In July of 2024, signatures for placing an anti-gerrymandering initiative on the November ballot were certified by the Ohio Secretary of State. The proposed initiative would have replaced a bipartisan redistricting commission with a citizens' redistricting commission. Though the initiative ultimately failed, polls leading up to the general election showed Ohioans strongly supported redistricting reform. Using a survey of likely voters in Ohio, the research presented here identifies the factors that explain support for redistricting reform. While there is a strong body of research on redistricting, this research is unique because the survey data come from likely voters during an actual redistricting campaign. The findings show that identifying threats to democracy as the most important election issue, awareness of the redistricting issue, identification with the Democratic Party, and liberal ideology are all positively associated with support for redistricting reform. The findings demonstrate how voters are influenced by partisanship on salient issues and how issue awareness interacts with partisanship to determine support for redistricting. This article concludes with a discussion of the context of the ballot initiative in Ohio.

This article examines the New Ethnicity movement through multiple lenses. First, it examines some of the objectives of the movement as articulated by its leaders and also looks at more recent scholarship on the lasting effects of the movement. During this ethnic reawakening of the 1970s, Polish American musical artists created songs with lyrics that reflected and reinforced Polish American ethnic identity. This paper examines two very different songs from this period: “My Melody of Love” by Bobby Vinton and “Love and Peace Polka” by Happy Louie (Dusseault). Then the immediate response to and lasting impact of these songs is examined through a survey primarily of Polish Americans. The cultural aspect of the New Ethnicity movement may endure, which helps to extend a theory of “latent ethnicity.” This means that the New Ethnicity movement's lasting legacy for Polonia may be the enduring impulse to preserve and promote ethnic identity through music, food, and other cultural means. This identity, while mostly latent, nonetheless exists, and can be activated in social and political life.

This article examines the Polish American vote in the 2024 US presidential election. First, it examines the history of the Polish American vote and considers whether there is still such a thing as a Polish American electorate. Then, utilizing a theory of identity priming, we test whether then-Vice President Kamala Harris's direct appeal to Polish American voters worked. The sample utilized consists of 1,278 students at a large Midwestern university, of whom nearly ten percent identify as Polish American. The results suggest some significant political differences between the Polish American and other respondents, including reactions to the Harris appeal. The paper concludes with a discussion of how the Polish American identity is maintained, through a theory of latent ethnicity.

In this research note we examine the effect of Taylor Swift's hypothetical endorsement of a Public policy position. We examine this in the context of the expanding literature on the effects of celebrity endorsements. Through a post-test only experimental survey design we test Swift's hypothetical endorsement of a policy position. We begin and conclude with analysis of why Swift's value as an endorser, as well as the value of other similarly situated endorsers may be particularly high.

Polish Americans celebrate their ethnic identity in myriad ways, including Pgczki Day celebrations, Dyngus Day parties, kol & eogon;dy singalongs, and dance and other performances. These types of events are examined in the context of theories of ethnicity persistence and dissipation, as well as through the lens of invented traditions. Results of a survey of 409 event participants are presented, which reveal that participants believe strongly in preserving Polish and Polish American culture, as well as the need for authenticity in these events. The role of food, drink, and polka music is examined, and distinctions are drawn among the various events based in part on the sponsoring organizations. Analysis is offered of differences between Polish American and non-Polish American participants, and some tentative thoughts are offered about the responses of various cohorts of Polish Americans. While for most Polish Americans, ethnic identity has become largely symbolic, it still can have consequences that go beyond mere celebration. A theory of latent ethnicity is presented, which argues that these events maintain ethnicity symbolically, and that Polish American ethnicity can then be awakened in everyday life, particularly during presidential elections.

In this article we examine the effect of Taylor Swift's hypothetical endorsement of a Public policy position. We examine this in the context of not just the expanding literature on the effects of celebrity endorsements, but also through the lens of Robert Cialdini's work on the seven factors of influence. Through a post-test only experimental survey design we test Swift's endorsement of a policy position, compared with the effects of social proof, scarcity, and authority. We find that Swift's endorsement is at least as influential as these other elements of influence, and possibly more so. We conclude with informed speculation about why Swift's value as an endorser may be particularly high. The survey was approved by BGSU’s Institutional Review Board (IRBNet ID Number: 2072943-2).

This study examines the 2020 decision by the Canadian football team previously known as the Edmonton Eskimos to change its name to the Edmonton Elks. The process of rebranding occurred during a time of unprecedented sociopolitical upheavals including economic uncertainties, multiple social justice movements, and a global health pandemic. To illuminate the complexities involved in effectively managing the process, the authors provide background on what makes Canadian professional football unique and how it is constructed as being essential to national identity. The study contextualizes the decision-making process historically and through a lens of contemporary social issues.

After examining the concept of festivals as ethnic practice and the scholarship on ethnic and heritage festivals among various ethnic groups in the US, including Cajuns and Czech, Scottish and German Americans, this paper utilizes a survey of Polish American festival organizers as well as public descriptions of Polish American festivals to determine why festival activists organize their events, what image of Polish American identity they try to project through their festivals, and how they account for issues of authenticity as Polish American neighborhoods continue to decline and the community becomes more diffused.

