Grants

Healthrural healthcarediabetes+1

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HelpAge International — Global Grants

global agingolder persons rightsinternational development

HelpAge International

Grants for programs supporting older people's rights, health, and economic security in developing countries.

$25K – $200K

2026-10-01

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Helping Hands for Honu'ea

National Park Service

United State Department of the Interior, National Park Service (NPS) Notice of Intent to Award. This is not a request for applications. This funding opportunity is to provide public notice of NPS's intention to fund the following project activities without full and open competition. Cooperative Agreement P17AC01306 with the University of Hawaii, a partner under the Hawaii-Pacific Islands Cooperative Ecosystem Studies Unit, for project titled "Helping Hands for Honu'ea"

Up to $34K

natural resources

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Helping Veterans with obstructive sleep apnea determine "what matters most" in choosing a treatment option: a randomized trial

NIH

Significance to VA: Obstructive sleep apnea (OSA) poses a treatment challenge to older Veterans. A common cause of daytime sleepiness and poor sleep quality and a risk factor for cardiovascular disease, cognitive impairment, and mortality, OSA is typically treated with medical devices (e.g., positive airway pressure, oral appliances). Unfortunately, therapy nonacceptance is common. Devices can be uncomfortable and device maintenance problematic, especially in the context of comorbidity (e.g., limited mobility). Typical OSA care begins with telling patients what is wrong with them rather than asking what matters most to them (i.e., their priorities). The objective of this trial is to evaluate the benefits of the Decide2Rest+ program—a 4 session program (patient decision aid plus sessions directed at treatment adherence) for improving patient reported outcomes (PROs) and aligning OSA care for older adults with their health priorities and values. Our central hypothesis is that it will improve the “inputs” (e.g., knowledge, patient priorities) needed to move towards patient priority-directed care, increase activities associated with this care (e.g., decisions that reflect each patient’s priorities), and optimize adherence and PROs. The rationale is that understanding how disease- specific treatments affect overall health and clarifying priorities are critical to improving the selection of treatments with features that matter most to the Veteran and are most likely to improve sleep quality for the Veteran and to engaging in behaviors necessary to adhere to a chosen therapy. The proposed program aims to improve sleep PROs among older Veterans with OSA by helping them align priorities with their care, which is a VA national priority. The work is also responsive to the 2024 VA/DoD Clinical Practice Guidelines for OSA and Insomnia, which recommend shared decision making when initiating OSA therapy. Innovation and Impact: This alternative, person-centered approach is a key aspect of the VA's “age-friendly” transformation and could set a different tone for OSA treatment and adherence among older Veterans. Our goal is to align OSA-related treatment decisions with patients’ health priorities to improve PROs and support’ use of OSA therapy in older Veterans newly diagnosed with OSA. Specific Aims: The aims of the study are (1) to determine whether the Decide2Rest+ program will improve patient-reported sleep disturbance and daytime sleepiness, (2) to determine whether Decide2Rest+ improves OSA device therapy acceptance/adherence, and 3) assess the impact of Decide2Rest+ on the congruency between decisions and health priorities/values. Methodology: We propose a 5-year multi-site randomized controlled trial of Veterans aged 50+ years with untreated OSA (n=128) comparing the Decide2Rest+ to an active-control program that includes behavioral adherence components from a clinical program that is currently used in our sleep center. We used a user- centered approach to develop and refine the decision aid. It provides a mechanism for helping patients clarify what treatment feature matter most to them, reflect upon decisional needs, and identify their health priorities. Path to Translation/Implementation: This phase II trial (T2) will assess the efficacy of the DecideRest+ program for improving PROs and acceptance/adherence to OSA therapy. We use the Ready, Willing, and Able Model as framework for guiding implementation. We will obtain input from Veterans and clinicians and collect implementation measures. In prior related projects that inform our line of research, we have used strategies that will facilitate implementation including sending OSA educational links through secure messages to patients, providing an OSA decision aid in waiting rooms of sleep clinics, and training providers to deliver our behavioral interventions using the training model for the VA’s cognitive behavioral therapy for insomnia rollout. The proposed project in combination with our prior research inform a future type 2 hybrid design trial that will test the effectiveness of the program and potential for implementation (T3).

