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CE25-029 - Pathways Between Child Maltreatment and Self-Directed Violence: A Longitudinal, Population-Based Study Using Machine Learning Approaches

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NCIPC - National Center for Injury Prevention and Control

This K01 award application is for Dr. Lindsey Palmer, a PhD-trained social worker whose overarching career goal is to become an independent violence prevention scientist, focused on promoting child health and well- being by advancing data-driven, evidence-based strategies to prevent maltreatment and its long-term consequences. This K01 will support three key areas of career development: 1) the application of machine learning approaches on violence prevention research, 2) cross-cutting violence prevention strategies, and 3) professional development and leadership. Dr. Palmer has assembled an interdisciplinary mentoring team comprised of Kristine Campbell, MD, MSc, a nationally recognized expert in pediatric child maltreatment with extensive experience collaborating with public agencies to develop cross-system prevention efforts; Fernando Wilson, PhD, an expert in the application of machine learning techniques on large-scale databases to examine health services and policy; Brooks Keeshin, MD, an internationally recognized expert in trauma assessment and suicide prevention; and Angela Fagerlin, PhD an expert in faculty enhancement, leadership and representation. Over the past decade, rates of self-directed violence (SDV) have risen sharply, particularly among 10- to 17-year-olds, with children and adolescents who have experienced maltreatment being at particularly heightened risk. A staggering 57% of children and adolescents who die by SDV have a history of alleged child maltreatment, which encompasses physical abuse, sexual abuse, emotional abuse, physical neglect, and exposure to intimate partner violence. These youths often face the compounded challenges of trauma, family dysfunction, and mental health issues. While child welfare system (CWS) involvement frequently signals heightened vulnerability, the pathways linking child maltreatment to SDV remain poorly understood. Contributing factors such as parental mental illness, substance use, overlapping forms of maltreatment, family instability are not well defined or understood. Additionally, there is limited evidence on the effectiveness of CWS interventions in reducing the risk of SDV for these children. This study’s Specific Aims include: 1) Determine the relationship between child maltreatment and SDV, specifically: Establish how the timing, type, and frequency of child maltreatment indicators are associated with SDV; and characterize the association between child maltreatment intervention and SDV; and 2) Leverage machine learning based approaches to identify direct and indirect pathways between child maltreatment and SDV, focusing on the progression of suicidal thoughts and behaviors over time. This study is significant and innovative because it will clarify the relationship between child maltreatment and SDV, identify high-risk subgroups, and examine if existing CWS interventions mitigate or exacerbate SDV risk, providing critical insights into the strengths and limitations of current maltreatment practices in reducing other forms of violence.

Up to $150K
2028-09-29
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

CE25-149 - The effect of Medicaid expansion on medications for opioid use disorder, mental health care, and overdose mortality among formerly incarcerated people

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NCIPC - National Center for Injury Prevention and Control

PROJECT SUMMARY/ABSTRACT People involved in the criminal legal system (CLS) face a disproportionately high burden of substance and opioid use disorders (SUD/OUD), which upon release from jail or prison is compounded by lack of access to care and results in extremely elevated post-release drug overdose mortality. Few interventions have been able to reduce overdose risk among CLS-involved people. A number of ongoing studies are testing strategies for linking CLS-involved people to medications for OUD (MOUD) in the community. However, lack of insurance for many CLS-involved people makes these care linkages unsustainable after study completion. Medicaid expansion provides an avenue to address healthcare needs for many CLS-involved people. Recent studies show that pre-release Medicaid enrollment increases post-release MOUD and reduces overdoses for CLS-involved people. However, benefits appear to accrue to white individuals and not to black individuals – a concerning inequity because overdose deaths are rapidly increasing among racially minoritized people in the US. Research to date, which has been ecological, has not been able to identify the mechanisms by which Medicaid enrollment may improve MOUD and overdose outcomes and why these benefits may differ across racialized groups. Large, longitudinal, individual level data can map the pathways through which Medicaid expansion benefits some groups but not others. While overdose prevention work among CLS-involved people deservedly focuses on MOUD access, the role of mental health treatment is also critical. Two-thirds of people with OUD have co-occurring mental health needs, a burden that is likely even higher among CLS-involved individuals. Hence, MOUD without mental health care may fall short in MOUD engagement and overdose prevention for CLS-involved individuals. In this application, we propose to conduct a quasi-experimental study, by leveraging the 2023 Medicaid expansion in North Carolina (NC), to examine racialized inequities in enrollment in Medicaid among CLS- involved individuals, as well as post-release MOUD and mental health care access. We will further examine the impact of enrollment in Medicaid and MOUD and mental health care access on fatal and non-fatal drug and opioid overdoses. We will use 13 years of Big Data (2013-2025) on all formerly incarcerated people in NC linked with Medicaid and death records, which our team already has access to through two ongoing studies focused on suicide and polydrug overdose prevention. Our study is aligned with RFA-CE-25-149’s Funding Option A. This study will be the first to examine the individual-level impact of Medicaid enrollment, MOUD access, and mental health services on drug and opioid overdoses among CLS-involved people. This study will further identify mechanistic factors that contribute to racialized inequities among CLS-involved people to help enhance and sustain linkage to care for all CLS-involved people, but especially racially minoritized individuals, thereby enhancing the impact of Medicaid expansion for all people.

