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Through co-transfection experiments, we explored that the abilities of OSCC cell proliferation, colony formation, invasion, and migration obviously reduced after miR-454 depletion, but these phenomena were mitigated to some extent after NR3C2 silencing. CONCLUSION The study illustrates that miR-454 acts as an active regulator to facilitate OSCC cells growth, colony formation, invasion, and migration by targeting NR3C2, which may afford a novel perspective and possibility for the targeted treatment of OSCC. © 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.BACKGROUND Our objective of the present study was to verify the speed and accuracy of fetal ultrasonic Doppler (fetal Doppler) in measuring heart rate of newborns at rest, including preterm, low birth weight infants, and its efficacy during neonatal resuscitation, including cases of neonatal asphyxia. METHODS A 3-lead electrocardiogram and fetal Doppler were used to measure resting heart rates in 100 newborns, including 48 preterm, low birth weight infants, at 0 to 72 hours after birth. Times to display heart rate were compared between electrocardiogram and fetal Doppler by the Bland-Altman analysis and Wilcoxon signed-rank test. The time required for the fetal Doppler to measure heart rate during neonatal resuscitation was also assessed. RESULTS In 100 newborns, the mean error of the resting heart rate in 1,293 measurement points was 0.07 beats/min. To display the heart rate, fetal Doppler required a median time of 5 seconds, and electrocardiogram required a median time of 10 seconds (p less then 0.001). During neonatal resuscitation, the heart rate was measured within 10 seconds in 18 of 21 cases (86%) and displayed with a median time of 5 seconds; this was measured in all neonatal asphyxia cases (9/9, 100%). CONCLUSIONS Fetal Doppler can accurately and rapidly measure heart rate in newborns and is useful for evaluating heart rate not only at rest, but also during neonatal resuscitation, especially in asphyxia. This article is protected by copyright. All rights reserved.BACKGROUND Hyperalgesia is a heightened pain response to a noxious stimulus and is a hallmark of many common neuropathic and chronic pain conditions. In a double-blind placebo-controlled drug-crossover trial the effects of concomitant and delayed minocycline treatment on the initiation and resolution of muscle hyperalgesia were tested. METHODS An initial cohort (n=10) received repeated injections (5 µg days 0, 2 and 4) of nerve growth factor (NGF) in the flexor carpi ulnaris muscle of the forearm and pressure pain thresholds were collected at day 0 (control), day 7 (peak) and day 14 (recovery). A second cohort (n=18) underwent an identical procedure, however, half received a placebo between days 0-7 before switching to minocycline from days 7-14 (P1/M2), while the remaining subjects received minocycline (day 0 200mg then 100mg b.i.d. for 7 days) before switching to placebo (M1/P2). RESULTS The initial cohort exhibited a diffuse muscular pain hypersensitivity with a decrease in pressure pain thresholds at day 7 before a partial return to normalcy at day 14. The P1/M2 treatment group exhibited an identical peak in hypersensitivity at day 7, however, after switching to minocycline in week 2 showed a significant reduction in muscle hyperalgesia compared to the initial cohort at day 14. The M1/P2 treatment group had significantly less (~50%) hyperalgesia at day 7 compared to the other groups. CONCLUSIONS This study indicates that the administration of minocycline can reduce experimentally induced muscle pain regardless of the time of administration. This article is protected by copyright. All rights reserved.BACKGROUND Aggressive periodontitis is characterized by the early-onset and rapid progression of periodontal destruction, and is closely associated with Aggregatibacter actinomycetemcomitans. Autophagy is a conserved process that is critical for removing damaged proteins, organelles, and even intracellular pathogens. Therefore, this study examined whether A. actinomycetemcomitans induces autophagy. In addition, the relationship among autophagy, bacterial internalization, and inflammatory molecules in periodontal aggressive inflammation was analyzed. METHODS The expression of autophagy-related proteins in human gingival tissue and THP-1 cells was assessed by Western blot analysis. The formation of light chain 3 (LC3) puncta was examined by confocal microscopy. The degree of bacterial internalization into the cells was determined by the viable cell count. Phagocytosis and ROS production were measured using confocal microscopy and flowcytometry. RESULTS When macrophages were infected with live A. actinomycetemcos reserved. This article is protected by copyright. All rights reserved.Nonalcoholic fatty liver disease (NAFLD) represents a burgeoning worldwide epidemic whose etiology reflects multiple interactions between environmental and genetic factors. Here we review the major pathways and dominant genetic modifiers known to be relevant players in human NAFLD and which may determine key components of the heritability of distinctive disease traits including steatosis and fibrosis. In addition, we have employed general assumptions which are based on known genetic factors in NAFLD to build a systems biology prediction model that includes functional enrichment. This new prediction model highlights additional complementary pathways that represent plausible intersecting signaling networks that we define here as a NAFLD-Reactome. We review the evidence connecting variants in each of the major known genetic modifiers (variants in PNPLA3, TM6SF2, MBOAT7, GCKR and HSD17B13) to NAFLD and expand the associated underlying mechanisms using functional enrichment predictions, based on both preclinical and cell based experimental findings. These major candidate gene variants function in distinct pathways, including substrate delivery for de-novo lipogenesis; mitochondrial energy utilization; lipid droplet assembly, lipolytic catabolism and fatty acid compartmentalization; and VLDL assembly and secretion. The NAFLD-Reactome model expands these pathways and allows for hypothesis testing as well as serving as a discovery platform for druggable targets across multiple pathways that promote NAFLD development and which influence several progressive outcomes. In conclusion, we summarize the strengths and weaknesses of studies implicating selected variants in the pathophysiology of NAFLD and highlight opportunities for future clinical research and pharmacologic intervention, as well as the implications for clinical practice. https://www.selleckchem.com/products/ps-1145.html This article is protected by copyright. All rights reserved.