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Transposable elements (TEs) are mobile DNA elements that comprise almost 50% of mammalian genomic sequence. TEs are capable of making additional copies of themselves that integrate into new positions in host genomes. This unique property has had an important impact on mammalian genome evolution and on the regulation of gene expression because TE-derived sequences can function as cis-regulatory elements such as enhancers, promoters and silencers. Now, advances in our ability to identify and characterize TEs have revealed that TE-derived sequences also regulate gene expression by both maintaining and shaping 3D genome architecture. Studies are revealing how TEs contribute raw sequence that can give rise to the structures that shape chromatin organization, and thus gene expression, allowing for species-specific genome innovation and evolutionary novelty., (© 2023. Springer Nature Limited.)

Background: Understanding how heterogeneous β-cell function impacts diabetes is imperative for therapy development. Standard single-cell RNA sequencing analysis illuminates some factors driving heterogeneity, but new strategies are required to enhance information capture., Results: We integrate pancreatic islet single-cell and bulk RNA sequencing data to identify β-cell subpopulations based on gene expression and characterize genetic networks associated with β-cell function in obese SM/J mice. We identify β-cell subpopulations associated with basal insulin secretion, hypoxia response, cell polarity, and stress response. Network analysis associates fatty acid metabolism and basal insulin secretion with hyperglycemic-obesity, while expression of Pdyn and hypoxia response is associated with normoglycemic-obesity., Conclusions: By integrating single-cell and bulk islet transcriptomes, our study explores β-cell heterogeneity and identifies novel subpopulations and genetic pathways associated with β-cell function in obesity., (© 2023. The Author(s).)

Transposable elements (TEs) encode regulatory elements that impact gene expression in multiple species, yet a comprehensive analysis of zebrafish TEs in the context of gene regulation is lacking. Here, we systematically investigate the epigenomic and transcriptomic landscape of TEs across 11 adult zebrafish tissues using multidimensional sequencing data. We find that TEs contribute substantially to a diverse array of regulatory elements in the zebrafish genome and that 37% of TEs are positioned in active regulatory states in adult zebrafish tissues. We identify TE subfamilies enriched in highly specific regulatory elements among different tissues. We use transcript assembly to discover TE-derived transcriptional units expressed across tissues. Finally, we show that novel TE-derived promoters can initiate tissue-specific transcription of alternate gene isoforms. This work provides a comprehensive profile of TE activity across normal zebrafish tissues, shedding light on mechanisms underlying the regulation of gene expression in this widely used model organism., (© 2022 Lee et al.; Published by Cold Spring Harbor Laboratory Press.)

Allele-specific expression (ASE) is a phenomenon in which one allele is preferentially expressed over the other. Genetic and epigenetic factors cause ASE by altering the final composition of a gene's product, leading to expression imbalances that can have functional consequences on phenotypes. Environmental signals also impact allele-specific expression, but how they contribute to this cross talk remains understudied. Here, we explored how genotype, parent-of-origin, tissue, sex, and dietary fat simultaneously influence ASE biases. Male and female mice from a F 1 reciprocal cross of the LG/J and SM/J strains were fed a high or low fat diet. We harnessed strain-specific variants to distinguish between two ASE classes: parent-of-origin-dependent (unequal expression based on parental origin) and sequence-dependent (unequal expression based on nucleotide identity). We present a comprehensive map of ASE patterns in 2853 genes across three tissues and nine environmental contexts. We found that both ASE classes are highly dependent on tissue and environmental context. They vary across metabolically relevant tissues, between males and females, and in response to dietary fat. We also found 45 genes with inconsistent ASE biases that switched direction across tissues and/or environments. Finally, we integrated ASE and QTL data from published intercrosses of the LG/J and SM/J strains. Our ASE genes are often enriched in QTLs for metabolic and musculoskeletal traits, highlighting how this orthogonal approach can prioritize candidate genes. Together, our results provide novel insights into how genetic, epigenetic, and environmental mechanisms govern allele-specific expression, which is an essential step toward deciphering the genotype-to-phenotype map., (© 2022 St. Pierre et al.; Published by Cold Spring Harbor Laboratory Press.)

The human reference genome is the most widely used resource in human genetics and is due for a major update. Its current structure is a linear composite of merged haplotypes from more than 20 people, with a single individual comprising most of the sequence. It contains biases and errors within a framework that does not represent global human genomic variation. A high-quality reference with global representation of common variants, including single-nucleotide variants, structural variants and functional elements, is needed. The Human Pangenome Reference Consortium aims to create a more sophisticated and complete human reference genome with a graph-based, telomere-to-telomere representation of global genomic diversity. Here we leverage innovations in technology, study design and global partnerships with the goal of constructing the highest-possible quality human pangenome reference. Our goal is to improve data representation and streamline analyses to enable routine assembly of complete diploid genomes. With attention to ethical frameworks, the human pangenome reference will contain a more accurate and diverse representation of global genomic variation, improve gene-disease association studies across populations, expand the scope of genomics research to the most repetitive and polymorphic regions of the genome, and serve as the ultimate genetic resource for future biomedical research and precision medicine., (© 2022. Springer Nature Limited.)

Parent-of-origin effects are unexpectedly common in complex traits, including metabolic and neurological traits. Parent-of-origin effects can be modified by the environment, but the architecture of these gene-by-environmental effects on phenotypes remains to be unraveled. Previously, quantitative trait loci (QTL) showing context-specific parent-of-origin effects on metabolic traits were mapped in the F 16 generation of an advanced intercross between LG/J and SM/J inbred mice. However, these QTL were not enriched for known imprinted genes, suggesting another mechanism is needed to explain these parent-of-origin effects phenomena. We propose that non-imprinted genes can generate complex parent-of-origin effects on metabolic traits through interactions with imprinted genes. Here, we employ data from mouse populations at different levels of intercrossing (F 0 , F 1 , F 2 , F 16 ) of the LG/J and SM/J inbred mouse lines to test this hypothesis. Using multiple populations and incorporating genetic, genomic, and physiological data, we leverage orthogonal evidence to identify networks of genes through which parent-of-origin effects propagate. We identify a network comprised of three imprinted and six non-imprinted genes that show parent-of-origin effects. This epistatic network forms a nutritional responsive pathway and the genes comprising it jointly serve cellular functions associated with growth. We focus on two genes, Nnat and F2r , whose interaction associates with serum glucose levels across generations in high-fat-fed females. Single-cell RNAseq reveals that Nnat expression increases and F2r expression decreases in pre-adipocytes along an adipogenic trajectory, a result that is consistent with our observations in bulk white adipose tissue., Competing Interests: JM, CS, JW, LY, LS, MM, CC, KF, JC, CS, HL No competing interests declared, (© 2022, Macias-Velasco et al.)

