MAYO CLINIC JACKSONVILLE (A NONPROFIT CORPORATION) - Florida Company Profile

GKPBCFV1QMM3

01JF4

2026-06-11

2025-06-13

2001-02-09

01JF4

Active

Non-Manufacturer

2025-06-13

2030-06-13

2026-06-11

DON COLDIRON

2025-06-13

5A021

MAYO CLINIC

36C24925P0108

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AWARD

PURCHASE ORDER

51105.00

51105.00

51105.00

Department of Veterans Affairs

2024-10-30

RATIFICATION OF AN UNAUTHORIZED COMMITMENT

621111: OFFICES OF PHYSICIANS (EXCEPT MENTAL HEALTH SPECIALISTS)

Q508: HEMATOLOGY & ONCOLOGY

36C26223C0234

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AWARD

DEFINITIVE CONTRACT

55414.00

55414.00

55414.00

Department of Veterans Affairs

2023-08-01

HUMANIZATION AND BINDING AFFINITY TESTING

541720: RESEARCH AND DEVELOPMENT IN THE SOCIAL SCIENCES AND HUMANITIES

AN42: HEALTH R&D SERVICES; HEALTH CARE - OTHER; APPLIED RESEARCH

75N91018P00618

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AWARD

PURCHASE ORDER

36000.00

36000.00

36000.00

Department of Health and Human Services

2018-09-13

SERVICES TO OBTAIN DNA SAMPLES AND PATIENT DATA FOR 1,100 RENAL CELL CARCINOMA CASES (RCC) FOR INCLUSION IN A GENOME-WIDE ASSOCIATION STUDY (GWAS)

541380: TESTING LABORATORIES

R499: SUPPORT- PROFESSIONAL: OTHER

2025-04-03

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Department of Defense

RESOLVING THE CRITICAL ROLE OF PINK1 EXPRESSION AND ACTIVITY IN PARKINSON'S DISEASE PATHOPHYSIOLOGY AND THERAPEUTIC INTERVENTION

813085.00

0.00

0.00

2025-04-03

View on USAspending

Department of Defense

RESOLVING THE CRITICAL ROLE OF PINK1 EXPRESSION AND ACTIVITY IN PARKINSON'S DISEASE PATHOPHYSIOLOGY AND THERAPEUTIC INTERVENTION

1186914.00

0.00

0.00

2025-04-08

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Department of Health and Human Services