2030-03-31

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Hematopoiesis

NHLBI - National Heart Lung and Blood Institute

Abstract Support is requested for a Keystone Symposia conference entitled “Hematopoiesis,” organized by Drs. Vijay G. Sankaran, Anna E. Beaudin and Esther Obeng, with scientific programming input from Keystone Symposia. The meeting will take place February 23–26, 2026 at the Keystone Resort in Keystone, Colorado, USA. Hematopoiesis is a fundamental biological process that underlies the production of all blood and immune cells, and consequently drives immune function, oxygen transport, and tissue homeostasis. Alterations in hematopoiesis can lead to a wide spectrum of disorders and conditions ranging from anemia to immunodeficiencies, inflammatory disorders and blood cancers. Given the vital role of hematopoiesis in health and disease, this conference will explore the molecular and cellular mechanisms that govern blood cell development and maintenance, highlight the latest technological advances in the field and underscore the broader

Up to $12K

2027-01-31

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Heme regulates neurocognition by modulating Tau pathology in sickle cell disease

NINDS - National Institute of Neurological Disorders and Stroke

Project Summary Majority of Individuals with sickle cell disease (SCD) experience neurocognitive complications including cerebrovascular lesions with poor performance in learning and memory functions. Cognitive impairment is a risk factor of dementia. The vascular contributions to cognitive impairment and dementia (VCID) in SCD have not been reported. Hemolysis within the cerebrovascular space representing severe anemia, is a strong predictor of neurocognitive impairment in SCD. Excess circulating free heme, a byproduct of intravascular hemolysis, is implicated for multiorgan complications in SCD. However, the mechanistic approaches interpreting the heme- driven pathogenesis of VCID linking cerebral microvasculature with cognitive impairment in SCD are lacking. In pilot studies, we discovered that heme instigates phosphorylation of microtubular associated protein Tau (pTau) in the cerebrovascular endothelium of transgenic SCD mice. Free heme activates endothelial toll-like receptor 4 (TLR4) and insulin growth factor binding protein 3 (IGFBP3) associated with Tau phosphorylation. Sickle bone marrow chimera mice deficient in TLR4 had reduced pTau associated with impeded IGFBP3 expression in the cerebrovascular endothelium. Moreover, heme induced the intercellular protein transporter, low-density lipoprotein receptor -1 (LRP1) in the microvessel adjacent astrocytes, where pTau was accumulated following heme challenge. Based on these preliminary data, we formulated the overarching hypothesis that heme triggers phosphorylation of endothelial Tau that is accumulated in the astrocytes via LRP1 and promotes neuroaxonal damage and cognitive impairment in SCD. In Aim 1, we will perform magnetic resonance angiography (MRA), diffusion tensor and weighted imaging (DTI/DWI), immunohistopatholgy, cognitive testing (Y-maze and novel object recognition), and bone marrow trasplantation (BMT) to assess the role of Tau in the development of heme-induced cognitive impairment in sickle mice. In Aim 2, we will determine whether TLR4-IGFBP3 signaling stimulates Tau phosphorylation. Aim 3 will determine the role of LRP1 in pTau accumulation and calcium signaling in the astrocytes. Overall, this study aims to determine the role of heme in the pathogenesis of neurovascular damage and cognitive impairment, delineating an innovative VCID pathway in SCD.

Up to $515K

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Hemogenic mesoderm heterogeneity, regulation, and function