Up to $349K
2028-09-29
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Cellular and circuit mechanisms underlying the generation, regulation, and flexibility of value representations in mouse medial prefrontal cortex

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NIMH - National Institute of Mental Health

Project Summary/Abstract Most sensory stimuli acquire value through learning and experience. While progress has been made in deline- ating the circuits involved in sensory value-guided behaviors, the cellular and circuit mechanisms that underlie how distinct value representations are formed during learning, regulated during behavior, and modified to ac- commodate changes in cue-outcome contingencies remain unclear. Resolving these open questions is a funda- mental challenge in neuroscience and will advance our understanding of how synaptic plasticity induced by reinforcement learning is maintained, yet behaviors remain adaptive. The overarching goal of this proposal is to seek a mechanistic understanding of the circuits underlying value-guided learning and action in the mouse me- dial prefrontal cortex (mPFC), a region essential for the imposition of value on sensory stimuli to guide behavior. Using an olfactory-based appetitive classical trace conditioning task in combination with high-density electro- physiological recordings and optogenetics, I will focus on how functionally distinct yet spatially intermingled pop- ulations of neurons encoding rewarded (conditioned stimuli, CS+) and unrewarded (CS-) odors interact within the local network to drive stable yet flexible reward-seeking behaviors. I will test the hypothesis that the CS+ and CS- populations form a mutually inhibitory circuit that underlies their behaviorally-opposing roles in reward-seek- ing (Aim 1, K99). I will investigate how the existence of a CS- population may represent a circuit mechanism to permit the maintenance of prior reinforcement despite the extinction of learned behavior, thus uncovering a pre- viously unappreciated role for the CS- ensemble in reinforcement learning (Aim 2, K99). In my R00 phase, I will interrogate the mechanisms by which CS+ and CS- representations arise during learning, testing the hypothesis that distinct inputs to the mPFC drive the reinforcement of odors predicting the presence or absence of reward (Aim 3a,b). Further, I will study how the CS+ and CS- representations are updated when cue-outcome contin- gencies are reversed (Aim 3c). Finally, I will model the mPFC circuit to reveal fundamental principles on value- guided learning, which will inform future experiments and also extend the insights that could be gained beyond that which is feasible by experimentation (Aim 3d). This work will have broad implications for various neuropsy- chiatric conditions in which adaptive value-guided learning is disrupted, including addiction and depression. Can- didate and Career Goals. I aim to establish an independent research program investigating the neural basis by which value representations are generated and flexibly regulated to support context-dependent behaviors. I have extensive experience in molecular and systems neuroscience and have developed foundational tools and in- sights for studying value learning. Career Development Plan. I will be trained by my mentors Drs. Richard Axel and Larry Abbott. Dr. Axel is a foremost leader in sensory neuroscience, who will guide me on all aspects of experimental design. Dr. Abbott is a world-renowned theorist who will provide training in the analysis and mod- eling of complex datasets. All mentors will provide career development training for my transition to independence.

