Summer Employment and Tobacco Use among College Students

Background: Research has shown that tobacco use among college students is influenced by the social environment, especially amonga subset of smokers known as social smokers. Although many college campuses now have tobacco-free policies that could restrictsocial use of tobacco products, these policies often do not extend to common places of summer employment for college students thathave similar social environments. Currently, no recommended tobacco policy exists for such summer programs, and little research hasbeen done to assess their need.Methods: The objective of this study was to examine trends in tobacco use among the college-aged summer employees of a non-profit organization. Participants included the college-aged summer employees of a seasonal non-profit organization based in the Appalachian region from May through August 2015. At the beginning and end of the summer employment period, an online cross-sectional survey was distributed to each eligible staff member to examine trends in tobacco use.Results: Among the 60 follow-up respondents, 22.8% (n=13) reported an overall increase in tobacco use over the summer, while 3.5%(n=2) reported a decrease in tobacco use and 73.7% (n=42) reported no change.Conclusions: These results indicate that college students are at risk of increasing their tobacco use during summer employment. There is a need for further research into the role of summer workplace influences on tobacco use among college students

Social functioning in schizotypy: How affect influences social behavior in daily life.

OBJECTIVE: Social deficits are already exhibited by people at risk for schizophrenia-spectrum disorders. Technological advances have made passive detection of social deficits possible at granular levels. METHOD: In this real-world study, we tested if schizotypy status (high/low) predicted two types of social behavior: (1) being around other people; and (2) actively socializing with others. We also examined if schizotypy influences relationships between social behavior and affect using subjective and objective instruments. RESULTS: Our findings revealed that socializing with others was significantly decreased in the high schizotypy group. Positive affect increased in social situations and predicted later social behavior in those low, but not high, in schizotypy. CONCLUSION: Decreased social behavior in schizotypy may be explained, in part, by these individuals being less incentivized than their peers to pursue social situations. Future studies should test this explanation in larger samples exhibiting elevated positive, negative, and disorganized schizotypy traits

Duoethnography as Transformative Praxis: Conversations about Nourishment and Coercion in the COVID-Era Academy

This article introduces the feminist praxis of duoethnography as a way to examine the COVID era. As a group of diverse, junior, midcareer, and senior feminist scholars, we developed a methodology to critically reflect on our positions in our institutions and social worlds. As a method, duoethnography emphasizes the dialogical intimacy that can form through anthropological work. While autoethnography draws on individual daily lives to make sense of sociopolitical dynamics, duoethnography emphasizes the relational character of research across people and practices. Taking the relational aspects of knowledge production seriously, we conceptualized this praxis as a transformative method for facilitating radical empathy, mobilizing our collective voice, and merging together our partial truths. As collective authors, interviewers, and interlocutors of this article, the anonymity of duoethnography allows us to vocalize details of the experience of living through COVID19 that we could not have safely spoken about publicly or on our ow

Body mass index change in gastrointestinal cancer and chronic obstructive pulmonary disease is associated with Dedicator of Cytokinesis 1

Background: There have been a number of candidate gene association studies of cancer cachexia-related traits, but no genome-wide association study (GWAS) has been published to date. Cachexia presents in patients with a number of complex traits, including both cancer and COPD. The objective of the current investigation was to search for a shared genetic aetiology for change in body mass index (ΔBMI) among cancer and COPD by using GWAS data in the Framingham Heart Study. Methods: A linear mixed effects model accounting for age, sex, and change in smoking status was used to calculate ΔBMI in participants over 40 years of age with three consecutive BMI time points (n = 4162). Four GWAS of ΔBMI using generalized estimating equations were performed among 1085 participants with a cancer diagnosis, 204 with gastrointestinal (GI) cancer, 112 with lung cancer, and 237 with COPD to test for association with 418 365 single-nucleotide polymorphisms (SNPs). Results: Two SNPs reached a level of genome-wide significance (P < 5 × 10−8) with ΔBMI: (i) rs41526344 within the CNTN4 gene, among COPD cases (β = 0.13, P = 4.3 × 10−8); and (ii) rs4751240 in the gene Dedicator of Cytokinesis 1 (DOCK1) among GI cancer cases (β = 0.10, P = 1.9 × 10−8). The DOCK1 SNP association replicated in the ΔBMI GWAS among COPD cases (βmeta-analyis = 0.10, Pmeta-analyis = 9.3 × 10−10). The DOCK1 gene codes for the dedicator of cytokinesis 1 protein, which has a role in myoblast fusion. Conclusions: In sum, one statistically significant common variant in the DOCK1 gene was associated with ΔBMI in GI cancer and COPD cases providing support for at least partially shared aetiology of ΔBMI in complex diseases

