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. Purpose:  Vessel leakage and loss of pericytes are early signs of diabetic retinopathy (DR), which leads to vision loss. Upregulation of the vascular endothelial growth factor (VEGF) during diabetes plays a key role in mediating these vascular lesions. The aim of this study is to investigate the effects of resveratrol, a natural plant‐derived phytoalexin, on vascular damage and VEGF induction in mouse retinas of early diabetes. Methods:  Diabetes was induced in C57BL/6 mice by five consecutive‐intraperitoneal injections of 55 mg/kg of streptozotocin (STZ). Animals injected with buffer only were used as controls. Beginning 1 month after the fifth injection of STZ or buffer, 20 mg/kg of resveratrol was administered by oral gavage daily for 4 weeks to diabetic and control mice, and all mice were killed 2 months after the injections. We assessed vessel leakage, pericyte loss and VEGF protein expression in mouse retinas of 2‐month diabetes compared with controls with or without resveratrol treatment. Results:  Diabetes led to increase vessel leakage, pericyte loss and VEGF protein level in the mouse retinas compared with controls; however, these changes were effectively blocked by resveratrol treatment. Conclusion:  Our data suggest that resveratrol is effective to decrease vascular lesions and VEGF induction in mouse retinas of early diabetes.

This Working Paper should not be reported as representing the views of the IMF. The views expressed in this Working Paper are those of the author(s) and do not necessarily represent those of the IMF or IMF policy. Working Papers describe research in progress by the author(s) and are published to elicit comments and to further debate. This paper examines equilibrium price relationships and price discovery between credit defaul swap (CDS), bond, and equity markets for emerging market sovereign issuers. Findings suggest that CDS and bond spreads converge despite various pressures that arise in the market. In most countries, however, we do not find any equilibrium price relationship between the bond and CDS markets and the equity markets. As for price discovery, our results are mixed. This stands in contrast to the empirical findings on corporate issuers in the United States and Europe.

Clusterin (CLU), a glycoprotein, is involved in apoptosis, producing two alternatively spliced isoforms in various cell types. The pro-apoptotic CLU appears to be a nuclear isoform (nuclear clusterin; nCLU), and the secretory CLU (sCLU) is thought to be anti-apoptotic. The detailed molecular mechanism of nCLU as a pro-apoptotic molecule has not yet been clear. In the current study, overexpressed nCLU induced apoptosis in human kidney cells. Biochemical studies revealed that nCLU sequestered Bcl-XL via a putative BH3 motif in the C-terminal coiled coil (CC2) domain, releasing Bax, and promoted apoptosis accompanied by activation of caspase-3 and cytochrome c release. These results suggest a novel mechanism of apoptosis mediated by nCLU as a pro-apoptotic molecule.

A signaling link between JNK and 14-3-3 and subsequent mitochondrial death pathway may partly act as an early signaling that promotes apoptotic cell death leading to AKI, and glutamine may at least partially prevent apoptosis via enhancing Hsp70 or GSH levels.