Pancreatic β-cells perform glucose-stimulated insulin secretion, a process at the center of type 2 diabetes etiology. Efforts to understand how β-cells behave in healthy and stressful conditions have revealed a wide degree of morphological, functional, and transcriptional heterogeneity. Sources of heterogeneity include β-cell topography, developmental origin, maturation state, and stress response. Advances in sequencing and imaging technologies have led to the identification of β-cell subtypes, which play distinct roles in the islet niche. This review examines β-cell heterogeneity from morphological, functional, and transcriptional perspectives, and considers the relevance of topography, maturation, development, and stress response. It also discusses how these factors have been used to identify β-cell subtypes, and how heterogeneity is impacted by diabetes. We examine open questions in the field and discuss recent technological innovations that could advance understanding of β-cell heterogeneity in health and disease.

We leverage the SM/J mouse to understand glycemic control in obesity. High-fat-fed SM/J mice initially develop poor glucose homeostasis relative to controls. Strikingly, their glycemic dysfunction resolves by 30 weeks of age despite persistent obesity. The mice dramatically expand their brown adipose depots as they resolve glycemic dysfunction. This occurs naturally and spontaneously on a high-fat diet, with no temperature or genetic manipulation. Removal of the brown adipose depot impairs insulin sensitivity, indicating that the expanded tissue is functioning as an insulin-stimulated glucose sink. We describe morphological, physiological, and transcriptomic changes that occur during the brown adipose expansion and remission of glycemic dysfunction, and focus on Sfrp1 (secreted frizzled-related protein 1) as a compelling candidate that may underlie this phenomenon. Understanding how the expanded brown adipose contributes to glycemic control in SM/J mice will open the door for innovative therapies aimed at improving metabolic complications in obesity., Competing Interests: Declaration of Interests The authors declare no competing interests., (Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.)

Maintenance of functional β-cell mass is critical to preventing diabetes, but the physiological mechanisms that cause β-cell populations to thrive or fail in the context of obesity are unknown. High fat-fed SM/J mice spontaneously transition from hyperglycemic-obese to normoglycemic-obese with age, providing a unique opportunity to study β-cell adaptation. Here, we characterize insulin homeostasis, islet morphology, and β-cell function during SM/J's diabetic remission. As they resolve hyperglycemia, obese SM/J mice dramatically increase circulating and pancreatic insulin levels while improving insulin sensitivity. Immunostaining of pancreatic sections reveals that obese SM/J mice selectively increase β-cell mass but not α-cell mass. Obese SM/J mice do not show elevated β-cell mitotic index, but rather elevated α-cell mitotic index. Functional assessment of isolated islets reveals that obese SM/J mice increase glucose-stimulated insulin secretion, decrease basal insulin secretion, and increase islet insulin content. These results establish that β-cell mass expansion and improved β-cell function underlie the resolution of hyperglycemia, indicating that obese SM/J mice are a valuable tool for exploring how functional β-cell mass can be recovered in the context of obesity., (© 2020 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)

Adipose is a dynamic endocrine organ that is critical for regulating metabolism and is highly responsive to nutritional environment. Brown adipose tissue is an exciting potential therapeutic target; however, there are no systematic studies of gene-by-environment interactions affecting function of this organ. We leveraged a weighted gene coexpression network analysis to identify transcriptional networks in brown adipose tissue from LG/J and SM/J inbred mice fed high- or low-fat diets and correlate these networks with metabolic phenotypes. We identified eight primary gene network modules associated with variation in obesity and diabetes-related traits. Four modules were enriched for metabolically relevant processes such as immune and cytokine response, cell division, peroxisome functions, and organic molecule metabolic processes. The relative expression of genes in these modules is highly dependent on both genetic background and dietary environment. Genes in the immune/cytokine response and cell division modules are particularly highly expressed in high fat-fed SM/J mice, which show unique brown adipose-dependent remission of diabetes. The interconnectivity of genes in these modules is also heavily dependent on diet and strain, with most genes showing both higher expression and coexpression under the same context. We highlight several genes of interest, Col28a1 , Cyp26b1 , Bmp8b , and Ngef , that have distinct expression patterns among strain-by-diet contexts and fall under metabolic quantitative trait loci previously mapped in an F 16 generation of an advanced intercross between LG/J and SM/J. Each of these genes have some connection to obesity and diabetes-related traits, but have not been studied in brown adipose tissue. Our results provide important insights into the relationship between brown adipose and systemic metabolism by being the first gene-by-environment study of brown adipose transcriptional networks.

U.S. immigrant parents encounter various challenges during the migration and resettlement process, such as acculturative stress and dissonance in parenting practices between the cultures in the U.S. and those in their country of origin. Although studies have established a link between increased perceived stress and reduced parenting self-efficacy in U.S.-born parents, which could be alleviated by levels of parental empowerment, little is known about this pathway in the context of migration. Guided by the Family Adjustment and Adaptation Response Model and with a focus on low-income immigrant parents of young children, we examined (1) the association between perceived stress and parenting self-efficacy, and (2) whether parental empowerment constitutes a buffer between perceived stress and parenting self-efficacy. Participants included foreign-born, low-income parents (n = 680) with preschool-aged children enrolled in Head Start of Greater Boston. Linear regression models were conducted to examine the relationship between perceived stress and parenting self-efficacy. An interaction term between perceived stress and empowerment was included to test the moderating effect of each dimension of parental empowerment (i.e., resource empowerment, critical awareness, and relational empowerment). Results showed higher perceived stress was associated with lower parenting self-efficacy and this relationship was moderated by relational empowerment. Findings suggest that relational empowerment can be an important resource for immigrant parents with high stress and a protective factor to improve self-efficacy in their parenting. These results pose important implications regarding how healthcare professionals and clinicians may support parents, for example, through the development of culturally sensitive parenting interventions and the creation of safe environments for parent-to-parent relationships., Competing Interests: Declarations. Competing Interests: The authors report there are no competing interests to declare., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: Iron is a critical component of metabolic homeostasis, but consumption of dietary iron has increased dramatically in the last 30 years, corresponding with the rise of metabolic disease. While the link between iron metabolism and metabolic health is well established, the extent to which dietary iron contributes to metabolic disease risk is unexplored. Further, it is unknown how dietary iron interacts with genetic background to modify metabolic disease risk., Methods: LG/J and SM/J inbred mouse strains were used to investigate the relationship between genetic background and metabolic function during an 8-week high iron diet. Glucose tolerance and adiposity were assessed, colorimetric assays determined levels of circulating metabolic markers, and hepatic iron content was measured. RNA sequencing was performed on white adipose tissue to identify genes differentially expressed across strain, diet, and strain X diet cohorts. Hepatic Hamp expression and circulating hepcidin was measured, and small nucleotide variants were identified in the Hamp genic region., Results: LG/J mice experienced elevated fasting glucose and glucose intolerance during the high iron diet, corresponding with increased hepatic iron load, increased circulating ferritin, and signs of liver injury. Adipose function was also altered in high iron-fed LG/J mice, including decreased adiposity and leptin production and differential expression of genes involved in iron and glucose homeostasis. LG/J mice failed to upregulate hepatic Hamp expression during the high iron diet, resulting in low circulating hepcidin levels compared to SM/J mice., Conclusions: This study highlights the importance of accounting for genetic variation when assessing the effects of diet on metabolic health, and suggests dietary iron's impact on liver and adipose tissue is an underappreciated component of metabolic disease risk., Competing Interests: All experiments were approved by the Institutional Animal Care and Use Committee at the Washington University School of Medicine (WUSM) in accordance with the National Institutes of Health (NIH) guidelines for the care and use of laboratory animals.Not applicable.The authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