NHLBI - National Heart Lung and Blood Institute

PROJECT SUMMARY / ABSTRACT The mammalian hematopoietic system develops in the early embryo through a series of spatio-temporally separated programs, each of which harbors different functional potential, culminating in the specification of the hematopoietic stem cell (HSC). The overall goal of our research is to understand the origins and development of each program in the embryonic hematopoietic system. Where does each developmental program originate from? How does it develop? Why is each different? And, is there clinical utility to embryonic cell types that are no longer found in adult donors? Dr. Sturgeon's prior work has focused on these questions, through the lens of human pluripotent stem cell (hPSC) directed differentiation, leading to the pivotal discovery of hematopoietic commitment occurring very early, within nacent mesoderm, referred to as hemogenic mesoderm (HM). The proposed research program builds upon Dr. Sturgeon's productive research track record to delineate the molecular and transcriptional mechanisms by which HM gives rise to the embryonic hematopoietic programs. Dr. Sturgeon has shown that HMs are found in multiple immunophenotypically distinct subsets, each of which are specified in ACTIVIN/NODAL- and/or WNT-dependent processes. Further, Dr. Sturgeon has found that each HM first gives rise to a hemogenic endothelial cell (HEC) population, in VEGF- and RA-dependent processes. HM express genes associated with early gastrulation, yet each HM is highly restricted, ultimately each giving rise to a specific hematopoietic program, such as yolk sac-like erythromyeloid progenitors (EMPs), or intra- embryonic-like definitive multipotent progenitors (MPPs). Finally, Dr. Sturgeon has found that hematopoietic lineages common across multiple HM populations harbor distinct functional properties from one another. Building off these groundbreaking findings, the research program is divided into 3 projects. The first project will delineate the signal, transcriptional, and epigenetic mechanisms underlying how each hematopoietic program is specified and functionally restricted. These studies will improve our ability to obtain progenitors from each program, including the HSC. The second project will define the mechanisms regulating how HECs give rise to different lineages. Finally, the third project will continue our studies on the translational potential of hematopoietic lineages from each developmental program. Collectively, these studies will provide us with a more comprehensive understanding of hematopoietic development. This is of fundamental importance to basic biology, and the insights generated from these studies will have clinical implications, such as the in vitro generation of HSCs or other embryonic hematopoietic lineages for a wide array of regenerative medicine applications.

Up to $1.2M

2033-01-31

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Henry Ford Health Community Health Investment

Henry Ford Health

Invests in community health programs in Southeast Michigan, addressing health equity, social determinants, and chronic disease in underserved communities.

$5K – $300K

health equitysocial determinantschronic disease+1

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Henry Luce Foundation Religion in Public Life Grants

Henry Luce Foundation

Supports understanding of religion's role in public life through academic research, journalism, and public programming. Major funder of religious studies.

$50K – $500K

religion in public liferesearchjournalism+1

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Henry M. Jackson Foundation — Elder Health Research

elder health researchclinical trialshealth services

Henry M. Jackson Foundation

Grants for research advancing healthcare for aging populations including clinical trials and health services research.

$50K – $300K

2026-11-01

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Hepatic Lymphatics and the Immune Response in Acute Liver Failure

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY Though the liver produces most of the lymph in the body, the role of hepatic lymphatics in liver disease is relatively less studied. While it is recognized that alterations in hepatic lymphatics cause ascites formation in chronic liver disease like cirrhosis, its contribution to acute liver failure (ALF), like that caused by drugs such as acetaminophen (APAP) are not well characterized. An APAP overdose is the most common cause of ALF in the United States, partly due to the short therapeutic window of the only FDA approved antidote, N-acetylcysteine (NAC). Excess APAP induces centrilobular necrosis, and a failure of inherent liver regeneration in a significant percentage of patients, especially after a severe overdose, causes ALF. Thus, insight into mechanisms of liver recovery which are compromised in patients with ALF, would allow their targeting to complement NAC treatment. One such beneficial phenomenon is the innate immune response induced by hepatocyte necrosis. Though interaction between the infiltrating immune cells and surviving hepatocytes facilitates their regeneration, repopulation of areas of necrosis also requires an orderly exit of the infiltrating immune cells to allow coordinated reestablishment of liver infrastructure and lymphatics to regain functional homeostasis. The lymphatic system is a central mode of immune cell emigration from tissues, and specific pro-resolving lipid mediators (SPMs) facilitate resolution of inflammation. However, their role in immune cell exit after acute APAP-induced ALF is unknown. Our preliminary data shows transient changes in hepatic lymphatics after APAP overdose with elevations in SPMs, which are known to facilitate lymphangiogenesis and immune cell clearance. Blocking lymphangiogenesis after an APAP overdose also extended hepatic residency of immune cells. Treatment with Wharton's Jelly mesenchymal stem cells (WJMSC) which are cleared for human use, also enhanced liver recovery in the mouse model with elevation in circulating VEGF-D, which activates lymphangiogenesis. This data led to the hypothesis that hepatic lymphatics play a critical role in immune cell clearance during liver recovery from an APAP overdose, a process facilitated by SPMs which could be targeted by WJMSC treatment to enhance liver recovery. This hypothesis will be tested by 1) evaluating mechanisms of immune cell clearance through hepatic lymphatics after acute APAP overdose, and 2) examining the role of SPMs and immune cell clearance as mechanisms facilitating recovery after delayed treatment with WJMSC. Collectively, we will define the molecular mechanisms responsible for efficient immune cell exit through hepatic lymphatics after reconstruction of areas of hepatic necrosis and study the consequence when this exit is compromised such as ALF. We will also evaluate a therapeutic intervention to enhance recovery, which can be rapidly translated to the clinic.

