Grants

Golden Field Office

The purpose of this notice is to provide potential applicants advance notice that the Office of Energy Efficiency and Renewable Energy (EERE), U.S. Department of Energy (DOE) intends to issue, on behalf of the Federal Energy Management Program (FEMP), a Funding Opportunity Announcement (FOA) entitled Assisting Federal Facilities with Energy Conservation Technologies (AFFECT) 2017 . (DE-FOA-0001667). This notice is issued so that interested parties are aware of the EERE s intention to issue this FOA in the near term. All of the information contained in this notice is subject to change. EERE may issue a FOA as described herein, may issue a FOA that is significantly different than the FOA described herein, or DOE may not issue a FOA at all. NO APPLICATIONS WILL BE ACCEPTED THROUGH THIS NOTICE. Please do not submit questions or respond to this Notice of Intent. Prospective applicants to the FOA should begin developing partnerships, formulating ideas, and gathering data in anticipation of the issuance of this FOA. It is anticipated that this FOA will be posted to EERE eXCHANGE in December 2016. The full NOI DE-FOA-0001672 can be found at https://eere-exchange.energy.gov.

$1 – $2

rolling

energyclean energy

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

Assisting Federal Facilities with Energy Conservation Technologies, Fiscal Year 2016

Golden Field Office

The purpose of this notice is to provide potential applicants advance notice that The Office of Energy Efficiency and Renewable Energy (EERE), U.S. Department of Energy (DOE) intends to issue, on behalf of the Federal Energy Management Program (FEMP), a Funding Opportunity Announcement (FOA) entitled Assisting Federal Facilities with Energy Conservation Technologies (AFFECT) 2016 . (DE-FOA-0001574). This notice is issued so that interested parties are aware of the EERE s intention to issue this FOA in the near term. All of the information contained in this notice is subject to change. EERE may issue a FOA as described herein, may issue a FOA that is significantly different than the FOA described herein, or DOE may not issue a FOA at all. NO APPLICATIONS WILL BE ACCEPTED THROUGH THIS NOTICE. Please do not submit questions or respond to this Notice of Intent. Prospective applicants to the FOA should begin developing partnerships, formulating ideas, and gathering data in anticipation of the issuance of this FOA. It is anticipated that this FOA will be posted to EERE eXCHANGE in May 2016.

$1 – $2

rolling

energyclean energy

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

Assistive Technology Act National Activities Data Analysis and Reporting Assistance

Administration for Community Living

Assistive Technology Act National Activities Data Analysis and Reporting Assistance

technology

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

Assistive Technology Alternative Financing Program

Administration for Community Living

The purpose of the Assistive Technology (AT) Alternative Financing Program (AFP) is to support programs that provide for the purchase of AT, such as a low-interest loan fund, an interest buy-down program, a revolving loan fund, a loan guarantee, or an insurance program, that results in the acquisition of AT devices and services. Applicants for the AT AFP grant awards are required to provide an assurance that, and information describing the manner in which, the AT AFP will expand and emphasize consumer choice and control. Applicants should incorporate credit-building activities in their programs, including financial education and information about other possible funding sources. Successful applicants must emphasize consumer choice and control and build programs that will provide financing for the full array of AT devices and services and ensure that all people with disabilities, regardless of type of disability or health condition, age, level of income, and residence, have access to the program.

$100K – $700K

2026-07-22

sciencetechnology

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

Assistive Technology Alternative Financing Program

Administration for Community Living

Assistive Technology Alternative Financing Program

2026-07-22

technology

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

Assistive Technology Alternative Financing Program

science_technology_and_other_research_and_development

Administration for Community Living

$100K – $700K

2026-07-22

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

Assistive Technology Programs

Administration for Community Living

Formula grants to states for assistive technology device demonstrations, lending, reutilization, and state financing activities for people with disabilities.

$250K – $1.5M

disability servicestechnologyassistive technology

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

Associated General Contractors Education & Research Foundation Construction Education Grants

Associated General Contractors Education & Research Foundation

Supports construction workforce development, safety education, and programs advancing careers in the construction industry.