The dramatic increase in global prevalence of metabolic disease is inexplicable when considering only environmental or only genetic factors, leading to the need to explore the possible roles of epigenetic factors. A great deal of progress has been made in this interdisciplinary field in recent years, with many studies investigating various aspects of the metabolic syndrome and its associated epigenetic changes. Rodent models of metabolic diseases have been particularly illuminating because of the ability to leverage tools such as genetic and environmental modifications. The current review summarizes recent breakthroughs regarding epigenetic markers in studies of obesity, Type II diabetes, and cardiovascular disease, the three major disorders associated with metabolic syndrome. We also discuss open questions and future directions for integrating genomic, epigenomic, and phenotypic big biodata toward understanding metabolic syndrome etiology.

The search for genetic risk factors in type-II diabetes has been hindered by a failure to consider dietary variables. Dietary nutrients impact metabolic disease risk and severity and are essential to maintaining metabolic health. Genetic variation between individuals confers differences in metabolism, which directly impacts response to diet. Most studies attempting to identify genetic risk factors in disease fail to incorporate dietary components, and thus are ill-equipped to capture the breadth of the genome's impact on metabolism. Understanding how genetic background interacts with nutrients holds the key to predicting and preventing metabolic diseases through the implementation of personalized nutrition. Dysregulation of iron homeostasis is associated with type-II diabetes, but the link between dietary iron and metabolic dysfunction is poorly defined. High iron burden in adipose tissue induces insulin resistance, but the mechanisms underlying adipose iron accumulation remain unknown. Hepcidin controls dietary iron absorption and distribution in metabolic tissues, but it is unknown whether genetic variation influencing hepcidin expression modifies susceptibility to dietary iron-induced insulin resistance. This review highlights discoveries concerning the axis of iron homeostasis and adipose function and suggests that genetic variation underlying dietary iron metabolism is an understudied component of metabolic disease.

Intervertebral disc degeneration (IDD) causes back pain and sciatica, affecting quality of life and resulting in high economic/social burden. The etiology of IDD is not well understood. Along with aging and environmental factors, genetic factors also influence the onset, progression and severity of IDD. Genetic studies of risk factors for IDD using human cohorts are limited by small sample size and low statistical power. Animal models amenable to genetic and functional studies of IDD provide desirable alternatives. Despite differences in size and cellular content as compared to human intervertebral discs (IVDs), the mouse is a powerful model for genetics and assessment of cellular changes relevant to human biology. Here, we provide evidence for early onset disc degeneration in SM/J relative to LG/J mice with poor and good tissue healing capacity respectively. In the first few months of life, LG/J mice maintain a relatively constant pool of notochordal-like cells in the nucleus pulposus (NP) of the IVD. In contrast, chondrogenic events are observed in SM/J mice beginning as early as one-week-old, with progressive fibrotic changes. Further, the extracellular matrix changes in the NP are consistent with IVD degeneration. Leveraging on the genomic data of two parental and two recombinant inbred lines, we assessed the genetic contribution to the NP changes and identified processes linked to the regulation of ion transport systems. Significantly, "transport" system is also in the top three gene ontology (GO) terms from a comparative proteomic analysis of the mouse NP. These findings support the potential of the SM/J, LG/J and their recombinant inbred lines for future genetic and biological analysis in mice and validation of candidate genes and biological relevance in human cohort studies. The proteomic data has been deposited to the ProteomeXchange Consortium via the PRIDE [1] partner repository with the dataset identifier PXD008784., (Copyright © 2018. Published by Elsevier B.V.)

Background/objectives: Elevated triglycerides predict insulin resistance and vascular disease in obesity, but how the inert triglyceride molecule is related to development of metabolic disease is unknown. To pursue novel potential mediators of triglyceride-associated metabolic disease, we used a forward genetics approach involving inbred mice and translated our findings to human subjects., Subjects/methods: Hemopexin (HPX) was identified as a differentially expressed gene within a quantitative trait locus associated with serum triglycerides in an F 16 advanced intercross between the LG/J and SM/J strains of mice. Hpx expression was evaluated in both the reproductive fat pads and livers of mice representing three strains, LG/J (n=25), SM/J (n=27) and C57Bl/6J (n=19), on high- and low-fat diets. The effect of altered Hpx expression on adipogenesis was studied in 3T3-L1 cells. Circulating HPX protein along with HPX expression were characterized in subcutaneous white adipose tissue samples obtained from a cohort of metabolically abnormal (n=18) and of metabolically normal (n=24) obese human subjects. We further examined the relationship between HPX and triglycerides in human atherosclerotic plaques (n=18)., Results: HPX expression in mouse adipose tissue, but not in liver, was regulated by dietary fat regardless of genetic background. HPX increased in concert with adipogenesis in 3T3-L1 cells, and disruption of its expression impaired adipocyte differentiation. RNAseq data from the adipose tissue of obese humans showed differential expression of HPX based on metabolic disease status (P<0.05), and circulating HPX levels were correlated with serum triglycerides in these subjects (r=0.33; P=0.03). HPX was also found in an unbiased proteomic screen of human atherosclerotic plaques and shown to display differential abundance based on the extent of disease and triglyceride content (P<0.05)., Conclusions: Our findings suggest that HPX is associated with triglycerides and provide a framework for understanding mechanisms underlying lipid metabolism and metabolic disease.

