Maranda L.,Albert Sherman Center |
Gupta O.T.,University of Texas Southwestern Medical Center
PLoS ONE | Year: 2016
Type 1 diabetes mellitus (T1DM) a chronic characterized by an absolute insulin deficiency requires conscientious patient self-management to maintain glucose control within a normal range. Family cohesion and adaptability, positive coping strategies, social support and adequate self-regulatory behavior are found to favorably influence glycemic control. Our hypothesis was that the responsible care of a companion animal is associated with these positive attributes and correlated with the successful management of a chronic illness such as type 1 diabetes. We recruited 223 youths between 9 and 19 years of age from the Pediatric Diabetes clinic at the University of Massachusetts Medical School, reviewed the status of their glycemic control (using three consecutive A1c values) and asked them questions about the presence of a pet at home, and their level of involvement with its care. Multivariate analyses show that children who care actively for one or more pets at home are 2.5 times more likely to have control over their glycemic levels than children who do not care for a pet, adjusting for duration of disease, socio-economic status, age and self-management [1.1 to 5.8], pWald = 0.032. A separate model involving the care of a petdog only yielded comparable results (ORa = 2.6 [1.1 to 5.9], pWald = 0.023). © 2016 Maranda, Gupta. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Lewandowski S.L.,University of Massachusetts Medical School |
Janardhan H.P.,University of Massachusetts Medical School |
Trivedi C.M.,University of Massachusetts Medical School |
Trivedi C.M.,Albert Sherman Center
Journal of Biological Chemistry | Year: 2015
Background: Histone-modifying genes play critical roles in the pathogenesis of human congenital heart disease. Results: HDAC3 recruits PRC2 complex to mediate epigenetic silencing of TGF-β1 in a deacetylase-independent manner within second heart field progenitor cells. Conclusion: HDAC3-mediated epigenetic silencing of TGF-β1 is required for normal heart development. Significance: This is the first report of HDAC-mediated epigenetic regulation of second heart field development. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc.
Wahl I.,University of Hamburg |
Lowe B.,University of Hamburg |
Bjorner J.B.,Copenhagen University |
Fischer F.,Charite - Medical University of Berlin |
And 9 more authors.
Journal of Clinical Epidemiology | Year: 2014
Objectives To provide a standardized metric for the assessment of depression severity to enable comparability among results of established depression measures. Study Design and Setting A common metric for 11 depression questionnaires was developed applying item response theory (IRT) methods. Data of 33,844 adults were used for secondary analysis including routine assessments of 23,817 in- and outpatients with mental and/or medical conditions (46% with depressive disorders) and a general population sample of 10,027 randomly selected participants from three representative German household surveys. Results A standardized metric for depression severity was defined by 143 items, and scores were normed to a general population mean of 50 (standard deviation = 10) for easy interpretability. It covers the entire range of depression severity assessed by established instruments. The metric allows comparisons among included measures. Large differences were found in their measurement precision and range, providing a rationale for instrument selection. Published scale-specific threshold scores of depression severity showed remarkable consistencies across different questionnaires. Conclusion An IRT-based instrument-independent metric for depression severity enables direct comparisons among established measures. The "common ruler" simplifies the interpretation of depression assessment by identifying key thresholds for clinical and epidemiologic decision making and facilitates integrative psychometric research across studies, including meta-analysis. © 2014 Elsevier Inc. All rights reserved.
Liu L.,Albert Sherman Center |
Nam M.,Albert Sherman Center |
Fan W.,Albert Sherman Center |
Akie T.E.,Albert Sherman Center |
And 4 more authors.
Journal of Clinical Investigation | Year: 2014
Sirtuin 3 (SIRT3), an important regulator of energy metabolism and lipid oxidation, is induced in fasted liver mitochondria and implicated in metabolic syndrome. In fasted liver, SIRT3-mediated increases in substrate flux depend on oxidative phosphorylation (OXPHOS), but precisely how OXPHOS meets the challenge of increased substrate oxidation in fasted liver remains unclear. Here, we show that liver mitochondria in fasting mice adapt to the demand of increased substrate oxidation by increasing their OXPHOS efficiency. In response to cAMP signaling, SIRT3 deacetylated and activated leucine-rich protein 130 (LRP130; official symbol, LRPPRC), promoting a mitochondrial transcriptional program that enhanced hepatic OXPHOS. Using mass spectrometry, we identified SIRT3-regulated lysine residues in LRP130 that generated a lysine-to-arginine (KR) mutant of LRP130 that mimics deacetylated protein. Compared with wild-type LRP130 protein, expression of the KR mutant increased mitochondrial transcription and OXPHOS in vitro. Indeed, even when SIRT3 activity was abolished, activation of mitochondrial transcription and OXPHOS by the KR mutant remained robust, further highlighting the contribution of LRP130 deacetylation to increased OXPHOS in fasted liver. These data establish a link between nutrient sensing and mitochondrial transcription that regulates OXPHOS in fasted liver and may explain how fasted liver adapts to increased substrate oxidation. © Copyright 2014 American Society for Clinical Investigation.