Research Question/Issue: Existing research on sovereign wealth funds (SWFs) has largely explored how they affect target firm value, overlooking the role they play in corporate governance. This paper examines the impact of SWFs' cross-border equity acquisitions on targets' corporate governance and the role the institutional environment of SWF countries plays in shaping this impact.Research Findings/Insights: We use a difference-in-differences approach and find that, on average, SWF investments are negatively related to target firms' corporate governance. This impact holds for small SWF cross-border equity investments only and is stronger for firms that are weakly governed and for those located in jurisdictions with weak shareholder protection. The negative relation is more pronounced when SWFs' home countries have lower-quality investor protection, corruption control, governmental effectiveness, and law enforcement than their host countries. We find further that SWF investments are positively associated with target firms' earnings management and negatively associated with investment efficiency. Finally, target firm value is found to decrease after SWF investments.Theoretical/Academic Implications: The evidence that SWFs' small equity investments are detrimental to target firms' corporate governance is broadly consistent with the view that SWFs are passive investors. Managers can exploit this passivity, as evidenced by higher earnings management, reduced investment efficiency, and lower firm value.Practitioner/Policy Implications: This study has important policy implications for investors, SWF managers, and policymakers. The passive role of SWFs in corporate governance should prompt minority shareholders to look for alternative monitoring mechanisms. Moreover, SWF managers may realize the need to target firms with strong corporate governance at the outset to compensate for the post-acquisition decline. Host country policymakers may need to condition SWF investments on commitments to improve the corporate governance of investee firms, which would be akin to the performance requirements imposed on inward foreign direct investment
Abstract. The present study aimed to investigate the effect of glutathione S-transferase A1 (GSTA1) on lung cancer cell viability, invasion and adhesion in the presence of nicotine in vitro. Furthermore, the effect of GSTA1 on the epithelial-mesenchymal transition (EMT), a process strongly associated with lung cancer metastasis, was examined. Human lung carcinoma A549 cells were treated with various concentrations of nicotine (0.01, 0.1, 1 and 10 µM) and levels of GSTA1 mRNA and protein were measured by reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. To knock down GSTA1 expression, GSTA1-small interfering RNA was transfected into A549 cells. Cell viability, invasion and adhesion abilities were determined by MTT, Transwell-Matrigel invasion and cell adhesion assays, respectively. The expression of the epithelial cell markers E-cadherin and keratin, and the mesenchymal cell markers vimentin and N-cadherin in A549 cells were examined by western blot analysis. The current study indicated that the expression of GSTA1 was increased in A549 cells following nicotine treatment. GSTA1 suppression inhibited the viability, invasion and adhesion of lung cancer cells. In addition, the increase in lung cancer cell viability, invasion and adhesion by nicotine was suppressed following GSTA1 knockdown. Furthermore, GSTA1 affected the expression of EMT markers in nicotine-treated or untreated lung cancer cells. Thus the present study demonstrates that GSTA1 promotes lung cancer cell invasion and adhesion and mediates the effect of nicotine on lung cancer cell metastasis in vitro. Furthermore, the results demonstrated that GSTA1 exerts its effect on lung cancer cell metastasis by promoting the EMT. IntroductionGlobally, lung cancer is the leading cause of cancer-associated mortality in men and the second leading cause of cancer-associated mortality in women (1). Recurrence and metastasis are the biggest obstacles to effective lung cancer treatment. Although treatments for lung cancer have improved over the past few decades, the 5-year survival rate is only ~16% (2). Thus, it is important to identify biomarkers associated with lung cancer metastasis in order to improve the therapeutic strategies available.Tumor metastasis is a complex process consisting of multiple biological steps (3) including increased motility, invasion into surrounding tissue, intravasation, entry and survival in the circulation, extravasation and eventual colonization of a distant site (4-6). The epithelial-mesenchymal transition (EMT) is a well-coordinated process that induces metastasis in epithelial cancer (7,8). Glutathione S-transferase A 1 (GSTA1) is an isoform of GST primarily involved in the detoxification of electrophilic compounds by undergoing conjugation with glutathione (9,10). Previous studies have demonstrated that the altered expression of GST genes increases the risk of prostate cancer and hepatocellular carcinoma (11)(12)(13)(14). Recently, Pan et al (15) identified the potential of GSTA1...
Background:Esophageal cancer is one of the worst malignant digestive neoplasms with poor treatment outcomes. Esophagectomy plays an important role and offers a potential curable chance to these patients. However, esophagectomy with radical lymphadenectomy is known as one of the most invasive digestive surgeries which are associated with high morbidity and mortality. The enhanced recovery after surgery (ERAS) protocol is a patient-centered, surgeon-led system combining anesthesia, nursing, nutrition, and psychology, which is designed for reducing complications, promoting recovery, and improving treatment outcomes. This systematic review and meta-analysis is aiming at how beneficial, and to what extent ERAS really will be.Methods:A systematic literature search will be performed through January 2018 using MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials, and Google Scholar for relevant articles published in any language. Randomized controlled trials, prospective cohort studies, and propensity-matched comparative studies will be included. All meta-analyses will be performed using Review Manager software. The quality of the studies will be evaluated using the guidelines listed in the Cochrane Handbook. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses statements will be followed until the findings of the systematic review and meta-analysis are reported.Results:The results of this systematic review and meta-analysis will be published in a peer-reviewed journal.Conclusion:Our study will draw an objective conclusion of the comparisons between ERAS and conventional care in aspects of perioperative outcomes and provide level I evidences for clinical decision makings.
Background/Aim: Most endoscopies performed in the United States utilize sedation. Anesthesia provides patient comfort and improved procedural quality but adds to the complexity of scheduling routine outpatient procedures. We aimed to assess the return of cognitive function after propofol administration in patients undergoing outpatient endoscopies. Patients and Methods: Cognitive recovery for patients undergoing endoscopy under monitored anesthesia care was evaluated using EncephalApp. Patients were tested before and after procedure and healthy controls were tested twice, 30 min apart. Results were tabulated in on state (on time) and off state (off time) and total time (on time + off time). The time difference between pre- and post-tests, “delta,” was calculated for on, off, and total times. Wilcoxon rank test was used to check the difference in mean delta of all three test times between cases and controls and to check for statistical significance. Results: The difference in mean time between cases and controls was significant for off ( P < 0.0001) and total ( P = 0.0002) times. No statistically significant difference was noted in mean time for on time ( P = 0.013) between cases and controls. Cognitive flexibility, a measure of on time, returned to baseline after procedural sedation even though psychomotor speed, a measure of off time and total time, had not. Conclusion: Cognitive flexibility returns to baseline within 30–45 min after propofol sedation despite delayed return of psychomotor speed and reaction time.
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