A5025320225- Muscle Physiology and Disorders
- Nutrition and Health in Aging
- Adipose Tissue and Metabolism
- Muscle metabolism and nutrition
- Exercise and Physiological Responses
- Mitochondrial Function and Pathology
- Diet and metabolism studies
- Autophagy in Disease and Therapy
- GDF15 and Related Biomarkers
- Thermoregulation and physiological responses
- Tissue Engineering and Regenerative Medicine
- Body Composition Measurement Techniques
- MicroRNA in disease regulation
- Cancer, Hypoxia, and Metabolism
- Muscle activation and electromyography studies
- Nuclear Structure and Function
- Liver Disease Diagnosis and Treatment
- Hormonal and reproductive studies
- Circular RNAs in diseases
- Intensive Care Unit Cognitive Disorders
- Knee injuries and reconstruction techniques
- Cardiovascular and exercise physiology
- ATP Synthase and ATPases Research
- Metabolism, Diabetes, and Cancer
- Radiomics and Machine Learning in Medical Imaging
University of Arkansas at Fayetteville
2015-2024
McMaster University
2023
Ochsner Medical Center
2020
Crouse Hospital
2015-2018
Southern Illinois University Edwardsville
2016
Stavros
2015
Texas A&M University
2015
University of South Carolina
2001-2014
University of Illinois Chicago
2003-2011
Advocate Christ Medical Center
2011
Cancer cachexia is largely irreversible, at least via nutritional means, and responsible for 20-40% of cancer-related deaths. Therefore, preventive measures are primary importance; however, little known about muscle perturbations prior to onset cachexia. associated with mitochondrial degeneration; yet, it remains be determined if degeneration precedes wasting in cancer our purpose was determine cancer-induced tumour-bearing mice.
Abstract Background Cancer cachexia occurs in approximately 80% of cancer patients and is a key contributor to cancer‐related death. The mechanisms controlling development tumour‐induced muscle wasting are not fully elucidated. Specifically, the progression underexplored. Therefore, we examined skeletal protein turnover throughout tumour‐bearing mice. Methods Lewis lung carcinoma (LLC) was injected into hind flank C57BL6/J mice at 8 weeks age with tumour allowed develop for 1, 2, 3, or 4...
Skeletal muscle interleukin-6 (IL-6) expression is induced by continuous contraction, overload-induced hypertrophy and during regeneration. The loss of IL-6 can alter skeletal muscle's growth extracellular matrix remodelling response to hypertrophy. Insulin-like factor-1 (IGF-1) gene related signalling through Akt/mTOR a critical regulator mass. significance the recovery from atrophy unclear. This study's purpose was determine effect on mouse gastrocnemius (GAS) mass hindlimb suspension...
Skeletal muscle mitochondrial degeneration is a hallmark of insulin resistance/obesity marked by lost function, enhanced ROS emission, and altered morphology which may be ameliorated physical activity (PA). However, no prior report has examined quality control regulation throughout biogenesis, fusion/fission dynamics, autophagy, permeability transition pore (MPTP) in obesity. Therefore, we determined how each process impacted Western diet (WD)-induced obesity whether voluntary PA alleviate...
Skeletal muscle is capable of robust self-repair following mild trauma, yet in cases traumatic volumetric loss (VML), where more than 20% a muscle's mass lost, this capacity overwhelmed. Current autogenic whole transfer techniques are imperfect, which has motivated the exploration implantable scaffolding strategies. In study, use an allogeneic decellularized skeletal (DSM) scaffold with and without addition minced (MM) autograft tissue was explored as repair strategy using lower-limb VML...
Abstract Background Muscle atrophy is a common pathology associated with disuse, such as prolonged bed rest or spaceflight, and detrimental health outcomes. There emerging evidence that disuse may differentially affect males females. Cellular mechanisms contributing to the development progression of remain elusive, particularly protein turnover cascades. The purpose this study was investigate initial muscle in male female mice using well‐established model hindlimb unloading (HU). Methods One...
Cancer-cachexia (CC) is a debilitating condition affecting up to 80% of cancer patients and contributing 40% cancer-related deaths. While evidence suggests biological sex differences in the development CC, assessments female transcriptome CC are lacking, direct comparisons between sexes scarce. This study aimed define time course Lewis lung carcinoma (LLC)-induced females using transcriptomics, while directly comparing differences.We found global gene expression gastrocnemius muscle mice...
Abstract Aim Obesity is classified as a metabolic disorder that associated with delayed muscle regeneration following damage. For optimal skeletal regeneration, inflammation along extracellular matrix remodelling and growth must be tightly regulated. Moreover, the regenerative process dependent on activation of myogenic regulatory factors ( MRF s) for myoblast proliferation differentiation. The purpose this study was to determine how obesity alters inflammatory protein synthetic signalling...
