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Central Carolina Community Foundation

Central Carolina Community Foundation ($200M in assets) supports nonprofits in SC through grants focused on education, community development, health, arts. Awards range from $2,000 to $75,000.

Life Over Violence Education Group

The Life Over Violence Education Group would like to host a festive event at 352 Martin Luther King Jr. Way August 25th, to empower youth, build relationships, and share healthy dialogue, to create positive change and life advancement in the community. The community event will be including free food, face painting, back to school supplies, poetry, music and activities for children.

Central Indiana Community Foundation

Central Indiana Community Foundation ($1.0B in assets) supports nonprofits in IN through grants focused on education, community development, arts, health. Awards range from $2,500 to $200,000.

Central Minnesota Community Foundation

Central Minnesota Community Foundation ($150M in assets) supports nonprofits in MN through grants focused on education, community development, health, arts. Awards range from $1,000 to $50,000.

Central New York Community Foundation

Central New York Community Foundation ($300M in assets) supports nonprofits in NY through grants focused on education, community development, health, arts. Awards range from $2,000 to $100,000.

European Commission - ERASMUS2027

Centres of Vocational Excellence. Call: Centres of Vocational Excellence. Programme: ERASMUS2027. Keywords: Agri-food, Agriculture, Air and water pollution control, Architecture and building, Arts, Biology, Building, Circular economy, Computer sciences - Operating systems (software development only), Craft skills, E-virtual, Education, Electricity, Electronics, Engineering and engineering trades, Entrepreneurship, Environmental protection, Food and drink processing, Foreign languages and cultures, Health, Health and welfare, Horticulture and gardening, Hotel and catering, ICT based learning, ICT's interoperability in education, Inclusion, Informal and non formal learning, Innovation in learning, teaching and assessment practices supported by digital technologies, Inter generational learning, Key competences, Life sciences, Manufacturing and processing, Medicine, Metal work, Mining and extraction, Road motor vehicla operations, Seafood biotechnology, Social Care, Social Media, Sports and leisure, Textiles, Tourism, Travel and tourism, Vocational training, aerospace and defence, construction, digitalisation, green skills, work-based learning. Open call from the EU Funding & Tenders Portal.

NINDS - National Institute of Neurological Disorders and Stroke

PROJECT SUMMARY Autonomic dysfunction remains underdiagnosed and misunderstood but is a significant healthcare burden that affects millions of people in the United States. Autonomic disturbances are present in 40% of neurodegenerative diseases like Parkinson’s disease, Alzheimer’s disease, and other dementias and is often coupled with higher markers of cerebrovascular pathology. In this context, cerebrovascular health and autonomic function may be linked, but the connection is unknown. Additionally, little is understood about the contribution of autonomic dysfunction in tandem with drivers of cerebrovascular pathology on vascular contributions to cognitive impairment and dementia (VCID). The overarching objective of this proposal is to elucidate the link between drivers of cerebrovascular pathology and autonomic dysfunction and identify the impact on VCID biomarkers. Our preliminary data demonstrate that elevated cerebral pulsatility is associated with greater VCID biomarkers (e.g. white matter hyperintensities, WMH) in cognitively normal adults, and our published data demonstrate that adults with lower cardiovascular responses to physiological stressors are associated with greater WMH in healthy adults. Therefore, the central hypothesis is that disrupted cerebral hemodynamics will associate with impaired autonomic function, and together these contribute to greater VCID biomarkers. To test this hypothesis, I will use state-of-the-art magnetic resonance imaging (MRI) and the novel 4D flow MRI technique to measure cerebral hemodynamics (e.g., cerebral pulsatility and cerebral blood flow, CBF) in collaboration with experts in the field of MRI (e.g., Dr. Wieben, Co-sponsor). Additionally, I will use gold-standard techniques to directly measure autonomic function (e.g., sympathetic nerve activity, SNA; baroreflex sensitivity, BRS; and cardiovascular responses). Lastly, I will assess VCID neuroimaging biomarkers (e.g. WMH and cerebrovascular reactivity, CVR), and evaluate the associations between cerebral hemodynamics or autonomic function and these VCID biomarkers. Aim 1 will examine cerebral hemodynamics in middle-aged adults with and without symptoms of autonomic dysfunction. Aim 2 will determine the impact of cerebral hemodynamics and autonomic function on VCID biomarkers in middle-aged adults with and without symptoms of autonomic dysfunction. Collectively, these data will determine the link between cerebral hemodynamic and autonomic function and their contributions to brain health. The proposed work, in conjunction with the comprehensive training plan, will assist in the development of a scientific niche in the field and ensure success through the transition from a predoctoral trainee to a postdoctoral fellowship position. In addition, outcomes from this project will have broader implications for how to prevent or treat autonomic dysfunction that could also benefit brain health.

