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The Shapes of Family Conflict: Differentiating Adaptive and Maladaptive Parent-Child Conflict in Daily Life

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NICHD - Eunice Kennedy Shriver National Institute of Child Health and Human Development

PROJECT SUMMARY The overall goal of this application is to provide the principal investigator with targeted training in advanced methods for capturing and analyzing daily family dynamics relevant to child mental health. In the long term, the applicant intends to establish an independent research career focused on how everyday family processes shape children’s development, with the goal of informing interventions that strengthen family functioning and support mental health. To support this trajectory, the proposed training plan includes focused development in three key areas: (1) interdisciplinary collaboration to integrate technology into the study of family interactions, (2) advanced statistical methods for analyzing large, multimodal datasets, and (3) the conceptualization and dissemination of findings on adaptive and maladaptive family processes in daily life. Together, these components will lay the groundwork for a research career focused on advancing the science of family processes and enhancing interventions that support child and family well-being. Children’s exposure to family conflict can significantly shape their development, influencing both mental health symptoms and how they manage conflict in the future. While some conflicts promote problem-solving and emotional growth, others escalate into maladaptive patterns that increase the risk for mental health symptoms. Yet, key questions remain about the core features that distinguish adaptive from maladaptive conflict. This study addresses that gap by examining how conflict unfolds in daily life, focusing on natural escalation within individual episodes as well as broader day-to-day conflict patterns over two months. Findings will identify the features that contribute to maladaptive conflict, shedding light on when and how conflict becomes harmful. By identifying these distinguishing features, this research will inform the development of targeted interventions aimed at supporting healthier family relationships. This project addresses two complementary aims, offering both detailed and broad perspectives on parent-child conflict. The first aim takes a “zoomed-in” approach, examining naturally occurring conflict episodes captured through at-home audio recordings. It focuses on specific features such as baseline intensity and the trajectory of escalation, and how these dynamics are linked to same-day and next-day changes in child mood and parent- child interactions. The second aim takes a “zoomed-out” view, using ecological momentary assessment surveys to track daily patterns of conflict intensity, frequency, and duration over a two-month period. This broader approach will examine how families’ overall conflict patterns relate to child mental health symptoms and parent-child relationship quality. By integrating these two levels of analysis, the project will provide a more complete picture of how parent-child conflict unfolds in everyday life—offering valuable insights to guide interventions that strengthen family relationships and promote child well-being.

Up to $46K

Deadline: 2027-07-14

Health

Understanding environmental mitochondrial health

open

NIEHS - National Institute of Environmental Health Sciences

Mitochondrial function is fundamental to health, as soberingly demonstrated by the wide range of debilitating pathologies and diseases faced by patients with genetically-based mitochondrial deficiencies. Chemical exposure can directly affect mitochondrial function in many different ways, and can also dramatically exacerbate underlying genetic conditions. Because mitochondrial toxicants are common among pollutants, understanding the detailed mechanisms by which these chemicals affect mitochondria, and their interactions with genetic differences, is a highly significant environmental health problem. Unfortunately, the molecular and cellular impacts of different, specific mechanisms of mitochondrial toxicity are poorly understood, and the interactions of such exposures with genetic deficiencies are even more obscure. These knowledge gaps hinder testing, regulatory, and personalized medicine efforts. We seek to understand 1) the biological pathways that respond to mitochondrial DNA damage, especially irreparable mitochondrial DNA damage; 2) the molecular and cellular consequences of different, specific kinds of stressor-mediated changes to mitochondrial integrity and function; 3) how the effects of mitochondrial toxicants change in the context of human mitochondrial disease genes. To address these knowledge gaps, we are employing a translational approach integrating a powerful mechanistic in vivo laboratory model, Caenorhabditis elegans, with cell culture experiments including cells from mitochondrial disease patients. We will continue to define the molecular and cellular outcomes of different kinds of mitochondrial toxicity, and to identify novel biological pathways that defend mitochondria and the mitochondrial genome. We will test how deficiencies in these genes, and genes known to cause mitochondrial disease, alter sensitivity to mitochondrial toxicants, in both C. elegans and patient-derived cells. We are developing powerful transgenic tools that allow us to measure key aspects of mitocondrial function and dysfunction, including energetics, morphology, and alterations to redox tone, in a cell-specific fashion and in vivo, in C. elegans. We are deriving iPSCs and differentiated, mitochondrial disease-relevant cells for testing gene-environment interactions. Given the prevalence of both mitochondrial gene variability and mitotoxicant exposure, understanding the detailed mechanisms by which mitotoxicants act, the impacts of the genetic deficiencies, and their interactive effects will be impactful for many people. Addressing these scientific challenges will be transformative for human health by providing mechanistic knowledge critical to understanding cellular and higher-level effects of mitochondrial toxicity, informing treatment and personalized intervention options, and developing appropriate testing and regulatory strategies.

Up to $1.0M

Deadline: 2034-01-31

Health

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