AbstractThis article explores how radio disc jockeys (DJs) and internet disc jockeys (IJs) who play polka music derived from Central and Eastern European music traditions are involved in the process of promoting and preserving ethnic identity in the United States.1 We surveyed DJs and IJs and found that they believe they are keeping an important tradition alive, promoting their ethnic culture, and sometimes teaching their audiences about the Polish, Czech, Slovenian, and German languages. These cultural gatekeepers believe the future of polka music is very challenging, in that there are diminishing numbers of people attending polka events in many of the regions where polka used to be popular. There is also a decline in the number of polka bands, and some DJs and IJs perceive a decline in the quality of both musicianship and singing in the European languages. There are, however, cultural conditions that make it possible for polka music to have an evolving and relevant future.

This paper presents a case study of Polish American Christmas events in Toledo, Ohio in 2013 through interviews and participant-observation ethnographic research.(1) It also briefly examines the history of the Polish American presence in Toledo, as well as the challenges the community faces now that its members no longer live in geographically concentrated neighborhoods. Despite the changing tastes of Toledoans both of Polish origin and other backgrounds, as well as controversies surrounding some Polish American events, a noticeable Polish American presence remains in the city and region, and is especially active around Christmas time.

U.S. celebrities endorse both ideas/issue positions and candidates for the Presidency. Presumably, they do this to influence their fans to agree with their positions and to support their preferred candidates. Using result from two non-probability samples of likely 2016 general election voters in Ohio this article demonstrates that familiarity and favorability are essential for a celebrity endorsement to have any effects. Celebrities with whom the public is merely familiar but not favorable toward may have a negative effect, while celebrities who are viewed favorably consistently have positive effects.

Chronic airway diseases are a significant cause of morbidity and mortality worldwide, and their prevalence is predicted to increase in the future. Respiratory viruses are the most common cause of acute pulmonary infection, and there is clear evidence of their role in acute exacerbations of inflammatory airway diseases such as asthma and chronic obstructive pulmonary disease. Studies have reported impaired host responses to virus infection in these diseases, and a better understanding of the mechanisms of these abnormal immune responses has the potential to lead to the development of novel therapeutic targets for virus-induced exacerbations. The aim of this article is to review the current knowledge regarding the role of viruses and immune modulation in acute exacerbations of chronic pulmonary diseases and to discuss exciting areas for future research and novel treatments.

Rhinoviruses cause the common cold and exacerbations of asthma. Animal models of infection have identified a protective role for interleukin-18 (IL-18). Following experimental rhinovirus infection, we observed increased respiratory symptoms in healthy and asthmatic subjects with low nasal and bronchial IL-18 levels.