NIAID - National Institute of Allergy and Infectious Diseases

ABSTRACT Viruses contain genetic material in DNA or RNA composed of nucleotides. For RNA, these nucleotides are A (adenine), C (cytosine), G (guanine), and U (uracil). Two nucleotides linked by a phosphate molecule, such as UA or CG, are called dinucleotides. Many RNA viruses, including flaviviruses, have evolved to mimic the low cytosine-phosphate-guanine (CG) dinucleotide content of vertebrate genomes to evade recognition by host zinc finger antiviral protein 1 (ZAP), which binds CG-rich or CG-enriched non-self RNA and targets it for degradation. Many viruses have also evolved reduced uracil-phosphate-adenine (UA) dinucleotide content to evade RNA- degrading enzymes and possibly ZAP. Enrichment of CG and UA dinucleotides in viral RNA is an emerging promising vaccine approach. In addition to vaccines, dinucleotide enrichment is an emerging approach for oncolytic viruses. A critical knowledge gap for the further rational development of safe and protective vaccines and effective oncolytic viruses is the lack of understanding of innate cellular immune responses to viruses carrying CG/UA-enriched RNA. Thus, in this project, we will study how peripheral and lymphoid dendritic cells (DCs) interact with CG-, UA-, and CG/UA-enriched viruses. Understanding interactions with DCs is significant because they are essential for initiating the early activation of inflammatory monocytes and adaptive T cell responses. Moreover, many viruses, such as flaviviruses like West Nile virus (WNV), have evolved to impair DC activation and DC-mediated stimulation of T cell antiviral responses. We will leverage characterized CG-, UA-, and CG/UA-enriched WNV variants, as well as the WNV–human peripheral DC–T cell interaction model. We will also use the conventional and ZAP knockout C57BL/6J mouse models to study interactions with lymphoid DCs. Unlike many human viruses, WNV is virulent in conventional C57BL/6J mice, which facilitates immune response studies. Classical virology and flow cytometry assays, bulk RNA-seq, and state-of-the-art single-cell RNA-seq will be used in the project. We will provide the first insights into how CG-, UA-, and CG/UA dinucleotide-enriched viruses interact with essential DC populations, and whether dinucleotide enrichment can overcome DC impairment and T cell dysfunction induced by wild-type virus infection. This project will advance the rational development of enriched vaccines and oncolytic viruses that selectively activate dinucleotide-specific beneficial immune pathways.

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY Antiretroviral drug therapy (ART) is the gold standard for HIV therapy for suppressing HIV infection. However, these small molecule drugs cannot eliminate the viral reservoir and thus, ART is a life-long therapy. Broadly neutralizing antibodies (bNAbs) could supplement ART and be used to reduce the viral reservoir through their Fc effector functions. While passive infusion of multiple active bNAbs can suppress viremia after ART is lifted, this strategy still requires the need for multiple infusions to maintain therapeutic concentrations of the bNAbs. We have been using adeno-associated virus (AAV) vectors to deliver HIV bNAbs, SIV bNAbs, and antibody-like inhibitors. AAV vectors provide means for long-term expression of bNAbs at concentrations capable of maintaining viral suppression via a one-time intramuscular administration. One issue that has been plaguing the field, especially in nonhuman primate models, is the development of host anti-drug antibodies and immune responses against the expressed bNAbs. We have recently demonstrated that targeting the immune checkpoint pathway is a promising target to limit the host immune response after vector administration. This work has resulted in consistent expression of two HIV bNAbs in rhesus macaques at concentrations thought to be in therapeutic range to suppress an HIV or SIV infection. Additionally, our work in developing eCD4-Ig, an antibody-like HIV entry inhibitor, has produced promising prophylaxis results in rhesus macaques against SHIV and SIV challenges. Because eCD4-Ig neutralizes all HIV-1, HIV-2, and SIV isolates and no escape mutations have been identified to date, it is a powerful inhibitor to combine with bNAbs for HIV and SIV therapy. Unlike ART, both antibodies and eCD4-Ig can kill infected cells, thus, providing a promising strategy to reduce and eliminate the viral reservoir. Therefore, we hypothesize combining AAV-delivered eCD4-Ig with antibodies would generate a unique viral reservoir upon suppression in the absence of ART, both characteristically and quantitatively. In Aim 1, we will optimize our AAV delivery strategy for multiple SIV antibodies and eCD4-Ig. In Aim 2, we will characterize and quantify the viral reservoir upon suppression when mediated by SIV bNAbs and eCD4-Ig compared to ART. In Aim 3, we will determine whether AAV-delivered SIV bNAbs and eCD4-Ig can increase the rate of viral reservoir decay compared to ART. These results would provide a foundation for AAV-delivered inhibitors as an alternative to ART and move the field closer to realizing an HIV cure.

