Effects of exercise on obesity-induced mitochondrial dysfunction in skeletal muscle

Obesity is known to induce inhibition of glucose uptake, reduction of lipid metabolism, and progressive loss of skeletal muscle function, which are all as- sociated with mitochondrial dysfunction in skeletal muscle. Mitochondria are dy- namic organelles that regulate cellular metabolism and bioenergetics, including ATP production via oxidative phosphorylation. Due to these critical roles of mitochon- dria, mitochondrial dysfunction results in various diseases such as obesity and type 2 diabetes. Obesity is associated with impairment of mitochondrial function (e.g., decrease in O2 respiration and increase in oxidative stress) in skeletal muscle. The bal- ance between mitochondrial fusion and fission is critical to maintain mitochondrial homeostasis in skeletal muscle. Obesity impairs mitochondrial dynamics, leading to an unbalance between fusion and fission by favorably shifting fission or reducing fusion proteins. Mitophagy is the catabolic process of damaged or unnecessary mito- chondria. Obesity reduces mitochondrial biogenesis in skeletal muscle and increases accumulation of dysfunctional cellular organelles, suggesting that mitophagy does not work properly in obesity. Mitochondrial dysfunction and oxidative stress are reported to trigger apoptosis, and mitochondrial apoptosis is induced by obesity in skeletal muscle. It is well known that exercise is the most effective intervention to protect against obesity. Although the cellular and molecular mechanisms by which exercise protects against obesity-induced mitochondrial dysfunction in skeletal mus- cle are not clearly elucidated, exercise training attenuates mitochondrial dysfunction, allows mitochondria to maintain the balance between mitochondrial dynamics and mitophagy, and reduces apoptotic signaling in obese skeletal muscle

Exercise Training Attenuates Ovariectomy-Induced Alterations in Skeletal Muscle Remodeling, Apoptotic Signaling, and Atrophy Signaling in Rat Skeletal Muscle

Purpose The effects of aerobic exercise training on soleus muscle morphology, mitochondria-mediated apoptotic signaling, and atrophy/hypertrophy signaling in ovariectomized rat skeletal muscle were investigated. Methods Female Sprague-Dawley rats were divided into control (CON), ovariectomy (OVX), and ovariectomy plus exercise (OVX+EX) groups. After ovarian excision, exercise training was performed using a rat treadmill at 20 m/min, 50 min/day, 5 days/week for 12 weeks. Protein levels of mitochondria-mediated apoptotic signaling and atrophy/hypertrophy signaling in the skeletal muscle (soleus) were examined through western immunoblot analysis. Results The number of myocytes and myocyte cross-sectional area (CSA) were increased and the extramyocyte space was decreased in the OVX group compared to those in the CON group. However, aerobic exercise training significantly increased myocyte CSA and decreased extramyocyte space in the OVX+EX group compared to those in the OVX group. The protein levels of proapoptotic signaling and muscle atrophy signaling were significantly increased, whereas the protein levels of muscle hypertrophy signaling were significantly decreased in the OVX group compared to that in the CON group. Aerobic exercise training significantly decreased the protein levels of proapoptotic signaling and increased the protein level of antiapoptotic protein in the OVX+EX group compared to that in the OVX group. Aerobic exercise training significantly increased the protein levels of hypertrophy signaling and decreased protein levels of atrophy signaling in the OVX+EX group compared to those in the OVX group. Conclusions Treadmill exercise improved estrogen deficiency-induced impairment in skeletal muscle remodeling, mitochondria-mediated apoptotic signaling, and atrophy/hypertrophy signaling in skeletal muscle

Focal Nodular Hyperplasia with Retraction of Liver Capsule: A Case Report

Focal nodular hyperplasia (FNH) is characterized by the presence a central scar with radiating fibrous septa. Our case had a capsular retraction, which was the result of an extension of the central scar to the surface. In addition, a hypointense scar on the T2-weighted image and a minimal enhancing central scar on the enhanced T1-weighted image, which was due to dense, sclerotic collagenous tissue, were observed. We report the first case of FNH with a capsular retraction