Our understanding of asthma control has evolved in recent years to include both the idea of current control (gauged mostly from symptoms) and a link with future risk, notably exacerbations.1Reddel H.K. Taylor D.R. Bateman E.D. Boulet L.P. Boushey H.A. Busse W.W. et al.American ThoracicSociety/European Respiratory Society Task Force on Asthma Control and ExacerbationsAn official American Thoracic Society/European Respiratory Society statement: asthma control and exacerbations: standardizing endpoints for clinical asthma trials and clinical practice.Am J Respir Crit Care Med. 2009; 180: 59-99Crossref PubMed Scopus (1547) Google Scholar Despite currently available therapies, many patients remain uncontrolled and asthma exacerbations, which are most frequently triggered by rhinovirus infections, remain a major unmet need.2Slejko J.F. Ghushchyan V.H. Sucher B. Globe D.R. Lin S.L. Globe G. et al.Asthma control in the United States, 2008-2010: indicators of poor asthma control.J Allergy Clin Immunol. 2014; 133: 1579-1587Abstract Full Text Full Text PDF PubMed Scopus (88) Google Scholar The development of human experimental models of rhinovirus-induced asthma exacerbations has led to important advances in our understanding of exacerbation pathogenesis3Message S.D. Laza-Stanca V. Mallia P. Parker H.L. Zhu J. Kebadze T. et al.Rhinovirus-induced lower respiratory illness is increased in asthma and related to virus load and Th1/2 cytokine and IL-10 production.Proc Natl Acad Sci U S A. 2008; 105: 13562-13567Crossref PubMed Scopus (406) Google Scholar; however, to date, studies have been limited through the inclusion of patients with well-controlled asthma only.3Message S.D. Laza-Stanca V. Mallia P. Parker H.L. Zhu J. Kebadze T. et al.Rhinovirus-induced lower respiratory illness is increased in asthma and related to virus load and Th1/2 cytokine and IL-10 production.Proc Natl Acad Sci U S A. 2008; 105: 13562-13567Crossref PubMed Scopus (406) Google Scholar It is therefore unknown how the level of control at the time of infection influences the severity of the exacerbation; however, studies of naturally occurring exacerbations support a relationship between control and exacerbation frequency.4Bateman E.D. Bousquet J. Busse W.W. Clark T.J. Gul N. Gibbs M. et al.GOAL Steering Committee and Investigators. Stability of asthma control with regular treatment: an analysis of the Gaining Optimal Asthma controL (GOAL) study.Allergy. 2008; 63: 932-938Crossref PubMed Scopus (91) Google Scholar, 5Bateman E.D. Reddel H.K. Eriksson G. Peterson S. Ostlund O. Sears M.R. et al.Overall asthma control: the relationship between current control and future risk.J Allergy Clin Immunol. 2010; 125 (608.e1-6): 600-608Abstract Full Text Full Text PDF PubMed Scopus (224) Google Scholar We therefore analyzed the relationship between the degree of baseline control in patients with asthma infected with rhinovirus-16 (RV16) and clinical measures of exacerbation severity following inoculation. A comparison of clinical outcomes between subjects with and without asthma including the same subjects as reported herein has been published elsewhere.6Jackson D.J. Makrinioti H. Rana B.M. Shamji B.W. Trujillo-Torralbo M.B. Footitt J. et al.IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo.Am J Respir Crit Care Med. 2014; 190: 1373-1382Crossref PubMed Scopus (10) Google Scholar Twenty-eight adult volunteers with asthma were recruited (Table I). The study was approved by a local research ethics committee (09/H0712/59), and all volunteers provided written informed consent to participate. The degree of asthma control at baseline was assessed using the Juniper Asthma Control Questionnaire (ACQ-7), with 3 control groups defined by ACQ cutoff scores of 0.75 or less for well-controlled (n = 12), 0.76 to 1.49 for partially controlled (n = 8), and 1.5 or more for uncontrolled asthma (n = 8), respectively.7Juniper E.F. Bousquet J. Abetz L. Bateman E.D. Identifying ‘well-controlled’ and ‘not well-controlled’ asthma using the Asthma Control Questionnaire.Respir Med. 2006; 100: 616-621Abstract Full Text Full Text PDF PubMed Scopus (735) Google Scholar For full inclusion/exclusion criteria, see this article's Methods section in the Online Repository at www.jacionline.org.Table IBaseline demographic and clinical characteristics of study volunteersCharacteristicWell-controlled ACQ score ≤0.75 (n = 12)Partially controlled ACQ score 0.76-1.49 (n = 8)Uncontrolled ACQ score ≥1.50 (n = 8)P valueAcross all groupsBetween groupsAge (y)33 ± 1238 ± 1036 ± 10.542—Sex (%).087— Female755025 Male255075White ethnicity (% of subjects)10 (83)5 (63)7 (88).426—Baseline FEV1 % of predicted value95 ± 1078 ± 782 ± 10.001Well vs part: .001Well vs un: .02Part vs un: 1.0Asthma severity (as defined by GINA).013Well vs part: .31Well vs un: .01Part vs un: .23 Mild asthma (% of subjects)8 (66.7)3 (37.5)0 (0) Moderate asthma (% of subjects)4 (33.3)5 (62.5)8 (100)Baseline histamine PC20 (mg/mL)1.55 ± 1.950.29 ± 0.611.78 ± 2.78.277—Baseline asthma control (ACQ score)0.56 ± 0.271.18 ± 0.151.86 ± 0.32<.001Well vs part: <.001Well vs un: <.001Part vs un: <.001Use of inhaled corticosteroids (% of subjects)4 (33)4 (50)7 (88).063—Dose of inhaled corticosteroids (beclometasone/equivalent) (μg) Median450350400.71— Interquartile range250-875200-875200-500IgE (IU/mL) Median95356152.183— Interquartile range65-212122-110552-710BAL eosinophilia (%) Median0.31.30.3.225— Interquartile range0-1.00.3-3.00-1.8BAL, Bronchoalveolar lavage; GINA, Global Initiative for Asthma; part, partially controlled; un, uncontrolled. Open table in a new tab BAL, Bronchoalveolar lavage; GINA, Global Initiative for Asthma; part, partially controlled; un, uncontrolled. Subjects were seen at baseline and on days 2, 3, 4, 5, 7, 10, and 42 postinoculation with RV16. Daily diary cards of upper and lower respiratory tract symptoms and FEV1 measurements were commenced 2 weeks before baseline sampling and continued for 6 weeks.6Jackson D.J. Makrinioti H. Rana B.M. Shamji B.W. Trujillo-Torralbo M.B. Footitt J. et al.IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo.Am J Respir Crit Care Med. 2014; 190: 1373-1382Crossref PubMed Scopus (10) Google Scholar The lower respiratory tract score was calculated from scores graded 0 to 3 for cough on waking; wheeze on waking; daytime cough; daytime wheeze; daytime chest tightness; daytime shortness of breath; nocturnal cough, wheeze, or shortness of breath.6Jackson D.J. Makrinioti H. Rana B.M. Shamji B.W. Trujillo-Torralbo M.B. Footitt J. et al.IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo.Am J Respir Crit Care Med. 2014; 190: 1373-1382Crossref PubMed Scopus (10) Google Scholar Bronchial mucosal lining fluid was sampled for measurement of a range of cytokines and chemokines including IL-4, IL-5, IL-6, IL-13, IL-33, CXCL10/IP-10, and CXCL11/ITAC using the technique of bronchosorption.6Jackson D.J. Makrinioti H. Rana B.M. Shamji B.W. Trujillo-Torralbo M.B. Footitt J. et al.IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo.Am J Respir Crit Care Med. 2014; 190: 1373-1382Crossref PubMed Scopus (10) Google Scholar This involves passing a specially designed probe with a synthetic absorptive tip down the operating port of a bronchoscope. Further details regarding study design, methodology, and statistical analyses are provided in this article's Online Repository at www.jacionline.org and have been previously published.6Jackson D.J. Makrinioti H. Rana B.M. Shamji B.W. Trujillo-Torralbo M.B. Footitt J. et al.IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo.Am J Respir Crit Care Med. 2014; 190: 1373-1382Crossref PubMed Scopus (10) Google Scholar Following RV16 infection, we observed an increase in upper and lower respiratory tract symptoms across all asthma control categories. However, those with uncontrolled asthma (ACQ score, ≥1.5) experienced significantly greater virus-induced respiratory symptoms than did those with superior baseline control. Specifically, although upper respiratory tract symptoms reached a similar magnitude across the groups, those with uncontrolled asthma experienced a more prolonged cold than did others with asthma (Fig 1, A). Analysis of lower respiratory tract symptom scores also revealed substantial differences between control categories: Those with uncontrolled asthma experienced a greater maximal level of lower respiratory tract symptoms on day 4 (P < .05) and a slower recovery with significant differences in symptoms observed on days 8 to 11 and 13 