Publications by authors named "Elena Fazio"

To investigate factors associated with infrequent dental use among older adults receiving home- and community-based services. This cross-sectional study analyzed responses from the 2014 National Survey of Older Americans Act participants who received home- and community-based services. Descriptive and multivariable analyses were conducted to examine the association between infrequent dental use and key sociodemographic and health indicators.

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In this issue of Alzheimer's & Dementia, Mashour et al. propose the intriguing hypothesis that some manifestations of late-stage dementia are reversible, albeit transiently. Calling this phenomenon paradoxical lucidity, their paper follows a 2018 workshop sponsored by the National Institute on Aging that assessed the state of knowledge on lucidity in dementia and identified areas ripe for further study.

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Progressive impairment of proteostasis and accumulation of toxic misfolded proteins are associated with the cellular aging process. Here, we employed chronologically aged yeast cells to investigate how activation of the unfolded protein response (UPR) upon accumulation of misfolded proteins in the endoplasmic reticulum (ER) affects lifespan. We found that cells lacking a functional UPR display a significantly reduced chronological lifespan, which contrasts previous findings in models of replicative aging.

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During homeostasis, the colonic epithelium is replenished every 3-5 days by rapidly cycling stem cells. However, various insults can lead to depletion of stem cells, and colonic epithelium can be regenerated from negative cells. While studies in the small intestine have addressed the lineage identity of the negative regenerative cell population, in the colon this question has remained unanswered.

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Article Synopsis
  • Pancreatitis is a serious disease of the pancreas that can lead to cancer called pancreatic ductal adenocarcinoma (PDAC).
  • ATF3 is a protein that helps control how cells respond to damage, and scientists found it plays a big role in how the pancreas reacts during pancreatitis.
  • When ATF3 is missing, pancreas cells don't change like they should during injury, which can cause more damage and inflammation.
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Metastatic epithelial ovarian cancer (EOC) cells can form multicellular spheroids while in suspension and disperse directly throughout the peritoneum to seed secondary lesions. There is growing evidence that EOC spheroids are key mediators of metastasis, and they use specific intracellular signalling pathways to control cancer cell growth and metabolism for increased survival. Our laboratory discovered that AKT signalling is reduced during spheroid formation leading to cellular quiescence and autophagy, and these may be defining features of tumour cell dormancy.

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The endoplasmic reticulum (ER) is the point of entry of proteins into the secretory pathway. Nascent peptides interact with the ER quality control machinery that ensures correct folding of the nascent proteins. Failure to properly fold proteins can lead to loss of protein function and cytotoxic aggregation of misfolded proteins that can lead to cell death.

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Recent genomics analysis of the high-grade serous subtype of epithelial ovarian cancer (EOC) show aberrations in the phosphatidylinositol 3-kinase (PI3K)/AKT pathway that result in upregulated signaling activity. Thus, the PI3K/AKT pathway represents a potential therapeutic target for aggressive high-grade EOC. We previously demonstrated that treatment of malignant ascites-derived primary human EOC cells and ovarian cancer cell lines with the allosteric AKT inhibitor Akti-1/2 induces a dormancy-like cytostatic response but does not reduce cell viability.

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Background: Stanniocalcin 2 (STC2) is a secreted protein activated by (PKR)-like Endoplasmic Reticulum Kinase (PERK) signalling under conditions of ER stress in vitro. Over-expression of STC2 in mice leads to a growth-restricted phenotype; however, the physiological function for STC2 has remained elusive. Given the relationship of STC2 to PERK signalling, the objective of this study was to examine the role of STC2 in PERK signalling in vivo.

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Background & Aims: Fibroblast growth factor 21 (FGF21) acts as a hormonal regulator during fasting and is involved in lipid metabolism. Fgf21 gene expression is regulated by peroxisome proliferator-activated receptor (PPAR)-dependent pathways, which are enhanced during pancreatitis. Therefore, the aim of this study was to investigate FGF21's role in pancreatic injury.

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Streptozotocin (STZ), a pancreatic beta cell toxin, is used to induce diabetic conditions by targeting the Glut-2 transporter. We have recently identified decreased Glut-2 expression in beta cells of mice lacking the transcription factor Mist1 (Mist1(KO)). Given the loss in Glut-2 expression, we examined whether Mist1(KO) beta cells have an increased resistance to STZ.

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Several animal models have been developed to investigate the pathobiology of pancreatitis, but few studies have examined the effects that altered pancreatic gene expression have in these models. In this study, the sensitivity to secretagogue-induced pancreatitis was examined in a mouse line that has an altered acinar cell environment due to the targeted deletion of Mist1. Mist1 is an exocrine specific transcription factor important for the complete differentiation and function of pancreatic acinar cells.

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Objectives: Racial and socioeconomic disparities in health have become a prominent feature of American society, though our understanding of the processes leading to such persistent disparities is still relatively limited. In this study, we focus on the impact of social and economic advantages and disadvantages over the life course on health disparities at older ages. In particular, we look at the roles of both cumulative and current financial resources and financial strains as determinants of a range of subjective and objective health assessments of physical conditions, functional impairment, and mental health.

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This article proposes several conceptual perspectives designed to advance our understanding of the material and experiential conditions contributing to persistent disparities in rates of morbidity and mortality among groups unequal in their social and economic statuses. An underlying assumption is that these disparities, which are in clear evidence at mid- and late life, may be anchored to earlier circumstances of the life course. Of particular interest are those circumstances resulting in people with the least privileged statuses having the greatest chances of exposure to health-related stressors.

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