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As an occupational group, clergy exhibit numerous physical health problems. Given the physical health problems faced by clergy, understanding where physical health falls within the priorities of seminary students, the ways students conceptualize physical health, and how seminary students do or do not attend to their physical health in the years immediately prior to becoming clergy, can inform intervention development for both seminary students and clergy. Moreover, understanding and shaping the health practices of aspiring clergy may be particularly impactful, with cascading effects, as clergy serve as important role models for their congregants. Drawing on 36 in-depth, qualitative interviews with first-year seminary students, this study examines the complex dynamics between religious frameworks related to physical health, explicit intentions to maintain healthy practices, and reported physical health behaviors. Our findings suggest that even students who deploy religious frameworks in relation to their physical health-and who, as a result, possess positive intentions to implement and maintain healthy behaviors-often report being unable to live up to their aspirations, especially in the face of barriers to health practices posed by the seminary program itself. After reviewing these findings, we offer suggestions for physical health focused interventions, including action and coping planning, which could be implemented at seminaries to reduce the intention-behavior gap and improve clergy health., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

The passive mechanical properties of the vertebrate heart are controlled in part by the composition of the extracellular matrix (ECM). Changes in the ECM, caused by increased blood pressure, injury or disease can affect the capacity of the heart to fill with blood during diastole. In mammalian species, cardiac fibrosis caused by an increase in collagen in the ECM, leads to a loss of heart function and these changes in composition are considered to be permanent. Recent work has demonstrated that the cardiac ventricle of some fish species have the capacity to both increase and decrease collagen content in response to thermal acclimation. It is thought that these changes in collagen content help maintain ventricle function over seasonal changes in environmental temperatures. This current work reviews the cellular mechanisms responsible for regulating collagen deposition in the mammalian heart and proposes a cellular pathway by which a change in temperature can affect the collagen content of the fish ventricle through mechanotransduction. This work specifically focuses on the role of transforming growth factor β1, MAPK signaling pathways, and biomechanical stretch in regulating collagen content in the fish ventricle. It is hoped that this work increases the appreciation of the use of comparative models to gain insight into phenomenon with biomedical relevance., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2022 The Author(s).)

Background: COVID-19 and its associated restrictions around in-person gatherings have created unprecedented challenges for religious congregations and those who lead them. While several surveys have attempted to describe how pastors and congregations responded to COVID-19, these provide a relatively thin picture of how COVID-19 is impacting religious life. There is scant qualitative data describing the lived reality of religious leaders and communities during the pandemic., Purpose and Methods: This paper provides a more detailed look at how pastors and congregations experienced and responded to COVID-19 and its associated restrictions in the early period of the pandemic. To do so, we draw from 26 in-depth interviews with church-appointed United Methodist pastors conducted between June and August 2020. Pastors were asked to describe how their ministry changed as a result of COVID-19 and interviews were analyzed using applied thematic analysis approaches to identify the most common emergent themes., Results: Pastors reported that COVID-19 fundamentally unsettled routine ways of doing ministry. This disruption generated both challenges and opportunities for clergy and their congregations. In the findings, we describe how clergy responded in key areas of ministry-worship and pastoral care-and analyze how the pandemic is (re)shaping the way that clergy understood their role as pastors and envisioned the future of the Church. We argue for the value of examining the pandemic as an "unsettled" cultural period (Swidler 1986) in which religious leaders found creative ways to (re)do ministry in the context of social distancing. Rather than starting from scratch, we found that pastors drew from and modified existing symbolic and practical tools to fit pandemic-related constraints on religious life. Notably, however, we found that "redoing" ministry was easier and more effective in some areas (worship) than others (pastoral care)., Conclusions and Implications: The impact of COVID-19 on pastors and congregations is complex and not fully captured by survey research. This study provides a baseline for investigating similarities and differences in the responses of pastors within and across denominations and traditions. It also provides a baseline for assessing whether changes in ministry implemented during the early stages of the pandemic remain in place in the post-COVID world., (© Religious Research Association, Inc. 2021.)

Rainbow trout (Oncorhynchus mykiss) live in environments where water temperatures range between 4 °C and 20 °C. Laboratory studies demonstrate that cold and warm acclimations of male trout can have oppositional effects on cardiac hypertrophy and the collagen content of the heart. The cellular mechanisms behind temperature-induced cardiac remodelling are unclear, as is why this response differs between male and female fish. Studies with cultured trout cardiac fibroblasts suggests that collagen deposition is regulated, at least in part, by mitogen-activated protein kinase (MAPK) cell signalling pathways. We, therefore, hypothesized that temperature-dependent cardiac remodelling is regulated by these signalling pathways. To test this, male and female trout were acclimated to 18 °C (warm) in the summer and to 4 °C (cold) in the winter and the activation of MAPK pathways in the hearts were characterized and compared to that of control fish maintained at 12 °C. In addition, cardiac collagen content, cardiac morphology and the expression of gene transcripts for matrix metalloproteinases (MMP) -9, MMP-2, tissue inhibitor of matrix metalloproteinases and collagen 1α were characterized. p38 MAPK phosphorylation increased in the hearts of female fish with cold acclimation and the phosphorylation of extracellular signal-regulated kinase increased in the hearts of male fish with warm acclimation. However, there was no effect of thermal acclimation on cardiac morphology or collagen content in either male or female fish. These results indicate that thermal acclimation has transient and sex-specific effects on the phosphorylation of MAPKs but also how variable the response of the trout heart is to thermal acclimation., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