between control groups (all P < .05) (Fig 1, B). Analysis of the total lower respiratory tract symptom score (summation of daily scores during the 14 days postinoculation, a more complete measure of exacerbation severity) demonstrated that those with uncontrolled asthma had a significantly greater mean score (59.8 ± 8.6) than did those with asthma with better baseline control (ACQ score, ≤0.75; total score, 21.3 ± 5.5 [P = .001]; ACQ score, 0.76-1.49; total score, 32.5 ± 6.3 [P = .02]) (Fig 1, C). Importantly, virus-induced increases in lower respiratory tract symptom scores were corrected for preinfection levels and were therefore over and above any baseline symptom for each subject (see this article's Methods section in the Online Repository). The relationship between baseline control and virus-induced symptom severity was mirrored by changes in lung function: Analysis of daily FEV1 measurements highlighted that those with uncontrolled asthma had significantly greater virus-induced falls in FEV1 from baseline: 24.6% ± 3.1% compared with 16.3% ± 1.7% for subjects with an ACQ score of 0.76 to 1.49 (P = .025), and 14.9% ± 2.0% for the well-controlled group (P = .021) (Fig 1, D). Taken together, those with uncontrolled asthma experienced a more severe and prolonged exacerbation than did those with asthma with better baseline control. Categorizing those with asthma by asthma severity (defined by the Global Initiative for Asthma8Global Initiative for AsthmaGlobal strategy for asthma management and prevention. Workshop report.www.ginasthma.comDate: 2004Google Scholar) rather than asthma control revealed significantly greater virus-induced lower respiratory tract symptoms in those with moderately severe asthma (n = 17) than in those with mild asthma (n = 11) (P = .01; Fig 1, E). However, analysis of those with moderately severe asthma alone demonstrated that the observed relationship between control and exacerbation severity persisted within this single severity category (r = 0.5; P = .04) (Fig 1, F). A significant relationship was also evident when the correlation was limited to those with asthma on inhaled corticosteroid therapy (r = 0.58; P = .02). Interestingly, no relationship in asthma was seen between lower respiratory tract symptoms and baseline FEV1 (r = −0.14; P = .49). Unfortunately, because of the small number of subjects in each control category, it has not been possible to address the potential for confounding factors further and future larger studies are required to investigate this. In addition, it should be noted that most of those with well-controlled asthma (8 of 12) had mild asthma. Measurement of a range of TH1 (CXCL10/IP-10 and CXCL11/ITAC), TH2 (IL-4, IL-5, IL-13, IL-33), and proinflammatory (IL-6) cytokines/chemokines in bronchial mucosal lining fluid was performed at baseline and on day 4 postinoculation and analyzed according to asthma control group (see Table E1 in this article's Online Repository at www.jacionline.org). Overall, there were no significant differences across control groups for these mediators; however, we were interested to note that the most marked virus-induced increases in the TH1/antiviral chemokines CXCL10/IP-10 and CXCL11/ITAC were seen in those with well-controlled asthma (Table E1). In addition, virus load (VL) was measured in nasal lavage samples at 6 time points between day 2 and day 10 postinoculation as well as in bronchoalveolar lavage on day 4. At each of these time points, median VL was numerically greater in those with uncontrolled asthma than in either of the other groups; however, these differences did not reach significance (Table E2 in this article's Online Repository at www.jacionline.org). To our knowledge, this study is the first to analyze the influence of asthma control on the outcome of a rhinovirus infection in asthma. We observed more severe exacerbations in those with uncontrolled asthma irrespective of asthma severity or treatment status. These results support findings by Bateman et al,5Bateman E.D. Reddel H.K. Eriksson G. Peterson S. Ostlund O. Sears M.R. et al.Overall asthma control: the relationship between current control and future risk.J Allergy Clin Immunol. 2010; 125 (608.e1-6): 600-608Abstract Full Text Full Text PDF PubMed Scopus (224) Google Scholar demonstrating the influence of control on the risk of future exacerbations, as well as findings of the Gaining Optimal Asthma controL study in which unscheduled health care utilization for exacerbations related to the level of control achieved rather than the treatment received.4Bateman E.D. Bousquet J. Busse W.W. Clark T.J. Gul N. Gibbs M. et al.GOAL Steering Committee and Investigators. Stability of asthma control with regular treatment: an analysis of the Gaining Optimal Asthma controL (GOAL) study.Allergy. 2008; 63: 932-938Crossref PubMed Scopus (91) Google Scholar We acknowledge that the small sample size (8-12 per group) makes it difficult to draw significant mechanistic conclusions from our study. However, the higher levels of TH2 cytokines and VL and the finding of less marked TH1/antiviral induction in subjects with asthma compared with healthy controls observed reproducibly in our earlier reports3Message S.D. Laza-Stanca V. Mallia P. Parker H.L. Zhu J. Kebadze T. et al.Rhinovirus-induced lower respiratory illness is increased in asthma and related to virus load and Th1/2 cytokine and IL-10 production.Proc Natl Acad Sci U S A. 2008; 105: 13562-13567Crossref PubMed Scopus (406) Google Scholar, 6Jackson D.J. Makrinioti H. Rana B.M. Shamji B.W. Trujillo-Torralbo M.B. Footitt J. et al.IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo.Am J Respir Crit Care Med. 2014; 190: 1373-1382Crossref PubMed Scopus (10) Google Scholar, 9Sykes A. Edwards M.R. Macintyre J. del Rosario A. Bakhsoliani E. Trujillo-Torralbo M.B. et al.Rhinovirus 16-induced IFN-α and IFN-β are deficient in bronchoalveolar lavage cells in asthmatic patients.J Allergy Clin Immunol. 2012; 129: 1506-1514.e6Abstract Full Text Full Text PDF PubMed Scopus (175) Google Scholar cannot explain why uncontrolled asthma is associated with greater rhinovirus infection–induced asthma symptoms, because trends in these responses did not reach statistical significance in the numbers studied (Table E1, Table E2). We plan to address this critical gap in knowledge in future studies using high throughput discovery approaches and greater numbers of poorly controlled subjects. Interestingly, a recent trial of inhaled IFN-β in asthma10Djukanović R. Harrison T. Johnston S.L. Gabbay F. Wark P. Thomson N.C. et al.INTERCIA Study GroupThe effect of inhaled IFN-β on worsening of asthma symptoms caused by viral infections: a randomized trial.Am J Respir Crit Care Med. 2014; 190: 145-154Crossref PubMed Scopus (215) Google Scholar identified significant improvements in the outcome of naturally occurring respiratory virus infections in those with more severe and poorly controlled asthma only. The data presented here extend our existing understanding of the link between the 2 domains of asthma control—current control and future risk—and further highlight the importance of maintaining adequate control in reducing the likelihood of severe asthma exacerbations. Inclusion and exclusion criteria have been previously published.E1Jackson D.J. Makrinioti H. Rana B.M.J. Shamji B.W.H. Trujillo-Torralbo M.-B. Footitt J. et al.IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo.Am J Respir Crit Care Med. 2014; 190: 1373-1382Crossref PubMed Scopus (457) Google Scholar Inclusion criteria for subjects with asthma:•Age 18 to 55 years•Patient-reported doctor diagnosis of asthma•PC20 histamine less than 8 μg/mL•Mild to moderate disease based on Global Initiative for Asthma criteriaE2Global Initiative for AsthmaGlobal strategy for asthma management and prevention. Workshop report.www.ginasthma.comDate: 2004Google Scholar•Worsening asthma symptoms with infection since last change in asthma therapy•Atopic on skin testing (≥1 positive skin prick test result on a panel of 10 aeroallergens) Exclusion criteria for subjects with asthma:•History of severe asthma•Smoking history over past 6 months or more than 5 pack-year history•Current symptoms of allergic rhinitis•Current or previous history of significant other respiratory disease•Any clinically relevant abnormality on screening or detected significant systemic disease•Asthma exacerbation or viral illness within the previous 6 weeks•Treatment with oral steroids in the previous 3 months•Current use of any nasal medication, oral or systemic antihistamine, antileukotrienes, anticholinergic, or anti-IgE therapy•Serum antibodies to RV-16•Pregnant or breast-feeding women•Contact with infants or elderly at home or at work Symptoms were assessed by daily diary cards as previously published,E1Jackson D.J. Makrinioti H. Rana B.M.J. Shamji B.W.H. Trujillo-Torralbo M.