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NIA - National Institute on Aging

SUMMARY Alzheimer’s disease (AD) is the most common form of dementia and the fifth leading cause of death among older adults in the United States. Unfortunately, available Food and Drug Administration (FDA)-approved therapeutics for treating AD only offer limited efficacy, largely due to our incomplete understanding of the underlying mechanisms that cause and drive the disease. Genome-wide association studies and immunohistochemistry both implicate neuroinflammation and immune dysfunction as key drivers of AD pathogenesis, but the availability of specific biomarkers to investigate and track the spatiotemporal dynamics and functional phenotypes of immune cells in AD remains extremely limited. Positron emission tomography (PET) is a highly sensitive molecular imaging modality well-suited for the longitudinal study of such biomarkers, with demonstrated utility for non-invasive, in vivo interrogation of biochemical processes. Existing PET biomarkers of neuroinflammation (e.g., the translocator protein 18kDa; TSPO) suffer from significant drawbacks, including non-specific expression across multiple cell types in the central nervous system (CNS) and an inability to distinguish between beneficial and harmful inflammatory processes. To address this unmet need, we identified G protein-coupled receptor 84 (GPR84) as a promising biomarker of pro-inflammatory innate immune responses in the context of AD. Specifically, my preliminary data showed that GPR84 expression is significantly upregulated in human myeloid cells following pro-inflammatory stimulation and in rodents after lipopolysaccharide challenge; upregulation is also observed in the brains of the 5xFAD AD mouse model. Excitingly, we developed two lead GPR84-specific PET radiotracers, [11C]GLPG-38 and [18F]MGX-110S, that cross the blood-brain barrier (BBB) in healthy rodents and enable sensitive detection of harmful inflammatory immune responses in vivo. In this proposal, I aim to evaluate the sensitivity and specificity of our two novel GPR84-PET radiotracers for quantifying pro-inflammatory immune responses in human cells and a mouse model of systemic and neuroinflammation (Aim 1). I will also assess radiotracer performance in the 5xFAD mouse model of AD and analyze the spatial overlap between radiotracer binding and immune cell markers in human AD postmortem brain tissues from multiple disease stages compared to healthy controls, employing in vitro autoradiography and advanced spatial biology techniques to further establish translational potential of each radiotracer (Aim 2). Successful completion of these aims will result in characterization of two novel GPR84-PET radiotracers, assessing their suitability for in vivo imaging of neuroinflammation and the specific innate immune cell populations they target. Ultimately, translation of these innovative PET radiotracers into clinical practice will significantly enhance our understanding of AD pathogenesis, facilitate targeted therapeutic development, and enable precise monitoring of treatment efficacy, ultimately paving the way for improved outcomes for patients with AD.

NIAID - National Institute of Allergy and Infectious Diseases

Project Summary This research project seeks to develop and characterize a novel mouse model to address the limitations of current systems for studying mucosal-associated invariant T (MAIT) cells. MAIT cells are a conserved subset of T lymphocytes that bridge innate and adaptive immunity by recognizing microbial metabolites presented by MR1 molecules. They play critical roles in infection control, cancer immunity, and tissue homeostasis. Despite their functional importance, MAIT cells are rare in commonly used laboratory mouse strains, including C57BL/6 (B6), which restricts their study under physiological conditions. Existing approaches, such as TCR transgenic mice or artificial expansion through infection, alter the natural TCR repertoire or rely on inflammation, complicating the study of MAIT cells' development and function. This proposal leverages a genetic engineering strategy to generate the MAIT-Boost Knock-In (MBKI) mouse model, which increases MAIT cell frequency while maintaining natural TCR diversity and thymic selection. By replacing Trav19 with Trav1 and Traj56 with Traj33, the MBKI model redirects TCRa recombination to favor the canonical Trav1-Traj33 configuration required for MAIT cell development. This approach is designed to boost MAIT cell numbers without the unintended consequences of existing models, offering a physiologically relevant system for studying their biology. The project aims to characterize the frequency, tissue distribution, and functional properties of MAIT cells in MBKI mice. It will also assess the broader impact of these modifications on TCRa rearrangement dynamics and other immune subsets, including gd T cells and iNKT cells. Finally, the MBKI model will be used to evaluate whether increased MAIT cell frequency enhances melanoma tumor control, addressing their potential for cancer immunotherapy. This work will provide fundamental insights into MAIT cell biology and create a platform for developing therapeutic strategies targeting infections, cancer, and immune dysregulation.

