Publications by authors named "Jarrod A. Call"

Article Synopsis
  • This study examined how two levels of low-intensity vibration training (0.6 g and 1.0 g) affected muscle and bone recovery in mice after a muscle injury known as volumetric muscle loss (VML).
  • Mice were divided into groups receiving either no treatment or varying levels of vibration training for 15 minutes a day over 8 weeks post-injury.
  • Results showed that bone structure improved with vibration training, particularly at the 1.0 g level, while muscle function showed less significant enhancement, suggesting that vibration training may be more beneficial for bone recovery than for muscle after VML.
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  • Prolonged bedrest and lack of physical activity after traumatic musculoskeletal injuries, particularly volumetric muscle loss (VML), can severely limit muscle adaptability and cause metabolic issues.
  • In a study with adult mice, activity restriction combined with VML increased carbohydrate usage and altered metabolic ratios, indicating lower capacity for fatty acid oxidation, while the overall muscle metabolome remained unchanged.
  • The findings suggest that VML injury leads to changes in fatty acid metabolism, which could be worsened by reduced activity, potentially leading to triglyceride accumulation in muscle.
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  • Peripheral nerve-crush injury promotes neuromuscular junction (NMJ) recovery, showing improved muscle function as nerve re-innervates, while volumetric muscle loss (VML) leads to permanent muscle function loss and chronic NMJ impairments.
  • In a study with adult mice, researchers compared the effects of nerve-crush versus VML on NMJ remodeling, monitoring recovery over time post-injury.
  • Results indicated that while nerve-crush injury allowed for complete recovery of muscle strength, VML resulted in persistent deficits, along with abnormal signaling and structural changes at the NMJ, with some noted sex differences in recovery rates.
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The objectives of this study were to determine the effect of COVID-19 on physical therapy (PT) mobilization of trauma patients and to determine if mobilization affected patient course in the ICU. This retrospective study included patients who were admitted to the ICU of a level II trauma center. The patients were divided into two groups, i.

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Skeletal muscle development is a highly ordered process orchestrated transcriptionally by the myogenic regulatory factors. However, the downstream molecular mechanisms of myogenic regulatory factor functions in myogenesis are not fully understood. Here, we identified the RNA-binding protein Musashi2 (Msi2) as a myogenin target gene and a post-transcriptional regulator of myoblast differentiation.

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  • Chronic hypoxia exacerbates muscle atrophy and weakness in mice, significantly reducing muscle mass and strength while impairing muscle regeneration abilities.
  • The study highlights the crucial role of hypoxia-inducible factor HIF-2α in muscle stem cell proliferation and regeneration, revealing negative effects on recovery post-injury.
  • Various experimental approaches, including the use of knockout mice and specific inhibitors, were utilized to investigate the molecular mechanisms driving these effects, with statistical analyses confirming the results.
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Hypophosphatasia (HPP) is a rare metabolic bone disorder characterized by low levels of tissue non-specific alkaline phosphatase (TNAP) that causes under-mineralization of the bone, leading to bone deformity and fractures. In addition, patients often present with chronic muscle pain, reduced muscle strength, and an altered gait. In this work, we explored dynamic muscle function in a homozygous TNAP knockout mouse model of severe juvenile onset HPP.

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Background: This study was designed to develop an understanding of the pathophysiology of traumatic muscle injury in the context of Western diet (WD; high fat and high sugar) and obesity. The objective was to interrogate the combination of WD and injury on skeletal muscle mass and contractile and metabolic function.

Methods: Male and female C57BL/6J mice were randomized into four groups based on a two-factor study design: (1) injury (uninjured vs.

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Introduction: Mitochondria are extremely important organelles in the regulation of bone marrow and brain activity. However, live imaging of these subcellular features with high resolution in scattering tissues like brain or bone has proven challenging.

Methods: In this study, we developed a two-photon fluorescence microscope with adaptive optics (TPFM-AO) for high-resolution imaging, which uses a home-built Shack-Hartmann wavefront sensor (SHWFS) to correct system aberrations and a sensorless approach for correcting low order tissue aberrations.

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The primary objective of this study was to determine if low- or high-resistance voluntary wheel running leads to functional improvements in muscle strength (i.e., isometric and isokinetic torque) and metabolic function (i.

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This study's objective was to investigate how contractile strength loss associated with a volumetric muscle loss (VML) injury affects the adjacent tibial bone structural and functional properties in male C57BL/6J mice. Mice were randomized into one of two experimental groups: VML-injured mice that were injured at age 12 weeks and aged to 20 weeks (8 weeks postinjury, VML) and 20-week-old age-matched uninjured mice (Uninjured-20). Tibial bone strength, mid-diaphysis cortical geometry, intrinsic material properties, and metaphyseal trabecular bone structure were assessed by three-point bending and microcomputed tomography (µCT).

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Volumetric muscle loss (VML) is associated with persistent functional impairment due to a lack of de novo muscle regeneration. As mechanisms driving the lack of regeneration continue to be established, adjunctive pharmaceuticals to address the pathophysiology of the remaining muscle may offer partial remediation. Studies were designed to evaluate the tolerance and efficacy of two FDA-approved pharmaceutical modalities to address the pathophysiology of the remaining muscle tissue after VML injury: (1) nintedanib (an anti-fibrotic) and (2) combined formoterol and leucine (myogenic promoters).