-B. Footitt J. et al.IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo.Am J Respir Crit Care Med. 2014; 190: 1373-1382Crossref PubMed Scopus (457) Google Scholar from 2 weeks before baseline sampling until 4 weeks postinoculation. The daily cold score was measured using the JacksonE3Jackson G.G. Dowling H.F. Spiesman I.G. Boand A.V. Transmission of the common cold to volunteers under controlled conditions, I: the common cold as a clinical entity.AMA Arch Intern Med. 1958; 101: 267-278Crossref PubMed Scopus (296) Google Scholar scale and summated from individual scores (sneezing, headache, malaise, chilliness, nasal discharge, nasal obstruction, sore throat, cough, fever) graded 0 (absent) to 3 (severe). The daily lower respiratory tract score was calculated from symptom scores (cough on waking; wheeze on waking; daytime cough; daytime wheeze; daytime chest tightness; daytime shortness of breath; nocturnal cough, wheeze, or shortness of breath), also graded 0 to 3. The same diary cards recorded home spirometry on waking each morning, recording the best of 3 recordings of FEV1 (Piko-1; nSpire). As previously reported,E1Jackson D.J. Makrinioti H. Rana B.M.J. Shamji B.W.H. Trujillo-Torralbo M.-B. Footitt J. et al.IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo.Am J Respir Crit Care Med. 2014; 190: 1373-1382Crossref PubMed Scopus (457) Google Scholar lower respiratory tract symptom scores were analyzed in 2-week blocks as the baseline and acute infection stages. Both contained a bronchoscopy on the fourth day of each 2-week block. Daily symptom scores during infection, corrected for baseline symptoms and the effects of bronchoscopy, were calculated by subtracting scores obtained during the baseline 2-week block from the corresponding days of the acute infection 2-week block. Total lower respiratory tract scores were calculated by summing the corrected daily scores for the 2-week infection period. The % change in morning FEV1 from baseline during infection was calculated for each subject as the % fall from the mean of the 7-day period before inoculation. Maximal fall from baseline (%) for each subject represented the greatest fall from baseline over the 2-week period following inoculation. RV-16 (100 TCID50) was diluted in 250 μL of 0.9% saline and inoculated into both nostrils using an atomizer (no. 286; De Vilbiss Co, Heston, United Kingdom) as described.E1Jackson D.J. Makrinioti H. Rana B.M.J. Shamji B.W.H. Trujillo-Torralbo M.-B. Footitt J. et al.IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo.Am J Respir Crit Care Med. 2014; 190: 1373-1382Crossref PubMed Scopus (457) Google Scholar Nasal lavage with sterile 0.9% sodium chloride was performed as previously publishedE1Jackson D.J. Makrinioti H. Rana B.M.J. Shamji B.W.H. Trujillo-Torralbo M.-B. Footitt J. et al.IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo.Am J Respir Crit Care Med. 2014; 190: 1373-1382Crossref PubMed Scopus (457) Google Scholar using a 10-mL syringe attached to a hollow nasal adapter (“olive”) used to obstruct the nostril and prevent leakage of lavage fluid. A total of 5 mL of sterile normal saline was instilled into the left nostril and the fluid withdrawn into the 10-mL syringe and flushed back into the nasal cavity 20 times over a 1-minute period. Fluid was collected, aliquoted, and stored at −80°C. All subjects were seronegative for RV16 at screening. Rhinovirus infection was confirmed by positive nasal lavage quantitative PCR for rhinovirus or seroconversion, defined as a titer of serum-neutralizing antibodies to RV16 of at least 1:4 at 6 weeks postinoculation. Serology was performed at screening, day 0, and day 42 postinfection. Full methods and serology results have been previously published.E1Jackson D.J. Makrinioti H. Rana B.M.J. Shamji B.W.H. Trujillo-Torralbo M.-B. Footitt J. et al.IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo.Am J Respir Crit Care Med. 2014; 190: 1373-1382Crossref PubMed Scopus (457) Google Scholar All data analyses were conducted using SPSS v20.0 (IBM Corp, New York, NY). Data are presented as mean (±SEM) values for normally distributed data or as median (interquartile range) values for nonparametric data. Differences between groups were analyzed by using unpaired t tests or Mann-Whitney tests. When differences were assessed between 3 asthma control groups, ANOVA and Kruskal-Wallis tests were performed for parametric and nonparametric comparisons, respectively. Within-group comparisons were analyzed with paired t tests or Wilcoxon's signed rank test. Correlations between data sets were examined using Pearson's correlation for normally distributed data and Spearman's rank correlation coefficient for nonparametric data. Differences were considered significant for all statistical tests at P values of less than .05. All reported P values are 2-sided.Table E1Cytokine and chemokine measurements in bronchial mucosal lining fluidCytokineACQ score ≤0.75n = 12 (baseline)n = 11 (day 4)ACQ score 0.76-1.49n = 7 (baseline)n = 6 (day 4)ACQ score ≥1.5n = 6 (baseline)n = 8 (day 4)P valueacross all groupsIL-4 (pg/mL) Baseline0.0 (0.0-1.3)0.6 (0.0-1.0)0.0 (0.0-0.2)NS Day 40.8 (0.0-2.1)0.3 (0.0-0.8)0.0 (0.0-0.9)NSIL-5 (pg/mL) Baseline0.0 (0.0-1.4)0.7 (0.6-1.2)0.3 (0.0-1.2)NS Day 40.7 (0.0-1.5)1.0 (0.6-2.2)1.6 (0.0-4.1)NSIL-6 (pg/mL) Baseline24.3 (12.9-56.1)28.3 (15.6-141.0)36.3 (17.5-135.8)NS Day 437.8 (12.8-122.7)49.8 (26.3-67.8)94.5 (40.3-1047.8)NSIL-13 (pg/mL) Baseline0.0 (0.0-1.4)0.8 (0.6-1.0)0.0 (0.0-0.9)NS Day 40.6 (0.0-1.1)0.8 (0.5-1.2)0.8 (0.0-2.8)NSIL-33 (ng/mL) Baseline1.81 (0.54-4.70)3.49 (1.53-5.48)2.05 (1.23-4.70)NS Day 40.92 (0.59-3.92)2.83 (1.14-4.46)2.96 (0.95-5.59)NSCXCL10/IP-10 (ng/mL) Baseline1.02 (0.45-1.76)0.86 (0.36-1.52)1.01 (0.65-1.17)NS Day 42.64 (1.73-5.27)∗P < .01 represents statistical significance for day 4 vs baseline.1.44 (0.85-4.45)†P < .05 represents statistical significance for day 4 vs baseline.1.96 (0.97-5.25)†P < .05 represents statistical significance for day 4 vs baseline.NSCXCL11/ITAC (pg/mL) Baseline18.6 (12.7-42.5)16.0 (11.4-34.0)23.9 (14.1-33.0)NS Day 4179.8 (64.9-527.7)∗P < .01 represents statistical significance for day 4 vs baseline.78.3 (18.3-972.6)†P < .05 represents statistical significance for day 4 vs baseline.64.1 (24.5-612.6)†P < .05 represents statistical significance for day 4 vs baseline.NSValues shown are at baseline and on day 4 postinoculation (medians and interquartile range). Bronchial sampling was not possible for 3 subjects at baseline and 5 subjects on day 4.NS, Not statistically significant.∗ P < .01 represents statistical significance for day 4 vs baseline.† P < .05 represents statistical significance for day 4 vs baseline. Open table in a new tab Table E2Virus loadBaseline ACQ scorePeak nasalDay 2 nasalDay 3 nasalDay 4 nasalDay 5 nasalDay 7 nasalDay 10 nasalDay 4 BAL≤0.75 n = 123.3 × 106 (6.8 × 105-6.1 × 106)5.4 × 104 (4887-5.9 × 105)1.7 × 106 (3.5 × 105-4.3 × 106)5.4 × 104 (1.6 × 105-1.5 × 106)3.7 (0-6.6 × 105)2447 (0-1.2 × 105)3809 (0-2.7 × 105)2572 (0-5.2 × 105)0.76-1.49 n = 88.1 × 106 (2.6 × 105-8.0 × 107)6213 (0-1.3 × 106)7.2 × 104 (6466- 1.6 × 107)3.0 × 104 (8811- 4.5 × 107)1.7 × 104 (1026- 3.6 × 105)2.1 × 104 (3366- 5.3 × 105)6971 (0-1.1 × 105)3458 (471-3.3 × 104)≥1.5 n = 89.4 × 106 (5.2 × 105-3.7 × 107)8.9 × 105 (82-4.3 × 106)9.3 × 106 (6.1 × 104-3.7 × 107)8.1 × 105 (1308-3.4 × 106)7.2 × 104 (2343-2.6 × 105)4.4 × 104 (5066-3.0 × 105)5.1 × 104 (1.3 × 104-2.1 × 105)9427 (322-8.2 × 105)Values represent medians and interquartile range (copies/mL). Peak value represents the maximal value for each subject. No group differences reached statistical significance.BAL, Bronchoalveolar lavage; NL, nasal lavage. Open table in a new tab Values shown are at baseline and on day 4 postinoculation (medians and interquartile range). Bronchial sampling was not possible for 3 subjects at baseline and 5 subjects on day 4. NS, Not statistically significant. Values represent medians and interquartile range (copies/mL). Peak value represents the maximal value for each subject. No group differences reached statistical significance. BAL, Bronchoalveolar lavage; NL, nasal lavage.

