College Students’ Use of Social Media and E-Cigarettes: How Correctly Identifying Platform Type Influences Findings

The purpose of this study was to examine how college students post or share JUUL-related content on social media. Using a sequential explanatory mixed-methods design, current JUUL users (n = 667) completed a cross-sectional survey in March of 2019, then 51 participants completed in-person follow-up interviews in April of 2019. Survey questions asked about JUUL-related social media postings and commenting history as well as demographic questions. Interview participants were asked to explain their survey responses and were then shown the survey results and asked for reasons why they and others did not post or comment about JUUL on social media. Qualitative data were coded independently by two coders using NVivo, and analyzed for themes. Survey participant (ages 18-24, mean age 20 years, 50.5% female, and 80.6% white) responses showed 81% had not posted a JUUL-focused comment on social media and had not posted a picture of themselves JUULing in the past year. However, interviewees reported they had continued to post about JUUL on social media but moved away from more public social media accounts (e.g., Facebook); private Instagram and Snapchat accounts were used to post both JUUL use and JUUL-focused content without risk of damaging their personal image to family or potential employers. How social media use questions are asked is critical for understanding college student promotion of JUULing and social norms. Young adults protect their social media presence by not including themselves in JUUL-focused content; thus, the spread of JUULing through private social media like Snapchat or Finstas may not be identified and young adults normalize JUUL use through memes or images

Immunoresponsive Gene 1 Augments Bactericidal Activity of Macrophage-Lineage Cells by Regulating β-Oxidation-Dependent Mitochondrial ROS Production

SummaryEvidence suggests the bactericidal activity of mitochondria-derived reactive oxygen species (mROS) directly contributes to killing phagocytozed bacteria. Infection-responsive components that regulate this process remain incompletely understood. We describe a role for the mitochondria-localizing enzyme encoded by Immunoresponsive gene 1 (IRG1) during the utilization of fatty acids as a fuel for oxidative phosphorylation (OXPHOS) and associated mROS production. In a zebrafish infection model, infection-responsive expression of zebrafish irg1 is specific to macrophage-lineage cells and is regulated cooperatively by glucocorticoid and JAK/STAT signaling pathways. Irg1-depleted macrophage-lineage cells are impaired in their ability to utilize fatty acids as an energy substrate for OXPHOS-derived mROS production resulting in defective bactericidal activity. Additionally, the requirement for fatty acid β-oxidation during infection-responsive mROS production and bactericidal activity toward intracellular bacteria is conserved in murine macrophages. These results reveal IRG1 as a key component of the immunometabolism axis, connecting infection, cellular metabolism, and macrophage effector function

The association of aggressive and chronic periodontitis with systemic manifestations and dental anomalies in a jordanian population: a case control study

<p>Abstract</p> <p><b>Background</b></p> <p>The relationship between dental anomalies and periodontitis has not been documented by earlier studies. Although psychological factors have been implicated in the etiopathogenesis of periodontitis, very little information has so far been published about the association of anxiety and depression with aggressive periodontitis. The aim of this study was to investigate the association of chronic periodontitis and aggressive periodontitis with certain systemic manifestations and dental anomalies.</p> <p><b>Methods</b></p> <p>A total of 262 patients (100 chronic periodontitis, 81 aggressive periodontitis and 81 controls), attending the Periodontology clinics at Jordan University of Science and Technology, Dental Teaching Centre) were included. All subjects had a full periodontal and radiographic examination to assess the periodontal condition and to check for the presence of any of the following dental anomalies: dens invaginatus, dens evaginatus, congenitally missing lateral incisors or peg-shaped lateral incisors. Participants were interrogated regarding the following: depressive mood, fatigue, weight loss, or loss of appetite; and their anxiety and depression status was assessed using the Hospital Anxiety and Depression (HAD) scale.</p> <p><b>Results</b></p> <p>Patients with aggressive periodontitis reported more systemic symptoms (51%) than the chronic periodontitis (36%) and control (30%) patients (<it>p </it>< 0.05). Aggressive periodontitis patients had a higher tendency for both anxiety and depression than chronic periodontitis and control patients. Dental anomalies were significantly (<it>p </it>< 0.05) more frequent among both of chronic and aggressive periodontitis patients (15% and 16%, respectively), compared to controls.</p> <p><b>Conclusion</b></p> <p>In this group of Jordanians, systemic symptoms were strongly associated with aggressive periodontitis, and dental anomalies were positively associated with both aggressive and chronic periodontitis.</p

Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes

T lymphocytes utilize amoeboid migration to navigate effectively within complex microenvironments. The precise rearrangement of the actin cytoskeleton required for cellular forward propulsion is mediated by actin regulators, including the actin‐related protein 2/3 (Arp2/3) complex, a macromolecular machine that nucleates branched actin filaments at the leading edge. The consequences of modulating Arp2/3 activity on the biophysical properties of the actomyosin cortex and downstream T cell function are incompletely understood. We report that even a moderate decrease of Arp3 levels in T cells profoundly affects actin cortex integrity. Reduction in total F‐actin content leads to reduced cortical tension and disrupted lamellipodia formation. Instead, in Arp3‐knockdown cells, the motility mode is dominated by blebbing migration characterized by transient, balloon‐like protrusions at the leading edge. Although this migration mode seems to be compatible with interstitial migration in three‐dimensional environments, diminished locomotion kinetics and impaired cytotoxicity interfere with optimal T cell function. These findings define the importance of finely tuned, Arp2/3‐dependent mechanophysical membrane integrity in cytotoxic effector T lymphocyte activities

Hypoxia increases neutrophil-driven matrix destruction after exposure to Mycobacterium tuberculosis.

The importance of neutrophils in the pathology of tuberculosis (TB) has been recently established. We demonstrated that TB lesions in man are hypoxic, but how neutrophils in hypoxia influence lung tissue damage is unknown. We investigated the effect of hypoxia on neutrophil-derived enzymes and tissue destruction in TB. Human neutrophils were stimulated with M. tuberculosis (M.tb) or conditioned media from M.tb-infected monocytes (CoMTB). Neutrophil matrix metalloproteinase-8/-9 and elastase secretion were analysed by luminex array and gelatin zymography, gene expression by qPCR and cell viability by flow cytometry. Matrix destruction was investigated by confocal microscopy and functional assays and neutrophil extracellular traps (NETs) by fluorescence assay. In hypoxia, neutrophil MMP-8 secretion and gene expression were up-regulated by CoMTB. MMP-9 activity and neutrophil elastase (NE) secretion were also increased in hypoxia. Hypoxia inhibited NET formation and both neutrophil apoptosis and necrosis after direct stimulation by M.tb. Hypoxia increased TB-dependent neutrophil-mediated matrix destruction of Type I collagen, gelatin and elastin, the main structural proteins of the human lung. Dimethyloxalylglycin (DMOG), which stabilizes hypoxia-inducible factor-1α, increased neutrophil MMP-8 and -9 secretion. Hypoxia in our cellular model of TB up-regulated pathways that increase neutrophil secretion of MMPs that are implicated in matrix destruction