Effects of Electronic (e)-Cigarette Vapor on Staphylococcal Virulence: Are E-Cigarettes Safer than Conventional Cigarettes?

In recent years, electronic (e)‐cigarettes have dramatically increased in popularity as an alternative to conventional cigarettes. Little is known about the effects of e‐cigarette vapor (EV) on bacteria that colonize the nasopharynx, including methicillin‐resistant Staphylococcusaureus (MRSA). As most cases of pneumonia can be traced to bacteria in a patient\u27s nasopharynx, increased virulence in potential pathogens could have direct consequences clinically for these patients. And because bacterial colonizers are spread between humans, increased virulence in one subject has implications for the community. There is accumulating evidence that exposure to cigarette smoke (CS) increases the pathogenicity of MRSA, as well as its dampening effects on the host immune system. EV exposure has also been demonstrated to increase MRSA virulence both invitro and in a murine model of pneumonia. In this chapter, we will compare the virulence changes reported in MRSA exposed to CS vs. those exposed to EV, as well as proposed mechanisms and therapeutic targets

Electronic cigarette inhalation alters innate immunity and airway cytokines while increasing the virulence of colonizing bacteria.

UnlabelledElectronic (e)-cigarette use is rapidly rising, with 20 % of Americans ages 25-44 now using these drug delivery devices. E-cigarette users expose their airways, cells of host defense, and colonizing bacteria to e-cigarette vapor (EV). Here, we report that exposure of human epithelial cells at the air-liquid interface to fresh EV (vaped from an e-cigarette device) resulted in dose-dependent cell death. After exposure to EV, cells of host defense-epithelial cells, alveolar macrophages, and neutrophils-had reduced antimicrobial activity against Staphylococcus aureus (SA). Mouse inhalation of EV for 1 h daily for 4 weeks led to alterations in inflammatory markers within the airways and elevation of an acute phase reactant in serum. Upon exposure to e-cigarette vapor extract (EVE), airway colonizer SA had increased biofilm formation, adherence and invasion of epithelial cells, resistance to human antimicrobial peptide LL-37, and up-regulation of virulence genes. EVE-exposed SA were more virulent in a mouse model of pneumonia. These data suggest that e-cigarettes may be toxic to airway cells, suppress host defenses, and promote inflammation over time, while also promoting virulence of colonizing bacteria.Key messageAcute exposure to e-cigarette vapor (EV) is cytotoxic to airway cells in vitro. Acute exposure to EV decreases macrophage and neutrophil antimicrobial function. Inhalation of EV alters immunomodulating cytokines in the airways of mice. Inhalation of EV leads to increased markers of inflammation in BAL and serum. Staphylococcus aureus become more virulent when exposed to EV

A technique for the measurement of realism in social situations

It is suggested that it might be useful to develop techniques which are specifically designed to examine the social aspects of experimental situations, in light of the increased emphasis and recognition given social phenomena in psychology in recent years. For this purpose the author attempts to modify level of aspiration techniques for use in sociometric situations. Concern is mainly with the concept of realism, which is operationally defined, on the basis of previous studies of the level of aspiration, as "that function of personality revealed by a technique designed to measure a subject's ability to designate accurately his expected performance in an activity in which he has had some experience and consequently some criterion on which -to base his designation." The attempt to measure this defined function in social situations was undertaken in the following way: 1. Asking each individual in a group to choose other individuals on the basis of a specified criterion. 2. Asking each individual to give the names of those individuals he expects to have chosen him. The individual's realism is estimated in terms of the discrepancy between the obtained and expected choices on the basis of three factors which were logically determined; Factor A, discrepancy between number expected and obtained; Factor B, discrepancy between correct expected choices and obtained choices in terms of the actual names of the individuals involved; and Factor C, the discrepancy between the mean sociometric status of the individuals he expected to choose him, and the mean sociometric status of those who did choose him. The process of derivation of the total R score is summarized below: Factor A - expected – obtained/(N – 1) x 100 - can be either + or -. Ignore this 'direction' until the expression of the R score. - converted to sigma score in terms of the distribution of A within the group, by formula: A – M(a)/Sigma(a) = Z(a) Factor B – 1 - correct expected choices/obtained choices x 100 - convert to sigma score Z(b) Factor C – [M(exp.) – M(obt)] x 100 - can be either + or -. Ignore direction until R - convert to sigma Z(c.) R score is given by the formula: WaZa + WbZb + WcZc/Wa + Wb + Wc Where Wa, Wb, and Wc are the weights derived from the beta coefficients obtained from the inter-correlations of the factors. Ineluded in the expression of the final R score for an individual, are the directions in which he tends on Factors A and C. This technique was applied to three groups at different age levels (7-8yrs., 21-31yrs., 59-86yrs.,) for the purpose of determining whether or not it was possible to obtain distributions of R scores for each of the groups; that is, whether the function measured could discriminate between individuals. This purpose was fulfilled. Certain general indications are presented, having to do with the patterning of the positive and negative directions on Factors A and C, various sociometric relationships, and a few others. There is also presented empirical evidence which is interpreted as a partial justification for the logical assumption that the technique is measuring a realism function similar to that reported in aspiration studies. Implications and suggestions for future research are discussed under these headings: "Technique," "Levels of Aspiration," and "Sociometry.”Arts, Faculty ofPhilosophy, Department ofGraduat

The workplace as a therapeutic landscape: Understanding the effects of COVID-19 on the wellbeing of food hospitality employees

This study investigated the pandemic-related modifications to food hospitality businesses in Ontario, Canada and their effects on the health and wellbeing of workers. Semi-structured interviews were conducted with 22 food hospitality employees in Ontario between June 2020 and May 2021 as part of the Food Retail Environment Study for Health and Economic Resiliency (FRESHER). Transcripts were analyzed inductively using grounded theory as a means of allowing themes to be distilled organically from this relatively new area of research. Therapeutic landscapes emerged as a framework for the resultant themes. The three main themes in this analysis are compromised based on the physical, social, and symbolic spaces of a therapeutic landscape: physical aspects of food hospitality businesses as influencers of wellbeing, social relationships as sources of support and stress, and symbols of fear and safety within food hospitality workplaces. Results indicate that, for food hospitality employees, the workplace was an imperfect therapeutic landscape with a mix of benefits and threats to wellbeing. Further study is needed to understand how these spaces might be reconstructed to better promote wellbeing

Hypoxia-inducible factor-1α inhibition modulates airway hyperresponsiveness and nitric oxide levels in a BALB/c mouse model of asthma

Hypoxia inducible factor (HIF)-1α is a master regulator of inflammation and is upregulated in alveolar macrophages and lung parenchyma in asthma. HIF-1α regulates select pathways in allergic inflammation, and thus may drive particular asthma phenotypes. This work examines the role of pharmacologic HIF-1α inhibition in allergic inflammatory airway disease (AIAD) pathogenesis in BALB/c mice, which develop an airway hyperresponsiveness (AHR) asthma phenotype. Systemic treatment with HIF-1α antagonist YC-1 suppressed the increase in HIF-1α expression seen in control AIAD mice. Treatment with YC-1 also decreased AHR, blood eosinophilia, and allergic inflammatory gene expression: IL-5, IL-13, myeloperoxidase and iNOS. AIAD mice had elevated BAL levels of NO, and treatment with YC-1 eliminated this response. However, YC-1 did not decrease BAL, lung or bone marrow eosinophilia. We conclude that HIF-1α inhibition in different genetic backgrounds, and thus different AIAD phenotypes, decreases airway resistance and markers of inflammation in a background specific manner