$5K – $100K

constructionworkforce developmentsafety education+1

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

Association of the Sugary Drink Excise Tax Policy and diabetes and associated cardiometabolic risk biomarkers in primary care patients (ASPIRE)

NIDDK - National Institute of Diabetes and Digestive and Kidney Diseases

PROJECT SUMMARY Sugar-sweetened beverage (SSB) consumption is a key contributor to obesity, diabetes, and cardiovascular disease (CVD) in the U.S. Seven U.S. municipalities have implemented SSB excise taxes to reduce consumption, yet the downstream impact of these taxes on diabetes and cardiometabolic health remains unknown. This study will leverage longitudinal electronic health record (EHR) data from the OCHIN network—a large, multi-state consortium of community health centers (CHCs)—to evaluate whether SSB excise tax implementation is associated with improvements in commonly assessed diabetes and cardiovascular risk biomarkers in real-world primary care settings. Using a quasi-experimental difference-in-differences design, we will compare changes in biomarker outcomes from pre- to post-tax periods in taxed versus matched non-taxed municipalities. We will also examine whether these effects differ across key individual-level subgroups, including by age, income, language preference, and food insecurity status. This work addresses a critical evidence gap regarding the health impacts of SSB taxation among low-income populations and will inform local, state, and national policy efforts, including proposals to restrict SSB purchases through SNAP. By evaluating clinical outcomes in the context of real-world tax implementation, this study will provide actionable insights into how policy interventions may influence diabetes and cardiometabolic health at scale.

Up to $781K

2031-02-28

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

Associations between actigraphy-derived circadian rest-activity rhythms and cancer-related fatigue: Insights from the Harvest for Health Clinical Trial

NCI - National Cancer Institute

PROJECT SUMMARY Cancer-related fatigue affects nearly all people undergoing cancer treatment and sometimes persists for months or years post-treatment. The etiology and pathophysiology of cancer-related fatigue are not well understood but may be related to disruption in circadian rhythms. Circadian rhythms describe the daily oscillations of metabolic, endocrine, and neuronal systems, all of which regulate energy levels. Behavioral interventions such as exercise and diet can regulate (or dysregulate) circadian rhythms, though circadian mechanisms are rarely leveraged in behavioral interventions. Ambulatory actigraphy data has become easy and inexpensive to collect, and there is a plethora of methods to analyze rest-activity rhythms from actigraphy data. However, timing is rarely incorporated into behavioral programs to address fatigue because the field has not yet defined unequivocal rest- activity rhythm parameters from actigraphy datasets that are associated with fatigue. Thus, the objective of this project is to quantify the associations between rest-activity rhythm parameters and persistent cancer-related fatigue using a battery of analysis methods. This study leverages the Harvest for Health study, which was a randomized controlled trial among older cancer survivors testing the effects of a 1-year gardening intervention vs. waitlist control. The dataset has actigraphy and fatigue data for 279 participants over two years. Participants wore an actigraph for 7 days and reported fatigue at baseline, 1 year, and 2 years. We will use traditional methods to quantify rest-activity rhythms (i.e., cosinar analysis, non-parametric measures) as well as novel hidden Markov modelling, based on a probabilistic framework. The hidden Markov models go beyond traditional methods in that they provide visual Day Profiles of activity and can quantify where in the day circadian disruptions are occurring. Aim 1 will assess the association between the rest-activity rhythm index parameters and fatigue from baseline to 1 and 2 years. We predict that higher hidden Markov-derived rhythm indices and other parameters that reflect stronger rest-activity rhythms will be associated with less fatigue. Aim 2 will assess the changes in rest-activity rhythm parameters over time. We predict that rest-activity rhythms will get stronger over time, as people get further from cancer treatment. Aim 3 will test the effects of the gardening intervention vs. control on Hidden Markov model-derived rhythm indices. We hypothesize that the gardening intervention will result in higher average rhythm index (stronger rest-activity rhythm) than the control at year 1. These findings will immediately be useful to researchers in the optimization of behavioral interventions (e.g., exercise, nutrition, sleep hygiene) to strengthen biological rhythms, address fatigue, and improve quality of life in cancer survivorship. The results and the resultant code to easily run hidden Markov models will inform future research and clinical applications. For example, these models will inform personalized recommendations for people struggling with fatigue based on a person’s rest-activity rhythm—should we focus efforts to improve sleep, encourage morning activity, minimize nutrient intake in the evening, or something else?—thereby accelerating people’s recovery from cancer.

