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Empirically, net capital inflows are pro-cyclical in developed countries and countercyclical in developing countries. That said, private inflows are pro-cyclical and public inflows are counter-cyclical in both groups of countries. The dominance of private (public) inflows in developed (developing) countries drives the difference in total net inflows. We rationalize these patterns using a dynamic stochastic two-sector model of a small open economy facing borrowing constraints. Private agents over-borrow because of the pecuniary externality arising from constraints. The government saves abroad to reduce aggregate debt, making the economy resilient to adverse shocks. Differences in borrowing constraints and shock processes across countries explain the empirical patterns of capital inflows.

In this paper we empirically explore the relationship between debt and output in a panel of 72 countries over the period 1970-2014 using a vector autoregression (VAR). We document two puzzling empirical findings that contrast with what is predicted by a standard small open economy model by Aguiar and Gopinath (2007), where debt and output endogenously respond to total factor productivity (TFP) shocks. First, developing countries' debt falls after a positive output shock, while the model predicts a debt expansion. Second, output declines in developed and developing countries after a debt shock, while the model predicts higher output. The relationship between debt and output depends on the sector taking on debt (households, firms, or governments) and the source of financing (domestic versus external) and differs across countries with varying degrees of economic development or different exchange rate regimes.

Jing-quan Zhang, Bo HongDepartment of Neurosurgery, Changhai Hospital, Second Military Medical University, Shanghai 200433, People's Republic of ChinaBackground: miR520a-3p has previously had its antitumorigenic role in various types of cancers revealed, and been predicted as a posttranscriptional regulator of the NFκB-subunit RELA gene. Thus, miR520a-3p could function in carcinogenesis through suppressing RELA.Methods: Expression of miR520a-3p and RELA mRNA was quantified in glioma and normal tissue, and the correlation between them was analyzed statistically. Also, receiver-operating characteristic (ROC)–curve analysis was performed. Effects of miR520a-3p on cell viability, colony formation, migration, and invasion wereexplored in vitro. Whether RELA was a direct target of miR520a-3p or not was analyzed. Finally, restoration of RELA on the effect of miR520a-3p overexpression on proliferation of glioblastoma cells was detected.Results: Data showed that miR520a-3p expression was aberrantly downregulated and associated with malignance in glioma tissue. Areas under ROC curves of miR520a-3p and RELA mRNA expression were 0.9483 and 0.5967, respectively. Also, miR520a-3p expression was statistically correlated with RELA mRNA level in grade III–IV glioma tissue. Transfection of miR520a-3p mimic significantly increased miR520a-3p expression, and resulted in significant suppression of proliferation, migration, and invasion of glioblastoma cells in vitro. miR520a-3p overexpression resulted in statistical downregulation of RELA, both in mRNA and protein levels. RELA was direct target of miR520a-3p. In addition, restoration of RELA significantly weakened the inhibitory effect of miR520a-3p overexpression on viability and EdU-labeled glioblastoma cells.Conclusion: These findings suggest that miR520a-3p should be helpful in auxiliary glioma diagnosis and can attenuate the proliferation and metastasis of glioblastoma through suppressing RELA, and thus could be an attractive therapeutic target to eliminate glioblastoma.Keywords: miR520a-3p, RELA, proliferation, migration, invasion, glioblastoma