Research Article| April 01 2014 "Another Polka Rockin' Weekend": Polish American Polka Music, Identity, and Traditional Values David James Jackson David James Jackson Search for other works by this author on: This Site Google Polish American Studies (2014) 71 (1): 37–52. https://doi.org/10.5406/poliamerstud.71.1.0037 Cite Icon Cite Share Icon Share Twitter Permissions Search Site Citation David James Jackson; "Another Polka Rockin' Weekend": Polish American Polka Music, Identity, and Traditional Values. Polish American Studies 1 January 2014; 71 (1): 37–52. doi: https://doi.org/10.5406/poliamerstud.71.1.0037 Download citation file: Zotero Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All Scholarly Publishing CollectiveUniversity of Illinois PressPolish American Studies Search Advanced Search The text of this article is only available as a PDF. Copyright 2014 by the Board of Trustees of the University of Illinois2014 Article PDF first page preview Close Modal You do not currently have access to this content.

Background: Rhinovirus (RV) is the most common cause for asthma exacerbations. Underlying mechanisms are poorly understood. A human model of experimental infection with RV has been introduced however published studies have thus far only recruited mild asthmatics. In order to be more representative of those who experience virus-induced exacerbations there is a need to establish the safety of this model in moderate asthma. Aim: To assess the safety of using the RV challenge model in subjects with moderate asthma treated with inhaled corticosteroids. Methods: Six subjects with moderately severe atopic asthma requiring maintenance inhaled corticosteroids were infected with RV16. Nasal lavage (NL) and clinic spirometry was performed on days 0,2,3,4,5,7,10. Symptom scores were recorded daily throughout the study. Clinical infection was confirmed using a combination of symptom scores, demonstration of RV16 RNA by RT-PCR in nasal lavage and at least a 4-fold increase in RV16 specific antibody titres on day 42. Results: All 6 subjects developed symptoms of a common cold 24-48 hours prior to an increase in lower respiratory symptoms. This was accompanied by a drop in morning FEV1 (mean fall of 25.6%). Whilst all subjects increased their use of bronchodilator, no subjects required oral corticosteroid therapy. RV16 was demonstrated in NL in all subjects. Conclusions: In this pilot study infection with RV16 in moderate asthma was well-tolerated resulting in a mild exacerbation. No unexpected adverse events or requirement for oral steroids occurred. The use of RV challenge in moderate asthma therefore appears safe. Results of future studies using this group of patients will better reflect those individuals with the greatest burden of disease.

