The Relation Between Self-Compassion, Body Image, and Mood: How Do Women Internalize Weight-Related Feedback?

Objective: Body dissatisfaction has been identified as a risk factor for depression and eating pathology, whereas, self-compassion has been associated with higher quality of life. This study sought to examine the relationship between negative body image and self-compassion as risk or protective factors for weight and body composition related feedback mood changes. Method: This deception study used a true-experimental, pre- and post-test design in a sample of 117 female graduate and medical students and college staff, aged 18 to 45 years; women diagnosed with eating disorders were excluded. After completing baseline questionnaires (including mood, body image, and self-compassion), patiicipants had their weight and body fat percentage measured. Changes in self-repmied mood were examined after patiicipants were given weight and body fat readings, respectively, that were either: (a) accurate; (A) (b) false higher (FH) by 5 pounds and 4 body fat percentage points; or (c) false lower (FL) by 5 pounds and 4 body fat percentage points. Results: The FH group repmied an average 14.6% mood reduction, whereas the FL and A feedback groups showed very little change in mood. In addition, self-compassion and body image served both as protective and as risk factors in the FH condition. Discussion: Findings suggest self-compassion and body image as impmiant targets of intervention for the prevention of depression and eating disorders because they may play an important role in how women subjectively experience weight and body fat related feedback

Transitioning into Academic Writing via a Soft CLIL Module on Immigration Issues

応用言語学における理論と実践 : 研究と教育を通し

The Lantern Vol. 61, No. 1, December 1993

• In Order to Succeed • Essay • Power of Human Self-Interest: Man vs. Car • In Setterich • Wandering Wanda • Maybe Kitchens • Saltiness • Homecoming • Perfect • Sincerely, Jen • A Midterm and a Paper • Prophet Junkie • Soundless Memo • After Ireland, Part 1https://digitalcommons.ursinus.edu/lantern/1142/thumbnail.jp

TFAP2 paralogs facilitate chromatin access for MITF at pigmentation and cell proliferation genes

Funding Information: This work was supported by grants from the National Institutes of Health (NIH) to RAC (R01-AR062457), a postdoctoral fellowship from the American Association for Anatomy to CK, and grants from the Research Fund of Iceland to ES (207067 & 217768). https://grants.nih.gov/grants/ funding/r01.htm https://www.anatomy.org https:// en.rannis.is/funding/research/icelandic-researchfund/ The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Publisher Copyright: © 2022 Kenny et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.In developing melanocytes and in melanoma cells, multiple paralogs of the Activating-enhancer-binding Protein 2 family of transcription factors (TFAP2) contribute to expression of genes encoding pigmentation regulators, but their interaction with Microphthalmia transcription factor (MITF), a master regulator of these cells, is unclear. Supporting the model that TFAP2 facilitates MITF's ability to activate expression of pigmentation genes, single-cell seq analysis of zebrafish embryos revealed that pigmentation genes are only expressed in the subset of mitfa-expressing cells that also express tfap2 paralogs. To test this model in SK-MEL-28 melanoma cells we deleted the two TFAP2 paralogs with highest expression, TFAP2A and TFAP2C, creating TFAP2 knockout (TFAP2-KO) cells. We then assessed gene expression, chromatin accessibility, binding of TFAP2A and of MITF, and the chromatin marks H3K27Ac and H3K27Me3 which are characteristic of active enhancers and silenced chromatin, respectively. Integrated analyses of these datasets indicate TFAP2 paralogs directly activate enhancers near genes enriched for roles in pigmentation and proliferation, and directly repress enhancers near genes enriched for roles in cell adhesion. Consistently, compared to WT cells, TFAP2-KO cells proliferate less and adhere to one another more. TFAP2 paralogs and MITF co-operatively activate a subset of enhancers, with the former necessary for MITF binding and chromatin accessibility. By contrast, TFAP2 paralogs and MITF do not appear to co-operatively inhibit enhancers. These studies reveal a mechanism by which TFAP2 profoundly influences the set of genes activated by MITF, and thereby the phenotype of pigment cells and melanoma cells.Peer reviewe

Analysis of zebrafish periderm enhancers facilitates identification of a regulatory variant near humanKRT8/18

Genome wide association studies for non-syndromic orofacial cleft (OFC) have identified single nucleotide polymorphisms (SNPs) at loci where the presumed risk-relevant gene is expressed in oral periderm. The functional subsets of such SNPs are difficult to predict because the sequence underpinnings of periderm enhancers are unknown. We applied ATAC-seq to models of human palate periderm, including zebrafish periderm, mouse embryonic palate epithelia, and a human oral epithelium cell line, and to complementary mesenchymal cell types. We identified sets of enhancers specific to the epithelial cells and trained gapped-kmer support-vector-machine classifiers on these sets. We used the classifiers to predict the effect of 14 OFC-associated SNPs at 12q13 near KRT18 . All the classifiers picked the same SNP as having the strongest effect, but the significance was highest with the classifier trained on zebrafish periderm. Reporter and deletion analyses support this SNP as lying within a periderm enhancer regulating KRT18 / KRT8 expression

Analysis of zebrafish periderm enhancers facilitates identification of a regulatory variant near human KRT8/18.

Genome-wide association studies for non-syndromic orofacial clefting (OFC) have identified single nucleotide polymorphisms (SNPs) at loci where the presumed risk-relevant gene is expressed in oral periderm. The functional subsets of such SNPs are difficult to predict because the sequence underpinnings of periderm enhancers are unknown. We applied ATAC-seq to models of human palate periderm, including zebrafish periderm, mouse embryonic palate epithelia, and a human oral epithelium cell line, and to complementary mesenchymal cell types. We identified sets of enhancers specific to the epithelial cells and trained gapped-kmer support-vector-machine classifiers on these sets. We used the classifiers to predict the effects of 14 OFC-associated SNPs at 12q13 near KRT18. All the classifiers picked the same SNP as having the strongest effect, but the significance was highest with the classifier trained on zebrafish periderm. Reporter and deletion analyses support this SNP as lying within a periderm enhancer regulating KRT18/KRT8 expression