Hard-to-serve youth and families residing in high-poverty communities often have multiple, interlocking needs. These needs necessitate complex service models. The complex model described in this article combines a unique approach to wraparound services with a coproduction framework and related theories. The model aims to improve outcomes for vulnerable youth and their families, simultaneously strengthening communities by employing residents and engaging participants in community service. Examples derived from current pilot projects illustrate co-production's importance for other child welfare initiatives. [ABSTRACT FROM AUTHOR]

Systems change in child welfare and cross-systems change involving other service sectors are needed in response to two developments: (1) New policy mandates (e.g., TANF, ASFA) and (2) Research on the co-occurring and interlocking needs of many child welfare families. A four-state initiative was structured in response to these needs. Collaborative learning and action research groups called design teams were structured to identify competencies and to develop new service delivery systems. Faculty facilitators representing social work education programs were assigned to these teams and charged with their development and evaluation. Facilitators served as linkage agents for university-community-state agency partnerships, and they promoted curriculum change. These study reports two sets of findings related to these design teams: (1) Findings from semi-structured interviews of design team members; and (2) Findings from the participatory action research completed by two faculty facilitators. Key themes related to design team processes are presented. Drawing on these emergent themes, components that help explain effective design team processes are identified. Selected implications for social work education programs and faculty also are identified. [ABSTRACT FROM AUTHOR]

Background: Screening, brief intervention, and referral to treatment (SBIRT) has been endorsed by the American Academy of Pediatrics as an evidence-based strategy to address risky substance use among adolescents in primary care. However, less than half of pediatricians even screen adolescents for substance use. The purpose of this study was to identify variation in SBIRT practice and explore how program directors' and clinicians' attitudes and perceptions of effectiveness, role responsibility, and self-efficacy impact SBIRT adoption, implementation, and practice in school-based health centers (SBHCs)., Methods: All 162 New York State SBHC program directors and clinicians serving middle and high school students were surveyed between May and June of 2013 (40% response rate)., Results: Only 22% of participants reported practicing the SBIRT model. Of the individual SBIRT model components, using a standardized tool to screen students for risky substance use, referring students with substance use problems to specialty treatment, and assessing students' readiness to change were practiced least frequently. Less than 30% of participants felt they could be effective at helping students reduce substance use, 63% did not believe it was their role to use a standardized screening tool, and 20-30% did not feel confident performing specific aspects of intervention and management. Each of these factors was correlated with SBIRT practice frequency (P < .05)., Conclusions: Findings from this study identify an important gap between an evidence-based SBIRT model and its adoption into practice within SBHCs, indicating a need for dissemination strategies targeting role responsibility, self-efficacy, and clinicians' perceptions of SBIRT effectiveness.

Objective: Sarcolipin (SLN) regulates muscle energy expenditure through its action on sarco/endoplasmic reticulum Ca(2+) -ATPase (SERCA) pump. It is unknown whether SLN-dependent respiration has relevance to human obesity, but whole-transcriptome gene expression profiling revealed that SLN was more highly expressed in myocytes from individuals with severe obesity (OB) than in lean controls (LN). The purpose of this study was to examine SLN-dependent cellular respiratory rates in LN and OB human muscles., Methods: Primary myocytes were isolated from muscle biopsy from seven LN and OB Caucasian females. Cellular respiration was assessed with and without lentivirus-mediated SLN knockdown in LN and OB myocytes., Results: SLN mRNA and protein abundance was greater in OB compared to LN cells. Despite elevated SLN levels in wild-type OB cells, respiratory rates among SLN-deficient cells were higher in OB compared to LN. Obesity-induced reduction in efficiency of SLN-dependent respiration was associated with altered sarcoplasmic reticulum phospholipidome., Conclusions: SLN-dependent respiration is reduced in muscles from humans with severe obesity compared to lean controls. Identification of the molecular mechanism that affects SLN efficiency might lead to interventions that promote an increase in skeletal muscle energy expenditure., (© 2015 The Obesity Society.)

Background: The laboratory mouse is the most commonly used model for studying variation in complex traits relevant to human disease. Here we present the whole-genome sequences of two inbred strains, LG/J and SM/J, which are frequently used to study variation in complex traits as diverse as aging, bone-growth, adiposity, maternal behavior, and methamphetamine sensitivity., Results: We identified small nucleotide variants (SNVs) and structural variants (SVs) in the LG/J and SM/J strains relative to the reference genome and discovered novel variants in these two strains by comparing their sequences to other mouse genomes. We find that 39% of the LG/J and SM/J genomes are identical-by-descent (IBD). We characterized amino-acid changing mutations using three algorithms: LRT, PolyPhen-2 and SIFT. We also identified polymorphisms between LG/J and SM/J that fall in regulatory regions and highly informative transcription factor binding sites (TFBS). We intersected these functional predictions with quantitative trait loci (QTL) mapped in advanced intercrosses of these two strains. We find that QTL are both over-represented in non-IBD regions and highly enriched for variants predicted to have a functional impact. Variants in QTL associated with metabolic (231 QTL identified in an F16 generation) and developmental (41 QTL identified in an F34 generation) traits were interrogated and we highlight candidate quantitative trait genes (QTG) and nucleotides (QTN) in a QTL on chr13 associated with variation in basal glucose levels and in a QTL on chr6 associated with variation in tibia length., Conclusions: We show how integrating genomic sequence with QTL reduces the QTL search space and helps researchers prioritize candidate genes and nucleotides for experimental follow-up. Additionally, given the LG/J and SM/J phylogenetic context among inbred strains, these data contribute important information to the genomic landscape of the laboratory mouse.

The transition to practice process is complex and facilitated by many formal and informal processes. The coronavirus disease 2019 global pandemic presented unique challenges for athletic trainers. An identity-specific focus is necessary to understand better the transition to practice process during the pandemic. To understand (1) what socializing factors influence a cohort of women athletic trainers who graduated from the same professional master's (PM) athletic training program as they transitioned to practice and (2) the unique challenges the women athletic trainers faced as they sought employment and transitioned into their first professional roles during the pandemic. Qualitative phenomenological cohort study. Semistructured, in-depth, 1-on-1 videoconference interviews. Six women (24.83 ±.96 years old) who graduated from the same PM athletic training program now working in various athletic training settings. We conducted semistructured interviews via Zoom (Zoom Video Communications). Interviews were transcribed, and a general phenomenological approach to analysis was used. Member checks, multiple analyst triangulation, and peer review were used to ensure trustworthiness. Three main themes emerged that describe the effects of the pandemic on the transition to practice of women athletic trainers: (1) personal identity, (2) relational identity, and (3) professional identity. Several subthemes were also identified to further illustrate the participants' lived experiences. Although some of the participants' socialization and transition to practice experiences were similar to other graduates described in the literature, the personal, relational, and professional identities of these women athletic trainers were influenced by the pandemic. The participants purposefully sought women mentors to assist them with navigating the challenges of developing a professional identity during the pandemic. There is a need to create gender-specific networks to support individuals during their growth from novice to professional. [ABSTRACT FROM AUTHOR]