NIMH - National Institute of Mental Health

HIV persists in central nervous system (CNS) reservoirs despite effective combination antiretroviral therapy (ART), contributing to chronic neuroinflammation and neuropathogenesis. While macrophages and microglia are known cellular reservoirs in the CNS, recent evidence suggests that infiltrating T cells also play a critical role in sustaining viral persistence. Limited access to human CNS tissues hampers our understanding of contributions of the CNS T cell reservoir in HIV neuropathogenesis. To closely examine the effects of HIV infection in the CNS, we will leverage a unique barcoded HIV system in a novel humanized mouse model to study CNS-resident viral reservoirs. Our preliminary data demonstrate that this barcoded HIV, which allows us to track and characterize virus that is being produced from different anatomic reservoirs, establishes a robust infection in both peripheral and CNS tissues, with RNA sequencing revealing upregulated type I interferon signaling and microglial activation, indicating HIV driven chronic neuroinflammation in vivo. Additionally, we have previously demonstrated in non-human primate (NHP) studies that HIV-specific chimeric antigen receptor (CAR) T cells that developed from gene modified hematopoietic stem/progenitor cells (HSPCs) can traffic to the CNS and reduce viral burden, indicating that there are ways to specifically deliver therapeutic antiviral T cells to the CNS. These findings highlight a need to define the mechanisms underlying T cell-mediated viral persistence in the CNS and to optimize CNS reservoir-targeted therapies. In these studies, we propose an integrated approach using barcoded HIV tracking, spatial transcriptomics, single-cell RNA sequencing, and integration site analysis to investigate the contributions of T cell populations in HIV persistence and inflammation in the CNS. Our central hypothesis is that T cells serve as key latent reservoirs in the CNS, promoting chronic immune activation, and that HSPC-derived CAR T cell therapy can effectively target and reduce these reservoirs. To test this hypothesis, we will: 1) Assess T cell reservoirs in the CNS during acute and chronic phase of HIV infection in humanized mice infected with barcoded HIV. 2) Investigate the contributions of T cell populations on CNS inflammation and neuropathogenesis during HIV infection. 3) Evaluate the antigen-specific T cell responses and therapeutic effects of CAR T cells on viral reservoir clearance and neuropathogenesis in the CNS. This study will provide critical insights into the role and consequences of T cell-mediated HIV persistence in the CNS and assess CAR T cells as a novel strategy for reservoir clearance and neuroinflammation reduction, advancing HIV cure strategies.