NIGMS - National Institute of General Medical Sciences

Abstract/Summary: The Fernández Lab seeks to understand how environmental cues and internal physiological states are processed by the nervous system to drive behavior. Our current research focuses on the circadian clock, which allows organisms to maintain internal temporal order and anticipate daily changes in their environment. While the molecular mechanisms underlying the circadian clock are well characterized, the processes by which clock neurons develop and establish connections with each other and with downstream pathways remain poorly understood. Drosophila is an excellent model due to the conservation of the molecular circadian clock and the presence of network motifs resembling those in mammals. Emerging evidence from both mammalian and invertebrate models suggest that core circadian clock genes, some of which are expressed prior to the initiation of the molecular clock, play critical in neuronal development and physiology beyond their established functions in molecular timekeeping mechanism. We recently showed that this is the case for the Drosophila clock gene cycle. When downregulated exclusively during development, cycle leads to altered clock neuron morphology and the loss of adult behavioral rhythms. Our ongoing and future research is aimed at understanding how clock neurons establish their connectivity patterns during development to form a synchronized network of neurons that drives rhythmicity, from gene expression to complex behaviors. Specifically, we will examine the developmental roles of the clock genes cycle and Clock in shaping the connectivity of the main circadian pacemaker neurons and other early-born clock neurons. Notably, these genes are expressed in clock neurons before molecular oscillations can be detected, and we will assess how their downregulation impacts gene expression pathways that influence early-developmental neuronal morphology and connectivity. Additionally, we will examine how various groups of clock neurons respond to key synchronizing signals throughout development, as well as to stimulation of other clock neuron classes. Our recent findings indicate that female circadian rhythms are more resilient to loss of synchronizing factors and suggest that the relative hierarchy of circadian oscillators is sexually dimorphic. We aim to determine the extent to which sexual dimorphism in circadian timekeeping emerges during development and the contributions of sex determination genes in establishing sex differences. Our research program aims to understand how clock neurons develop, communicate, and form precise connections to generate a functional network that drives timekeeping. Our results will contribute to a broader understanding of the mechanisms underlying neuronal development and behavioral plasticity.

NIDDK - National Institute of Diabetes and Digestive and Kidney Diseases

Project Summary Despite recent advances in diabetes treatment and technology (e.g., automated insulin delivery [AID] systems), achieving recommended glycemic targets is still difficult for people with type 1 diabetes (T1D) and, worrisomely, T1D confers substantial cardiorenal risk even when conventional glycemic targets are achieved. The sodium- glucose cotransporter inhibitors (SGLTi) are antihyperglycemic medications that have demonstrated significant cardiorenal benefits in people with and without type 2 diabetes, including reductions in kidney disease progression and hospitalization for heart failure. SGLTi medications have been tested in people with T1D and shown beneficial effects on glycemic control; however, they also contribute to an increased risk of ketoacidosis that has drastically limited their clinical utility in this population. AID systems pair continuous glucose monitors (CGM) and insulin pumps with control algorithms that automatically modulate insulin delivery in real-time. Continuous ketone monitoring (CKM) is a rapidly evolving technology with the potential to prevent ketoacidosis by tracking ketone levels, transmitting results to a dedicated smartphone or device, and providing early warnings of ketone elevations. A combined CKM/CGM biowearable sensor (Abbott Diabetes Care; Alameda, CA) is currently in clinical testing for commercial use and has the potential to be integrated into closed-loop AID systems. The current proposal will specifically address this by developing a “ketone-aware” AID system that receives dual input from the CKM/CGM sensor and subsequently optimizes glycemic control while minimizing ketosis. Our study aims are as follows: 1. We will refine and implement the Ketone-Aware Predictive Algorithm (kAPA), a ketone-aware algorithm with its roots in our recent SGLTi + AID crossover trial. Using archival data and CKM characteristics, we will model ketone elevation and measurement in our well-known simulation environment that is FDA-accepted for preclinical testing of AID systems. In parallel, we will create a kAPA model predictive AID controller and refine it in silico before implementing kAPA into our established DiAS prototyping platform. 2. We will demonstrate the feasibility and safety of kAPA in people with T1D by conducting a 36-hour supervised pilot study to demonstrate acceptable real-time ketosis control while taking sotagliflozin 200 mg; 3. We will demonstrate that kAPA improves glycemic control and minimizes ketosis by conducting a 12- week randomized, single-blind, placebo-controlled crossover clinical trial comparing kAPA + sotagliflozin to AID + placebo in people with T1D. Successful completion of this project will develop a proactive, ketone-aware AID system that can optimize glycemic control, minimize ketosis, and allow for safe administration of SGLTi medications in people with T1D.

