Aging-Aware Request Scheduling for Non-Volatile Main Memory

Modern computing systems are embracing non-volatile memory (NVM) to implement high-capacity and low-cost main memory. Elevated operating voltages of NVM accelerate the aging of CMOS transistors in the peripheral circuitry of each memory bank. Aggressive device scaling increases power density and temperature, which further accelerates aging, challenging the reliable operation of NVM-based main memory. We propose HEBE, an architectural technique to mitigate the circuit aging-related problems of NVM-based main memory. HEBE is built on three contributions. First, we propose a new analytical model that can dynamically track the aging in the peripheral circuitry of each memory bank based on the bank's utilization. Second, we develop an intelligent memory request scheduler that exploits this aging model at run time to de-stress the peripheral circuitry of a memory bank only when its aging exceeds a critical threshold. Third, we introduce an isolation transistor to decouple parts of a peripheral circuit operating at different voltages, allowing the decoupled logic blocks to undergo long-latency de-stress operations independently and off the critical path of memory read and write accesses, improving performance. We evaluate HEBE with workloads from the SPEC CPU2017 Benchmark suite. Our results show that HEBE significantly improves both performance and lifetime of NVM-based main memory.Comment: To appear in ASP-DAC 202

Teaching the Academic Word List in Foreign Language Speaking Classes

WOS: 00043485270039

Quercetin-induced cell death in human papillary thyroid cancer (B-CPAP) cells

In this study, we have investigated the antiproliferative effect of quercetin on human papillary thyroid cancer cells and determined the apoptotic mechanisms underlying its actions. We have used different concentrations of quercetin to induce apoptosis and measured cell viability. Apoptosis and cell cycle analysis was determined by flow cytometry using Annexin V and propidium iodide. Finally, we have measured changes in caspase-3 and cleaved poly(ADP-ribose) polymerase (PARP) protein expression levels as hallmarks of apoptosis and Hsp90 protein expression level as a marker of proteasome activity in treated and control cells. Quercetin treatment of human papillary thyroid cancer cells resulted in decreased cell proliferation and increased rate of apoptosis by caspase activation. Furthermore, it was demonstrated that quercetin induces cancer cell apoptosis by downregulating the levels of Hsp90. In conclusion, we have shown that quercetin induces downregulation of Hsp90 expression that may be involved in the decrease of chymotrypsin-like proteasome activity which, in order, induces inhibition of growth and causes cell death in thyroid cancer cells. Thus, quercetin appears to be a promising candidate drug for Hsp90 downregulation and apoptosis of thyroid cancer cells

Increased plasma malondialdehyde and protein carbonyl levels and lymphocyte DNA damage in patients with angiographically defined coronary artery disease

We investigated the oxidative modifications of lipids, proteins and DNA, three potential molecular targets of oxidative stress, in 30 patients with angiographically defined coronary artery disease (CAD) and 30 healthy control subjects. In addition, we examined relationships between these oxidative modifications and the severity of vascular lesions in patients with CAD. Malondialdehyde (MDA) and protein carbonyl (PC) levels, as well as ferric reducing antioxidant power (FRAP), were measured in the plasma. DNA damage was evaluated as single strand breaks (SSBs), formamidopyrimidine glycosylase (Fpg) and endonuclease III (E-III)-sensitive sites by the cornet assay in DNA isolated from lymphocytes. MDA and PC levels increased, but FRAP values decreased, in patients as compared to controls. However, these values did not vary with the number of affected coronary vessels and were not correlated with Duke score, a parameter of the severity of vascular lesions in patients with CAD. We also found that lymphocyte DNA damage (SSBs, Fpg and E-III sites) were increased in patients. Although there were no significant differences in SSBs values ill patients grouped according to affected vessel number, Fpg and E-III sites increased. We also detected significant correlations between Duke scores and SSBs and Fpg sites. Serum cholesterol, triglyceride and LDL-cholesterol levels were found to increase, but HDL-cholesterol levels decreased in CAD patients, but these lipids were not correlated with Duke scores. The results of this Study reinforce the presence of increased combined oxidative modifications in lipid, protein and DNA in patients with CAD. However, lymphocyte DNA damage seems to be a more reliable assay than MDA and PC determinations to detect the severity of vascular lesions in patients. (C) 2005 The Canadian Society of Clinical Chemists. All rights reserved