NIDA - National Institute on Drug Abuse

PROJECT SUMMARY Opioid receptors not only mediate pain relief but also act as the targets of potent exogenous opioids that are devastatingly addictive and cause overdose deaths. The principal target for both analgesia and addiction of exogenous opioids is the µ-opioid receptor (µOR). While traditionally thought to be regulated exclusively by opioids, recent work from our group has detailed an unexpected layer of complexity: endogenous neuromodulators such as endocannabinoids and oxytocin – classically associated with their own independently signaling receptors that regulate mood, pain, inflammation, and social behavior – can directly work to allosterically modulate µOR signaling. This unanticipated ligand-mediated crosstalk opens an entirely new dimension in opioid receptor pharmacology and suggests that targeting these pathways could yield novel interventions for opioid use disorder (OUD) and related conditions. The central goal of this project is to elucidate, at atomic resolution, the molecular mechanisms by which endogenous neuromodulators influence µOR structure and function. We will employ state-of-the-art cryo-electron microscopy (cryoEM) approaches to determine high- resolution structures of µOR in both its active and inactive states, bound to cannabinoids and neuropeptides like oxytocin. Critically, we will advance methodological innovations in time-resolved cryoEM to directly visualize the intermediate conformational states and the full activation/inactivation pathway of the receptor as it transitions between these endpoints. This will allow us, for the first time, to construct “molecular movies” that reveal the stepwise mechanisms by which natural modulators influence receptor activation, allostery, and signaling bias. Through these detailed structural insights, we aim to identify previously unrecognized allosteric sites and intermediate states that serve as "control points" for selective pharmacological intervention. These discoveries will inform the rational design of new therapeutic strategies that harness or mimic the brain’s own modulatory systems, offering a pathway to safer, more targeted treatments for OUD, pain, and overdose. In summary, this project will not only clarify the molecular basis of opioid receptor regulation in the brain, but will also set the stage for mechanism-driven drug discovery to address the current opioid crisis and advance our broader understanding of GPCR biology.

NCI - National Cancer Institute

PROJECT SUMMARY The Fanconi anemia (FA) pathway is involved in several key processes required to maintain genome stability. It promotes the repair of DNA lesions, such as inter-strand crosslinks (ICLs) and DNA double strand breaks. It is also involved in protecting nascent DNA from degradation and preventing the accumulation of single-strand DNA (ssDNA) gaps during DNA replication. FA pathway proteins also favor the resolution of RNA-DNA hybrids (R-loops), which form as a result of transcription. Mutations in FA pathway genes cause Fanconi anemia, a genetic disorder associated with bone marrow failure, developmental abnormalities, and an increased risk of hematological malignancies and solid tumors. Mutations in FA pathway genes also predispose to hereditary breast and ovarian cancer, and they have been observed in more than a third of somatic tumors. Current treatments for cancers with FA pathway defects often involve the use of DNA crosslinking agents or PARP inhibitors. However, these treatments can lose effectiveness over time as cancer cells develop resistance. To improve therapeutic outcomes, it is therefore critical to systematically define factors required for the survival of FA pathway-deficient cancer cells. In preliminary work, we conducted high-throughput genetic interaction studies to identify dependencies of mammalian cells deficient for FA pathway genes. This work identified synthetic lethal interactions between the FA pathway and the DNA repair genes GEN1, CIP2A and RHNO1. The main goals of this proposal are to characterize mechanistically the synthetic lethal relationships between these genes and the FA pathway and determine their relevance in cancer. In particular, we propose 1) to investigate the genetic dependency of cells deficient in the FA pathway on GEN1, CIP2A and RHNO1; 2) to define the endogenous sources of replication stress that sensitize cells deficient in the FA pathway to the loss of GEN1, CIP2A and RHNO1; 3) to explore the loss of GEN1, CIP2A or RHNO1 as a cancer vulnerability in the context of FA pathway deficiency and FA gene mutations. Our approach will utilize state-of-the-art CRISPR combinatorial knockout and base editing screens, coupled with functional characterization of genetic interactions and mutations using molecular and cell biology assays. We expect that these studies will advance our understanding of the interactions of the FA pathway with other DNA damage response pathways and identify vulnerabilities that could be exploited for the development of personalized therapies for FA pathway-deficient tumors.