Up to $411K

2028-02-29

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

Associations of Movement and Sleep Behaviors through the Cardiovascular-Kidney-Metabolic Stage Progression (CARDIA CKMoverS)

NHLBI - National Heart Lung and Blood Institute

ABSTRACT Cardiovascular-Kidney-Metabolic (CKM) syndrome is a progressive condition with a four-stage grading approach caused by the interplay between obesity, diabetes, chronic kidney disease, and cardiovascular disease (CVD). There is a high burden of poor CKM health in US adults. The progression from metabolically healthy to advanced CKM stages (subclinical or clinical CVD and kidney failure) takes several decades to develop. As such, few studies are capable of understanding the natural lifelong disease progression of CKM. The Coronary Artery Risk Development in Young Adults (CARDIA) study provides a unique opportunity to study CKM stage progression in a cohort with 40 years of continuous follow-up since early adulthood (18-30 years), including repeated assessments of physical activity and sleep. The Year 40 in-person exam is scheduled for 2026 and 2027 when participants will be 59 to 71 years old. We propose a four-year CARDIA ancillary study, CARDIA Moving through Cardiovascular-Kidney-Metabolic Syndrome (CKMoverS) Study, to obtain 7 days of accelerometry measures to be paired with the existing data collected from early adulthood through the start of older adulthood to capture, for the first time, CKM progression states in an estimated 3,103 Black and White men and women expected to return for the Year 40 exam (11th CARDIA exam). We will add gold standard accelerometry measures to assess movement behaviors (sedentary behavior, light intensity physical activity, and moderate to vigorous intensity physical activity [MVPA]) to the CARDIA Year 40 exam. This will advance knowledge on the benefits of light intensity physical activity which compose a significant portion of the 24-hour day but cannot be accurately measured by self-report. CARDIA CKMoverS is a vital opportunity to significantly enhance the scope of CARDIA by clarifying novel associations and future intervention targets between movement behaviors and CKM disease progression during the critical life transition of midlife into older adulthood. CARDIA CKMoverS will address the limited evidence of risk factors associated with accelerated CKM progression and lifestyle behaviors to target earlier stages of CKM to reduce risk and limit advancement to CVD. To address this goal we will quantify the burden and rate of accelerated CKM progression across 40 years of adulthood, examine the role and critical window(s) of reported MVPA and sedentary behavior with accelerated CKM progression risk, and given recent evidence suggests that the optimal period in life to intervene on health is midlife, we will estimate the 20-year associations of accelerometer-determined sedentary and physical activity (light to vigorous intensity) and sleep movement behaviors across midlife on CKM progression risk. Finally, we will fill knowledge gaps regarding risk factors of CKM by examining if these associations are moderated by several sociodemographic risk factors. CARDIA CKMoverS will address current evidence gaps and provide empirical evidence for the critical widows for lifestyle modifications to intervene within the progression of CKM and attenuate the projected disease burden.

Up to $788K

2030-03-31

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

Asthma and Allergic Diseases Cooperative Research Centers

National Institutes of Health

Asthma and Allergic Diseases Cooperative Research Centers

research

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

Asthma and Allergic Diseases Cooperative Research Centers

National Institutes of Health

<p>The National Institute of Allergy and Infectious Diseases (NIAID) seeks to advance its mission through the continued support of the Asthma and Allergic Diseases Cooperative Research Centers (AADCRC). The AADCRC program serves as the cornerstone of NIAID's efforts to promote clinical and basic research in diseases including asthma, upper airway allergic/inflammatory diseases, food and drug allergies, atopic dermatitis, and other allergic diseases. The overarching goals of this program are to investigate mechanisms underlying the onset, progression, treatment modalities, and mechanisms of treatment response for the diseases of interest. Goals of the program may include exploring disease mechanisms and/or treatment modalities in small clinical trials/observational studies or immune pathway-focused projects using primarily human materials. The AADCRC is the only NIAID program that is designed to promote multi-center, multidisciplinary, translational research in asthma and allergic diseases. Grant authorities that allow NIAID to forecast this opportunity are as follows: Sections 301 and 405 of the Public Health Service Act as amended (42 USC 241 and 284) and under Federal Regulations 42 CFR Part 52 and 2 CFR Part 200.</p>