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An often-overlooked component of traumatic skeletal muscle injuries is the impact on the nervous system and resultant innervation of the affected muscles. Recent work in a rodent model of volumetric muscle loss (VML) injury demonstrated a progressive, secondary loss of neuromuscular junction (NMJ) innervation, supporting a role of NMJ dysregulation in chronic functional deficits. Terminal Schwann cells (tSCs) are known to be vital for the maintenance of NMJ structure and function, in addition to guiding repair and regeneration after injury.

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Article Synopsis
  • Volumetric muscle loss (VML) injuries lead to irreversible tissue loss, causing problems with muscle performance and metabolism, which has been traditionally studied under non-physiological conditions.* -
  • Researchers proposed a new method called "CK Clamp," using creatine kinase and phosphocreatine to evaluate mitochondrial function under realistic ATP:ADP ratios in VML-injured muscles.* -
  • The study found that VML-injured muscles exhibited significantly reduced mitochondrial respiration rates and electron conductance compared to uninjured muscles, validating the CK Clamp's effectiveness for assessing muscle bioenergetics.*
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Introduction: Musculoskeletal injury (MSKI) risk is increased following mild traumatic brain injury (mTBI). Increased MSKI risk is present up to 2 years following post-mTBI return-to-duty/activity relative to both non-mTBI peers and to their pre-mTBI selves across a range of populations, including military service members, and professional, college and high school athletes. Despite the well documented increased post-mTBI MSKI risk, the underlying neuromuscular mechanisms contributing to this increased risk have yet to be definitively determined.

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Context: Aberrant movement patterns among individuals with concussion history have been reported during sport-related movement. However, the acute postconcussion kinematic and kinetic biomechanical movement patterns during a rapid acceleration-deceleration task have not been profiled and leaves their progressive trajectory unknown. Our study aimed to examine single-leg hop stabilization kinematics and kinetics between concussed and healthy-matched controls acutely (≤7 d) and when asymptomatic (≤72 h of symptom resolution).

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Volumetric muscle loss (VML) is the traumatic loss of skeletal muscle, resulting in chronic functional deficits and pathological comorbidities, including altered whole-body metabolic rate and respiratory exchange ratio (RER), despite no change in physical activity in animal models. In other injury models, treatment with β receptor agonists (e.g.

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Exercise benefits many organ systems, including having a panacea-like effect on the brain. For example, aerobic exercise improves cognition and attention and reduces the risk of brain-related diseases, such as dementia, stress, and depression. Recent advances suggest that endocrine signaling from peripheral systems, such as skeletal muscle, mediates the effects of exercise on the brain.

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New Findings: What is the central question of this study? First, how does physical rehabilitation influence recovery from traumatic muscle injury? Second, how does physical activity impact the rehabilitation response for skeletal muscle function and whole-body metabolism? What is the main finding and its importance? The most salient findings were that rehabilitation impaired muscle function and range of motion, while restricting activity mitigated some negative effects but also impacted whole-body metabolism. These data suggest that first, work must continue to explore treatment parameters, including modality, time, type, duration and intensity, to find the best rehabilitation approaches for volumetric muscle loss injuries; and second, restricting activity acutely might enhance rehabilitation response, but whole-body co-morbidities should continue to be considered.

Abstract: Volumetric muscle loss (VML) injury occurs when a substantial volume of muscle is lost by surgical removal or trauma, resulting in an irrecoverable deficit in muscle function.

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Context: Neuromuscular function is altered acutely following concussion and theoretically linked to the subsequent postconcussion musculoskeletal injury risk. Existing research has only examined voluntary muscle activation, limiting mechanistic understanding. Therefore, our study aimed to examine voluntary and involuntary muscle activation between college-aged, concussed individuals when symptom-free and healthy matched controls.

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Objective: Balance impairments may suggest somatosensory disruption beyond concussion clinical recovery, but somatosensory subsystems have never been directly assessed. Our objective was to examine somatosensory function between individuals with a concussion and healthy matched-controls at acute (<7 days) and asymptomatic (<72 hours of being symptom-free) time points.

Setting: Laboratory.

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Volumetric muscle loss (VML) injuries represent a majority of military service member casualties and are common in civilian populations following blunt and/or penetrating traumas. Characterized as a skeletal muscle injury with permanent functional impairments, there is currently no standard for rehabilitation, leading to lifelong disability. Toward developing rehabilitative strategies, previous research demonstrates that the remaining muscle after a VML injury lacks similar levels of plasticity or adaptability as healthy, uninjured skeletal muscle.

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A Western diet (WD), high in sugars and saturated fats, impairs learning and memory function and contributes to weight gain. Mitochondria in the brain provide energy for neurocognitive function and may play a role in body weight regulation. We sought to determine whether a WD alters behavior and metabolic outcomes in male and female rodents through impacting hippocampal and hypothalamic mitochondrial bioenergetics.

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