NIDA - National Institute on Drug Abuse

Project Summary Millions of individuals are affected with substance use disorders (SUD), posing a significant burden on these individuals, their families, and communities. There is a substantial comorbidity between SUD and HIV infection. HIV is also a risk factor for SUD because of the increased use of opioid pain medications that may lead to opioid addiction. The Single-Cell Opioid Responses in the Context of HIV (SCORCH) consortium was formed to gain insights into cellular and molecular responses in different brain regions to SUD and HIV by collecting single-cell transcriptomic and epigenomic data in affected brain regions from hundreds of human donors, as well as from animal models. It has been observed that SUD and HIV comorbidity may exacerbate cellular dysfunction beyond the effects of each condition alone, and the data generated by the SCORCH consortium provide opportunities for a comprehensive characterization of cellular states across conditions including control, HIV, OUD, and HIV+OUD. Preliminary data show substantial heterogeneity in molecular phenotypes across samples with the same exposure, e.g., HIV and SUD. Our premise is that the identifications of genetic variants mediating the effects of exposures to HIV and SUD will offer a unique angle to understand how different cell types in different brain regions respond to the exposures, and such understanding through genetic heterogeneity among individuals can lead to novel insights and clinical applications. We will apply state-of-the-art integrative methods to investigate how genetic variants affect molecular phenotypes in different cell types across brain regions with different exposure. We will accomplish this goal through three specific aims. The first aim will analyze total read counts from a transcript/isoform or peak using Bayesian methods that explicitly model shared genetic effects to borrow information across cell types and brain regions to increase statistical power. We will perform eQTL, caQTL, and isoQTL analyses. We will also leverage the multi-omic data to infer gene regulation networks and conduct grQTL analysis. The second aim will consider allele-specific analysis to complement analyses based on total counts. We will then combine allele-specific results with total read count results. To further improve statistical power, we will integrate SCORCH data with external data sets, computationally predicted effect sizes for genetic variants, and transfer known QTLs. We will develop gene expression and chromatin accessibility imputation models to facilitate genome-wide association studies. We will work with the SCORCH team to share our results with the broader scientific community. This project will be co-led by Dr. Hongyu Zhao, Dr. Mark Gerstein, and Dr. Ke Xu, who have complementary expertise covering statistical genetics/genomics, computational biology, single-cell analysis, SUD genetics, and HIV research.

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY The persistence of latent viral reservoirs is a major obstacle to curing HIV, as it causes viral rebound when antiretroviral therapy (ART) is interrupted. Current strategies for an HIV cure, such as "shock and kill," "block and lock," broadly neutralizing antibodies, chimeric antigen receptors, and therapeutic vaccines, focus largely on subtype B and overlook Africa, which bears the highest burden of HIV. Africa, home to two-thirds of global HIV cases, has significant genetic diversity in HIV subtypes, including HIV-1, recombinant forms, and HIV-2. HIV-2, found mainly in West Africa, constitutes 10–20% of regional HIV cases, yet little is known about its latent reservoirs, particularly in dual HIV-1/2 infections. This study aims to address this gap by investigating HIV-2 latent reservoirs and their interactions with HIV-1 in dual infections, focusing on a cohort in Ghana. A cohort of 74 virologically suppressed individuals with dual infections will be used. The team’s expertise includes developing assays to quantify viral DNA and RNA specific to HIV-2. Aim 1 focuses on quantifying reservoir sizes in CD4+ T-cell subsets (central, transitional, and effector memory) and monocytes across HIV-1, HIV-2, and dual infections. Previous studies have explored reservoirs in ART-naïve people living with HIV-2 but not in virologically suppressed or dual-infected individuals. Methods include cell-associated DNA PCR, RNA analysis, quantitative viral outgrowth assays (QVOA) and intact proviral DNA assay (IPDA). Aim 2 will create an HIV-2 latency model using cell lines like Jurkat and THP-1 and test latency-reversing agents (LRAs) on ex-vivo samples from virologically suppressed people. The team will adapt existing fluorescence-based tools for HIV-2 and measure viral reactivation using gag mRNA quantification. The outcomes will provide critical insights into the HIV-2 reservoir and its impact on HIV-1 in dual infections, laying the groundwork for cure strategies that extend to the USA and globally, as HIV-2 has been identified in other regions, including the USA, due to migration. Understanding HIV-2 reservoir dynamics and latency reactivation will inform the development of new ways to tackle HIV-1 which will benefit PWH in the USA as well. Findings from the study could advance global HIV cure research on reservoir characteristics, measurement tools, and therapeutic approaches that address different viral subtypes and dual infections. The proposal aligns with exploratory R21 mechanisms and has the potential to significantly advance HIV cure research in the USA and globally.

