Background Polychlorinated biphenyls (PCBs) are persistent environmental pollutants which are detectable in the serum of all American adults. Amongst PCB congeners, PCB 153 has the highest serum level. PCBs have been dose-dependently associated with obesity, metabolic syndrome, and nonalcoholic fatty liver disease (NAFLD) in epidemiological studies. Objective The purpose of this study is to determine mechanisms by which PCB 153 worsens diet-induced obesity and NAFLD in male mice fed a high fat diet (HFD). Methods Male C57BL6/J mice were fed either control or 42% milk fat diet for 12 weeks with or without PCB 153 co-exposure (50 mg/kg i.p. × 4). Glucose tolerance test was performed, and plasma and tissues were obtained at necropsy for measurements of adipocytokine levels, histology and gene expression. Results In control diet-fed mice, addition of PCB 153 had minimal effects on any of the measured parameters. However, PCB 153 treatment in high fat-fed mice was associated with increased visceral adiposity, hepatic steatosis and plasma adipokines including adiponectin, leptin, resistin and plasminogen activator inhibitor-1 levels. Likewise, co-exposure reduced expression of hepatic genes implicated in β-oxidation while increasing the expression of genes associated with lipid biosynthesis. Regardless of diet, PCB 153 had no effect on insulin resistance or tumor necrosis factor alpha levels. Conclusion PCB 153 is an obesogen which exacerbates hepatic steatosis; alters adipocytokines; and disrupts normal hepatic lipid metabolism when administered with HFD, but not control diet. Because all U.S. adults have been exposed to PCB 153, this particular nutrient-toxicant interaction potentially impacts human obesity/NAFLD.

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Objective Cytokeratin 18 (CK18) is a novel serologic biomarker for occupational liver disease. The purpose of this study is to determine the prevalence of CK18 elevation in elastomer/polymer workers exposed to acrylonitrile, 1,3 butadiene, and styrene. Methods 82 chemical workers were evaluated. CK18 was determined by ELISA and pro-inflammatory cytokines were measured by multi-analyte chemiluminescent detection. Results 39% (32 of 82) had elevated CK18 levels which were not explained by alcohol or obesity, except in potentially 4 cases. The pattern of CK18 elevation was consistent with toxicant-associated steatohepatitis (TASH) in the majority of cases (78%). TNFα, IL-6, IL-8, MCP-1, and PAI-1 were increased in these workers compared to those with normal CK18 levels. Conclusions These results suggest a high prevalence of occupational liver disease and TASH in elastomer/polymer workers with elevated pro-inflammatory cytokines.

After rotator cuff repair, a clinically significant improvement in patient-reported outcomes, range of motion, and strength was seen up to 1 year after surgery, but not beyond this. This information is important not only to establish appropriate patient expectations but also to determine a time frame for outcome collection after surgery to better define value in orthopaedic care.