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ation. This article is protected by copyright. All rights reserved.The farnesoid X receptor (FXR)-fibroblast growth factor 19 (FGF19) axis has provided promising therapeutic targets for nonalcoholic steatohepatitis (NASH), with obeticholic acid (OCA), the first-in-class FXR agonist, showing fibrosis improvement in two human trials.(1,2) FXR regulates bile acid, lipid, and glucose metabolism by controlling a broad transcriptional repertoire in the intestine and the liver. FGF19, the most prominent FXR target gene in the intestine, is released into portal circulation and binds to the FGF receptor 4 (FGFR4) on the surface of hepatocytes. This article is protected by copyright. All rights reserved.Infrared-A (IRA), which can penetrate deeply into the human skin, is a major component of solar radiation and is recognized to promote photoaging of human dermis. To our knowledge, however, the cellular and molecular consequences of human epidermis exposure to IRA have not been clarified. Thus, we investigated whether IRA inhibits the proliferation of normal human epidermal keratinocytes (NHEKs). selleckchem IRA irradiation resulted in cell cycle arrest at G1 and a dose-dependent reduction in the proliferation of NHEKs. We found that mechanistic target of rapamycin complex 1 (mTORC1) was initially inactivated during IRA irradiation due to the formation of stress granules (SGs), and this inactivation was maintained for at least 6 hours after irradiation due to Akt dephosphorylation. Furthermore, repeated exposure of human skin equivalents to IRA led to marked thinning of the epidermal cell layer. In conclusion, IRA irradiation inhibits mTORC1 activity possibly through two molecular mechanisms involving SG formation in the early phase and subsequent Akt dephosphorylation. This sequential mechanism seems to cause G1 cell cycle arrest and a reduction in cell proliferation, supporting the hypothesis that the decreased proliferation of basal keratinocytes that occurs during skin aging might be partly attributable to IRA radiation. This article is protected by copyright. All rights reserved.Increasing evidence supports a positive association between periodontal disease and total cancer risk. We evaluated the association of clinically assessed periodontal disease and a consequence, edentulism with total cancer mortality in participants without a prior cancer diagnosis in a U.S. nationally representative population. Included were 6,034 participants aged ≥40 years without a prior cancer diagnosis who participated in the National Health and Nutrition Examination Survey III. Periodontal health was measured by trained dentists. Cancer deaths (n = 702) were ascertained during a median of 21.3 years of follow-up. Cox proportional hazards regression was used to estimate the association of periodontal disease and edentulism with total cancer mortality using no periodontal disease/dentate as the reference and adjusting for potential demographic, lifestyle including smoking and social factor confounders. Fifteen percent had periodontitis and 17% were edentulous. Periodontitis was not statistically significantly associated with risk of total cancer death after multivariable adjustment. Edentulism was associated with an increased risk of cancer mortality (hazard ratio = 1.50, 95% confidence interval = 1.12-2.00) after multivariable adjustment, including in men and women and in each racial/ethnic group studied. The positive association was observed in overweight/obese participants but not participants with normal body mass index, more strongly in prediabetic/diabetic participants than in participants without diabetes and in ever cigarette smokers but not in never cigarette smokers. In this U.S. nationally representative population, those with edentulism, but not periodontal disease, had a higher risk of total cancer death, especially in those with shared risk factors for periodontal disease and cancer. © 2020 UICC.Listeria monocytogenes is often responsible for postprocessing contamination of ready-to-eat (RTE) products including cooked ham. As an emerging technology, atmospheric cold plasma (ACP) has the potential to inactivate L. monocytogenes in packaged RTE meats. The objectives of this study were to evaluate the effect of treatment time, modified atmosphere gas compositions (MAP), ham formulation, and post-treatment storage (1 and 7 days at 4 °C) on the reduction of a five-strain cocktail of L. monocytogenes and quality changes in ham subjected to in-package ACP treatment. Initial average cells population on ham surfaces were 8 log CFU/cm2 . The ACP treatment time and gas composition significantly (P 6 log reduction) when samples were stored in MAP1. However, there were significant changes in lipid oxidation and color after post-treatment storage. In conclusion, the antimicrobial efficacy of ACP is strongly influenced by gas composition inside the package and post-treatment storage. PRACTICAL APPLICATION Surface contamination of RTE ham with L. monocytogenes may occur during processing steps such as slicing and packaging. In-package ACP is an emerging nonthermal technology, which can be used as a postpackaging decontamination step in industrial settings. This study demonstrated the influence of in-package gas composition, treatment time, post-treatment storage, and ham formulation on L. monocytogenes inactivation efficacy of ACP. Results of present study will be helpful to optimize in-package ACP treatment and storage conditions to reduce L. monocytogenes, while maintaining the quality of ham. © 2020 Institute of Food Technologists®.ETV6-RUNX1 (E/R) fusion gene, arising in utero from translocation t(12;21)(p13q22), is the most frequent alteration in childhood acute lymphoblastic leukemia (ALL). However, E/R is insufficient to cause overt leukemia since it generates a clinically silent pre-leukemic clone which persists in the bone marrow but fails to out-compete normal progenitors. Conversely, pre-leukemic cells show increased susceptibility to transformation following additional genetic insults. Infections/inflammation are the most accredited triggers for mutations accumulation and leukemic transformation in E/R+ pre-leukemic cells. However, precisely how E/R and inflammation interact in promoting leukemia is still poorly understood. Here we demonstrate that IL6/TNFα/ILβ pro-inflammatory cytokines cooperate with BM-MSC in promoting the emergence of E/R+ Ba/F3 over their normal counterparts by differentially affecting their proliferation and survival. Moreover, IL6/TNFα/ILβ-stimulated BM-MSC strongly attract E/R+ Ba/F3 in a CXCR2-dependent manner.