The form and function of the rainbow trout heart can remodel in response to various stressors including changes in environmental temperature and anemia. Previous studies have hypothesized that changes in biomechanical forces experienced by the trout myocardium as result of such physiological stressors could play a role in triggering the remodeling response. However, there has been no work examining the influence of biomechanical forces on the trout myocardium or of the cellular signals that would translate such a stimuli into a biological response. In this study, we test the hypothesis that the application of biomechanical forces to trout cardiac fibroblasts activate the cell signaling pathways associated with cardiac remodeling. This was done by cyclically stretching cardiac fibroblasts to 10% equibiaxial deformation at 0.33 Hz and quantifying the activation of the p38-JNK-ERK mitogen activated protein kinase (MAPK) pathway. After 20 min, p38 MAPK phosphorylation was elevated by 4.2-fold compared to control cells ( P <0.05) and after 24 h of stretch, p38 MAPK phosphorylation remained elevated and extracellular-regulated kinase 1/2 was phosphorylated by 2.4-fold compared to control ( P <0.05). Together, these results indicate that mechanotransductive pathways are active in cardiac fibroblasts, and lead to the activation of cell signaling pathways involved in cardiac remodeling., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2020. Published by The Company of Biologists Ltd.)

Warm acclimation of rainbow trout can cause a decrease in the collagen content of the heart. This ability to remove cardiac collagen is particularly interesting considering that collagen deposition in the mammalian heart, following an injury, is permanent. We hypothesized that collagen removal can be facilitated by microRNA-29b (miR-29b), a highly conserved, small, non-coding RNA, as a reduction in this microRNA has been reported during the development of fibrosis in the mammalian heart. We also used a bioinformatics approach to investigate the binding potential of miR-29b to the seed sequences of vertebrate collagen isoforms. Cultured trout cardiac fibroblasts were transfected with zebrafish mature miR-29b mimic for 7 days with re-transfection occurring after 3 days. Transfection induced a 17.8-fold increase in miR-29b transcript abundance ( P <0.05) as well as a 54% decrease in the transcript levels of the col1a3 collagen isoform, compared with non-transfected controls ( P <0.05). Western blotting demonstrated that the level of collagen type I protein was 85% lower in cells transfected with miR-29b than in control cells ( P <0.05). Finally, bioinformatic analysis suggested that the predicted 3'-UTR of rainbow trout col1a3 has a comparatively higher binding affinity for miR-29b than the 3'-UTR of col1a1 Together, these results suggest that miR-29b is a highly conserved regulator of collagen type I protein in vertebrates and that this microRNA decreases collagen in the trout heart by targeting col1a3 ., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2019. Published by The Company of Biologists Ltd.)

The collagen content of the rainbow trout heart increases in response to cold acclimation and decreases with acclimation to warm temperatures. This ability to remodel the myocardial extracellular matrix (ECM) makes these fish useful models to study the cellular pathways involved in collagen regulation in the vertebrate heart. Remodelling of the ECM in the mammalian heart is regulated, in part, by myofibroblasts which arise from pre-existing fibroblasts in response to transforming growth factor-β1 (TGF-β1). We have previously demonstrated that treatment of cultured rainbow trout cardiac fibroblasts with human TGF-β1 causes an increase in collagen production. Here, we showed that repetitive treatment of rainbow trout cardiac fibroblasts with a physiologically relevant concentration of human recombinant TGF-β1 results in a ∼29-fold increase in phosphorylated small mothers against decapentaplegic 2 (pSmad2); a 2.9-fold increase in vinculin protein, a 1.2-fold increase in cellular size and a 3-fold increase in filamentous actin (F-actin). These are common markers of the transition of fibroblasts to myofibroblasts. Cells treated with TGF-β1 also had highly organized cytoskeletal α-smooth muscle actin, as well as increased transcript abundances of mmp-9 , timp-2 and col1a1 Furthermore, using gelatin zymography, we demonstrated that TGF-β1 treatment causes a 5.3-fold increase in gelatinase activity. Together, these results suggest that trout cardiac fibroblasts have the capacity to differentiate into myofibroblasts and that this cell type can increase extracellular collagen turnover via gelatinase activity. Cardiac myofibroblasts are, therefore, likely involved in the remodelling of the cardiac ECM in the trout heart during thermal acclimation., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2018. Published by The Company of Biologists Ltd.)

Cold acclimation of rainbow trout, Oncorhynchus mykiss , causes collagen to increase within the extracellular matrix (ECM) of the myocardium, while warm acclimation has the opposite effect. The mechanism responsible for this remodelling response is not known. In mammals, transforming growth factor beta-1 (TGF-β1) stimulates collagen deposition within the myocardial ECM. Therefore, we hypothesized that TGF-β1 regulates trout myocardial ECM turnover and predicted that TGF-β1 would induce collagen deposition in cultured rainbow trout cardiac fibroblasts. We found that treatment of trout cardiac fibroblasts with 15 ng ml -1 human recombinant TGF-β1 caused an increase in total collagen at 48 and 72 h and an increase in collagen type I protein after 7 days. We also found that TGF-β1 treatment caused an increase in the transcript abundance of tissue inhibitor of metalloproteinase 2 ( timp-2 ) and matrix metalloproteinase 9 ( mmp-9 ) at 24 h. Cells treated with TGF-β1 also had lower levels of the gene transcript for mmp-2 after 48 h and higher levels of the gene transcript for collagen type I α1 ( col1a1 ) after 72 h. These changes in gene expression suggest that the increase in collagen deposition is due to a decrease in the activity of matrix metalloproteinases and an increase in collagen synthesis. Together, these results indicate that TGF-β1 is a regulator of ECM composition in cultured trout cardiac fibroblasts and suggest that this cytokine may play a role in regulating collagen content in the trout heart during thermal acclimation., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2017. Published by The Company of Biologists Ltd.)