NIAID - National Institute of Allergy and Infectious Diseases

ABSTRACT Members of the IL-17 family (IL-17A-F) and its cognate receptors (IL-17RA-RE) mediate physiologically important immune responses, however, they can also drive inflammatory diseases, such as allergic asthma in case of IL-25. Despite its emerging clinical need, no drugs against IL-25 or its signaling pathway are currently clinically available. Our long-term goal is to identify small molecule inhibitors of the IL-25 pathway to probe and prevent IL-25-mediated diseases. The goal of this exploratory R21 application is to establish and validate a high throughput screening (HTS) system as well as relevant orthogonal assays that will enable successful IL-25 small molecule drug discovery using HTS-based hit identification and a defined hit advancement strategy. One major barrier for small molecule drug (SMD) development targeting IL-25 (and other members of the IL-17 family) is that the defined part of the signaling cascade relies on a series of hierarchically acting protein interactions that are inherently difficult for targeted drug development: IL-25 initiates signaling via binding and dimerization of IL-17 receptor RA- and RB-chains, which leads to recruitment/ dimerization of the common IL- 17R adaptor ACT1, followed by recruitment/ dimerization of TRAF6. IL-25 and IL-17RA/RB define the IL-25- specific signaling pathway, while ACT1 defines the common IL-17R family pathway. TRAF6, in turn, defines the boundary between various IL-17R family members and common, IL-17R-non-specific downstream pathways. Thus, signaling events up-stream of ACT1 represent a ‘drug target window’ that defines IL-25-specific inhibitors. Signaling events between ACT1 and TRAF6 represent a ‘drug target window’ that defines common inhibitors of the IL-17 family, including IL-17A as major driver of Th17 immune responses and inflammatory diseases. To overcome limitations related to targeted drug development, we developed a unique, cellular high throughput screening (HTS) platform that retains the advantages of phenotypic screening, i.e. the testing of complex responses in the natural environment of cells and, at the same time, eliminates non-specific compounds, thereby mitigating the major disadvantage of phenotypic screening. In this application, we propose (i) to validate already established reporter cell lines on robots in HTS/ 386 well- format and perform a small 3.6k pilot screen to test and calibrate our screening tool and (ii) to establish and validate a set of orthogonal assays that are suitable to advance IL-25-inhibitory compounds in a full-scale drug discovery campaign. We expect that establishment of these key components of HTS-based drug discovery (along with medicinal chemistry, pharmacology and clinical support by collaborators) will put us in an ideal position for future work to (i) identify specific IL-25-inhibitory small molecule compounds and (ii) develop them towards lead compounds with suitable drug-like properties to be used as probes and starting point for future drug development.