2027-05-21

Health

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

Asthma and Allergic Diseases Cooperative Research Centers

National Institutes of Health

The National Institute of Allergy and Infectious Diseases (NIAID) seeks to advance its mission through the continued support of the Asthma and Allergic Diseases Cooperative Research Centers (AADCRC). The AADCRC program serves as the cornerstone of NIAID's efforts to promote clinical and basic research in diseases including asthma, upper airway allergic/inflammatory diseases, food and drug allergies, atopic dermatitis, and other allergic diseases. The overarching goals of this program are to investigate mechanisms underlying the onset, progression, treatment modalities, and mechanisms of treatment response for the diseases of interest. Goals of the program may include exploring disease mechanisms and/or treatment modalities in small clinical trials/observational studies or immune pathway-focused projects using primarily human materials. The AADCRC is the only NIAID program that is designed to promote multi-center, multidisciplinary, translational research in asthma and allergic diseases. Grant authorities that allow NIAID to forecast this opportunity are as follows: Sections 301 and 405 of the Public Health Service Act as amended (42 USC 241 and 284) and under Federal Regulations 42 CFR Part 52 and 2 CFR Part 200.

2027-05-21

Healthhealthcare

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

Asthmatic lgE release is due to substance P released by sensory neurons

NIAID - National Institute of Allergy and Infectious Diseases

Project Summary Asthma and asthmatic symptoms continue to pose a significant health burden to the USA, demonstrating the need to understand how the primary asthmatic effector molecule, immunoglobulin (Ig) E (IgE), is produced. While IgE production can lead to protective immunity in response to venoms and multicellular pathogens, its overproduction in response to benign substances underlies its role in asthmatic inflammation. IgE is secreted from B lineage cells in the presence of cognate antigen and activates mast cells and basophils to release potent inflammatory molecules that act directly on the airway wall and attract inflammatory cells to the lungs. Emerging evidence demonstrates that asthmatic inflammation sensitizes another cell type, neurons. Once sensitized, neurons release a host of neuropeptides that enhance asthmatic inflammation. This application aims to investigate how the release of neuropeptides from sensory neurons drives B cell fate, maturation, and class switch recombination to IgE. The overall objective of this application is to investigate how sensory neuron release of the neuropeptide substance P stimulates B cell IgE release in asthma. Our preliminary work shows that substance P is preferentially released in response to Alternaria alternata induction of asthma in mice and that sensory neuron depletion reduces substance P release and IgE production. Supplementation of substance P back into the lungs of sensory neuron-ablated mice restores the asthmatic phenotype. Also, substance P knockout mice (those that do not produce substance P) produce less IgE in response to A alternata compared to WT littermates. This occurs via substance P binding to Mrgpra1 receptors on B cells and ultimately controls transcription factors to steer cell fate, maturation, and class switch recombination. We will investigate this novel mechanism of IgE overproduction in two aims. AIM 1 will test how substance P regulates B cell class switch recombination via specific transcriptional regulation in vitro with protein analysis, flow cytometry, and IgE germline and circular transcripts. In addition, the asthmatic phenotype in vitro using murine and human B cells and in vivo using adoptive transfer techniques. AIM 2 will investigate the maturation of B cells induced by substance P using in vitro and in vivo protein analysis and flow cytometry. This contribution is significant because it is expected to elucidate how integrated neuroimmune regulation augments IgE production and dysregulation in asthma. Such knowledge can inform the development of new strategies that will help reduce the growing problem of chronic asthmatic disease, directly in line with the mission statement of the NIH, to reduce the burden of human disease.

Up to $245K

2028-06-30

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

Astrocyte Response to Glymphatic Shear Force

NINDS - National Institute of Neurological Disorders and Stroke

Our overall hypothesis is that astrocyte endfeet at perivascular regions act as sensory cells, responding to shear forces along the glia limitans. We propose to quantify the sensitivity of mouse and human astrocytes in basal and reactive states to these forces and to determine the extent to which the transduction mechanisms that we have identified contribute to brain hemorrhage and cerebral edema. For this, we will use a combination of techniques that include Ca2+ imaging in microfluidics devices to quantify forces and responses, pharmacological and genetic deletion to identify molecular players, imaging of brain slices to gauge response to osmotic stimuli, and super-resolution microscopy to localize endfoot proteins and their colocalization with each other in regions of infarct. These studies are based on our recent publication showing that mouse astrocytes are highly sensitive to shear stress when the mechanosensor Piezo1 is activated, and are designed to quantify this sensitivity and how it can be modulated by other factors. In addition to evaluation of forces that astrocyte endfeet feel, these studies are expected to have high impact in the understanding of conditions that regulate glymphatic flow and normally clear amyloid and other debris from brain extracellular space. Such understanding could ultimately lead to conditions that restore normal glymphatic function in aging and neurological disease such as Alzheimers.