Up to $127K
2028-03-31
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Characterization of striatal dopamine dynamics in Shank3-/- mice during postnatal development

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NIMH - National Institute of Mental Health

Abstract Autism spectrum disorders (ASD) are neurodevelopmental conditions marked by early-emerging deficits in social behavior, restricted interests, and motor abnormalities. Converging genetic and clinical evidence implicates dysfunction of the dopaminergic (DA) system as a core feature of ASD pathophysiology. DA signaling is essential for the maturation of striatal circuits, which govern reward processing, motor learning, and emotional regulation. However, the developmental origins of dopaminergic dysfunction in ASD, and how genetic risk factors affect striatal DA signaling in vivo during early life, remain unknown. Mutations in SHANK3 are among the most penetrant genetic causes of ASD, and Shank3-deficient mice exhibit early striatal circuit abnormalities, impaired social behavior, and DA neuron dysfunction. Preliminary evidence suggests that loss of Shank3 disrupts DA neuron excitability and alters dopamine release dynamics in the nucleus accumbens (NAc) during ethologically relevant behaviors. However, technical challenges have historically limited in vivo monitoring of DA signaling in developing mouse pups, preventing direct investigation of this hypothesis. To address this gap, we have developed a novel fiber photometry platform optimized for postnatal mice (~P15) using tapered optical fibers, enabling stable, high-resolution recordings of striatal DA dynamics and neural activity during maternal and social interactions. We will combine this in vivo imaging approach with whole-cell electrophysiology and genetic tools to define the impact of Shank3 loss on the maturation of dopaminergic circuits. Aim 1 will quantify in vivo DA signaling in the NAc of P15 Shank3-/- and conditional DA neuron-specific Shank3 knockout mice during maternal and social interaction paradigms. Aim 2 will assess intrinsic excitability and HCN channel function in VTA DA neurons projecting to the NAc, comparing global and DA neuron-specific Shank3 knockouts to isolate cell- autonomous mechanisms of dysfunction. Together, these studies will provide the first real-time characterization of postnatal DA circuit dynamics in a genetically validated ASD model and identify a mechanistic link between Shank3 loss, HCN channel dysfunction, and DA signaling abnormalities. The proposed work will not only establish an innovative platform for studying DA function in early development but also define therapeutic targets for SHANK3-related disorders and other forms of ASD with disrupted striatal dopamine signaling.

Up to $437K
2028-05-31
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Characterizing intracortical feedforward and feedback sensory processes in ASD

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NIMH - National Institute of Mental Health

Project Summary Autism spectrum disorder (ASD) is a neurodevelopmental disorder long associated with functional connectivity abnormalities that are widespread throughout the brain. Despite countless studies on the topic, no single unifying model of functional connectivity abnormalities in ASD has emerged to date. Enthusiasm for studying functional connectivity differences in ASD has subsided in light of evidence of alterations that are more heterogeneous than some of the earlier hypotheses suggested, and because the links of these alterations to neural mechanisms of ASD have been challenging to map. Yet, one related theme that has garnered support has been that functional connectivity in ASD is increased in the bottom-up (or "feedforward") direction and decreased in the top-down (or "feedback) direction. Here, we propose to test a hypothesis that the functional characteristics of ASD are rooted in a fundamental imbalance between feedforward and feedback influences. This hypothesis stems from our preliminary data and prior studies, and it is motivated by many aspects of the ASD phenotype: These include increased perceived salience of sensory stimuli and evidence of reduced top-down control in ASD, which manifest across a range of atypical behaviors characteristic of the disorder. Thus far, mapping feedforward and feedback inputs non-invasively in the human brain has been methodologically challenging. Here we propose a multimodal neuroimaging approach, which combines (a) effective connectivity measures using millisecond temporal resolution magnetoencephalography (MEG) with (b) highly novel submillimeter-resolution layer- specific 7T functional MRI. We will use these advanced techniques to characterize feedforward and feedback flow of information along the auditory cortical hierarchy, in 90 ASD and 60 neurotypical (NT) adults, ages 21- 35, with average or above average IQ. Using our multimodal research design, which is firmly rooted in laminar neurophysiological recordings in non- human primates, we will pursue the following Specific Aims: (1) Test the hypothesis that feedforward inputs are abnormally increased in ASD relative to NT individuals; (2) Test the hypothesis that feedback inputs are abnormally decreased in ASD relative to NT individuals; (3) Test the hypothesis that the extent to which feedforward and feedback inputs in the ASD group are indeed different, is predictive of ASD severity and the extent of auditory processing deficits, assessed behaviorally. We expect that the results of this study will lead to a substantially more detailed, comprehensive, and mechanistically motivated framework for the wide range of functional connectivity abnormalities observed in ASD.