ABSTRACT Insulin resistant diabetes, currently at epidemic levels in developed countries, begins the skeletal muscle and is linked to altered protein turnover. microRNAs downregulate targeted mRNA translation decreasing amount of translated protein, thereby regulating many cellular processes. Regulation miRNAs their function insulin resistance largely unexplored. The purpose this study was identify effects on contents with potential functions We examined miRs ‐1, ‐16, ‐23, ‐27, ‐133a, ‐133b,...
Muscle atrophy is a hallmark of cancer cachexia resulting in impaired function and quality life the immediate cause death for 20-40% patients. Multiple microRNAs (miRNAs) have been identified as being involved muscle development atrophy; however, less known specifically on miRNAs cachexia. The purpose this investigation was to examine miRNA profile skeletal induced by uncover potential with catabolic condition. Phosphate-buffered saline (PBS) or Lewis lung carcinoma cells (LLC) were injected...
Obesity is a known risk factor for the development of hepatic disease; obesity-induced fatty liver can lead to inflammation, steatosis, and cirrhosis associated with degeneration mitochondria. Lifestyle interventions such as physical activity may ameliorate this condition. The purpose study was investigate regulation mitochondrial autophagy quality control in following Western diet-induced obesity voluntary activity. Eight-week-old C57BL/6J mice were fed diet (WD) or normal chow (NC,...
Cancer cachexia (CC) is a devastating syndrome characterized by weight loss, reduced fat mass and muscle that affects approximately 80% of cancer patients responsible for 22%–30% cancer-associated deaths. Understanding underlying mechanisms the development CC are crucial to advance therapies treat improve outcomes. multi-organ results in extensive skeletal adipose tissue wasting; however, can impair other organs such as liver, heart, brain, bone well. A considerable amount research focuses...
Cancer-cachexia (CC) is a wasting condition directly responsible for 20-40% of cancer-related deaths. The mechanisms controlling development CC-induced muscle are not fully elucidated. Most investigations focus on the postcachectic state and do examine progression condition. We recently demonstrated mitochondrial degenerations precede in time course CC. However, extent perturbations before CC unknown. Therefore, we performed global gene expression analysis to enhance understanding...
Cancer-associated bodyweight loss (cachexia) is a hallmark of many cancers and associated with decreased quality life increased mortality. Hepatic function can dramatically influence whole-body energy expenditure may therefore significantly health during cancer progression. The purpose this study was to examine alterations in markers hepatic metabolism physiology cachexia Male C57BL/6J mice were injected 1 × 10 6 Lewis Lung Carcinoma cells dissolved 100 μL PBS allowed develop for 1, 2, 3, or...
Overloading healthy skeletal muscle produces myofibre hypertrophy and extracellular matrix remodelling, these processes are thought to be interdependent for producing growth. Inflammatory cytokine interleukin-6 (IL-6) gene expression is induced in overloaded muscle, the loss of this IL-6 induction can attenuate hypertrophic response overload (OV). Although OV may an important regulator inflammatory satellite cell proliferation, less known about its role regulation remodelling. The purpose...
Abstract Background Disuse decreases muscle size and is predictive of mortality across multiple pathologies. Detriments to mitochondrial function are hypothesized underlie disuse‐induced atrophy. Little data exist on early mechanisms contributing onset these pathologies, nor it known how they differ between sexes. The purpose this study was examine differential conserved responses quality control in male female mice during the development progression Methods One hundred C57BL/6J (50 50...
Our study demonstrates divergent tumor development and tissue wasting within 3- 4-wk mice, where approximately half the mice developed large tumors subsequent cachexia. Unlike previous male studies, metabolic perturbations precede onset of cachexia, females appear to exhibit protections from cachexia development. data provide novel evidence for cachectic in tumor-bearing female compared with CC suggesting different mechanisms between sexes.
Previously, we demonstrated that high-volume resistance exercise stimulates mitochondrial protein synthesis (a measure of biogenesis) in lean but not obese Zucker rats. Here, examined factors involved regulating biogenesis the same animals. PGC-1α was 45% higher following animals compared with sedentary counterparts. Interestingly, exercised greater PPARδ both (47%) and (>200%) AMPK phosphorylation (300%) CPT-I (30%) were elevated by only, indicating improved substrate availability/flux....
PGC-1α4 is a novel regulator of muscle hypertrophy; however, there limited understanding the regulation its expression and role in many (patho)physiological conditions. Therefore, our purpose was to elicit signalling mechanisms regulating gene Pgc1α4 examine response stimuli associated with altered mass.IL-6 knockout mice pharmacological experiments C2C12 myocytes were used identify transcription. To conditions, obese lean Zucker rats with/without resistance exercise (RE), ageing...
We present data suggesting that mitochondria-based interventions may mitigate disuse atrophy. However, the efficacy of vary depending on specific target intervention and sex organism. Females appear to be more responsive increased mitochondrial catalase as a potential therapeutic for mitigating