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

PROJECT SUMMARY/ABSTRACT Development of novel contraceptive strategies is central to the mission of the Contraceptive Research Branch of the NICHD. This goal is driven by a global need for effective contraceptive methods to address: 1) the glut of unintended pregnancies (~45% of US pregnancies in 2011); 2) the high rate of elective abortion (1.15M unintended pregnancies ended in abortion in 2011 in the US); and 3) the high risk of maternal mortality (~830 women/day worldwide die due to pregnancy or childbirth complications). In a search for novel male contraceptive drug targets, we identified RBM46, which is a germ cell-specific RNA binding protein expressed by germ cells on the basement membrane of seminiferous tubules (outside the blood-testis-barrier), and is essential for spermatogenesis. Indeed, Rbm46 knockout mice are sterile and have no other phenotype, raising the distinct possibility that targeting RBM46 could lead to safe and effective male contraception by blocking spermatogenesis at the differentiating spermatogonial stage. Thus, we propose to develop drugs that target degradation of RBM46 as a means of oral, non-hormonal male contraception, which will significantly advance additional safe and reversible options for male contraception towards the clinic. Specifically, we will combine: 1) exceptional expertise in drug screening and development at UTSA and UT Health San Antonio; 2) leading expertise in male reproduction, spermatogenesis, and infertility at UTSA and ECU; 3) close proximity to one of two NIH-designated Marmoset Breeding Colonies, maintained at the Southwest National Primate Research Center; 4) growing and ongoing experience collecting and assessing marmoset sperm; 5) published experience in the use of cutting- edge single-cell genomics to assess normality of spermatogenic cell types; and 6) documented expertise with spermatogonial stem cell (SSC) transplantation. In Aim 1, we will identify small molecules that bind RBM46 and could be used to develop PROTACs. In Aim 2, we will produce initial RBM46 PROTACs and validate that they degrade the protein in vitro. In Aim 3, we will use medicinal chemistry to optimize the drug-like characteristics of top validated RBM46 PROTACs. In Aims 4 and 5, we will determine whether optimized RBM46 PROTACs induce reversible contraception in vivo using mice and marmosets, respectively. Together, these Aims are designed to advance RBM46 degradation as a novel strategy to achieve reversible, non-hormonal male contraception and provide key results to justify further preclinical investigation and eventual commercialization.

NIAID - National Institute of Allergy and Infectious Diseases

Proposal Summary Neural regulation of sleep, appetite and energy homeostasis is critical to an animal’s survival and under stringent evolutionary pressure. Despite the prevalence of disorders associated with metabolism and sleep, the neural and genetic processes that regulate interactions between these two systems is unclear. This proposal will investigate how sleep is regulated by blood feeding in the disease vector mosquito Aedes aegypti. We will systematically define sleep in mosquitos, and determine the dietary amino acids that promote sleep. We will then screen neuropeptides for regulators of sleep to test for neuromodulators required for sleep following a blood meal. These experiments leverage decades of sleep analysis in fruit flies, to define sleep in a blood feeding insect. The findings have potential to identify conserved regulators of sleep-feeding interactions, as well as providing the first investigation of how macronutrients regulate sleep in a blood-feeding insect. Further, the methodology used to define sleep can be readily applied to other mosquito species. Therefore, the completion of this work will establish Ae. aegypti as a model for studying dietary regulation of sleep.

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY The bacterial family that is particularly associated with infections of the gut are Enterobacteriaceae. One significant but understudied family member, Providencia alcalifaciens, has been linked to sporadic foodborne outbreaks of diarrhea and isolated from stool samples from persons with diarrhea. P. alcalifaciens is also part of the human oral, sputum and gut microbiomes of healthy individuals. What distinguishes commensal from enteropathogenic P. alcalifaciens? Most diarrheal isolates harbor a large plasmid ranging in size from 128 kb - 181 kb that encodes a type III secretion system (T3SS) that is closely related to, and functionally interchangeable with, the invasion-associated T3SS (T3SS1) of Salmonella enterica serovar Typhimurium. Of the plasmid- carrying isolates, a subset invades non-phagocytic host cells in cellulo. The primary objective of this application is to define what role this genomic and phenotypic heterogeneity plays in P. alcalifaciens pathogenesis. A comparative genomic analysis identified nine genes in the 40 kb type III gene cluster on the plasmid as statistically associated with the invasion phenotype. In Specific Aim 1, we will use in silico, in vitro and in cellulo analysis to determine if these predicted genes are the molecular drivers of invasiveness in P. alcalifaciens. In Specific Aim 2, we will establish an oral-challenge murine model to assess bacterial colonization and host response in the gut upon infection with invasive and non-invasive P. alcalifaciens isolates. These results will define the contribution of intestinal epithelial cell invasion to P. alcalifaciens enteropathogenesis via the natural route of infection. The potential impact of our proposed work is high because it will be the first to decipher the genetic and molecular basis of pathogenicity of P. alcalifaciens, and the first systematic assessment of P. alcalifaciens virulence determinants in a small animal model.

