Aims: We reported the attenuation of diabetes-induced renal dysfunction by exposure to multiple low-dose radiation (LDR) at 25 mGy every other day by suppressing renal oxidative damage. We here explored the optimal conditions of LDR to protect the kidney from diabetes. Main methods: Male C57BL/6J mice with type I diabetes were induced with multiple injections of low-dose streptozotocin. Diabetic mice received whole body X-irradiation at a dose of 12.5, 25 or 50 mGy every other day for either 4 or 8 weeks. Age-matched normal mice were similarly irradiated at the dose of 25 mGy for 4 or 8 weeks. The renal function and histopathological changes were examined at the 4th and 8th weeks of the study. Key findings: Diabetes induced renal dysfunction is shown by the decreased creatinine and increased microalbumin in the urine. Renal oxidative damage, detected by protein nitration and lipid oxidation, and remodeling, reflected by increased expression of connective tissue growth factor, collagen IV and fibronectin, were significantly increased in diabetic mice. All these renal pathological and function changes in diabetic mice were significantly attenuated by exposure to LDR at all regimens, among which, however, exposure to LDR at 12.5 mGy for 8 weeks provided the best protective effect on the kidney of diabetic mice. Significance: Our results suggest that whole-body LDR at 12.5 mGy every other day for 8 weeks is the optimal condition of LDR to protect the kidney from diabetes. (C) 2014 Elsevier Inc. All rights reserved.

The complete convergence is obtained for the moving average processes associated to heavy-tailed distributions via integral test. As the applications, two versions of Chover's law of the iterated logarithm are deduced. (C) 2014 Elsevier Inc. All rights reserved.

We propose and demonstrate a reconfigurable microwave photonic filter (MPF) based on tunable dispersion-induced power fading (DIPF) in a dispersive element A multi-wavelength optical signal is used to generate the multi-taps of the MPF. A polarization modulator (PolM), a polarization controller (PC), and a polarizer are cascaded to build a new modulator which can be regarded as an intensity modulator, a phase modulator, or an intensity and phase hybrid modulator by adjusting the PC. A dispersive element is followed after the PC to generate the DIPF which is controllable by tuning the PC. In this way, the MPF is reconfigurable and tunable. The proposed method is theoretically analyzed and experimentally verified. The simulated results fit well with the experimental ones. (C) 2014 Elsevier B.V. All rights reserved.

This paper considers optimal solutions of interval linear programming problems, in a unified framework. Necessary and sufficient conditions for checking (A, b)-strong optimality and (A, b, c)-strong optimality of interval linear programming with inequality constraints are developed. The features of the proposed methods are illustrated by some examples. (C) 2013 Elsevier B.V. All rights reserved.

Objectives The goal of this study was to evaluate the pharmacodynamic effects of switching patients from ticagrelor to prasugrel. Background Clinicians may need to switch between more potent P2Y(12) inhibitors because of adverse effects or switch to the use of a once-daily dosing regimen due to compliance issues. Methods After a 3-to 5-day run-in phase with a ticagrelor 180-mg loading dose (LD) followed by a ticagrelor 90-mg twice-daily maintenance dose (MD), aspirin-treated patients (N = 110) with stable coronary artery disease were randomized to continue ticagrelor or switch to prasugrel 10-mg once-daily MD, with or without a 60-mg LD. Pharmacodynamic assessments were defined according to P2Y(12) reaction unit (PRU) (P2Y(12) assay) and platelet reactivity index (vasodilator-stimulated phosphoprotein phosphorylation assay) at baseline (before and after the run-in phase) and 2, 4, 24, and 48 h and 7 days after randomization. Results Platelet reactivity was significantly greater at 24 and 48 h after switching to prasugrel versus continued therapy with ticagrelor, although to a lesser extent in those receiving an LD. Mean PRU remained significantly higher in the combined prasugrel groups versus the ticagrelor group (least-squares mean difference: 46 [95% confidence interval 25 to 67]) and did not meet the primary noninferiority endpoint (upper limit of the confidence interval <= 45), although PRU in the prasugrel cohort was lower at 7 days than at 24 or 48 h. Accordingly, rates of high on-treatment platelet reactivity were higher at 24 and 48 h in both prasugrel groups. At 7 days, there was no difference in high on-treatment platelet reactivity rate between the combined prasugrel and ticagrelor groups. Conclusions Compared with continued ticagrelor therapy, switching from ticagrelor to prasugrel therapy was associated with an increase in platelet reactivity that was partially mitigated by the administration of an LD. (C) 2014 by the American College of Cardiology Foundation

Background & Aims: Alcoholic liver disease is associated with inflammation and cell death. Heme oxygenase-1 (HO-1) is a stress-inducible enzyme with anti-apoptotic and anti-inflammatory properties. Here we tested the hypothesis that induction of HO-1 or treatment with a carbon monoxide releasing molecule (CORM) during chronic ethanol exposure protects and/or reverses ethanol-induced liver injury. Methods: Female C57BL/6J mice were allowed free access to a complete liquid diet containing ethanol or to pair-fed control diets for 25 days. Mice were treated with cobalt protoporphyrin (CoPP) to induce HO-1 expression during ethanol feeding or once liver injury had been established. Mice were also treated with CORM-A1, a CO-releasing molecule (CORM), after ethanol-induced liver injury was established. The impact of HO-1 induction on ethanol-induced cell death was investigated in primary cultures of hepatocytes. Results: Induction of HO-1 during or after ethanol feeding, as well as treatment with CORM-A1, ameliorated ethanol-induced increases in AST and expression of mRNAs for inflammatory cytokines. Treatment with CoPP or CORM-A1 also reduced hepatocyte cell death, indicated by decreased accumulation of CK18 cleavage products and reduced RIP3 expression in hepatocytes. Exposure of primary hepatocyte cultures to ethanol increased their sensitivity to TNF alpha-induced cell death; this response was attenuated by necrostatin-1, an inhibitor of necroptosis, but not by caspase inhibitors. Induction of HO-1 with CoPP or CORM-3 treatment normalized the sensitivity of hepatocytes to TNF alpha-induced cell death after ethanol exposure. Conclusions: Therapeutic strategies to increase HO-1 and/or modulate CO availability ameliorated chronic ethanol-induced liver injury in mice, at least in part by decreasing hepatocellular death. (C) 2014 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.