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NINDS - National Institute of Neurological Disorders and Stroke

There have been great advances in microscopic and non-invasive optical neuroimaging technologies, which allow neuroscientists to visualize molecular, cellular and systems-level brain physiology and functions. For the last five years, these technological efforts have been greatly facilitated by the BRAIN Initiative, which also supports the pipeline to commercialization. However, this fast growth has widened the gap between the developers and the neuroscience community in need. This is because to properly use these novel tools, it is important to understand the underlying physical principles and have the practical skills in data collection and analysis. Furthermore, each technique comes with its limitations, and understanding these limitations is critical for avoiding unconscious bias. Thus, although instrumentation may be available, the researchers are often not fully utilizing these tools due to the lack of proper training. To this end, we propose a two-week Summer School program in Neurovascular Imaging Across Scales in Animals and Humans run by the Boston University (BU) Neurophotonics Center. This program will offer hands- on, practical training in a number of optical imaging technologies applicable to in vivo studies in awake behaving animals. In addition, we include a macroscopic, non-invasive optical imaging modality applicable to humans. These technologies will be taught and exemplified in the context of specific neuroscience questions developed by trainees. These questions will be centered on neurovascular brain physiology in heath and disease addressing the mission of NINDS. The program will target graduate students and postdoctoral fellows in the beginning of their research projects who started using one of these imaging technologies and want to acquire practical “know-how” skills and gain exposure to other imaging technologies applicable to neurovascular studies. Our primary goal is to create an innovative educational program using neurophotonics as an enabler to understand neurovascular brain function in health and disease. This program will also contribute to broad dissemination of neurophotonics technologies, increase visibility of these tools within the neuroscience community, and promote the emerging interdisciplinary field of neurophotonics and the deliverables of the BRAIN Initiative. The program alumni will fill an acute nation-wide need for neuroscience investigators skilled in state- of-the-art neurophotonics technologies. In addition, we expect the key aspects of our innovative training approach to be translated to other interdisciplinary graduate and postgraduate education programs at BU and beyond. Our best practices and measured impacts of experiential learning will be disseminated to peer institutions and to graduate education stakeholders. Our primary goal is to create an innovative educational program using neurophotonics as an enabler to understand neurovascular brain function in health and disease. This program will also contribute to broad dissemination of neurophotonics technologies, increase visibility of these tools within the neuroscience community, and promote the emerging interdisciplinary field of neurophotonics and the deliverables of the BRAIN Initiative. The program alumni will fill an acute nation-wide need for neuroscience investigators skilled in state- of-the-art neurophotonics technologies. In addition, we expect the key aspects of our innovative training approach to be translated to other interdisciplinary graduate and postgraduate education programs at BU and beyond. Our best practices and measured impacts of experiential learning will be disseminated to peer institutions and to graduate education stakeholders.

New Mexico Department of Finance and Administration

The Colonias Infrastructure Fund provides grants to communities along the US-Mexico border for basic infrastructure including water systems, wastewater treatment, housing, and roads in historically underserved colonias communities.

New Mexico Indian Affairs Department

The Tribal Infrastructure Fund provides grants to New Mexico's pueblos, tribes, and nations for critical infrastructure projects including water and wastewater systems, roads, public buildings, and broadband connectivity.

Regional Council Capital Fund - RC 2

New York Insitute of Technology STEM Capital

Labor

On October 21, 2021, New York State (NYS) Governor Kathy Hochul announced a commitment of $11.1 million in federal workforce development investment to expand the Disability Resource Coordinators (DRCs) network across several Local Workforce Development Areas (LWDAs). This program builds on previous programs like the Disability Employment Initiative (DEI) and Disability Program Navigator, and aims to improve education, training and employment outcomes for individuals with disabilities, including those receiving Social Security benefits, by scaling up services and enhancing support across nearly all LWDAs in NYS.A key partner in the NY SCION effort is the New York Employment Services System (NYESS) under the NYS Office of Mental Health (OMH), which commits $1 million annually to support employment services in participating LWDAs for individuals with disabilities. Through this collaboration, DRCs connect individuals with disabilities to Career Center services, employment referrals, and benefits advisement. NY SCION is currently active in 27 LWDAs, including New York City, covering 48 counties, and has helped more than 11,000 individuals with disabilities access career services to date. The program's ambitious goal is to serve 45,000 individuals with disabilities, significantly improving access to sustainable employment and career pathways.