The autonomous and active Long-Interspersed Element-1 (LINE-1, L1) and the non-autonomous Alu retrotransposon elements, contributing to 30% of the human genome, are the most abundant repeated sequences. With more than 90% of their sequences being methylated in normal cells, these elements undeniably contribute to the global DNA methylation level and constitute a major part of circulating-cell-free DNA (cfDNA). So far, the hypomethylation status of LINE-1 and Alu in cellular and extracellular DNA has long been considered a prevailing hallmark of ageing-related diseases and cancer. This study demonstrated that errors in LINE-1 and Alu methylation level measurements were caused by an excessive input quantity of genomic DNA used for bisulfite conversion. Using the minuscule DNA amount of 0.5 ng, much less than what has been used and recommended so far (500 ng-2 μg) or 1 μL of cfDNA extracted from 1 mL of blood, we revealed hypermethylation of LINE-1 and Alu in 407 tumour samples of primary breast, colon and lung cancers when compared with the corresponding pair-matched adjacent normal tissue samples (P < 0.05–0.001), and in cfDNA from 296 samples of lung cancers as compared with 477 samples from healthy controls (P < 0.0001). More importantly, LINE-1 hypermethylation in cfDNA is associated with healthy ageing. Our results have not only contributed to the standardized bisulfite-based protocols for DNA methylation assays, particularly in applications on repeated sequences but also provided another perspective for other repetitive sequences whose epigenetic properties may have crucial impacts on genome architecture and human health. [ABSTRACT FROM AUTHOR]

Different sheep breeds show distinct phenotypic plasticity in fat deposition in the tails. The genetic background underlying fat deposition in the tail of sheep is complex, multifactorial, and may involve allele-specific expression (ASE) mechanism to modulate allelic expression. ASE is a common phenomenon in mammals and refers to allelic imbalanced expression modified by cis-regulatory genetic variants that can be observed at heterozygous loci. Therefore, regulatory processes behind the fat-tail formation in sheep may be to some extent explained by cis- regulatory variants, through ASE mechanism, which was investigated in the present study. An RNA-Seq-based variant calling was applied to perform genome-wide survey of ASE genes using 45 samples from seven independent studies comparing the transcriptome of fat-tail tissue between fat- and thin-tailed sheep breeds. Using a rigorous computational pipeline, 115 differential ASE genes were identified, which were narrowed down to four genes (LPL, SOD3, TCP1 and LRPAP1) for being detected in at least two studies. Functional analysis revealed that the ASE genes were mainly involved in fat metabolism. Of these, LPL was of greater importance, as 1) observed in five studies, 2) reported as ASE gene in the previous studies and 3) with a known role in fat deposition. Our findings implied that complex physiological traits, like fat-tail formation, can be better explained by considering various genetic mechanisms, which can be more finely mapped through ASE analyses. The insights gained in this study indicate that biallelic expression may not be a common mechanism in sheep fat-tail development. Hence, allelic imbalance of the fat deposition-related genes can be considered a novel layer of information for future research on genetic improvement and increased efficiency in sheep breeding programs. [ABSTRACT FROM AUTHOR]

Background: Percocypris pingi (Tchang) was classified as Endangered on the Red List of China′s Vertebrates in 2015 and is widely distributed in the Upper Yangtze River. Although breeding and release into wild habitats have been performed for this commercially important fish in recent years, low genetic diversity has been found in wild populations. Genomic resources are strongly recommended before formulating and carrying out conservation strategies for P. pingi. Thus, there is an urgent need to conserve germplasm resources and improve the population diversity of P. pingi. To date, the whole genome of P. pingi has not been reported. Results: In our study, we constructed the first chromosome-level genome of P. pingi by high-throughput chromosome conformation capture (Hi-C) technology and PacBio long-read sequencing. The assembled genome was 1.7 Gb in size, with an N50 of 17,692 bp and a GC content from circular consensus sequencing of 37.67%. The Hi-C results again demonstrated that P. pingi was tetraploid (n = 98), with the genome consisting of 24-type and 25-type chromosomes. Chr.19 of the 24-type chromosomes in P. pingi resulted from the fusion of chr.19 and chr.22 in zebrafish. The divergence times between 24-type and 25-type chromosomes was around 6.1 million years ago. A total of 25,198 and 25,291 protein-coding genes were obtained from the 24-type and 25-type chromosomes, respectively. The ploidy of P. pingi is an allotetraploid. A total of 8,741 genes of P. pingi were clustered into 4,378 gene families that were shared with 14 other species, and the P. pingi genome had 68 unique gene families. Phylogenetic analyses indicated that P. pingi was most closely related to Schizothorax oconnori, and the genes were clustered on one branch. We identified 166 significantly expanded gene families and 173 significantly contracted gene families in P. pingi. The most enriched positive protein-coding genes, such as Bmp-4, Etfdh, homeobox protein HB9, and ATG3, were screened. Conclusion: Our study provides a high-quality chromosome-anchored reference genome for P. pingi and provides sufficient information on the chromosomes, which will lead to valuable resources for genetic, genomic, and biological studies of P. pingi and for improving the genetic diversity, population size, and scientific conservation of endangered fish and other key cyprinid species in aquaculture. [ABSTRACT FROM AUTHOR]

Building Cultures of Care in schools has profound potential to support students' mental health and academic success. This is critical as students' mental and behavioral challenges are rising, and teachers report stress and burn out. To inform work in other communities, we examine the Culture of Care initiative in a tri-county region of one US state. We take a Developmental Evaluation approach, documenting the journey, including successes, challenges, adaptations, and initial outcomes over 3 years encompassing the covid-19 pandemic. In Year 1, 12 school district administrators and partners responsible for initiative launch reflected on keys to success, early outcomes, and challenges through interviews. In Year 3, 62 educators, local administrators, and community partners who implemented the initiative participated in open-ended surveys and focus groups. Results from content analysis revealed evidence of a systems approach to integrating multiple components of trauma-informed and restorative school practices into a unified initiative to create educational cultures of care. Strengths stemmed from a regional, relationship-based approach uniting educational leaders and a team of coaches across multiple districts, coupled with tailored strategies for individual schools, and adaptability to emergent needs. Challenges included escalating student needs, difficulty learning new practices, staff turnover, stress and fatigue, variability in buy-in across schools, and challenges to community and family partnerships. Yet, participants consistently pointed to indicators of success, including transformation in staff perspectives and practices, and more positive learning environments. Further research is needed to capture students' and families' perspectives and to examine equitable educational and mental health outcomes for students. [ABSTRACT FROM AUTHOR]