Up to $426K

2028-01-31

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Hepatitis C Virus Trafficking in Hepatocytes

NIAID - National Institute of Allergy and Infectious Diseases

RESEARCH ABSTRACT: HEPATITIS C VIRUS TRAFFICKING IN HEPATOCYTES Many viruses have evolved distinct pathways of transmitting their infection between cells. This viral spread involves canonical pathways that release unprotected virions from the infected cell (thus potentially exposing the virion to neutralizing antibodies) and/or pathways that shield the virion from the humoral response (cell-cell spread, syncytia formation, and the release of virions in extra-cellular vesicles). Viral egress pathways that evade the humoral response are especially important to understand given the potential importance of manipulating viral susceptibility to this critical arm of adaptive immunity. Most viruses of the Flaviviridae appear to use both mechanisms of viral egress. We and others previously characterized the pathway of canonical hepatitis C virus (HCV) release, while canonical dengue virus (DENV) secretion has also been well characterized. In contrast, noncanonical pathways of virion spread in the Flaviridae are poorly understood. Our lab has a longstanding interest in Flaviviridae entry and spread. In our prior funding period, we developed a multi-pronged analysis (host genetics, pharmacological inhibition and single particle imaging) of polarized hepatoma organoids to characterize HCV entry and egress. The work established the most complete, detailed pathway of HCV entry, in addition to extensive preliminary data on HCV cell-cell spread. We expanded these studies into the non-canonical spread of DENV, focusing on a process we discovered years ago: DENV-induced lipophagy, which is the selective autophagic mobilization of lipid droplet stores to stimulate lipid metabolism. This process has been associated with the non-canonical release of DENV into extra-cellular vesicles. We have identified a central cellular player in this process: the selective autophagy adaptor NBR1. In this R01 renewal application, we will focus on extending and expanding our studies on HCV and DENV non-canonical virion spread. In the case of HCV, we developed quantitative cell-cell spread assays and identified putative cellular secretion pathways and cargo adaptors that modulate cell-cell spread. We propose to characterize the significance of these pathways using imaging of our 3-dimensional polarized hepatoma spheroid system. Additionally, we will collaborate for an ultra-structural analysis of HCV-infected hepatocyte cell-cell junctions cryoelectron microscopy tomography (cryo-ET). For DENV non-canonical spread, we will validate a rove for NBR1 and lipophagy in the cell-cell spread of DENV. We will then characterize the pathway of non-canonical release of DENV virions. Finally, we will perform ultrastructural analysis of the NBR1-dependent DENV containing extra-cellular vesicles using cryo-ET. The specific aims are: Aim 1. Characterize the pathway(s) of HCV cell-cell spread in infected hepatocytes. Aim 2. Characterize the NBR1-dependent pathway of non-canonical DENV egress.

Up to $480K

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Hepatotoxicity of Legacy and Replacement PFAS: Role of BRUCE-Mitochondrial Interactions