National Aeronautics and Space Administration

Next Gen STEM (NGS) NASA Aerospace Skilled Technical Workforce Hubs (NAS_Hub)

NIA - National Institute on Aging

Peripheral artery disease (PAD) is a progressive condition marked by the narrowing and blockage of arteries supplying the legs, often leading to debilitating leg pain and significant walking impairment known as claudication. While standard therapies exist, their effectiveness is limited, and there remains a critical need for treatments that enhance limb perfusion and function while reducing reliance on costly interventions. Recent clinical trials have suggested that stem cell therapy may hold promise for PAD treatment, yet results have been mixed, with ongoing barriers regarding the optimal cell type, delivery method, and therapeutic targeting. In this proposal, we overcome these barriers by using an autologous cellular preparation (adipose stromal vascular fraction, or SVF), and by targeting the inflow collateral vessels and employing a novel access and delivery strategy to enhance perfusion. We have developed and validated a minimally-invasive porcine model of hindlimb ischemia (percutaneous catheter-based coil occlusion of the iliofemoral and popliteal arteries) which recapitulates key aspects of human PAD and can be a platform for PAD therapy development. We have demonstrated that transvenous periarterial administration (around the porcine aortic trifurcation) of SVF increases long-term arterial inflow to the ischemic hindlimb and improves treadmill performance with respect to sham-treated ischemic hindlimbs. The objective of our proposal is to compare regenerative, cell-based regimens for PAD treatment (including SVF and SVF-derived exosomes) in a clinically relevant animal model of hindlimb ischemia whose size, anatomy, physiology, and comorbidities closely mirror those of human PAD patients. Our central hypothesis is that: (i) delivery of SVF into the peri-arterial region of the aortic trifurcation, in our porcine hindlimb ischemia model, will increase arteriogenesis and improve hemodynamic and functional endpoints more effectively than either intra-arterial SVF delivery or sham treatment; and (ii) SVF vs. SVF-derived exosomes, delivered peri-arterially in the same model, will provide equivalent benefits on the same endpoints. We will test this central hypothesis in three Specific Aims: Aim 1 will compare the effect of transvenous/peri-arterial (aortic trifurcation region) SVF delivery vs. intra- arterial SVF delivery on arteriogenesis, hindlimb perfusion, treadmill performance, and histological endpoints in our porcine model of hindlimb ischemia; Aim 2 will compare the effect of transvenous/peri-arterial (aortic trifurcation region) delivery of SVF vs. exosomes derived from SVF on arteriogenesis, hindlimb perfusion, treadmill performance, and histological endpoints; and Aim 3 will investigate the mechanisms by which SVF or exosomes delivered to the retroperitoneum around the aortic trifurcation drive arteriogenesis. Successful performance of this research proposal should lead to development of arterial inflow-enhancing therapies which would be useful in PAD patients, particularly ones who are not fit, not appropriate, or not willing to undergo a major revascularization procedure.

COLUMBIA PIPE & SUPPLY LLC

Distribution and Conditioning Systems and Equipment and Components

DEPT OF DEFENSE.DEPT OF THE NAVY.NAVSUP.NAVSUP WEAPON SYSTEMS SUPPORT.NAVSUP WSS PHILADELPHIA.NAVSUP WEAPON SYSTEMS SUPPORT

NIIN:013145838/ACTUATOR,ELECTRO-ME

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY The fungal pathogen Histoplasma capsulatum infects and thrives within phagocytes of the immune system. Results from a genetic screen indicate that peroxisome organelles play a critical role in facilitating Histoplasma proliferation in macrophages. Preliminary work demonstrated that the known peroxisomal functions of fatty acid β-oxidation, the glyoxylate cycle, and catalase destruction of reactive oxygen are all dispensible for Histoplasma pathogenesis indicating that peroxisomes play a novel role. This proposal will uncover new peroxisome functions by definition of the peroxisome proteome and metabolome in pathogenic-phase fungal cells. Candidate peroxisomal functions will be validated by functional tests to determine their contributions to Histoplasma’s intramacrophage proliferation. This work will uncover new peroxisomal functions and reveal novel mechanisms for fungal exploitation of the macrophage.