Asthma is a heterogeneous condition and it is vital to accurately predict responders to targeted therapies. However, difficulties in measuring IL5 and IL13 have forced reliance on indirect markers of Th2 inflammation with limited success. Using the human model of experimental rhinovirus (RV) induced asthma exacerbation (AE) and new techniques to absorb nasal (nasosorption) and bronchial (bronchosorption) mucosal lining fluid (MLF), we explored Th2 inflammation during a RV-induced AE. Methods: 32 mild-to-moderate asthmatics and 14 healthy subjects were inoculated with RV-16. Bronchoscopies were performed 2 weeks prior to inoculation and on d4 post-inoculation. Cytokines were measured in both bronchial and nasal samples at baseline and on d4 with further nasal sampling on days 2,3,5,7,10 and 42. Results: Nasal IL5 and IL13 were significantly increased in asthma during infection compared to baseline (p Conclusion: RV induced Th2 inflammation correlated with AE severity. Nasal Th2 inflammation correlated with bronchial levels whilst baseline Th2 levels predicted the magnitude of Th2 induction during the AE. Nasosorption is a non-invasive, rapid technique capable of measuring Th2 inflammation directly. It may be possible to use this technique as a biomarker to guide therapy with anti-IL5 and anti-IL13 mAb treatments.

Background Rhinovirus (RV) infection is the most common cause of asthma exacerbations (AE). Mechanisms underlying this remain poorly understood. A human model of experimental RV induced AE has been developed however published studies have only recruited subjects with mild, well-controlled asthma naive to inhaled corticosteroid (ICS) therapy. The influence of asthma severity and baseline control on outcome remains unknown. For these studies to be more representative of those who experience virus-induced AE there is a need to establish the safety of using this model in subjects with moderate, poorly-controlled asthma and to investigate clinical outcomes. Method 48 adults - 14 healthy, 14 mild asthmatic, and 18 moderate asthmatic (defined by GINA) were recruited and inoculated nasally with RV-16. Daily symptom scores and spirometry were recorded throughout the study. Asthma control at baseline was recorded using the ACQ. Nasal lavage (NL) for viral shedding was performed on days 0, 2, 3, 4, 5, 7, 10. Clinical infection was confirmed by demonstration of RV16 RNA by RT-PCR in NL and/or serum titre of RV-16 specific antibodies greater than 1:4 on d42. Results 11/14 healthy, 11/14 mild asthmatic and 17/18 moderate asthmatic volunteers met criteria for infection. Both groups of asthmatics developed greater lower respiratory symptoms, falls in FEV1, and airway hyper-responsiveness (AHR) compared to healthy volunteers (all P=<0.01). These changes were significantly greater in the moderate asthmatics than in the mild asthmatics (P=<0.05). Poorly-controlled asthmatics experienced greater chest symptoms (P=<0.01) and RV-induced falls in lung function (P=<0.05) compared to subjects with well-controlled asthma. Conclusion RV infection results in more severe chest symptoms and falls in lung function in moderate asthma than in mild asthma. Within the moderate group the poorly-controlled asthmatics experienced the most severe exacerbations. This occurred despite therapy with ICS. This is the first study to experimentally inoculate both moderate, poorly-controlled and milder well-controlled asthmatics. Both severity and baseline control appear to influence the outcome of virus-induced AE. Measures to improve control will significantly reduce the likelihood of a severe virus-induced AE and lessen the healthcare costs associated with them.