Effects of Acute Exercise on Mitochondrial Function, Dynamics, and Mitophagy in Rat Cardiac and Skeletal Muscles

Purpose This study aimed to investigate the effects of single-bout exercise on mitochondrial function, dynamics (fusion, fission), and mitophagy in cardiac and skeletal muscles. Methods Fischer 344 rats (4 months old) were randomly divided into the control (CON) or acute exercise (EX) group (n=10 each). The rats performed a single bout of treadmill exercise for 60 minutes. Mitochondrial function (e.g., O2 respiration, H2O2 emission, Ca2+ retention capacity), mitochondrial fusion (e.g., Mfn1, Mfn2, Opa1), mitochondrial fission (e.g., Drp1, Fis1), and mitophagy (e.g., Parkin, Pink1, LC3II, Bnip3) were measured in permeabilized cardiac (e.g., left ventricle) and skeletal (e.g., soleus, white gastrocnemius) muscles. Results Mitochondrial O2 respiration and Ca2+ retention capacity were significantly increased in all tissues of the EX group compared with the CON group. Mitochondrial H2O2 emissions showed tissue-specific results; the emissions showed no significant differences in the left ventricle or soleus (type I fibers) but was significantly increased in the white gastrocnemius (type II fibers) after acute exercise. Mitochondrial fusion and fission were not altered in any tissues of the EX group. Mitophagy showed tissue-specific differences: It was not changed in the left ventricle or white gastrocnemius, whereas Parkin and LC3II were significantly elevated in the soleus muscle. Conclusions A single bout of aerobic exercise may improve mitochondrial function (e.g., O2 respiration and Ca2+ retention capacity) in the heart and skeletal muscles without changes in mitochondrial dynamics or mitophagy

Immersive Insights: A Hybrid Analytics System for Collaborative Exploratory Data Analysis

In the past few years, augmented reality (AR) and virtual reality (VR) technologies have experienced terrific improvements in both accessibility and hardware capabilities, encouraging the application of these devices across various domains. While researchers have demonstrated the possible advantages of AR and VR for certain data science tasks, it is still unclear how these technologies would perform in the context of exploratory data analysis (EDA) at large. In particular, we believe it is important to better understand which level of immersion EDA would concretely benefit from, and to quantify the contribution of AR and VR with respect to standard analysis workflows. In this work, we leverage a Dataspace reconfigurable hybrid reality environment to study how data scientists might perform EDA in a co-located, collaborative context. Specifically, we propose the design and implementation of Immersive Insights, a hybrid analytics system combining high-resolution displays, table projections, and augmented reality (AR) visualizations of the data. We conducted a two-part user study with twelve data scientists, in which we evaluated how different levels of data immersion affect the EDA process and compared the performance of Immersive Insights with a state-of-the-art, non-immersive data analysis system.Comment: VRST 201

Impaired Design Fluency Is a Marker of Pathological Cognitive Aging; Results from the Korean Longitudinal Study on Health and Aging

ObjectiveaaWe investigated neuropsychological markers that can be used to discriminate pathological cognitive aging from normal cognitive aging. MethodsaaWe administered frontal lobe function tests including the Wisconsin Card Sorting Test (WCST), digit span test, lexical fluency test, fixed condition design fluency test, and Trail Making Test B (TMT-B) to 92 individuals with pathological cognitive aging (PCA) and 222 individuals with normal cognitive aging (NCA). We examined the main effects of participants ’ diagnoses (PCA, NCA) and age (65-69 years old, 70-74 years old and 75 years old or over) on their test performance using multivariate analysis of variance. ResultsaaThe main effects of both the diagnosis (F=2.860, p=0.002) and the age group (F=2.484, p<0.001) were significant. The PCA group showed lower performance on the backward digit span test (F=14.306, p<0.001), fixed condition design fluency test (F=8.347, p=0.004) and also exhibited perseverative errors in the WCST (F=4.19, p=0.042) compared with the NCA group. The main effect of the diagnosis on the backward digit span test and the fixed condition design fluency test remained significant after Bonferroni correction