The accumulation of visceral adipose tissue (VAT) is strongly associated with cardiovascular disease and diabetes. In contrast, individuals with increased subcutaneous adipose tissue (SAT) without corresponding increases in VAT are associated with a metabolic healthy obese phenotype. These observations implicate dysfunctional VAT as a driver of disease processes, warranting investigation into obesity-induced alterations of distinct adipose depots. To determine the effects of obesity on adipose gene expression, male mice (n = 4) were fed a high-fat diet to induce obesity or a normal laboratory diet (lean controls) for 12–14 mo. Mesenteric VAT and inguinal SAT were isolated for bulk RNA sequencing. AT from lean controls served as a reference to obesity-induced changes. The long-term high-fat diet induced the expression of 169 and 814 unique genes in SAT and VAT, respectively. SAT from obese mice exhibited 308 differentially expressed genes (164 upregulated and 144 downregulated). VAT from obese mice exhibited 690 differentially expressed genes (262 genes upregulated and 428 downregulated). KEGG pathway and GO analyses revealed that metabolic pathways were upregulated in SAT versus downregulated in VAT while inflammatory signaling was upregulated in VAT. We next determined common genes that were differentially regulated between SAT and VAT in response to obesity and identified four genes that exhibited this profile: elovl6 and kcnj15 were upregulated in SAT/downregulated in VAT while trdn and hspb7 were downregulated in SAT/upregulated in VAT. We propose that these genes in particular should be further pursued to determine their roles in SAT versus VAT with respect to obesity. NEW & NOTEWORTHY: A long-term high-fat diet induced the expression of more than 980 unique genes across subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT). The high-fat diet also induced the differential expression of nearly 1,000 AT genes. We identified four genes that were oppositely expressed in SAT versus VAT in response to the high-fat diet and propose that these genes in particular may serve as promising targets aimed at resolving VAT dysfunction in obesity. [ABSTRACT FROM AUTHOR]

The rat, Rattus norvegicus, has provided an important model for investigation of a range of characteristics of biomedical importance. Here we survey the origins of this species, its introduction into laboratory research, and the emergence of genetic and genomic methods that utilize this model organism. Genomic studies have yielded important progress and provided new insight into several biologically important traits. However, some studies have been impeded by the lack of a complete and accurate reference genome for this species. New sequencing and genome assembly methods applied to the rat have resulted in a new reference genome assembly, GRCr8, which is a near telomere-to-telomere assembly of high base-level accuracy that incorporates several elements not captured in prior assemblies. As genome assembly methods continue to advance and production costs become a less significant obstacle, genome assemblies for multiple inbred rat strains are emerging. These assemblies will allow a rat pangenome assembly to be constructed that captures all the genetic variations in strains selected for their utility in research and will overcome reference bias, a limitation associated with reliance on a single reference assembly. By this means, the full utility of this model organism to genomic studies will begin to be revealed. [ABSTRACT FROM AUTHOR]

Meta-analysis is used to aggregate the effects of interest across multiple studies, while its methodology is largely underexplored in mediation analysis, particularly in estimating the total mediation effect of high-dimensional omics mediators. Large-scale genomic consortia, such as the Trans-Omics for Precision Medicine (TOPMed) program, comprise multiple cohorts with diverse technologies to elucidate the genetic architecture and biological mechanisms underlying complex human traits and diseases. Leveraging the recent established asymptotic standard error of the R-squared (R2)-based mediation effect estimation for high-dimensional omics mediators, we have developed a novel meta-analysis framework requiring only summary statistics and allowing inter-study heterogeneity. Whereas the proposed meta-analysis can uniquely evaluate and account for potential effect heterogeneity across studies due to, for example, varying genomic profiling platforms, our extensive simulations showed that the developed method was more computationally efficient and yielded satisfactory operating characteristics comparable to analysis of the pooled individual-level data when there was no inter-study heterogeneity. We applied the developed method to 5 TOPMed studies with over 5800 participants to estimate the mediation effects of gene expression on age-related variation in systolic blood pressure and sex-related variation in high-density lipoprotein (HDL) cholesterol. The proposed method is available in R package MetaR2M on GitHub. Author summary: We have developed a novel meta-analysis framework to combine the estimates of the total mediation effect of high-dimensional omics mediators on complex traits from multiple studies in large-scale genomic consortia. By applying the developed method to genome-wide gene expression data from five studies with over 5,800 participants, we were able to demonstrate that our approach is not only computationally efficient but also yields reliable results. We illustrate how certain genes and biological pathways can influence age-related changes in blood pressure and sex differences in high-density lipoprotein (HDL) cholesterol levels. Our new tool, available as an R package MetaR2M on GitHub, makes it easier for researchers to analyze such complex data. This could lead to a better understanding of the genetic architecture and biological mechanisms underlying complex human traits and diseases. [ABSTRACT FROM AUTHOR]

Background: Indigenous buffaloes, as the important livestock species contributing to economy of the country, are the lifeline of livelihood in Nepal. They are distributed across diverse geographical regions of the country and have adapted to various feeding, breeding, and management conditions. The larger group of these native buffalo breeds are present in narrow and stiff hilly terrains. Their dispersal indicates a possible environmental adaptation mechanism, which is crucial for the conservation of these breeds. Results: We utilized whole-genome sequencing (WGS) to investigate the genetic diversity, population structure, and selection signatures of Nepalese indigenous buffaloes. We compared 66 whole-genome sequences with 118 publicly available sequences from six river and five swamp buffalo breeds. Genomic diversity parameters indicated genetic variability level in the Nepalese buffaloes comparable to those of Indian breeds, and population genetic structure revealed distinct geography-mediated genetic differentiation among these breeds. We used locus-specific branch length analysis (LSBL) for genome-wide scan, which revealed a list of potentially selected genes in Lime and Parkote breeds that inhabit the hilly region. A gene ontology (GO) analysis discovered that many GO terms were associated with cardiac function regulation. Furthermore, complementary analyses of local selection signatures, tissue expression profiles, and haplotype differences identified candidate genes, including KCNE1, CSF1R, and PDGFRB, related to the regulation of cardiac and pulmonary functions. Conclusions: This study is a comprehensive WGS-based genetic analysis of the native Nepalese buffalo breeds. Our study suggested that the Nepalese "hilly" buffaloes, especially the Lime and Parkote breeds, have undergone some characteristic genetic changes and evolved increased cardiac and pulmonary function for their adaptation to the steep hilly terrains of the country. [ABSTRACT FROM AUTHOR]

Witnessing that the appearance of female trainers has been regarded as a potential cause of appearance-based discrimination and a source of bodily capital, this study examined the influence of female trainers' appearance on the process of occupational socialization. We invited eight research participants for in-depth interviews, including female trainers, Pilates instructors, and male fitness center owners with training experience. We followed the grounded theory analysis method to derive meaningful insights from the collected data. The results indicate that the physical appearance of female trainers had various effects on their perceived value as bodily capital during the preparatory and adaptation periods. However, it became a constraining factor during the conflict period as they experienced bodily changes in their late 20s. Eventually, their physical appearance hindered female trainers from maintaining their careers and decreased the percentage of female trainers who reached maturity period. Ultimately, the culture of lookism had a mixed impact on women's occupational socialization, revealing its discriminatory undertones. Although some women profited from the culture, lookism disadvantaged others. Finally, we suggested that a possible solution would be the enactment of the anti-discrimination law for better protection. [ABSTRACT FROM AUTHOR]

