Exercise prevents obesity-induced cognitive decline and white matter damage in mice.

Obesity in the western world has reached epidemic proportions, and yet the long-term effects on brain health are not well understood. To address this, we performed transcriptional profiling of brain regions from a mouse model of western diet (WD)-induced obesity. Both the cortex and hippocampus from C57BL/6J (B6) mice fed either a WD or a control diet from 2 months of age to 12 months of age (equivalent to midlife in a human population) were profiled. Gene set enrichment analyses predicted that genes involved in myelin generation, inflammation, and cerebrovascular health were differentially expressed in brains from WD-fed compared to control diet-fed mice. White matter damage and cerebrovascular decline were evident in brains from WD-fed mice using immunofluorescence and electron microscopy. At the cellular level, the WD caused an increase in the numbers of oligodendrocytes and myeloid cells suggesting that a WD is perturbing myelin turnover. Encouragingly, cerebrovascular damage and white matter damage were prevented by exercising WD-fed mice despite mice still gaining a significant amount of weight. Collectively, these data show that chronic consumption of a WD in B6 mice causes obesity, neuroinflammation, and cerebrovascular and white matter damage, but these potentially damaging effects can be prevented by modifiable risk factors such as exercise

Modifiers of healthy aging: evaluating the effect of diet and physical inactivity on age-dependent dysfunction of the neurovascular system.

The goal of this project was to construct Gene Ontology (GO) ‘slims,’ high level sets of terms to support data aggregation, to provide a new computational pipeline to better understand sets of genes that are dysfunctional in cancer, with a focus on immune system processes and developmental processes. We used functional annotation data in the Mouse Genomic Informatics (MGI) system for mouse, computationally selected the most informative terms, and consulted with biologists to confirm their relevance. The completed immune system process GO slim of 34 terms covered 1519 out of 1842 total GO immune terms that covered 5257 annotations (73% of annotations to immune system processes overall). Eighty-three excluded terms with direct annotations were grouped as “other immune system process.” The completed developmental system GO slim of 44 terms had the coverage of 3959 out of 5775 total GO immune terms that covered 21219 annotations (84% of annotations to developmental processes overall). Six hundred twenty five excluded terms with direct annotations were grouped as “other developmental processes.” Cancer gene sets of interest were then analyzed using the constructed GO slims to identify which categories of the immune system processes and developmental processes were over or under-represented

Reparo: A Fast RAID Recovery Scheme for Ultra-large SSDs

A recent ultra-large SSD (e.g., a 32-TB SSD) provides many benefits in building cost-efficient enterprise storage systems. Owing to its large capacity, however, when such SSDs fail in a RAID storage system, a long rebuild overhead is inevitable for RAID reconstruction that requires a huge amount of data copies among SSDs. Motivated by modern SSD failure characteristics, we propose a new recovery scheme, called reparo, for a RAID storage system with ultra-large SSDs. Unlike existing RAID recovery schemes, reparo repairs a failed SSD at the NAND die granularity without replacing it with a new SSD, thus avoiding most of the inter-SSD data copies during a RAID recovery step. When a NAND die of an SSD fails, reparo exploits a multi-core processor of the SSD controller in identifying failed LBAs from the failed NAND die and recovering data from the failed LBAs. Furthermore, reparo ensures no negative post-recovery impact on the performance and lifetime of the repaired SSD. Experimental results using 32-TB enterprise SSDs show that reparo can recover from a NAND die failure about 57 times faster than the existing rebuild method while little degradation on the SSD performance and lifetime is observed after recovery. © 2021 Association for Computing Machinery.1

RealWear

NAND flash memory has revolutionized how we manage data in modern digital systems, significant improvements are needed in flash-based storage systems to meet the requirements of emerging data-intensive applications. In this paper, we address the problem of NAND aging markers that represent the wearing degree of NAND cells. Since all flash operations are affected by the wearing status of NAND cells, an accurate NAND aging marker is critical to develop flash optimization techniques. From our evaluation study, we first show that the existing P/E cyclebased aging marker (PeWear) is inadequate to estimate the actual aging status of NAND blocks, thus losing opportunities for further optimizations. To overcome the limitations of PeWear, we propose a new NAND aging marker, RealWear, based on extensive characterization studies using real 3D TLC flash chips. By considering multiple variables that can affect the NAND cell wear, RealWear can accurately indicate the actual wear status of NAND blocks during run time. Using three case studies, we demonstrate that RealWear is effective in enhancing the lifetime and performance of a flash storage system. Our experimental results showed that RealWear can extend the lifetime of individual NAND blocks by 63% and can reduce the GC overhead by 21%. Furthermore, RealWear significantly mitigates read latency fluctuations, guaranteeing that the read latency can be bounded with at most 2 read retry operations. © 2021 Copyright is held by the owner/author(s).N