NIDA - National Institute on Drug Abuse

PROJECT SUMMARY The initiating factor for opioid use disorder often stems from comorbid neuropsychiatric conditions including anxiety, depression, and post-traumatic stress disorder. Experience of extreme or traumatic stress is often the underlying factor responsible for these neuropsychiatric conditions and, thus, investigation into the neural mechanisms by which stress impacts the brain is essential for determining the mechanisms responsible for the initiation of substance use disorders. Our preliminary data demonstrates that stress exposure leads to increased cytokine release and heightened activity of the noradrenergic locus coeruleus (LC), a key region responsible for the integration of stress signaling that projects norepinephrine to numerous downstream brain areas. The prelimbic cortex of the medial prefrontal cortex (PrL) is one such region that receives over 90% of its noradrenergic innervation from the LC and plays a major role in drug seeking and reward-related behaviors. Thus, the overall goal of this project is to establish the circuit mechanisms of stress-related norepinephrine release in the PrL and the role of these projections in oral oxycodone seeking behaviors. These experiments will use cutting edge techniques including chemogenetics, in vivo electrophysiology, and fiber photometry with GRAB sensors to monitor neuronal activity and transmitter release across this circuit in response to stress and drug stimuli. Three main experiments have been designed to address the hypothesis that stress-evoked increases in neuroimmune activity in the LC initiate neuronal activation and downstream NE release to mediate stress- induced drug seeking behavior. First, chemogenetic suppression of neuroimmune activity in the LC will be paired with in vivo electrophysiology during stress to monitor the impact of microglial reactivity on neuronal activity within this region (Aim1, K99). The second experiment will utilize GRABNE sensors in the PrL to determine the time-course of norepinephrine release in response to stress cues. These studies will also use adrenergic receptor antagonists microinjected into the PrL during stress-cue reinstatement to determine the mechanisms by which NE is acting in this region to impact drug seeking behaviors (Aim2, K99). The final experiment will use translationally relevant compounds to determine if the reversal of stress-induced neuroimmune reactivity can prevent the deleterious effects observed as a consequence of stress (Aim3, R00). Taken together, these studies will expand our understanding of the circuit mechanisms responsible for stress-related opioid seeking behaviors and determine the therapeutic potential of clinically available pharmaceuticals all while providing extensive training in innovative preclinical techniques. The combined technical training and career development opportunities supported by this application will facilitate further independent projects designed to address unanswered questions regarding the neural mechanisms responsible for opioid use to develop novel treatment targets for comorbid stress and substance use disorders.

Town of Greensboro

North Caroline Wastewater System

North Seattle Boys & Girls Club

Add 23 state-of-the-art computers in the newly renovated Teen Center in North Seattle. Increase technology access and provide more hands-on academic and STEM-based tech education programs to 400 youth.

WE STAY NOS QUEDAMOS INC

Sited at 2 local community gardens and within the courtyard of NQ's headquarters, each will include solar canopies, rainwater harvesting systems, and broadband access, establishing three local microgrids.

International Trade Commission

Notice is hereby given that the U.S. International Trade Commission has received a complaint entitled Certain Disposable and Other Closed-System Electronic Nicotine Delivery Systems (ENDS) Devices and Components Thereof, DN 3875; the Commission is soliciting comments on any public interest issues raised by the complaint or complainant's filing pursuant to the Commission's Rules of Practice and Procedure.