Up to $825K
2030-12-31
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Characterizing PrEP Need and Use in Eswatini: Individual and Programmatic Insights Through Data Triangulation and Novel Epidemiological Methods

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NIMH - National Institute of Mental Health

PROJECT SUMMARY/ABSTRACT Background. In Eswatini, adult HIV prevalence is over 31%, and national adult HIV incidence is the highest in the world at 7.77 new infections per 1,000 persons annually. While the country has almost met UNAIDS’ 95-95- 95 goals for epidemic control, HIV incidence is declining at a glacial pace, pointing to the need for comprehensive HIV prevention programs. Eswatini’s scale-up of HIV pre-exposure prophylaxis (PrEP) began in 2018, with nearly 100,000 individuals initiating PrEP in-country since. The proposed study will develop better methods to determine who could most benefit from PrEP (i.e., PrEP need) in Eswatini, and whether that need is being met at programmatic and individual levels, to inform future implementation of HIV prevention programs. Aims. In line with the NIMH Division of AIDS Research’s strategic priorities, this study will 1) compare models for predicting who could most benefit from PrEP in Eswatini; 2) compare novel PrEP-to-Need Ratios (PnRs) to original PnRs at the facility level; and 3) examine individual-level prevention-effective persistence and trajectories over time. Approach. This research will use data from the 2021 Eswatini Population-based HIV Impact Assessment (N=11,199) and Eswatini’s HIV-1 Recent Infection Surveillance (N~32,780) to build machine learning models to predict both recent and long-term but newly diagnosed HIV infections, providing insight into vulnerable subpopulations most in need of PrEP. Using routinely collected health facility data (N=150 facilities), PnRs will be created that account for heterogeneity in infection timing (i.e., recent vs. long-term), as well as subpopulation variability. Facilities will be compared over time. Lastly, using data from the DYnamics of Contraception in Eswatini (DYCE) Study (N=321), changes in PrEP need over time, relative to changes in use of PrEP and other prevention methods, will be assessed using an operationalization of prevention-effective persistence. Latent class analysis will be used to detect actionable differences between classes of prevention-effective persistence trajectories. Each aim is designed to identify gaps in HIV prevention efforts and guide the continued scale-up of PrEP in Eswatini to ultimately reduce HIV incidence. Training. Ms. Wallach’s training plan leverages her quantitative analysis and HIV research experience to advance her skills and launch her career as an independent HIV investigator. Her training goals are to develop a deep, nuanced understanding of PrEP need, gain experience working with and triangulating various data sources, gain skills in machine learning methods and latent class analysis, gain experience with longitudinal data analysis, and build capacity for effective research communication and dissemination. Under the guidance of her Primary Sponsor, Ms. Wallach will receive tailored mentorship from a team of experienced HIV researchers who work with the included data sources, conduct PrEP-related research, and have expertise in the advanced epidemiologic methods herein. Training will occur at Columbia University, a high-caliber institution with specialized research programs, including in infectious disease epidemiology, and that houses ICAP, a global health and HIV implementation and research organization.

Up to $50K
2028-02-29
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Characterizing the effects of the kynurenine pathway on blood-brain barrier disruption and CD14+CD16+ monocyte function in people with HIV and comorbid depression

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NIMH - National Institute of Mental Health