This paper proposes dovetailing the concept of youth-adult partnership with youth participatory action research to generate a methodology of youth-adult participatory action research. Within contemporary education, deficit-oriented discourses of hopelessness and demoralisation among 'at risk' young people and their teachers, particularly those in marginalised and/or high poverty communities, pervade the literature. However, scholarship suggests that negative emotions do not tend to stem from a sense of hopelessness but one of uncertainty, which is typically caused by a lack of accurate information and thus provides a starting point for investigations through integrating reason and emotion. Embedded in Fraser's conceptualisation of justice as parity of participation, coupled with Freire's notion of intergenerational dialogue and a critical-democratic conceptualisation of engagement, youth-adult participatory action research seeks to generate communities of praxis in which students, teachers and researchers form explicit tripartite partnerships as co-investigators and co-learners. As they jointly explore their shared concerns, the members of the community mobilise their collective power and agency to co-design context-specific solutions and in so doing, transform the negative emotion and disenfranchisement stemming from uncertainty into a critical hope for more optimistic futures than those alluded to by the 'at risk' and 'disengaged' policy tags. [ABSTRACT FROM AUTHOR]

External ear hole closure in LG/J mice represents a model of regenerative response. It is accompanied by the formation of a blastema-like structure and the re-growth of multiple tissues, including cartilage. The ability to regenerate tissue is heritable. An F34 advanced intercross line of mice (Wustl:LG,SM-G34) was generated to identify genomic loci involved in ear hole closure over a 30-day healing period. We mapped 19 quantitative trait loci (QTL) for ear hole closure. Individual gene effects are relatively small (0.08 mm), and most loci have co-dominant effects with phenotypically intermediate heterozygotes. QTL support regions were limited to a median size of 2 Mb containing a median of 19 genes. Positional candidate genes were evaluated using differential transcript expression between LG/J and SM/J healing tissue, function analysis and bioinformatic analysis of single-nucleotide polymorphisms in and around positional candidate genes of interest. Analysis of the set of 34 positional candidate genes and those displaying expression differences revealed over-representation of genes involved in cell cycle regulation/DNA damage, cell migration and adhesion, developmentally related genes and metabolism. This indicates that the healing phenotype in LG/J mice involves multiple physiological mechanisms.

Parents influence children's obesity risk factors but are infrequently targeted for interventions. This study targeting low-income parents integrated a community-based participatory research approach with the Family Ecological Model and Empowerment Theory to develop a childhood obesity intervention. This article (1) examines pre- to postintervention changes in parents' empowerment; (2) determines the effects of intervention dose on empowerment, and (3) determines whether changes in parent empowerment mediate previous changes identified in food-, physical activity-, and screen-related parenting. The pre-post quasi-experimental design evaluation demonstrated positive changes in parent empowerment and empowerment predicted improvement in parenting practices. The integrated model applied in this study provides a means to enhance intervention relevance and guide translation to other childhood obesity and health disparities studies.

Background: This study aimed to explore the relationship between the changes in parent-related factors and preschoolers exceeding screen time (ST) recommendations. Methods: A longitudinal analysis using 2-year follow-up data from 4 kindergartens (n = 409) was conducted in Zhejiang, China, from 2019 to 2021. Multivariate logistic regression models were used to determine the potential parental modifiable predictors. Results: The significant associations of baseline ST, change in screen accessibility, and the interaction of preschooler ST with maternal ST change with preschooler follow-up ST were observed. For preschool-aged children with baseline ST ≤ 1 hour per day, the follow-up of preschoolers with ST > 1 hour per day increased significantly when parental clarity of their ST rules decreased or remained low. For preschool children with baseline ST > 1 hour per day, follow-up ST increased significantly when their father kept ST >2 hours per day, when the screen accessibility became or remained easy, or when parental awareness of the ST decreased. Conclusions: Changes in parental correlates played an important role in preschooler ST based on 2-year longitudinal data. Early interventions should focus on improving the clarity of parental rules and perceptions, as well as on reducing parental ST and accessibility of home screens. [ABSTRACT FROM AUTHOR]

Objective: According to the Family Ecological Model (FEM), parenting behaviours are shaped by the contexts in which families are embedded. In the present study, we utilize the FEM to guide a mixed-methods community assessment and summarize the results. Additionally, we discuss the utility of the FEM and outline possible improvements., Design: Using a cross-sectional design, qualitative and quantitative methods were used to examine the ecologies of parents’ cognitions and behaviours specific to children’s diet, physical activity and screen-based behaviours. Results were mapped onto constructs outlined in the FEM., Setting: The study took place in five Head Start centres in a small north-eastern city. The community assessment was part of a larger study to develop and evaluate a family-centred obesity prevention programme for low-income families., Subjects: Participants included eighty-nine low-income parents/caregivers of children enrolled in Head Start., Results: Parents reported a broad range of factors affecting their parenting cognitions and behaviours. Intrafamilial factors included educational and cultural backgrounds, family size and a lack of social support from partners. Organizational factors included staff stability at key organizations, a lack of service integration and differing school routines. Community factors included social connectedness to neighbours/friends, shared norms around parenting and the availability of safe public housing and play spaces. Policy- and media-related factors included requirements of public assistance programmes, back-to-work policies and children’s exposure to food advertisements., Conclusions: Based on these findings, the FEM was refined to create an evidence-based,temporally structured logic model to support and guide family-centred research in childhood obesity prevention.

Parent-of-origin effects occur when the phenotypic effect of an allele depends on whether it is inherited from the mother or the father. Several phenomena can cause parent-of-origin effects, but the best characterized is parent-of-origin-dependent gene expression associated with genomic imprinting. The development of new mapping approaches applied to the growing abundance of genomic data has demonstrated that imprinted genes can be important contributors to complex trait variation. Therefore, to understand the genetic architecture and evolution of complex traits, including complex diseases and traits of agricultural importance, it is crucial to account for these parent-of-origin effects. Here, we discuss patterns of phenotypic variation associated with imprinting, evidence supporting its role in complex trait variation and approaches for identifying its molecular signatures.

Prevention of childhood obesity is a national priority. Parents influence young children's healthy lifestyles, so it is paradoxical that obesity interventions focus primarily on children. Evidence and theory suggest that including parents in interventions offers promise for effective childhood obesity prevention. This case study engaged parents' as co-researchers in the design, implementation and evaluation of an intervention for low-income families with a child enrolled in Head Start. Parent engagement mechanisms include: (1) targeted partnership development (2) operationalizing a Community Advisory Board (CAB) that was the key decision making body; (3) a majority of CAB members were parents who were positioned as experts, and (4) addressing structural barriers to parent participation. Lessons learned are provided for future research, and practice.