NIAID - National Institute of Allergy and Infectious Diseases

ABSTRACT Allergic diseases have increased dramatically to become the most common human disorders in developed countries. Despite improved clinical diagnosis and management, they are the leading cause of work and school absences. The prevalence of food allergy is rising for unclear reasons, with prevalence estimates in the developed countries around 10%. Peanut allergy affects 1–2% of the population in Westernized nations and is a leading cause of food-induced anaphylaxis. Specifying and maintaining elimination diets places a significant burden on patients, families and healthcare systems. The possibility of anaphylactic responses by sensitized individuals complicates food manufacturing, as the products should be free of unmarked allergy triggers, including peanuts, tree nuts, wheat, soy, fish, shellfish, eggs and milk. Thus, there is an unmet need to identify allergen features and find proteins which could cause cross-reactions in sensitive individuals among the vast number of proteins now catalogued in proteome databases. A first version of a novel machine learning (ML) tool, AllergenAI, which used only amino acid sequences in three allergen protein databases, SDAP 2.0, COMPARE and AlgPred, achieved robust results. To further improve this ML model, we will use Alphafold-2 to model all proteins in these three databases and incorporate the 3D structural information into AllergenAI (Aim1). The predictive abilities of AllergenAI will be experimentally assessed in Aim2, by analyzing the features scores for well-studied vicilin allergens, which are among the most common allergens (with over 20 entries in the Structural Database of Allergenic Proteins (SDAP), including the major allergen Ara h 1 of peanuts and its homologues in tree nuts, legumes and cotton). The program’s ability to distinguish homologues in the very broad vicilin protein family that could cause cross-reactions with IgE in allergic patient sera will be tested. The weight parameters of AllergenAI will be fine-tuned by using a Large Language Model (LLM) ESM-2 in Aim 3. The optimized AllergenAI will be benchmarked by comparison to other prediction methods for allergenic proteins that are based on sequence alone. We hypothesize that artificial intelligence (AI) technologies that made dramatic improvements in recent years will clarify the problem of “what makes a protein allergenic”. The application of AI technology to allergen research is novel. Our combined experimental and computational approach will yield a powerful new method to identify potential allergenic characteristics in new proteins and help design better immunotherapies for allergenic diseases. The source code for the optimized AllergenAI model, documentation for use and example input files will be made available from our SDAP 2.0 website, which is used extensively by researchers and clinicians throughout the world.

NIAID - National Institute of Allergy and Infectious Diseases

Project Summary/Abstract The immune system can be categorized into innate and adaptive immunity. Innate immune cells detect and respond according to danger associated signals and initiate a coordinated antigen-specific response by the adaptive system to eliminate threats such as viruses, bacteria and tumor cells. Immunosuppressive drugs inhibit adaptive responses and are used following organ transplantation to prevent acute transplant rejection but do not generally target innate immunity. It was recently discovered that innate cells can be licensed to detect foreign allogenic tissue and initiate responses against the transplant in the absence of danger- associated signals. Additionally, innate cells show accelerated activation responses following re-exposure to the identical foreign tissue, called innate memory or trained immunity. These findings suggest that innate cells are chronically stimulated and activated following transplantation, and it is possible that persistent innate responses participate in or drive chronic transplant rejection, the main reason for graft loss. Little is known about the mechanisms that control and modulate innate allo-activity and no therapeutic is clinically available to resolve persistent innate alloimmunity following transplantation. In this proposal, we hypothesize that Semaphorin 3F (SEMA3F)-Neuropilin 2 (NRP2) interactions on monocytes can inhibit and/or resolve persistent innate alloimmune responses following transplantation. In preliminary experiments, we find that monocytes express NRP2 following initial alloimmune activation in recipients of fully MHC mismatched cardiac allografts. We also find that the administration of the NRP2-ligand SEMA3F prolongs allograft survival in models of cardiac transplantation. In Aim 1, we will assess SEMA3F- induced innate responses following transplantation and we will employ transcriptomics and confirmatory protein-based methods to define SEMA3F-dependent signaling networks within monocytic subsets. In Aim 2, we will use a monocyte-specific tamoxifen-inducible NRP2 KO mouse model and evaluate intrinsic effects of NRP2 signaling on monocyte responses following transplantation. We predict that the administration of SEMA3F prolongs allograft survival by inhibiting monocyte and macrophage alloimmune memory responses. We also predict that deletion of NRP2 from monocytes results in accelerated graft rejection and that SEMA3F- NRP2 interactions are required for long term graft survival. If successful, the impact and relevance of these studies are the identification of SEMA3F as a novel immunoregulatory ligand that suppresses innate immunity following transplantation, the identification of NRP2 as a co-inhibitory receptor on innate cells, and that they enable the development of immunomodulatory drugs that resolve persistent innate alloimmune responses post transplantation.