HIV is a major public health concern with 39.9 million people living with HIV as of 2023. Depression is the most common neuropsychiatric comorbidity seen in this population, affecting 30-50% of people with HIV (PWH), a prevalence almost two times greater than the general population. Depression in PWH is associated with increased morbidity and mortality. Thus, understanding the neurobiological mechanisms underlying depression in PWH is highly important. We propose that HIV-associated depression is mediated by activation of the kynurenine pathway (KP). Recent data from our group show that increased quinolinic acid (QUIN) and decreased kynurenic acid (KynA), both KP metabolites, are associated with depression and anhedonia severity in women with HIV, suggesting a role for the KP in depression pathogenesis in PWH. However, the mechanisms by which the KP drive depression pathogenesis are not characterized. We will examine mechanisms by which the KP contributes to depression in PWH. We hypothesize that the KP is mediating HIV-associated depression pathogenesis through its effects on the blood-brain barrier (BBB) and CD14+CD16+ monocyte function, which have both been implicated in depression and HIV neuropathogenesis. We will investigate this hypothesis with the following aims: Specific Aim 1: Assess the effect of KP metabolites on BBB permeability and function of CD14+CD16+ monocytes matured and infected with HIV in vitro. We will characterize mechanisms through which KP metabolites increase in vitro BBB permeability and transmigration and inflammatory function of CD14+CD16+ monocytes matured and infected with HIV in vitro. We will test effects of KYN, QUIN, and KynA on BBB permeability and TJP as a mechanism for BBB disruption. We will examine transmigration and inflammatory mediator production of KYN-treated in vitro matured and HIV-infected human CD14+CD16+ monocytes. Hypotheses: 1) QUIN, but not KynA, increases BBB permeability by altering BBB TJP; 2) KYN increases migration across the BBB and inflammatory mediators of CD14+CD16+ monocytes. Specific Aim 2. Examine the associations between peripheral KP activity, in vitro BBB permeability, CD14+CD16+ monocyte transmigration, and depressive symptom severity in PWH and PWoH. We will enroll 70 virally suppressed PWH and 70 PWoH and evaluate them for depression/anhedonia severity. Using plasma and PBMC from participants, we will assess peripheral KP activity, BBB permeability, and CD14+CD16+ monocyte transmigration. Multivariate analyses will determine associations of KP metabolites, BBB permeability, and PBMC transmigration with depression/ anhedonia severity in both groups. Hypothesis: Increased peripheral QUIN, decreased KynA, increased BBB permeability, and increased CD14+CD16+ monocyte transmigration will correlate with greater depression/ anhedonia severity in PWH. Impact: Understanding the effects of KP dysregulation on BBB integrity and monocyte function in the context of HIV and depression may identify targets to mitigate depression in PWH, enhancing quality of life and survival.

Up to $50K
2028-03-24
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Characterizing the role of anandamide in trauma-related hyperarousal during the menopause transition

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NIMH - National Institute of Mental Health

Posttraumatic stress disorder (PTSD) is a debilitating mental health condition that disproportionately affects women, particularly those from underserved populations who face higher rates of trauma exposure. PTSD is associated with trauma-related hyperarousal (TRH), which is characterized by increased psychophysiological hyperarousal, including exacerbated fear-potentiated startle, deficits in fear extinction, and increased skin conductance response to trauma reminders. Despite evidence perimenopausal women exhibit peak PTSD prevalence rates and greater symptom severity compared to younger, reproductive-aged women, the biological mechanisms underlying this increased vulnerability to the psychological consequences of hormonal variation remain unclear. The current study aims to investigate the role of the endocannabinoid system, specifically anandamide (AEA), in modulating the severity of TRH during the menopause transition in Black women. The proposed research will test the hypothesis that lower AEA concentrations over the menopause transition will be associated with decreased estradiol concentrations and increased TRH. We will employ a combination of psychological assessments, fear conditioning paradigms, and biological measures to provide a comprehensive understanding of the mechanisms driving TRH exacerbation during perimenopause. The findings from this research have the potential to inform the development of targeted interventions for trauma-exposed women during this critical period of vulnerability. In addition, the F32 fellowship under the guidance of a distinguished mentoring team will provide the applicant with essential training in clinical and translational women's health research, neuroendocrinology, psychophysiology, advanced statistical methods, and scientific communication. This training will be crucial for the applicant's career development as an independent researcher focused on investigating the impact of trauma on women's health across the lifespan, particularly in underserved populations who suffer disproportionately from the adverse health impacts of trauma exposure.

Up to $83K
2029-03-31
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Chemi-Knock: Achieving rapidly inducible loss-of-function in live animal brains during memory consolidation

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NIMH - National Institute of Mental Health