Department of Cultural Affairs and Special Events

TERRA FOUNDATION FOR AMERICAN ART

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

Abstract The Child Health Research Career Development Award (CDRCDA) Program was first established at Children’s National Hospital in 2000, and over the past 24 years, we have successfully trained 30 Scholars. The purpose of the program is to facilitate the development of successful basic, translational, and clinical research careers for junior faculty members in pediatrics across the T0-T4 spectrum. The rationale for the program is that while many opportunities exist to use molecular biology, biomedical engineering, and translational science to advance treatment of pediatric diseases, the comprehensive scientific knowledge and practical experience that are required to capitalize on these opportunities are often deficient among young pediatrician-investigators who have recently finished clinical training. The CHRCDA addresses this need by providing protected time for nascent scientists during their initial academic appointment. In our program, scholars: 1) take coursework in basic, translational, or clinical science areas relevant to their research; 2) learn state-of-the art laboratory and computational methodologies; 3) develop preliminary data under the supervision of established mentors that will lead to submission of independent NIH grant applications; and 4) learn to effectively advance accomplishments in basic, translational, and clinical research into improvements in child health. To accomplish these goals, the CHRCDA scholars spend at least 75% effort honing these skills under the mentorship of established mentors over a 3-4 year period. During this period, each of the above tasks will be addressed in a systematic fashion, including participation in a core curriculum in research methodology and biostatistics, training in responsible conduct of research, and performance of increasingly independent research under senior investigators. We fund 2-3 Scholars annually and match these scholars with senior mentors within four scientific affinity groups: neuroscience, molecular genetics, cancer and immunology, and biomedical engineering. The administrative structure includes a Principal Investigator/Program Director, a Training Director, an Executive Committee, and an external Advisory Committee. The outcomes of this program are measured by the products of the scholars’ subsequent academic careers: publications and independent external grant support. Recent innovations to our program include: expansion of funded research to include T2-T4 science with recruitment of a cadre of appropriate mentors, new pipeline programs to increase our pool of candidates including two R38 awards to fund research among pediatric residents and significant capital investments including the new Children’s National Research and Innovation campus. This administrative supplement is necessary to sustain the CDRCDA program during an unanticipated funding gap, ensuring uninterrupted support for scholars and continued program operations until a future funding opportunity is released.

API Food Fight Club

API Food Fight Club will partner with other community organizations to host the Chinatown-International District Block Party featuring Asian Pacific American music, arts, food, and culture. It will be held August 3, 2019 from 3 pm - 9pm at 900 S King St.

NIMH - National Institute of Mental Health

PROJECT SUMMARY In a dynamic environment, learning is an evolutionary advantage. When faced with a novel situation, animals that adapt their behavior appropriately may live to reproduce another day. Associative learning requires linking distinct events across time, such as a sensory event with a motor command that results in the desired outcome. How are flexible sensorimotor associations implemented in the brain? The brain regions supporting the encoding of these events are broadly distributed suggesting that learning- related plasticity would benefit from neural mechanisms that operate across multiple timescales and brain regions. Ascending neuromodulatory systems—with their broad projection architecture and multiple timescales of activity—fulfill these criteria and could serve as a potent mechanism to link the different sensory, motor and outcome components. More specifically, the cholinergic basal forebrain (CBF) is the ideal candidate to support rapid learning-related plasticity across multiple cortical regions. This builds on a robust literature showing a pleiotropic role of the CBF to establish both sensory and motor cortical plasticity. Additionally, CBF neurons respond precisely to reinforcement, movement, and sensory events. The overall hypothesis is that the CBF phasic activity serves as a ‘teaching’ signal, locally integrating distinct events, and then projecting conjoint signals (i.e., sensory-motor contingencies) to recipient regions on the timescale of contingency acquisition. The mentored phase will exploit a novel behavioral approach that isolates the timing of acquisition of novel sensorimotor contingencies combined with state-of-the-art optical and physiological tools to test this specific hypothesis. Aim 1 will determine the spatiotemporal dynamics of cholinergic signaling to the Auditory Cortex (AC) and Motor Cortex (MC) during early task acquisition. Aim 2 will identify the causal role of CBF in associative audiomotor acquisition. In the R00 phase this framework will be expanded to implicit learning, when previously acquired sensorimotor contingencies are subject to rapid changes. Aim 3 will determine the role of CBF in implicit learning of auditory regularities. Using a combination of state-of the art optical tools, cell-type specific and temporally precise optogenetics and custom computational analysis and tools, this project unveils the role of cholinergic inputs to distinct cortical targets in learning. There is growing evidence that hearing loss and dementia are tightly linked. Cholinergic circuits play a prominent role in essential cognitive functions which are impacted during cognitive decline. Interestingly, it is one of the earliest regions to exhibit neurodegeneration in Alzheimer’s disease. Understanding how cortical networks are modulated by cholinergic inputs to produce the appropriate behavior will advance our understanding of basic cognitive functions and help develop targeted approaches to fend-off cognitive decline.