Genetic Association and Risk Scores in a Chronic Obstructive Pulmonary Disease Meta-analysis of 16,707 Subjects

The heritability of chronic obstructive pulmonary disease (COPD) cannot be fully explained by recognized genetic risk factors identified as achieving genome-wide significance. In addition, the combined contribution of genetic variation to COPD risk has not been fully explored. We sought to determine: (1) whether studies of variants from previous studies of COPD or lung function in a larger sample could identify additional associated variants, particularly for severe COPD; and (2) the impact of genetic risk scores on COPD. We genotyped 3,346 single-nucleotide polymorphisms (SNPs) in 2,588 cases (1,803 severe COPD) and 1,782 control subjects from four cohorts, and performed association testing with COPD, combining these results with existing genotyping data from 6,633 cases (3,497 severe COPD) and 5,704 control subjects. In addition, we developed genetic risk scores from SNPs associated with lung function and COPD and tested their discriminatory power for COPD-related measures. We identified significant associations between SNPs near PPIC (P = 1.28 X 10-8) and PPP4R4/SERPINA1 (P = 1.0131028) and severe COPD; the latter association may be driven by recognized variants in SERPINA1. Genetic risk scores based on SNPs previously associated with COPD and lung function had a modest ability to discriminate COPD (area under the curve, ~0.6), and accounted for a mean 0.9–1.9% lower forced expiratory volume in 1 second percent predicted for each additional risk allele. In a large genetic association analysis, we identified associations with severe COPD near PPIC and SERPINA1. A risk score based on combining genetic variants had modest, but significant, effects on risk of COPD and lung function

Common Genetic Polymorphisms Influence Blood Biomarker Measurements in COPD

Implementing precision medicine for complex diseases such as chronic obstructive lung disease (COPD) will require extensive use of biomarkers and an in-depth understanding of how genetic, epigenetic, and environmental variations contribute to phenotypic diversity and disease progression. A meta-analysis from two large cohorts of current and former smokers with and without COPD [SPIROMICS (N = 750); COPDGene (N = 590)] was used to identify single nucleotide polymorphisms (SNPs) associated with measurement of 88 blood proteins (protein quantitative trait loci; pQTLs). PQTLs consistently replicated between the two cohorts. Features of pQTLs were compared to previously reported expression QTLs (eQTLs). Inference of causal relations of pQTL genotypes, biomarker measurements, and four clinical COPD phenotypes (airflow obstruction, emphysema, exacerbation history, and chronic bronchitis) were explored using conditional independence tests. We identified 527 highly significant (p 10% of measured variation in 13 protein biomarkers, with a single SNP (rs7041; p = 10−392) explaining 71%-75% of the measured variation in vitamin D binding protein (gene = GC). Some of these pQTLs [e.g., pQTLs for VDBP, sRAGE (gene = AGER), surfactant protein D (gene = SFTPD), and TNFRSF10C] have been previously associated with COPD phenotypes. Most pQTLs were local (cis), but distant (trans) pQTL SNPs in the ABO blood group locus were the top pQTL SNPs for five proteins. The inclusion of pQTL SNPs improved the clinical predictive value for the established association of sRAGE and emphysema, and the explanation of variance (R2) for emphysema improved from 0.3 to 0.4 when the pQTL SNP was included in the model along with clinical covariates. Causal modeling provided insight into specific pQTL-disease relationships for airflow obstruction and emphysema. In conclusion, given the frequency of highly significant local pQTLs, the large amount of variance potentially explained by pQTL, and the differences observed between pQTLs and eQTLs SNPs, we recommend that protein biomarker-disease association studies take into account the potential effect of common local SNPs and that pQTLs be integrated along with eQTLs to uncover disease mechanisms. Large-scale blood biomarker studies would also benefit from close attention to the ABO blood group

Global urban environmental change drives adaptation in white clover

Urbanization transforms environments in ways that alter biological evolution. We examined whether urban environmental change drives parallel evolution by sampling 110,019 white clover plants from 6169 populations in 160 cities globally. Plants were assayed for a Mendelian antiherbivore defense that also affects tolerance to abiotic stressors. Urban-rural gradients were associated with the evolution of clines in defense in 47% of cities throughout the world. Variation in the strength of clines was explained by environmental changes in drought stress and vegetation cover that varied among cities. Sequencing 2074 genomes from 26 cities revealed that the evolution of urban-rural clines was best explained by adaptive evolution, but the degree of parallel adaptation varied among cities. Our results demonstrate that urbanization leads to adaptation at a global scale