Using a sample of ERP adopters among Chinese publicly listed firms and a one-group pre- and post-test design, this study examines the impact of dominant shareholdings on the relationship between Enterprise Resources Planning (ERP) systems and earnings quality. We use the absolute value of discretionary accruals as a proxy for earnings quality. We predict and find that as the dominant shareholdings increase, Chinese firms show a decrease in the absolute value of total discretionary accruals after ERP implementations. Furthermore, we find that after ERP implementations, discretionary short-term accruals decrease with higher dominant shareholdings, while discretionary long-term accruals increase with higher dominant shareholdings. Our study contributes to research and practice by documenting that dominant shareholdings in China can influence the impact of ERP implementations on earnings quality, suggesting that dominant shareholdings may induce dominant shareholders' self-serving incentives to influence firms' financial reporting via ERP implementations.
Background
Metformin is commonly considered the first-line therapy for type 2 diabetes (T2D) and also had potential treating utility in other areas; however, ~20% of patients experience intolerance with unclear underlying mechanisms. In the present study, we performed the full-length 16S rRNA (V1-V9) for the fecal samples and bioinformatics analysis to study the mechanisms of the metformin intolerance combining the gut flora and host.
Results
The results showed that Barnesiella (p=0.046) and Parabacteroides goldsteinii (p=0.016), which transforming primary into secondary bile acid (SBA), were higher in the TS than T group, and were eliminated in the TSa group, which might lead to the accumulation of primary bile acids (PBA) such as cholic acid (CA), the change of GLI1 gene, and following diarrhea in the TSa group. Lactobacillus brevis (p=0.024) and Lactobacillus plantarum (p=0.026) were up-regulated in TSa than TS group. The two flora might cause the changes of genes including FOXA2, HTR7, GADPH, and intolerance relief, which might be a worthwhile future direction for preventing metformin intolerance.
Conclusions
These results hinted that the differential flora and co-regulation of them with the host might be intolerance-related. Our results partly provided theoretical support for intolerance prevention.
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