Recent Publications

Hepatic steatosis associated with decreased β-oxidation and mitochondrial function contributes to cell damage in obese mice after thermal injury.
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Hepatic steatosis associated with decreased β-oxidation and mitochondrial function contributes to cell damage in obese mice after thermal injury.

Cell Death Dis. 2018 05 01;9(5):530

Authors: Diao L, Auger C, Konoeda H, Sadri AR, Amini-Nik S, Jeschke MG

Abstract
Severely burned patients who are morbidly obese have poor clinical outcomes with aggravated metabolic consequences, a higher incidence of multiple organ dysfunction/failure, and significantly increased morbidity and mortality. The underlying mechanisms of these adverse outcomes are essentially unknown. Since the liver is one of the central metabolic organs, we hypothesized that thermal injury in obese patients leads to substantially increased lipolysis, hepatic fat infiltration, resulting in profound hepatic cellular and organellar alterations, consequently causing liver damage and severely augmented metabolic dysfunction. We tested this hypothesis using an obese mouse model subjected to a 20% total body surface area burn injury. C57BL/6 mice were randomly divided into low-fat diet (LFD) and high-fat diet (HFD) sham and burn groups (n = 6 per group) and fed for 16 weeks. 7 days after the thermal injury portal and cardiac blood were taken separately and liver tissue was collected for western blotting and immunohistochemical analysis. Gross examination of the liver showed apparent lipid infiltration in HFD fed and burned mice. We confirmed that augmented ER stress and inhibition of Akt-mTOR signaling dysregulated calcium homeostasis, contributed to the decrease of ER-mitochondria contact, and reduced mitochondrial β-oxidation in HFD fed and burned mice, leading to profound hepatic fat infiltration and substantial liver damage, hence increased morbidity and mortality. We conclude that obesity contributes to hepatic fat infiltration by suppressing β-oxidation, inducing cell damage and subsequent organ dysfunction after injury.

PMID: 29748608 [PubMed - indexed for MEDLINE]

Peripheral nerve injuries, pain, and neuroplasticity.
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Peripheral nerve injuries, pain, and neuroplasticity.

J Hand Ther. 2018 Apr - Jun;31(2):184-194

Authors: Osborne NR, Anastakis DJ, Davis KD

Abstract
INTRODUCTION: Peripheral nerve injuries (PNIs) cause both structural and functional brain changes that may be associated with significant sensorimotor abnormalities and pain.
PURPOSE OF THE STUDY: The aim of this narrative review is to provide hand therapists an overview of PNI-induced neuroplasticity and to explain how the brain changes following PNI, repair, and during rehabilitation.
METHODS: Toward this goal, we review key aspects of neuroplasticity and neuroimaging and discuss sensory testing techniques used to study neuroplasticity in PNI patients.
RESULTS: We describe the specific brain changes that occur during the repair and recovery process of both traumatic (eg, transection) and nontraumatic (eg, compression) nerve injuries. We also explain how these changes contribute to common symptoms including hypoesthesia, hyperalgesia, cold sensitivity, and chronic neurogenic pain. In addition, we describe how maladaptive neuroplasticity as well as psychological and personality characteristics impacts treatment outcome.
DISCUSSION AND CONCLUSION: Greater understanding of the brain's contribution to symptoms in recovering PNI patients could help guide rehabilitation strategies and inform the development of novel techniques to counteract these maladaptive brain changes and ultimately improve outcomes.

PMID: 29706196 [PubMed - indexed for MEDLINE]