Up to $462K

2028-04-30

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

Astrocyte-mediated tonic inhibition in a mouse model of Lewy body dementia

NIA - National Institute on Aging

Abstract Lewy body dementia (LBD) is the second most common form of dementia after Alzheimer’s disease (AD), affecting over 1.4 million Americans. The causes of LBD remain largely unknown, and there is currently no cure. This application aims to explore the mechanisms that underlie the genetic link between LBD and mutations in GBA1, the gene that encodes the lysosomal enzyme glucocerebrosidase (GCase). Homozygous recessive mutations in GBA1 cause Gaucher disease, the most common lysosomal storage disorder, which is often associated with parkinsonism and cognitive impairment. Heterozygous GBA1 mutations, however, represent the strongest genetic risk factor for both LBD and Parkinson’s disease (PD), and are linked to more severe cognitive impairment and more rapid cognitive decline. Despite the role of GBA1 mutations in promoting α-synuclein (αSyn) pathology, little is known about how these mutations contribute to the pathophysiology of LBD. Using an astrocyte specific Gba1 conditional knockout (Gba1CKO) mouse model, we have found that astrocyte Gba1 deficiency induces hippocampus dependent mild cognitive impairment. By crossing Gba1CKO mice with the well- characterized Thy1-αSyn (Line 61) mouse model of LBD, which overexpresses human wild-type αSyn, we provide evidence that astrocyte Gba1 deficiency exacerbates LBD-related αSyn accumulation, cognitive impairment and motor symptoms. Gba1CKO mice further demonstrate an increase in levels of hippocampal astrocyte GABA transporter GAT-3, a reduction in extrasynaptic GABAAR-mediated tonic inhibition in CA1 pyramidal neurons, and a defect in autophagy-lysosome degradation. Based on these preliminary findings, we hypothesize that GBA1 deficiency disrupts astrocyte GAT-3-mediated GABA uptake and tonic inhibition, leading to increased neuronal excitability and more severe αSyn accumulation during the prodromal phase of LBD. Three specific aims are proposed: Aim 1 will determine whether GAT-3 upregulation contributes to impaired tonic inhibition and neuronal hyperexcitability in Gba1CKO mice; Aim 2 will assess whether GAT-3 upregulation is caused by autophagy-lysosome dysfunction in Gba1CKO mice; Aim 3 will examine whether impaired tonic inhibition exacerbates neuronal hyperexcitability and αSyn pathology in the Gba1CKO:Thy1-αSyn LBD model mice. The successful completion of this project will reveal a novel astrocyte-mediated mechanism for LBD pathogenesis and inform the development of more effective therapies.

Up to $452K

2027-12-31

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

Astronomy and Astrophysics Research Grants

U.S. National Science Foundation

Astronomy and Astrophysics Research Grants

2026-11-16

research

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

Astronomy and Astrophysics Research Grants

U.S. National Science Foundation

The Astronomy and Astrophysics Research Grants (AAG) Program is an inclusive and flexible funding opportunity to support research in the astronomical sciences. The Program provides individual investigator and collaborative research grants for observational, theoretical, laboratory, and archival data studies in astronomy and astrophysics. The Program also considers proposals for projects and tools that enable or enhance astronomical research. Proposals may span multiple disciplines and/or areas of study and may utilize multiple techniques.