NIEHS - National Institute of Environmental Health Sciences

Epidemiological studies have shown a strong association between exposure to PFAS (Per- and Poly- fluoroalkyl Substances) and liver toxicity. Particularly, legacy C8-PFAS members, PFOS (perfluorooctane sulfonate) and PFOA (perfluorooctanoic acid), are highly toxic, with PFOS estimated to be approximately 10 times more toxic than PFOA in ecotoxicity models. Consequently, PFAS replacements such as GenX and PFBS are marketed as safe alternatives, although growing evidence indicates that these substitutes also exhibit toxic effects. Lab animal model studies have shown hepatotoxic effects of both legacy and replacement PFAS members, characterized by Metabolic dysfunction-associated steatotic liver disease (MASLD) and its severe form Metabolic dysfunction- associated steatohepatitis (MASH), the two chronic liver diseases affecting an estimated 80-100 million Americans. The broader objective of this project is to understand the underlying mechanisms of PFAS hepatotoxicity in MASLD/MASH. In this context, our initial studies have shown that PFAS exposure of mice downregulates hepatic BRUCE, an autophagy inhibitor, resulting in development of MASLD in WT, and more severe MASLD and even progression to MASH in BRUCE liver-knockdown (BKO) mice. Using primary hepatocytes, we found PFAS-induced BRUCE reduction compromised mitochondrial (mt) functions (respiration, fatty acid oxidation/FAO, and ATP production) and suppressed mitophagy in WT and more so in BKO mice. Pharmacological restoration of mt function in mice prevented PFAS-induced MASLD/MASH. Guided by these compelling preliminary data and scientific premise, we hypothesize that PFAS degradation of BRUCE in hepatocytes induces excessive autophagy (resulting in cytotoxicity) and inhibits mitophagy (resulting in accumulation of damaged mitochondria), leading to release of mtDAMPs to activate inflammation/ fibrosis, thereby facilitating progression from MASLD to MASH. We will test this by three specific aims. Aim 1 (ex vivo) is to determine the human-relevant PFAS doses that modulate BRUCE levels for homeostatic vs cytotoxic autophagy and how BRUCE in turn regulates autophagy. Aim 2 (ex vivo) will investigate BRUCE-driven mitophagy pathway specific to PFAS exposure at human-relevant doses. Aim 3 (ex vivo and in vivo) will involve ex vivo simulation experiments to characterize the role of PFAS-induced, BRUCE-dependent hepatocyte- released mt DAMPs in activation of immune and fibrogenic cells using co-culture assays. Next, we will perform in vivo intervention to validate the role of PFAS-damaged mitochondria in driving MASH progression in mouse models. Furthermore, human relevance of the delineated mechanisms will be ascertained and validated using iPSC-derived human liver organoid system. Impact: This project will advance our understanding of autophagy/mitophagy-centric mechanisms with therapeutic potential in the context of PFAS-induced liver disease MASLD/MASH.

Up to $3.9M

2030-06-09

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HER2 PET imaging to assess HER2 heterogeneity and predict response to HER2-targeted therapy in biliary tract cancer

NCI - National Cancer Institute

ABSTRACT The management of metastatic biliary tract cancer (BTC) has been transformed over the past 5 years, with FDA approval of anti-PD-1/PD-L1 antibodies and several molecularly targeted therapies. Despite these advances, most patients with metastatic BTC still die from their disease. The HER2 receptor tyrosine kinase (encoded by the ERBB2 gene) is implicated in the pathogenesis of several cancer types, and drugs that target HER2 have an established role in the management of breast, lung, colorectal, and esophagogastric cancers. While ERBB2 amplification and/or mutations are present in up to 30% of metastatic BTCs, older HER2-targeted antibodies and kinase inhibitors had only modest clinical activity in patients with BTCs. Unprecedented clinical activity was recently demonstrated with a new generation of HER2-targeted therapies in breast and lung cancers resistant to older HER2-targeted therapies, including HER2-low breast cancer and ERBB2-mutated lung cancer. The current proposal is based on 1) durable responses to next-generation HER2-directed therapies in a subset of patients with HER2-expressing BTC; 2) preliminary data indicating frequent mutational discordance of ERBB2 and heterogeneity of HER2 expression in paired primary and metastatic tumors collected from individual patients with BTCs; and 3) loss of ERBB2 expression at progression on HER2 targeted therapies in paired samples from patients with BTCs. Based on these preliminary data, we hypothesize that pre-existing HER2 expression heterogeneity will be a common mechanism of resistance to a novel HER2-targeted bispecific antibody in BTC and that molecular imaging can identify patients with biliary tract tumors most likely to achieve durable responses. To test this hypothesis, we will leverage a largest-of-its-kind prospective molecular characterization effort and a novel molecular imaging platform (89Zr-ss-pertuzumab PET) to define the prevalence of HER2 expression heterogeneity in BTC, its association with ERBB2 mutational status, and its impact on HER2-targeted bispecific antibody therapy response. We will accomplish these translational objectives through three broad approaches: 1) We will perform molecular analyses of paired primary and metastatic tumors collected from patients with BTC; 2) We will explore the extent of lesion-to-lesion HER2 heterogeneity in metastatic BTC using a bespoke HER2 PET imaging platform (89Zr-ss-pertuzumab PET); and 3) We will use 89Zr-ss-pertuzumab PET and tumors collected before treatment and at the time of disease progression on HER2-targeted bispecific antibody therapy to study the impact of HER2 genomic and expression heterogeneity on depth of response to this novel drug class. Mechanisms of HER2-targeted therapy resistance will be functionally explored using patient-derived BTC organoid and xenograft models. Given the promising clinical activity of novel HER2-directed therapies in patients with BTC, we predict that the studies proposed will directly influence the design of future clinical trials of HER2- targeted therapies and establish the clinical utility of HER2 PET as a predictive biomarker of response in patients.