Seattle Asian American Film Festival

The Seattle Asian American Film Festival will screen free films at Hing Hay Park, 423 Maynard Avenue South on two successive Saturdays, August 18th and 25th, 2018. The films are targeted to Asian Americans in the surrounding community with the film on August 18th being screened in it's original Chinese language. The screening on August 25th will focus on the Japanese American internment during WWII. The films will be preceded by live performances and arts and crafts.

Department of Cultural Affairs and Special Events

COMMUNITY ARTS ACCESS PROGRAM - CITY MATCH

City of Newark

The City of Newark provides grants to nonprofit organizations and community groups for programs and projects that improve quality of life for Newark residents, including youth services, senior programs, arts, and neighborhood development.

Department of Public Health

This grant opportunity allows Skilled Nursing Facilities (SNFs), non-profit organizations, consumer advocacy organizations, and more to apply for funding to execute projects to improve the lives of SNF residents. Examples of projects include, but are not limited to, developing and implementing methods to increase Person-Centered Care, Infection Control Training, Arts and Engagement projects, and other topics. Examples of projects that will not be approved for CMP funding include, but are not limited to, research-only projects, projects with an indirect benefit to nursing residents, capital improvements to a facility, duplication of CMS requirements, paying for nursing home staff salaries, or high-dollar, complex technology, such as but not limited to engagement technology, telemedicine, alert systems, virtual reality, artificial intelligence, etc.  Applicants must use the template provided on the CDPH website. Projects may vary in length up to a maximum of 36 months. Award size is dependent on project request up to the allowable amount.  Keywords: Civil Money Penalty, CMP, CDPH, CMS, Skilled Nursing Facility, Reinvestment, Public Health, SNF

National Endowment for the Humanities

CLASSICAL EDUCATION AND THE AMERICAN EXPERIMENT ? THE DECLARATION OF INDEPENDENCE AT 250 [IN 2025-2026, THE GREAT HEARTS INSTITUTE WILL CELEBRATE THE 250TH ANNIVERSARY OF THE DECLARATION OF INDEPENDENCE BY EXPLORING ITS ENDURING CONNECTION TO CLASSICAL EDUCATION. THE GREAT HEARTS CELEBRATE AMERICA PROJECT, "CLASSICAL EDUCATION AND THE AMERICAN EXPERIMENT: THE DECLARATION OF INDEPENDENCE AT 250, SEEKS TO DEEPEN OUR UNDERSTANDING OF THE AMERICAN MIND THROUGH A YEAR-LONG SERIES OF EVENTS, INITIATIVES, AND PUBLICATIONS. THE 250TH ANNIVERSARY OF AMERICA'S FOUNDING PRESENTS A UNIQUE AND TIMELY OPPORTUNITY TO ENGAGE THE CLASSICAL EDUCATION COMMUNITY NATIONWIDE. THROUGH A YEAR-LONG INITIATIVE, THE GREAT HEARTS INSTITUTE WILL HIGHLIGHT THE ESSENTIAL ROLE OF CIVIC LEARNING?ROOTED IN THE GREAT TEXTS AND IDEAS OF THE AMERICAN TRADITION?AS A CORNERSTONE OF CLASSICAL LIBERAL ARTS EDUCATION IN THE UNITED STATES.]

Cleveland Foundation

One of America's oldest community foundations, providing grants for arts, education, economic development, and neighborhood revitalization across Greater Cleveland.