Summary Exercise improves whole-body metabolic health through adaptations to various tissues including adipose tissue, but the effects of exercise training on the lipidome of white (WAT) and brown (BAT) adipose tissue are unknown. Here, we utilized MS/MSALL shotgun lipidomics to determine the molecular signatures of exercise-induced adaptations to subcutaneous WAT (scWAT) and BAT. Three weeks of exercise-training decreased specific molecular species of phosphatidic acid (PA), phosphatidylcholines (PC), phosphatidylethanolamines (PE), and phosphatidylserines (PS) in scWAT and increased specific molecular species of PC and PE in BAT. Exercise also decreased most triacylglycerols (TAGs) in scWAT and BAT. In summary, exercise-induced changes to the scWAT and BAT lipidome were highly specific to certain molecular lipid species, indicating that changes in tissue lipid content reflects selective remodeling in scWAT and BAT of both phospholipids and glycerol lipids in response to exercise training, thus providing a comprehensive resource for future studies of lipid metabolism pathways.

Various previous studies established that the amphiphilic tri-block copolymer known as poloxamer 188 (P188) or Pluronic-F68 can stabilize the plasma membrane following a variety of injuries to multiple mammalian cell types. This characteristic led to proposals for the use of P188 as a therapeutic treatment for various disease states, including muscular dystrophy. Previous studies suggest that P188 increases plasma membrane integrity by resealing plasma membrane disruptions through its affinity for the hydrophobic lipid chains on the lipid bilayer. P188 is one of a large family of copolymers that share the same basic tri-block structure consisting of a middle hydrophobic propylene oxide segment flanked by two hydrophilic ethylene oxide moieties [poly(ethylene oxide)80-poly(propylene oxide)27-poly(ethylene oxide)80]. Despite the similarities of P188 to the other poloxamers in this chemical family, there has been little investigation into the membrane-resealing properties of these other poloxamers. In this study we assessed the resealing properties of poloxamers P181, P124, P182, P234, P108, P407, and P338 on human embryonic kidney 293 (HEK293) cells and isolated muscle from the mdx mouse model of Duchenne muscular dystrophy. Cell membrane injuries from glass bead wounding and multiphoton laser injury show that the majority of poloxamers in our panel improved the plasma membrane resealing of both HEK293 cells and dystrophic muscle fibers. These findings indicate that many tri-block copolymers share characteristics that can increase plasma membrane resealing and that identification of these shared characteristics could help guide design of future therapeutic approaches.

Objectives: As the United States (U.S.) population rapidly ages, the incidence of Alzheimer's Disease and Related Dementias (ADRDs) is rising, with racial/ethnic minorities affected at disproportionate rates. Much research has been undertaken to test, sequence, and analyze genetic risk factors for ADRDs in Caucasian populations, but comparatively little has been done with racial/ethnic minority populations. We conducted a scoping review to examine the nature and extent of the research that has been published about the genetic factors of ADRDs among racial/ethnic minorities in the U.S.Design: Using an established scoping review methodological framework, we searched electronic databases for articles describing peer-reviewed empirical studies or Genome-Wide Association Studies that had been published 2005–2018 and focused on ADRD-related genes or genetic factors among underrepresented racial/ethnic minority population in the U.S.Results: Sixty-six articles met the inclusion criteria for full text review. Well-established ADRD genetic risk factors for Caucasian populations including APOE, APP, PSEN1, and PSEN2 have not been studied to the same degree in minority U.S. populations. Compared to the amount of research that has been conducted with Caucasian populations in the U.S., racial/ethnic minority communities are underrepresented.Conclusion: Given the projected growth of the aging population and incidence of ADRDs, particularly among racial/ethnic minorities, increased focus on this important segment of the population is warranted. Our review can aid researchers in developing fundamental research questions to determine the role that ADRD risk genes play in the heavier burden of ADRDs in racial/ethnic minority populations.

Various injuries to the neural tissues can cause irreversible damage to multiple functions of the nervous system ranging from motor control to cognitive function. The limited treatment options available for patients have led to extensive interest in studying the mechanisms of neuronal regeneration and recovery from injury. Since many neurons are terminally differentiated, by increasing cell survival following injury it may be possible to minimize the impact of these injuries and provide translational potential for treatment of neuronal diseases. While several cell types are known to survive injury through plasma membrane repair mechanisms, there has been little investigation of membrane repair in neurons and even fewer efforts to target membrane repair as a therapy in neurons. Studies from our laboratory group and others demonstrated that mitsugumin 53 (MG53), a muscle-enriched tripartite motif (TRIM) family protein also known as TRIM72, is an essential component of the cell membrane repair machinery in skeletal muscle. Interestingly, recombinant human MG53 (rhMG53) can be applied exogenously to increase membrane repair capacity both in vitro and in vivo. Increasing the membrane repair capacity of neurons could potentially minimize the death of these cells and affect the progression of various neuronal diseases. In this study we assess the therapeutic potential of rhMG53 to increase membrane repair in cultured neurons and in an in vivo mouse model of neurotrauma. We found that a robust repair response exists in various neuronal cells and that rhMG53 can increase neuronal membrane repair both in vitro and in vivo. These findings provide direct evidence of conserved membrane repair responses in neurons and that these repair mechanisms can be targeted as a potential therapeutic approach for neuronal injury.

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