Up to $715K

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Herb Alpert Award in the Arts

Herb Alpert Foundation

Unrestricted grants to mid-career artists in dance, film/video, music, theater, and visual arts.

$50K – $75K

2026-07-31

artsmid-career

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Hereditary Hemorrhagic Telangiectasia (HHT) Center

Health Resources and Services Administration

The purpose of the Hereditary Hemorrhagic Telangiectasia (HHT) Center Program is to reduce illness and death related to HHT by partnering with clinical center to expand access and coordination of care; creating innovative strategies that support clinicians with identifying and diagnosing HHT cases; and developing a de-identified, aggregate patient data registry to better understand this rare disease and its treatment outcomes.

Up to $2.9M

2026-07-10

Healthhealthcare

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Hereditary Hemorrhagic Telangiectasia (HHT) Center

Health Resources and Services Administration

Hereditary Hemorrhagic Telangiectasia (HHT) Center

2026-07-10

general

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HERITABLE, EPIGENETIC EFFECTS OF PATERNAL ALCOHOL USE ON FASD PHENOTYPES

NIAAA - National Institute on Alcohol Abuse and Alcoholism

Project Summary & Abstract PROJECT SUMMARY & ABSTRACT Despite evidence that poor paternal health increases the risk of pregnancy loss and that maternal alcohol use correlates with paternal drinking, all public health messaging addressing fetal alcohol spectrum disorders (FASDs) exclusively targets women. The Golding lab and other researchers examining paternal epigenetic effects propose that the exclusive emphasis on maternal health has created a significant blind spot in our efforts to understand the origins of FASDs and that paternal drinking is an entirely unexplored source of variation in alcohol-related birth defect penetrance and severity. Published preclinical studies from the Golding lab demonstrate that chronic preconception male alcohol exposures cause dose-dependent effects on offspring fetoplacental growth and craniofacial patterning. Emerging research reveals that these effects on offspring development arise as part of a heritable response to paternal oxidative stress, promoting the epigenetic inheritance of mitochondrial dysfunction. The offspring of alcohol-exposed fathers exhibit deficits in mitochondrial function, including alterations in mitochondrial structure, increased inflammatory cytokines, a reduced NAD+/NAHD ratio, and increased mitophagy, the removal of damaged mitochondria. Notably, these deficits interact with maternal alcohol exposures to exacerbate FASD outcomes and persist into adulthood. Individuals diagnosed with FASDs exhibit an increased incidence of age-related diseases and a reduced life expectancy. This proposal posits that some FASD adverse health outcomes are linked to paternal epigenetic effects on mitochondrial health. This proposal will test the hypothesis that paternal systemic mitochondrial stress induced by chronic alcohol exposure alters sperm-inherited noncoding RNAs, which provoke lasting epigenetic changes in offspring mitochondrial function and the emergence of FASD outcomes. The research outlined in this proposal will use transgenic mouse models to exacerbate and track the epigenetic transmission of mitochondrial dysfunction from parents to offspring, through fetal life and into adulthood. Published studies from the Golding lab demonstrate that chronic male alcohol use induces mitochondrial stress in the liver and epididymis – the portion of the male reproductive tract where sperm mature. This paternal mitochondrial stress correlates with the enrichment of sperm-inherited microRNAs, influencing the antioxidant response and mitochondrial function. This proposal will determine the function of these sperm-inherited noncoding RNAs and their relationship to the emergence of FASD phenotypes. Maternal education on the benefits of dietary folic acid intake and the dangers of drug use during pregnancy has helped significantly increase children's health. However, 50% of the information necessary to optimize the chances of achieving a healthy pregnancy may be missing because the father's lifestyle choices are not deemed important. The research outlined in this grant proposal will address this knowledge gap.

Up to $607K

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Heritage Documentation programs

National Park Service

he objective of the Agreement is to promote the purposes of NHPA by the NPS and CAMM undertaking activities requiring the sharing of their knowledge, skills and resources. NPS and CAMM will undertake activities that promote greater public and private participation in historic preservation programs and activities nationwide. The parties will also undertake activities directed at assisting State and local governments, Federal agencies, Indian tribes, and Native Hawaiians in expanding and improving their existing historic preservation programs and activities.

other

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Heritage Management Assistance Agreement

National Park Service

This announcement is not a request for applications. This announcement is to provide public notice of the National Park Service s intention to award financial assistance for the following project activities without competition.

