal ENS development through its effects on macrophages. Using a mouse model, we found that exposure to vancomycin in the first 10 days of life, but not in adult mice, resulted in an expansion of pro-inflammatory colonic macrophages by increasing the recruitment of bone-marrow-derived macrophages. Single-cell RNA sequencing of neonatal colonic macrophages revealed that early-life vancomycin exposure was associated with an increase in immature and inflammatory macrophages, consistent with an influx of circulating monocytes differentiating into macrophages. Lineage tracing confirmed that vancomycin significantly increased the non-yolk-sac-derived macrophage population. Consistent with these results, early-life vancomycin exposure did not expand the colonic macrophage population nor decrease enteric neuron density in CCR2-deficient mice. Collectively, these findings demonstrate that early-life vancomycin exposure alters macrophage number and phenotypes in distinct ways compared with vancomycin exposure in adult mice and results in altered ENS development
Determinants of the variability in corporate effective tax rates: Evidence from longitudinal data
Firms' Off-Balance Sheet and Hybrid Debt Financing: Evidence from Their Book-Tax Reporting Differences
We match large U.S. corporations' tax returns during 1989-2001 to their financial statements to construct a firm-level proxy of firms' use of off-balance sheet and hybrid debt financing. We find that firms with less favorable prior-period Standard & Poor's (S&P) bond ratings or higher leverage ratios in comparison to their industry report greater amounts of interest expense on their tax returns than to investors and creditors on their financial statements. These between-firm results are consistent with credit-constrained firms using more structured financing arrangements. Our within-firm tests also suggest that firms use more structured financing arrangements when they enter into contractual loan agreements that provide incentives to manage debt ratings. Specifically, we find that after controlling for S&P bond rating and industry-adjusted leverage, our sample firms report greater amounts of interest expenses for tax than for financial statement purposes when they enter into performance pricing contracts that use senior debt rating covenants to set interest rates. Furthermore, we find that the greatest book-tax reporting changes occur when firms become closer to violating these debt rating covenants. These latter findings are consistent with firms' contractual debt covenants influencing their use of off-balance sheet and hybrid debt financing. Copyright University of Chicago on behalf of the Institute of Professional Accounting, 2005.
HIV-1 viral load and CD4 cell count in untreated children with vertically acquired asymptomatic or mild disease.
Background: Plasma HIV-1 RNA levels are high in vertically infected infants. Information in older children is limited, particularly in those who have not received antiretroviral therapy.
Objectives: To describe the relationships between HIV-1 RNA, age and CD4 cell count in untreated vertically infected children.
Design: HIV-1 RNA was measured in 70 children [median age, 3.5 years (range, 0.4-11.9 years); median CD4 cell count, 881 x 10(6)/l (interquartile range, 576-1347 x 10(6) cells/l)] enrolled in a randomized placebo-controlled trial comparing immediate with deferred zidovudine in asymptomatic or mildly symptomatic vertically infected children (PENTA-1 trial). Short-term variability was assessed by comparing HIV-1 RNA at -2 and 0 weeks (prior to randomization). The relationship between age and HIV-1 RNA, and CD4 cell count was analysed using data from all children prior to randomization and sequential samples from 35 remaining on placebo for up to 105 weeks, by fitting mixed linear models.
Results: The within-individual SD in viral load was 0.26 log(10) copies/ml. The median plasma HIV-1 RNA at enrolment was 4.61 log(10) (range, 2.3-6.56 log(10) copies/ml), significantly higher in children aged less than or equal to 2 years (median, 5.23 log(10) copies/ml) than in those aged > 2 years (4.51 log(10) copies/ml; P < 0.0001). Mean HIV-1 RNA fell by 0.38 log(10) copies/ml per year up to 2 years of age, by 0.21 log(10) copies/ml per year from 2 to 4 years of age, and by 0.03 log(10) copies/ml per year from 4 to 6 years of age reaching a nadir of 4.25 log(10) copies/ml at 6 years. Mean log(10) CD4 cell count declined steadily with age and was not significantly correlated with HIV-1 RNA, although there was some evidence that the rate of log(10) CD4 cell decline was negatively correlated with the initial rate of HIV-1 RNA decline. No mutations associated with resistance to zidovudine were observed.
Conclusions: Age is a key factor in the interpretation of both viral load and CD4 cell count in vertically infected children