PROJECT SUMMARY Memory consolidation is an important process in memory retention, whereby short-term memories are transformed into long-term ones. Memory retention is facilitated when novel or salient experiences occur within 1-2 hours before or after memory encoding. Novelty-induced memory consolidation relies on the locus coeruleus-hippocampus pathway and involves the de novo synthesis of an–as–yet–unidentified group of proteins known as plasticity-related proteins (PRPs) in the hippocampus. These PRPs are thought to play a critical role in memory consolidation by stabilizing synaptic plasticity. However, the precise mechanism through which these newly synthesized PRPs facilitate the consolidation of synaptic plasticity and memory in the hippocampus remains unclear. This uncertainty primarily arises from the limited availability of loss-of-function techniques capable of perturbing the function of the target PRP with a minute temporal resolution and selectively within this memory process. This project aims to develop innovative molecular tool, using chemical-based manipulation, that enable the rapid and precise inactivation of endogenous target proteins in specific cell types during memory consolidation without genetic modification. Specifically, upon a chemical trigger, our new tool is designed to relocate a target PRP from its active site to other subcellular locations within a timeframe of minutes. This relocation can be achieved in specific neuron types in the hippocampus of freely moving rats undergoing memory tasks. To demonstrate the utility of this tool, we have selected activity-regulated cytoskeleton associated protein (ARC), one of the major PRPs, as a model target. Success in this endeavor will not only shed light on the elusive molecular mechanisms of memory consolidation by identifying key PRPs but also potentially reveal new pharmacological targets to improve memory retention. Moreover, the flexible and modular nature of this genetically encoded tool opens the door to its use in a broad range of biological applications beyond memory research.

Up to $428K
2028-04-30
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Chronic Illness Self-Management in Children and Adolescents (R01)

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National Institutes of Health

-Purpose. The purpose of this Funding Opportunity Announcement (FOA) issued by the National Institute of Nursing Research (NINR), the National Institute of Child Health and Human Development (NICHD), the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), the National Cancer Institute (NCI), and the Office of Dietary Supplements (ODS) is to solicit research to improve self-management and quality of life in children and adolescents with chronic illnesses. Biobehavioral studies of children in the context of family and family-community dynamics are encouraged. Children diagnosed with a chronic illness and their families have a long-term responsibility for self-management. The child with the chronic illness will have a life-long responsibility to maintain and promote health and prevent complications. Research related to biological/ technological factors, as well as, sociocultural, environmental, and behavioral mechanisms that contribute to successful and ongoing self-management of chronic illnesses in children is also encouraged. This FOA is restricted to studies of chronic illnesses in children and adolescents ages 8 to 21 grouped by developmental stages according to the discretion of the investigator. Studies of chronic mental illness or serious cognitive disability are beyond the scope of this FOA. -Mechanism of Support. This FOA will utilize the NIH Research Project Grant (R01) award mechanism and runs in parallel with FOAs of identical scientific scope, PA-07-099, that solicit applications under the R21 mechanism, and PA-07-098, that solicit applications under the R03 mechanism. -Funds Available and Anticipated Number of Awards. Awards issued under this FOA are contingent upon the availability of funds and the submission of a sufficient number of meritorious applications.

rolling
Education

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Chronic Illness Self-Management in Children and Adolescents (R03)

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National Institutes of Health

-Purpose. The purpose of this Funding Opportunity Announcement (FOA) issued by the National Institute of Nursing Research (NINR), the National Institute of Child Health and Human Development (NICHD), the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), the National Cancer Institute (NCI), and the Office of Dietary Supplements (ODS) is to solicit research to improve self-management and quality of life in children and adolescents with chronic illnesses. Biobehavioral studies of children in the context of family and family-community dynamics are encouraged. Children diagnosed with a chronic illness and their families have a long-term responsibility for self-management. The child with the chronic illness will have a life-long responsibility to maintain and promote health and prevent complications. Research related to biological/ technological factors, as well as, sociocultural, environmental, and behavioral mechanisms that contribute to successful and ongoing self-management of chronic illnesses in children is also encouraged. This FOA is restricted to studies of chronic illnesses in children and adolescents ages 8 to 21 grouped by developmental stages according to the discretion of the investigator. Studies of chronic mental illness or serious cognitive disability are beyond the scope of this FOA.

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Education

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Chronic Illness Self-Management in Children and Adolescents (R21)

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National Institutes of Health

-Purpose. The purpose of this Funding Opportunity Announcement (FOA) issued by the National Institute of Nursing Research (NINR), the National Institute of Child Health and Human Development (NICHD), the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), the National Cancer Institute (NCI), and the Office of Dietary Supplements (ODS) is to solicit research to improve self-management and quality of life in children and adolescents with chronic illnesses. Biobehavioral studies of children in the context of family and family-community dynamics are encouraged. Children diagnosed with a chronic illness and their families have a long-term responsibility for self-management. The child with the chronic illness will have a life-long responsibility to maintain and promote health and prevent complications. Research related to biological/ technological factors, as well as, sociocultural, environmental, and behavioral mechanisms that contribute to successful and ongoing self-management of chronic illnesses in children is also encouraged. This FOA is restricted to studies of chronic illnesses in children and adolescents ages 8 to 21 grouped by developmental stages according to the discretion of the investigator. Studies of chronic mental illness or serious cognitive disability are beyond the scope of this FOA. -Mechanism of Support. This FOA will use the NIH Exploratory/Developmental (R21) grant mechanism and runs in parallel with FOAs of identical scientific scope, PA-07-097, that solicits applications under the R01 mechanism, and PA-07-098, that solicits applications under the R03 mechanism. -Funds Available and Anticipated Number of Awards. Awards issued under this FOA are contingent upon the availability of funds and the submission of a sufficient number of meritorious applications.

