Background and Aims NAFLD and its more‐advanced form, steatohepatitis (NASH), is associated with obesity and is an independent risk factor for cardiovascular, liver‐related, and all‐cause mortality. Available human data examining hepatic mitochondrial fatty acid oxidation (FAO) and hepatic mitochondrial turnover in NAFLD and NASH are scant. Approach and Results To investigate this relationship, liver biopsies were obtained from patients with obesity undergoing bariatric surgery and data clustered into four groups based on hepatic histopathological classification: Control (CTRL; no disease); NAFL (steatosis only); Borderline‐NASH (steatosis with lobular inflammation or hepatocellular ballooning); and Definite‐NASH (D‐NASH; steatosis, lobular inflammation, and hepatocellular ballooning). Hepatic mitochondrial complete FAO to CO2 and the rate‐limiting enzyme in β‐oxidation (β‐hydroxyacyl‐CoA dehydrogenase activity) were reduced by ~40%–50% with D‐NASH compared with CTRL. This corresponded with increased hepatic mitochondrial reactive oxygen species production, as well as dramatic reductions in markers of mitochondrial biogenesis, autophagy, mitophagy, fission, and fusion in NAFL and NASH. Conclusions These findings suggest that compromised hepatic FAO and mitochondrial turnover are intimately linked to increasing NAFLD severity in patients with obesity.

ObjectiveTo compare rates of injury and concussion among non-elite (lowest 60% by division of play) Bantam (ages 13–14 years) ice hockey leagues that disallow body checking to non-elite Bantam leagues that allow body checking.MethodsIn this 2-year cohort study, Bantam non-elite ice hockey players were recruited from leagues where policy allowed body checking in games (Calgary/Edmonton 2014–2015, Edmonton 2015–2016) and where policy disallowed body checking (Kelowna/Vancouver 2014–2015, Calgary 2015–2016). All ice hockey game-related injuries resulting in medical attention, inability to complete a session and/or time loss from hockey were identified using valid injury surveillance methodology. Any player suspected of having concussion was referred to a study physician for diagnosis and management.Results49 body checking (608 players) and 33 non-body checking teams (396 players) participated. There were 129 injuries (incidence rate (IR)=7.98/1000 hours) and 54 concussions (IR=3.34/1000 hours) in the body checking teams in games. After policy change, there were 31 injuries (IR=3.66/1000 hours) and 17 concussions (IR=2.01/1000 hours) in games. Policy disallowing body checking was associated with a lower rate of all injury (adjusted incidence rate ratio (IRR)=0.44; 95% CI: 0.27 to 0.74). The point estimate showed a lower rate of concussion (adjusted IRR=0.6; 95% CI: 0.31 to 1.18), but this was not statistically significant.ConclusionPolicy change disallowing body checking in non-elite Bantam ice hockey resulted in a 56% lower rate of injury. There is growing evidence that disallowing body checking in youth ice hockey is associated with fewer injuries.

for assimilation and thus exert a lower thermic effect of food (diet-induced thermogenesis) (3)(4)(5). Individuals that assimilate dietary fat effi ciently to meet their needs between meals have an advantage in enduring starvation. Thus, genes conferring this trait may be selected through evolution. During times of continuous abundance, however, individuals thrifty of energy substrates and high in metabolic effi ciency are prone to accumulating fuel surpluses in adipose and other tissues ( 6, 7 ). In humans, excessive fat accumulation is associated with metabolic diseases, including obesity, hepatic steatosis, and insulin resistance, which plague many industrialized parts of the world ( 8, 9 ).The absorption of dietary fat involves the resynthesis of digested triacylglycerol in enterocytes, mainly through a pathway catalyzed by acyl CoA:monoacylglycerol acyltransferase (MGAT) ( 10 ). Three related genes have been identifi ed that code for MGAT; among them, only Mogat2 is highly expressed in the small intestine of both mice and humans ( 11-15 ). Thus, Mogat2 probably encodes the intestinal MGAT activity, although Mogat3 is also found in the distal intestine in humans ( 14 ).Consistent with a role of MGAT2 in promoting conservation of dietary fat, mice lacking the enzyme ( Mogat2 Ϫ / Ϫ ) are resistant to obesity and other metabolic disorders induced by high-fat feeding ( 16,17 ؊ / ؊ mice expended energy and lost weight like wild-type controls. To determine whether MGAT2 defi ciency protects against obesity in the absence of high-fat feeding, we crossed Mogat2 ؊ / ؊ mice with genetically obese Agouti mice. MGAT2 defi ciency increased energy expenditure and prevented these mice from gaining excess weight. Our results suggest that MGAT2 modulates energy expenditure through multiple mechanisms, including one independent of dietary fat; these fi ndings also raise the prospect of inhibiting MGAT2 as a strategy for combating obesity and related metabolic disorders resulting from excessive calorie intake. Abbreviations: DGAT, diacylglycerol acyltransferase; MGAT, monoacylglycerol acyltransferase; RER, respiratory exchange ratio.

Introduction: In collaboration with the Alberta Medical Association's Physician Learning Program we developed individualized physician reports and held a group feedback session on rheumatoid arthritis (RA) performance measures (PM) to facilitate treat-to-target (T2T) strategies and evaluated physician experiences with this process. Methods: 5 PMs addressing T2T concepts from an established Canadian quality framework were operationalized for physician practice reports at 2 university-affiliated rheumatology clinics. Rheum4U, a quality improvement and research platform, was the data source. The audit results were reviewed in a facilitated group feedback session. Rheumatologists provided experiential feedback on the process through survey and/or an interview. Transcripts from interviews were analyzed using a 6-step thematic analysis. Results: 11 of 12 eligible rheumatologists consented to receive practice reports and provided feedback through surveys (n = 5) and interviews (n = 6). The practice reports from Rheum4U

ObjectivesThe objective of this study is to evaluate the effect of policy change disallowing body checking in adolescent ice hockey leagues (ages 15–17) on reducing rates of injury and concussion.MethodsThis is a prospective cohort study. Players 15–17 years-old were recruited from teams in non-elite divisions of play (lower 40%–70% by division of play depending on year and city of play in leagues where policy permits or prohibit body checking in Alberta and British Columbia, Canada (2015–18). A validated injury surveillance methodology supported baseline, exposure-hours and injury data collection. Any player with a suspected concussion was referred to a study physician. Primary outcomes include game-related injuries, game-related injuries (>7 days time loss), game-related concussions and game-related concussions (>10 days time loss).Results44 teams (453 player-seasons) from non-body checking and 52 teams (674 player-seasons) from body checking leagues participated. In body checking leagues there were 213 injuries (69 concussions) and in non-body checking leagues 40 injuries (18 concussions) during games. Based on multiple multilevel mixed-effects Poisson regression analyses, policy prohibiting body checking was associated with a lower rate of injury (incidence rate ratio (IRR): 0.38 (95% CI 0.24 to 0.6)) and concussion (IRR: 0.49; 95% CI 0.26 to 0.89). This translates to an absolute rate reduction of 7.82 injuries/1000 game-hours (95% CI 2.74 to 12.9) and the prevention of 7326 injuries (95% CI 2570 to 12083) in Canada annually.ConclusionsThe rate of injury was 62% lower (concussion 51% lower) in leagues not permitting body checking in non-elite 15–17 years old leagues highlighting the potential public health impact of policy prohibiting body checking in older adolescent ice hockey players.