$50K

Education

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Heritage Oak Riparian Restoration and Streambank Stabilization

Fish and Wildlife Service

Restore and enhance the riparian ecosytem on private fallow and marginal land to prevent river sedimentation, enhance riparian corridors wtih native plants to maximize recovery of listed, threatened, endangered and sensitive birds species.

Environmentalsustainability

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Hermes Foundation Skills & Craft Grants

Hermes Foundation

Supports artisan skills preservation, biodiversity, and social solidarity through French luxury philanthropy.

$10K – $250K

artisan skillsbiodiversitysocial solidarity

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HERO Appendix E: Space Radiobiology and Human Health Countermeasures Topics

NASA Johnson Space Center

This National Aeronautics and Space Administration (NASA) Research Announcement (NRA), entitled Human Exploration Research Opportunities (HERO) 2016, solicits applied research in support of NASA s Human Research Program. Research response area NRA NNJ16ZSA001N-SRHHC Space Radiobiology and Human Health Countermeasures Topics is Appendix E of the Human Exploration Research Opportunities (HERO) NRA (NNJ16ZSA001N). Proposals are solicited by NASA in the areas of Evaluation of Current Clinical Markers as Surrogate Endpoints for Space Radiation-Induced Cardiovascular Disease; Evaluation of Animal Model Systems and Common Pathways in Understanding Space Radiation-Induced Late CNS Outcomes and Cardiovascular Disease; Approaches to Evaluate Sex Dependence and Quality Effects on Space Radiation Carcinogenesis; Galactic Cosmic Ray (GCR) Simulator Validation Experiments: Dose-Rate Dependence; In-Flight Cognitive and Behavioral Central Nervous System Risks from Space Radiation; and Combined Effects of Simulated Weightlessness and Space Radiation on Cardiovascular Structure and Function. Please note that the last topic is being jointly solicited by HRP and NASA s Space Biology (SB) Program. Awards range from under $150K per year for focused, limited efforts to $600K per year for extensive activities. Awards will be made as grants. The period of performance for an award is one to four years. All categories of United States (U.S.) institutions are eligible to submit proposals in response to this NRA. The solicitation uses a two-step proposal process. Proposals that do not conform to the standards outlined in the solicitation will be declared noncompliant and will be handled in accordance with the NASA Federal Acquisition Regulation Supplement. On or about March 22, 2017, the NRA will be available electronically through NASA Solicitation and Proposal Integrated Review and Evaluation System (NSPIRES) by going to http://nspires.nasaprs.com A virtual Pre-Proposers Conference is scheduled for March 31, 2017, and more details will be posted shortly alongside the solicitation on NSPIRES. Appendix E Step-1 pre-proposals are due April 24, 2017. Invited Appendix E Step-2 proposals are due July 17, 2017. All categories of United States (U.S.) institutions are eligible to submit proposals in response to the NRA. Principal Investigators may collaborate with universities, Federal Government laboratories, the private sector, and state and local government laboratories. In all such arrangements, the applying entity is expected to be responsible for administering the project according to the management approach presented in the proposal. NASA s policy is to conduct research with non-U.S. organizations on a cooperative, no exchange-of-funds basis. Electronically submitted Step-1 pre-proposals are required. This is a broad agency announcement as specified in FAR 6.102 (d) (2).

sciencetechnology

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Heron's Nest Community Kitchen Phase 1

Shared Spaces Foundation

Heron's Nest is a volunteer-led project focused on repatriating a 3.5 acre parcel of land to the Duwamish Tribe. To do this, the land will be purchased and placed in a trust held by Duwamish Tribal Services. Our goal for this land is to provide community accessible facilities including workshop, class, and meeting spaces, a recycling facility, office space, storage, and short term accommodations for tribal members. An important element of our plan is the development of an outdoor kitchen facility. We have preliminary plans to build the kitchen in the shape and style of a traditional Duwamish Longhouse with cedar beams and roof. With this funding award we will complete the first phase of the outdoor kitchen which includes finalizing the design and completing the permitting processes. Phase 1 of this project will be completed by December 29, 2023.

Up to $30K