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Healthy versus Unhealthy Adipose Tissue Expansion: the Role of Exercise
Benjamin M. Meister,Soon-Gook Hong,Junchul Shin,Meghan Rath,Jacqueline Sayoc,박준영 대한비만학회 2022 The Korean journal of obesity Vol.31 No.1
Although the hallmark of obesity is the expansion of adipose tissue, not all adipose tissue expansion is the same. Expansion of healthy adipose tissue is accompanied by adequate capillary angiogenesis and mitochondria-centered metabolic integrity, whereas expansion of unhealthy adipose tissue is associated with capillary and mitochondrial derangement, resulting in deposition of immune cells (M1-stage macrophages) and excess production of pro-inflammatory cytokines. Accumulation of these dysfunctional adipose tissues has been linked to the development of obesity comorbidities, such as type 2 diabetes, hypertension, dyslipidemia, and cardiovascular disease, which are leading causes of human mortality and morbidity in modern society. Mechanistically, vascular rarefaction and mitochondrial incompetency (for example, low mitochondrial content, fragmented mitochondria, defective mitochondrial respiratory function, and excess production of mitochondrial reactive oxygen species) are frequently observed in adipose tissue of obese patients. Recent studies have demonstrated that exercise is a potent behavioral intervention for preventing and reducing obesity and other metabolic diseases. However, our understanding of potential cellular mechanisms of exercise, which promote healthy adipose tissue expansion, is at the beginning stage. In this review, we hypothesize that exercise can induce unique physiological stimuli that can alter angiogenesis and mitochondrial remodeling in adipose tissues and ultimately promote the development and progression of healthy adipogenesis. We summarize recent reports on how regular exercise can impose differential processes that lead to the formation of either healthy or unhealthy adipose tissue and discuss key knowledge gaps that warrant future research.
Golf Swing Rotational Velocity: The Essential Follow-Through
Katherine M. Steele,Eugene Y. Roh,Gordhan Mahtani,David W. Meister,Amy L. Ladd,Jessica Rose 대한재활의학회 2018 Annals of Rehabilitation Medicine Vol.42 No.5
Objective To evaluate if shoulder and pelvic angular velocities differ at impact or peak magnitude between professional and amateur golfers. Golf swing rotational biomechanics are a key determinant of power generation, driving distance, and injury prevention. We hypothesize that shoulder and pelvic angular velocities would be highly consistent in professionals. Methods Rotational velocities of the upper-torso and pelvis throughout the golf swing and in relation to phases of the golf swing were examined in 11 professionals and compared to 5 amateurs using three-dimensional motion analysis.Results Peak rotational velocities of professionals were highly consistent, demonstrating low variability (coefficient of variation [COV]), particularly upper-torso rotational velocity (COV=0.086) and pelvic rotational velocity (COV=0.079) during down swing. Peak upper-torso rotational velocity and peak X-prime, the relative rotational velocity of upper-torso versus pelvis, occurred after impact in follow-through, were reduced in amateurs compared to professionals (p=0.005 and p=0.005, respectively) and differentiated professionals from most (4/5) amateurs. In contrast, peak pelvic rotational velocity occurred in down swing. Pelvic velocity at impact was reduced in amateurs compared to professionals (p=0.019) and differentiated professionals from most (4/5) amateurs. Conclusion Golf swing rotational velocity of professionals was consistent in pattern and magnitude, offering benchmarks for amateurs. Understanding golf swing rotational biomechanics can guide swing modifications to help optimize performance and prevent injury.
Jennifer Holder-Murray,Stephen A Esper,Michael L Boisen,Julie Gealey,Katie Meister,David S Medich,Kathirvel Subramaniam 대한마취통증의학회 2019 Korean Journal of Anesthesiology Vol.72 No.4
Background: Enhanced recovery protocols (ERP) provide optimal perioperative care for surgical patients. Postoperative nausea and vomiting (PONV) is common after colorectal surgery (CRS). We aim to compare the efficacy of aprepitant to a cost-effective alternative, perphenazine, as components of triple antiemetic prophylaxis in ERP patients. Methods: Patients who underwent ERP CRS at a single institution from July 2015 to July 2017 were evaluated retrospectively. Only subjects who received aprepitant (Group 1) or perphenazine (Group 2) preoperatively for PONV prophylaxis were included. Patient characteristics, simplified Apfel PONV scores, perioperative medications, and PONV incidence were compared between the groups. PONV was defined as the need for rescue antiemetics on postoperative days (POD) 0–5. Results: Five hundred ninety-seven patients underwent CRS of which 498 met the inclusion criteria. Two hundred thirty- one (46.4%) received aprepitant and 267 (53.6%) received perphenazine. The incidence of early PONV (POD 0–1) was comparable between the two groups: 44.2% in Group 1 and 44.6% in Group 2 (P = 0.926). Late PONV (POD 2–5) occurred less often in Group 1 than Group 2, respectively (35.9% vs. 45.7%, P = 0.027). After matching the groups for preoperative, procedural, and anesthesia characteristics (164 pairs), no difference in early or late PONV could be demonstrated between the groups. Conclusions: The incidence of PONV remains high despite most patients receiving three prophylactic antiemetic medications. Perphenazine can be considered a cost-effective alternative to oral aprepitant for prophylaxis of PONV in patients undergoing CRS within an ERP.
Arab, K.,Park, Y.,Lindroth, Anders M.,Schafer, A.,Oakes, C.,Weichenhan, D.,Lukanova, A.,Lundin, E.,Risch, A.,Meister, M.,Dienemann, H.,Dyckhoff, G.,Herold-Mende, C.,Grummt, I.,Niehrs, C.,Plass, C. Cell Press 2014 Molecular cell Vol.55 No.4
DNA methylation is a dynamic and reversible process that governs gene expression during development and disease. Several examples of active DNA demethylation have been documented, involving genome-wide and gene-specific DNA demethylation. How demethylating enzymes are targeted to specific genomic loci remains largely unknown. We show that an antisense lncRNA, termed TARID (for TCF21 antisense RNA inducing demethylation), activates TCF21 expression by inducing promoter demethylation. TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation. GADD45A in turn recruits thymine-DNA glycosylase for base excision repair-mediated demethylation involving oxidation of 5-methylcytosine to 5-hydroxymethylcytosine in the TCF21 promoter by ten-eleven translocation methylcytosine dioxygenase proteins. The results reveal a function of lncRNAs, serving as a genomic address label for GADD45A-mediated demethylation of specific target genes.