NIAID - National Institute of Allergy and Infectious Diseases

Summary Regulation of immune responses is critical to provide beneficial immunity against pathogens and cancer, while avoiding autoimmune diseases and immunopathology. A population of memory-phenotype CD8+ T cells, expressing the transcription factor Helios” has been proposed to play a key role in preventing excessive and autoimmune responses following vaccination or infection. However, the precise identity of these Helios+ “regulatory” CD8+ T cells, the factors controlling their differentiation and maintenance, and the exact ways in which they contribute to immune homeostasis are highly controversial. In this exploratory proposal, we develop model systems intended to dissect the development, homeostasis and specificity of these CD8+ T cells, position ourselves for future studies on the physiological role and therapeutic potential of Helios+ CD8+ T cells.

AXON ENTERPRISE INC

Engineering and Research and Technology Based Services-Computer services-System and system component administration services-Technical support or help desk services

Columbia Gorge Community College

Promote an inclusive academic library environment by developing a knowledge organization system that dismantles systems of oppression enforced by traditional Eurocentric classification schemas, updating collections to be more reflective of the global majority, and providing technology that bridges the digital divide and affords all students access to advanced technology and/or distance learning courses.

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY / ABSTRACT This MPI R21 proposal directly addresses the objectives of the INvestigation of Co-occurring conditions across the Lifespan to Understand Down syndromE (INCLUDE) Project, emphasizing the creation of innovative biological resources to advance Down syndrome (DS) research. DS is linked to widely dysregulated immune responses, including susceptibility to autoimmunity and infections, but most current research has focused on B cell hyperactivity and interferon-driven pathways, leaving the role of inadequate thymic selection—marked by reduced thymic output and premature thymic involution—largely uncharacterized. Our proposal posits that a fundamental gap in DS research is the absence of a comprehensive understanding of how these thymic defects drive peripheral immune dysfunction. To address this, we will build a well-annotated, deeply profiled biorepository of thymic samples from individuals with trisomy 21 and age-matched disomic controls, enabling a systematic examination of thymic education processes that may underlie the broader immunopathology seen in DS. Although murine models of DS have offered important insights into the genetics and pathology of trisomy 21, they are inherently limited by the fact that the extra copy of human chromosome 21 cannot be fully and precisely replicated in mice. Thymic development, in particular, depends heavily on self-antigens specific to each species, as immature thymocytes are “educated” through interactions with the host’s unique set of self-genes. By establishing a biorepository of human DS thymic tissue, we will circumvent these issues, enabling precise investigations into how an extra copy of chromosome 21 disrupts thymic selection and predisposes individuals with DS to immune dysfunction. To this end, we propose the following two goals. First, through a close collaboration with the Primary Children’s Hospital in Salt Lake City, we will create a comprehensive repository of thymic samples from infants with trisomy 21 and age-matched controls. All samples will undergo HLA genotyping, biological sex determination, and a thorough phenotypic analysis of both T-lineage and non–T- lineage cells, evaluating each thymocyte subset’s responsiveness to T cell receptor (TCR) stimuli at critical developmental checkpoints. Second, we will sequence the TCR repertoire at each developmental stage— evaluating both diversity and amino acid composition—and then compare these results with our existing in- house TCR datasets from individuals with autoimmune diseases and carriers of polymorphisms in genes critical for TCR repertoire formation. This approach will help us pinpoint meaningful similarities or differences among these groups. By filling critical knowledge gaps related to T-lineage ontogeny, our findings may reveal whether this underexplored aspect of thymic development in DS contributes to the documented immune dysfunction.

NIA - National Institute on Aging

Project Abstract Healthy aging may be a case of mind over matter. Experiments in systems ranging from worms to mice have established that neural states, which humans often associate with the feelings and motivations behind our behaviors, may be as influential as physical experiences in promoting a long and healthy life. One major motivational drive for animals is hunger, which promotes feeding. Feeding can be generated by the physiological need to consume nutrients as well as the hedonic properties of food. While brain circuits and mechanisms that regulate feeding have been described, it is unclear how they contribute to the generation of motive forces that drive feeding, and ultimately impact aging. Based on visually identified and quantified behaviors exhibited by hungry flies, we have found that flies exhibit distinct and measurable hunger drives that can be homeostatic (i.e., need-based) or hedonic (i.e., pleasure-based). These can be distinguished, at least in part, using sophisticated feeding behavior metrics that have shown homeostatic feeding is best represented by the number of feeding events on a protein rich food, while hedonic feeding is characterized by the duration of feeding events on a highly palatable food. We have discovered specific regions of the fly brain that influence feeding duration on palatable food but not the number of protein food events, suggesting that they are involved specifically in hedonic feeding. While the direct manipulation of homeostatic hunger has been shown to extend lifespan, preliminary data from our laboratory indicate that hedonic drive shortens fly lifespan. To understand how hedonic feeding is generated by the brain and manipulate this hedonic perception, we will determine how the identified hedonic neural circuitry encodes a hedonic hunger state in Aim 1. For Aim 2, we will identify how different levels of hedonic perception influences aging in Drosophila. The proposed study will provide key insight into how the brain weighs environmental cues to drive hedonic feeding behavior and how hedonic feeding impacts lifespan in various environmental contexts. Additionally, we will manipulate these cues to determine the cellular mechanisms through which feeding neural states can affect healthy aging.