2026-11-16

sciencetechnology

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

Astronomy and Astrophysics Research Grants

science_technology_and_other_research_and_development

U.S. National Science Foundation

2026-11-16

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

Asymmetric CRISPR Approach for Nucleic Acid Quantification

NIBIB - National Institute of Biomedical Imaging and Bioengineering

Abstract The quantitative detection of nucleic acids plays an increasingly important role in the early detection and screening of cancers. Although the real-time quantitative PCR method has become the gold standard for nucleic acid quantification, its reliance on expensive equipment and trained personnel limits its use in resource-limited settings. Recently, CRISPR technology has emerged as a simple and powerful tool for highly sensitive and specific nucleic acid detection when combined with nucleic acid pre-amplification. However, due to the incorporation of the pre-amplification step, CRISPR-based detection methods require multiple operations and lack the quantitative detection capabilities needed for nucleic acid targets. Therefore, developing a simple and sensitive CRISPR approach for the quantitative detection of nucleic acid biomarkers (e.g., microRNAs) remains a challenge. Recent studies have demonstrated that exosomal microRNAs (exo-miRNAs) are promising liquid biopsy biomarkers for detecting cancer progression and assessing therapy efficacy with high sensitivity and specificity. However, current methods for exo-miRNA detection often require expensive equipment and specialized expertise, hindering their widespread clinical application. Here, we propose to study an asymmetric CRISPR approach for the quantitative detection of nucleic acids (e.g., exo-miRNAs). Furthermore, we will integrate the asymmetric CRISPR assay into a microfluidic chip to develop an asymmetric CRISPR diagnostic platform for exo-miRNA profiling in clinical blood samples. As an example application, we will adapt our asymmetric CRISPR diagnostic platform for the non-invasive early detection of breast cancer—the most commonly diagnosed cancer in the world—and rigorously validate its clinical application. Ultimately, the success of our proposed project will enable clinical translation, facilitating the development of a simple, sensitive, nucleic acid-based molecular detection method for early cancer detection and personalized medicine.

Up to $644K

2030-01-31

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

Asymptomatic TB Transmission, Infectiousness, and Immunology

NIAID - National Institute of Allergy and Infectious Diseases

SUMMARY Tuberculosis (TB) is the leading cause of death due to an infectious agent. Progress in controlling the TB epidemic has fallen short of milestones and new strategies for TB control are urgently needed. Asymptomatic TB, defined as microbiological evidence of TB in people without symptoms, has recently been recognized as common (>50% of prevalent TB) and probably a significant source of M. tuberculosis (Mtb) transmission and driver of the epidemic. There are important knowledge gaps that impede interventions to target asymptomatic TB including: 1) Determining the spectrum of asymptomatic TB infectiousness and risk factors for increased infectiousness and Mtb transmission, 2) Discovering host determinants and mechanisms associated with different outcomes in the natural history of asymptomatic TB (e.g., progression to more infectious TB versus self- resolution of disease), and 3) Developing cost-effective tools to screen for people with asymptomatic TB, especially those who are most infectious or more likely to progress to infectious states. To address these knowledge gaps, this proposal will investigate infectiousness and transmission related to asymptomatic TB, disease trajectories, pathogenesis, and detection in Nairobi, Kenya, a setting with a high burden of TB. Two premises underly our proposed study: 1) Among people with AsxTB, there is a highly infectious (“superspreader”) phenotype who drive Mtb transmission; 2) The untreated clinical course of AsxTB differs between persons, includes self-resolution of TB, and is regulated by unknown clinical and immunologic factors. We will assess infectiousness (cough aerosol culture status), Mtb transmission (investigations of household and non-household contacts to identify recent transmission), immunologic pathways, and cough and biometric profiles (using personal mobile devices). Aim 1 will enroll 10,000 participants in a community-based TB prevalence survey to identify people with asymptomatic TB and symptomatic TB, estimate infectiousness based on cough aerosol culture status, and investigate household and non-household contacts for evidence of transmission using interferon-gamma dependent and independent responses. Aim 2 will follow 7500 participants for 18 months to understand the natural history of asymptomatic TB and investigate the host mechanisms associated with different TB outcomes using single-cell and bulk RNA-Seq. Aim 3 will discover personal-device based cough and biometric profiles to detect asymptomatic TB in the ambulatory setting using machine learning models. Finally, immunologic, clinical, and biometric datasets will be integrated to develop a comprehensive prediction model. This proposal’s multidisciplinary and complementary team will leverage their expertise and experience to construct a new model of asymptomatic TB pathogenesis and natural history, generate evidence on its contribution to transmission, and develop detection methods with potential for public health impacts.

Up to $653K

2031-06-30

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

At Home in the World: Building a Livable Seattle

350 Seattle

The 350 Seattle organization will host a community forum to discuss the need for affordable housing and to explore intersections between the issues of housing, climate protection, and social justice. It will be held at Seattle First Baptist Church located at 1111 Harvard Ave on October 27, 2018 from 1pm - 5pm.

Up to $5K