NIA - National Institute on Aging

PROJECT SUMMARY This proposal aims to develop advanced statistical and computational methods for analyzing immune data to enhance our understanding of the immune system’s role in aging and age-related diseases. Aging is accompanied by significant changes in the immune system, increasing susceptibility to infections, chronic inflammation, and other health challenges. Understanding the heterogeneity of immune profiles and their associations with aging outcomes holds great promise for predicting disease risk and identifying therapeutic targets. Large-scale studies such as the Health and Retirement Study (HRS) provide invaluable data on the elderly population. However, immune data obtained from flow cytometry present unique analytical challenges. These data are compositional, highly skewed, and prone to substantial measurement errors, rendering standard analyses unreliable. Existing methods for supervised and unsupervised analysis of immune data frequently fall short in adjusting for covariates, identifying key immune features, capturing nonlinear relationships, and integrating multiple data sources, resulting in significant gaps in our understanding of immune aging. This proposal addresses these challenges through innovative methodologies. In Aim 1, we will develop a robust nonparametric framework to denoise immune cell frequency data. This framework is free from distributional assumptions and adaptable to diverse data types, enhancing the accuracy of subsequent analyses. In Aim 2, we will create a model-based clustering framework to identify immune subgroups, with a special focus on adjusting for covariates and identifying key drivers of heterogeneity between clusters. In Aim 3, we will develop novel semi-parametric methods to integrate multiple sources of immune biomarkers and associate them with aging outcomes, emphasizing biological interpretability and feature selection. In Aim 4, we will build an open- source software package to ensure the accessibility and wide dissemination of these methods. Motivated by and applied to HRS data, these methods aim to uncover immune signatures in the elderly and clarify their relationship with age-related outcomes. The research will deliver powerful tools for immune data analysis and transformative insights into the interplay between immunity and aging.

NIAID - National Institute of Allergy and Infectious Diseases

Abstract: The cytokine IFN-g controls both protective and pathogenic host responses during infection and inflammation. By activating cell autonomous antimicrobial mechanisms, this cytokine mediates host resistance mechanisms that control pathogen replication. Much less is known about how the same cytokine regulates sickness associated behaviors such as anorexia and whole-body weight loss. We have recently published data indicating that IFN-g regulates the systemic levels of the stress hormone GDF-15 which is important for appetite suppression and weight loss during infection. In turn, GDF15 is required for hepatic production of FGF21 and the consequent generation of ketone bodies, including beta-hydroxybutyric acid. Recently, a previously unrecognized biochemical pathway of “reverse proteolysis”, mediated by the enzyme CNDP2 (carnosine dipeptidase 2) has been shown to generate a novel class of anorexigens through chemical conjugation of either beta-hydroxybutyric (BHB) acid or lactic acid to amino acids bearing hydrophobic side chains. While a role for this new pathway has recently been demonstrated in the context of appetite suppression following metformin therapy or physical exercise, its relevance to sickness associated anorexia during infection and inflammation has not been examined. Here, we present preliminary data showing that BHB-amino acid but not lactoyl-amino acid conjugates are elevated in the serum of T. gondii-infected mice. Furthermore, the in vivo expression of CNDP2 transcripts is upregulated during infection and this induction is dependent on IFN-g receptor signaling. Thus, we hypothesize that IFN-g mediates suppression of food intake and sickness associated weight loss, in part, by inducing CNDP2 in immune cells, thus, elevating circulating levels of this novel class of metabolite-derived anorexigens during infection. Specific Aim 1 will test the hypothesis that IFN-g signaling induces CNDP2-mediated generation of BHB-amino acids by immune cells during T. gondii infection. Specific Aim 2 will critically interrogate the role and function of CNDP2 in regulating the sickness associated anorexia and weight loss during T. gondii infection. Completion of this project will provide novel and fundamental insights into how inflammation and immune cytokines control sickness associated anorexia and weight loss during infection and inflammation. These insights may provide avenues to promote health by decreasing disease sequelae that result from hyperactivation of immune response and the ensuing disruption of metabolic homeostasis in the host.

National Park Service

NPS Cooperative Ecosystems Studies Units (CESU) Master Cooperative Agreements

U.S. National Science Foundation

NSF STEM K-12

U.S. National Science Foundation

NSF-DFG Lead Agency Opportunity in Chemistry and Chemical Process and Transport Systems

DEPT OF DEFENSE.DEPT OF THE NAVY.NAVSUP.NAVSUP WEAPON SYSTEMS SUPPORT.NAVSUP WSS MECHANICSBURG.NAVSUP WEAPON SYSTEMS SUPPORT MECH

NUT, STEM RETAINING

DEPT OF DEFENSE.DEPT OF THE NAVY.NAVSUP.NAVSUP WEAPON SYSTEMS SUPPORT.NAVSUP WSS MECHANICSBURG.NAVSUP WEAPON SYSTEMS SUPPORT MECH

NUT,HEX