Lusted Water District

Distribution System Improvements

City of Joseph

Distribution System Improvements 2022

Lakewood Homeowners Inc.

Distribution System Replacement Feasibility Study

Christmas Valley Domestic Water Supply District

Distribution System Replacement Phase 3

Ask Reply, Inc. d/b/a B2GNow

Engineering and Research and Technology Based Services

U.S. National Science Foundation

Division of Integrative Organismal Systems Core Programs

Department of Defense

DoD SBIR Phase I awards fund feasibility studies for innovative defense technologies. Topics released monthly covering AI/ML, cybersecurity, autonomous systems, data analytics, and more. Requires U.S. small business with <500 employees. Post-reauthorization solicitations expected March-April 2026.

Department of Defense

DoD STTR Phase I requires partnership with a U.S. research institution. Small business performs 40%+ of work, research institution 30%+. Topics released monthly covering AI/ML, cybersecurity, autonomous systems, and more. Post-reauthorization solicitations expected March-April 2026.

State Water Resources Control Board

The Division of Financial Assistant (DFA), State Water Board manages the DWSRF program and prioritizes financing for projects that address the most serious human health risks, are necessary to comply with SDWA, and assist public water systems (PWS) most in need on per household basis. Periodically funding programs that help provide clean and safe water are used in combination with the DWSRF program. Eligible  community water systems (CWS) currently may receive principle forgiveness (PF)/grant from $2,000,000 up to 100% of total eligible project cost depending on the project types, community served by the CWS, and residential water rates as a percentage of MHI. Financing terms varies from 0% interest to half of California's average general obligation bond rate for the previous calendar year. Repayment may be amortized for 30 to 40 years or the useful life of he financed construction facilities.  Construction of water systems' infrastructures (treatment facilities, water sources, storages, and distribution systems) and contingency of change orders are common eligible construction cost. Additional eligible construction cost examples are value appraisal and land purchase for right-of-way and easements, planning and design, administration, and construction management. Applications for the DWSRF program and associated funding are accepted on a continuous basis. After DFA receives a complete application, a detailed technical, environmental, legal, and financial review is conducted to determine the applicant’s eligibility for DWSRF and associated drinking water funding.

State Water Resources Control Board

The Division of Financial Assistant (DFA), State Water Board manages the DWSRF program and prioritizes financing for projects that address the most serious human health risks, are necessary to comply with SDWA, and assist public water systems (PWS) most in need on per household basis. Periodically funding programs that help provide clean and safe water are used in combination with the DWSRF program. Eligible small community water systems (SCWS) serving a small disadvantage community (DAC) and small severely disadvantage communities (SDAC), eligible non-transient non-community water systems (NTNC) serving a small DAC or small SDAC, and public water systems (PWS) extending service to small DACs andsmall SDACs may receive the maximum principle forgiveness (PF)/grant of $500,000. Other public water systems may receive loan or partial loan with subsidized interest rate and maximum term for repayable of five or ten years. Planning costs may include the preparation of planning/design documents such as Feasibility studies and project reports, plans and specifications, engineering and specifications, environmental documents, capital improvement plans, etc. Other costs such as legal costs and fees, environmental review, TMF assessments, water rate studies, and test wells are also eligible for funding under planning projects. Applications for the DWSRF program and associated funding are accepted on a continuous basis. After DFA  receives a complete application, a detailed technical, environmental, legal, and financial review is conducted to determine the applicant’s eligibility for DWSRF and associated drinking water funding.

EDF

DRT Power Systems Capital