Background: Ineffective family interventions for the prevention of childhood obesity have, in part, been attributed to the challenges of reaching and engaging parents. With a particular focus on parent engagement, this study utilized community-based participatory research to develop and pilot test a family-centered intervention for low-income families with preschool-aged children enrolled in Head Start., Methods: During year 1 (2009-2010), parents played an active and equal role with the research team in planning and conducting a community assessment and using the results to design a family-centered childhood obesity intervention. During year 2 (2010-2011), parents played a leading role in implementing the intervention and worked with the research team to evaluate its results using a pre-post cohort design. Intervention components included: (1) revisions to letters sent home to families reporting child body mass index (BMI); (2) a communication campaign to raise parents' awareness of their child's weight status; (3) the integration of nutrition counseling into Head Start family engagement activities; and (4) a 6-week parent-led program to strengthen parents' communication skills, conflict resolution, resource-related empowerment for healthy lifestyles, social networks, and media literacy. A total of 423 children ages 2-5 years, from five Head Start centers in upstate New York, and their families were exposed to the intervention and 154 families participated in its evaluation. Child outcome measures included BMI z-score, accelerometer-assessed physical activity, and dietary intake assessed using 24-hour recall. Parent outcomes included food-, physical activity- and media-related parenting practices and attitudes., Results: Compared with pre intervention, children at post intervention exhibited significant improvements in their rate of obesity, light physical activity, daily TV viewing, and dietary intake (energy and macronutrient intake). Trends were observed for BMI z-score, sedentary activity and moderate activity. Parents at post intervention reported significantly greater self-efficacy to promote healthy eating in children and increased support for children's physical activity. Dose effects were observed for most outcomes., Conclusions: Empowering parents to play an equal role in intervention design and implementation is a promising approach to family-centered obesity prevention and merits further testing in a larger trial with a rigorous research design.

Physical activity (PA) parenting, or strategies parents use to promote PA in children, has been associated with increased PA in children of all ages, including preschool-aged children. However, little is known about the circumstances under which parents adopt such behaviors. This study examined family ecological factors associated with PA parenting. Low-income parents (N = 145) of preschool-aged children (aged 2 to 5 years) were recruited from five Head Start centers in upstate New York. Guided by the family ecological model (FEM), parents completed surveys assessing PA parenting and relevant family and community factors. Hierarchical regression analysis identified independent predictors of PA parenting. Parent depressive symptoms, life pressures that interfere with PA and perceived empowerment to access PA resources were associated with PA parenting. Community factors, including neighborhood play safety and social capital, were not independently associated with PA parenting in the multivariate model. Together, family ecological factors accounted for a large proportion of the variance in PA parenting (R (2) = .37). Findings highlight the need to look beyond cognitive predictors of PA parenting in low-income families and to examine the impact of their broader life circumstances including indicators of stress.

Phubbing is not only a consequence of technological advancements but also represents an entirely novel aspect of social conduct, impacting students' academic performance and the sustainability of development. The purpose of the study is to identify the relationship between students’ level of phubbing, academic engagement and academic performance and offer practical solutions for managing and controlling students’ level of phubbing. We measured students’ level of phubbing, academic engagement and academic performance. The study involved 513 undergraduate and graduate students of Peter the Great Polytechnic University. The study also uses the Phubbing Scale, student attendance records of face-to-face classes, records of completed tasks in Moodle, motivation questionnaire. According to the results, there is no significant difference between men and women. The degree of phubbing showed a robust connection to behavioral engagement, emotional engagement, cognitive engagement, and academic performance. Additionally, the extent of phubbing played a mediating role in the link between behavioral engagement, emotional engagement, cognitive engagement, and academic performance. So that all hypothesizes are supported. As a tool to control the level of phubbing we propose to organize and conduct additional seminars for first-year students in order to get acquainted with such a concept as phubbing, to discuss how this habit can have a negative effect on the academic and professional success of future specialists and to form “mindfulness” among students. [ABSTRACT FROM AUTHOR]

The purpose of this study was to describe the acculturation of six British physical education (PE) preservice teachers (PSTs). The research questions we sought to answer were: (a) What were the PSTs' values, beliefs, and perspectives regarding PE? and (b) What factors shaped the PSTs' values, beliefs, and perspectives during their acculturation? We collected data with three types of formal interviewing and employed standard interpretive techniques to reduce the data to themes. Key findings were that the PSTs aspired to a career teaching secondary PE, possessed a balanced orientation to teaching curricular PE and coaching extracurricular sport, and espoused a mostly traditional multi-activity curriculum that was dominated by sport. The main attractors to a career in PE were the opportunity to maintain a connection with sport and working with youth. The key shaper of the PSTs' perspectives was their apprenticeships of observation. These findings should aid sport pedagogy faculty in their efforts to produce stronger initial teacher education programs. [ABSTRACT FROM AUTHOR]

This paper draws on critical discourse analysis to examine how health and physical education (HPE) curricula from Sweden, Norway, South Africa, Australia, and New Zealand may influence possibilities for the enactment of social justice in schools. The findings highlight the presence of social justice intentions across the five curricula as related to embodied movement experiences, social cohesion, and activism. That said, the findings simultaneously suggest that the language used to orient teaching towards social justice objectives is often elusive. In this paper, we contend that despite the presence of social justice intentions in these five HPE curricula, the articulation and function of the language within the curriculum documents do not necessarily support the enactment of this in practice. To conclude, we therefore suggest that more work is needed to ensure that curricula and other supporting artefacts and resources can better support both teachers' practice and students' learning in raising awareness of, and addressing, social justice outcomes in HPE. [ABSTRACT FROM AUTHOR]

The recent emergence of primary school generalist teachers with physical education (PE) expertise has addressed calls for some form of specialisation in primary PE provision in Ireland (Marron et al., 2018). It was hoped that these teachers could advance the quality of PE taught within schools, through their own teaching and by supporting colleagues (Ní Chróinín, 2018). Despite PE specialism graduates (PESGs) developing teaching orientations and high self-efficacy to teach PE during their professional socialisation, it is unclear how their skills are applied within schools. This study examined the organisational socialisation of PESGs through a micropolitical lens, drawing on the research of Kelchtermans and Ballet (2002a , 2002b). Adopting a critical realist approach enabled us to explore teachers' complex teaching realities. Semi-structured interviews were conducted with 11 graduates of the four-year Bachelor of Education with a major specialism in PE. Reflexive thematic analysis of interview data identified that PESGs had limited opportunities to apply their PE skills due to the conflicting custodial orientations of their schools. Due to PESGs' professional interests, they were more likely to assimilate with the existing school culture as early career teachers, even if it overlooked their PE expertise. The outsourcing of PE provision to external coaches, and PESGs' identity as novice teachers, also undermined their potential contribution as PE experts. Although some PESGs have positively used their knowledge to direct whole-school PE provision, more structured opportunities may be necessary to support the continued development of PESGs as teachers and leaders of PE. [ABSTRACT FROM AUTHOR]