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Education

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Circuit Mechanisms of Social Attachment in the Prairie Vole Medial Amygdala

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NIMH - National Institute of Mental Health

Project Summary / Abstract Enduring social bonds are essential for human health and well-being, yet their underlying neural mechanisms remain elusive due to limitations in traditional model organisms. Prairie voles, which naturally form lifelong pair bonds, offer a powerful system for investigating how the brain encodes stable social states. The medial amygdala (MeA) is functionally connected to a broad network of brain regions that collectively governs social behavior. Specifically, the MeA relays pheromonal cues that are critical for guiding context- appropriate behavior selection, yet how this region contributes to the behavior transition from a naïve to a bonded state in prairie voles is unknown. This proposal investigates how molecularly defined circuits in the MeA contribute to the emergence and maintenance of attachment behavior. Using single-cell RNA sequencing, I identified a sex-biased neuronal population that downregulates the neuropeptide gene Tac1 following pair bond formation. Intriguingly, the mouse equivalent of this population drives both affiliative and aggressive behaviors, and Tac1 itself has been linked to aggression control. In prairie voles, a bonded animal exhibits selective affiliation toward its partner and aggression toward all other opposite-sex conspecifics – a behavioral dichotomy that may be orchestrated by this population. I propose to characterize how this population is integrated into broader brain circuits of prairie voles and to monitor its activity during the formation of a pair bond. These experiments will clarify whether and how this population might serve as a neural substrate for the internal state of bondedness. Ultimately, this research may shed light on fundamental principles of social attachment and offer insight into how disruptions in such processes contribute to psychiatric illness. In addition to the proposed research, this application outlines a comprehensive training plan to prepare Dr. Wang for an independent career as a neuroscientist and psychiatrist. She will be mentored by Dr. Dev Manoli (UCSF), an expert in the molecular genetics and social behavior of prairie voles, and co-mentored by Dr. Michael Brainard (UCSF), a leader in the neurophysiology of complex behavior, and Dr. Vikaas Sohal (UCSF), who specializes in quantitative neural data analysis and circuit-level manipulations. Dr. Wang will also receive guidance on advanced molecular tool development from Dr. Nadav Ahituv (UCSF) and Dr. Josh Huang (Duke). Her career development is strongly supported by the UCSF Department of Psychiatry and Behavioral Sciences, which is committed to transitioning her to a full-time faculty position.

Up to $210K
2031-04-30
health research

Free to search & build · $99 one-time to unlock the application pack · No subscription

Clinical Research on Mental Illnesses in Older Adults (R01)

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National Institutes of Health

-Purpose. The purpose of this Funding Opportunity Announcement (FOA) issued by the National Institute of Mental Health (NIMH), National Institutes of Health (NIH), is to invite grant applications for clinical research that will reduce the burden of mental illnesses on older adults. The NIMH has a long-standing commitment to studying mental illnesses in older individuals. The intent of this FOA is to intensify investigator-initiated research in this area, to attract new investigators to the field, and to enhance interdisciplinary approaches to research. -Mechanism of Support. This FOA will utilize the NIH Research Project Grant (R01) award mechanism. Applications of identical scientific scope are solicited also under the NIH Small Research Grant (R03), the NIH Exploratory/Developmental Grant (R21), and the NIMH Clinical Exploratory Research Grant (R34) award mechanisms, responding to FOAs PA-06-180, PA-06-181, and PA-06-248, respectively. -Funds Available and Anticipated Number of Awards. Because the nature and scope of the proposed research will vary from application to application, it is anticipated that the size and duration of each award will also vary. The total amount awarded and the number of awards will depend upon the mechanism numbers, quality, duration, and costs of the applications received.

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Healthhealthcare

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