Introduction An improved method for sampling nasal mucosal lining fluid (MLF), termed nasosorption, utilises a synthetic absorptive matrix (SAM) (Accuwick Ultra, Pall). Conventionally, Whatman9s filter paper has been used for absorption of nasal MLF, but this natural cellulose source has the capacity to bind mediators, causing eluted fluid to have decreased and variable detectable levels of mediators. Nasal lavage has the problem of diluting MLF and this also causes detectable levels of mediators to be low. Strips of Accuwick are effective for nasosorption in adults following nasal allergen challenge and for sampling children with active rhinitis. However, Accuwick is no longer manufactured and we wished to validate an alternative SAM (Leukosorb, Pall). Methods Sputum supernatant (40 μl) from a subject with COPD as well as a standard preparation of cytokines was spiked onto Accuwick and Leukosorb strips. Following elution by spin filter centrifugation, the MesoScale Diagnostics (MSD) multi-immunoassay platform was used to assess levels of IFN-γ, IL-10, IL-12 p70, IL-6, IL-8, and TNFα. After absorption to Accuwick and Leukosorb, elution was compared with and without buffer (PBS with BSA (1%) and Triton X (1%)), prior to immunoassay of the recovered sample. Results Without buffer the recovery of 7 cytokines after the sputum supernatant was applied to Accuwick was a mean of 17.6% (range 1–100%), while recovery was a mean of 20.2% (range 2.9–92.5%) using Leukosorb. Addition of the buffer prior to elution of the fluid increased mean recovery to 61.8% when employing the Leukosorb system. Finally, in a direct comparison when employing Leukosorb and Accuwik for nasosorption in different nostrils after nasal allergen challenge in a single subject, Leukosorb resulted in higher detectable IL-5 levels in MLF. Conclusion Leukosorb appears to be a superior alternative to Accuwick Ultra for nasosorption in terms of recovery of cytokines. Addition of a buffer containing detergent and protein prior to elution significantly increases recovery. SAM has the potential to be employed in the upper and lower respiratory tract to sample undiluted MLF.

Viral respiratory infections are the most common cause of an acute asthma exacerbation in both children and adults and represent a significant global health burden. An increasing body of evidence supports the hypothesis that these infections cause a greater degree of morbidity in asthmatic subjects than in the healthy population, emphasizing a discrepancy in the antiviral response of asthmatics. In this review we discuss why such a discrepancy might exist, examining the role of the bronchial epithelium as well as the main inflammatory cells, mediators, and molecular pathways that are involved in the immune response. In addition, the potential impact of virus-induced asthma exacerbations on airway remodelling is reviewed and we explore which therapeutic options might be of benefit in preventing the deterioration of asthma control seen following viral infection.