STANDARDIZING AND HARMONIZING BEHAVIORAL AND SOCIAL SCIENCE RESEARCH FACTORS IN ALZHEIMER'S DISEASE THROUGH ONTOLOGY-BASED APPROACHES - ABSTRACT BEHAVIORAL AND SOCIAL SCIENCE RESEARCH (BSSR) IS INSTRUMENTAL IN COMPREHENDING ALZHEIMER'S DISEASE AND RELATED DEMENTIA (ADRD) AND ITS FAR-REACHING IMPLICATIONS FOR INDIVIDUALS, FAMILIES, AND COMMUNITIES. BSSR INVESTIGATES HOW BEHAVIORAL AND SOCIAL DETERMINANTS, ENCOMPASSING FACTORS LIKE PHYSICAL ACTIVITY, COGNITIVE ENGAGEMENT, DIET, AND SOCIAL INTERACTIONS, INFLUENCE THE RISK OF DEVELOPING AD. THIS EXPLORATION AIMS TO UNCOVER NON-PHARMACOLOGICAL INTERVENTIONS THAT CAN MANAGE SYMPTOMS AND ENHANCE THE WELL-BEING OF INDIVIDUALS WITH AD/ADRD, INCLUDING COGNITIVE STIMULATION PROGRAMS, BEHAVIORAL THERAPIES, SOCIAL ENGAGEMENT INITIATIVES, AND CAREGIVER TRAINING. MOREOVER, BSSR DELVES INTO THE SOCIAL, CULTURAL, AND ENVIRONMENTAL ELEMENTS CONTRIBUTING TO HEALTH DISPARITIES, INFORMING TAILORED INTERVENTIONS AND POLICIES FOR VARIOUS POPULATIONS, ESPECIALLY UNDERSERVED AND MINORITY COMMUNITIES. COLLECTIVELY, THIS RESEARCH ENRICHES OUR UNDERSTANDING OF ADRD AND GUIDES THE DEVELOPMENT OF INTERVENTIONS, SUPPORT SYSTEMS, AND POLICIES TO ENHANCE THE LIVES OF THOSE AFFECTED BY THE DISEASE. YET, THERE ARE CHALLENGES IMPEDING THE INTEGRATION OF ADRD-RELATED BSSR DATA. A CRITICAL ISSUE IS THE ABSENCE OF FORMAL REPRESENTATIONS FOR BSSR DATA AND LIMITED TOOLS TO LINK COMPREHENSIVE BSSR INFORMATION FROM DIVERSE SOURCES. THIS HAMPERS THE HOLISTIC CONSIDERATION OF BSSR FACTORS IN AD-RELATED RESEARCH, UNDERMINING EVIDENCE-BASED CARE AND SUPPORT. IN RESPONSE TO PAR-23-182, WE PROPOSE PIONEERING ONTOLOGY-BASED APPROACHES TO FORMALLY REPRESENT ADRD-RELATED BSSR FACTORS IN A STANDARDIZED MANNER. WE WILL DEVELOP NATURAL LANGUAGE PROCESSING (NLP) METHODS TO EXTRACT AND NORMALIZE BSSR DATA FROM ELECTRONIC HEALTH RECORDS (EHRS) AND LITERATURE. OUR PROJECT AIMS TO INTEGRATE STRUCTURED AND UNSTRUCTURED DATA ACROSS VARIOUS RESEARCH SILOS, CULMINATING IN A COMPREHENSIVE AND NORMALIZED KNOWLEDGE GRAPH INCORPORATING BSSR FACTORS FOR ADRD COHORTS. MORE SPECIFICALLY, IN AIM 1, WE WILL DEVELOP THE BEHAVIORAL SOCIAL DATA AND KNOWLEDGE ONTOLOGY FOR ADRD (BSO-AD) TO STANDARDIZE BSSR FACTORS. WE WILL ALSO ASSESS THE BSO-AD FOR CORRECTNESS AND SUITABILITY, REFINING IT BASED ON EVALUATION SCORES. AIM 2 EMPLOYS NLP TECHNOLOGIES, INCLUDING STATE-OF-THE-ART LARGE LANGUAGE MODELS, TO EXTRACT AND NORMALIZE BSSR-RELATED INFORMATION FROM CLINICAL NOTES AND LITERATURE. THIS NLP SYSTEM WILL ENSURE SEMANTIC INTEROPERABILITY AND CONSISTENCY IN ENTITY RECOGNITION AND NORMALIZATION. IN AIM 3, WE WILL CREATE A KNOWLEDGE GRAPH (KG) TO INTEGRATE ANNOTATED BSSR FACTORS FROM STRUCTURED AND UNSTRUCTURED SOURCES, SUPPORTING ADRD-RELATED RESEARCH AND APPLICATIONS. WE WILL EVALUATE THE ONTOLOGY AND KG THROUGH DEMONSTRATION STUDIES AND DISSEMINATE THESE RESOURCES TO THE RESEARCH COMMUNITY, PROMOTING COLLABORATIVE RESEARCH EFFORTS. IN SUMMARY, OUR PROJECT AIMS TO BRIDGE THE GAP IN ADRD-RELATED BSSR DATA INTEGRATION BY STANDARDIZING REPRESENTATION, ENABLING EFFICIENT EXTRACTION, AND FOSTERING COLLABORATION WITHIN THE RESEARCH COMMUNITY. THIS ENDEAVOR WILL ADVANCE OUR UNDERSTANDING OF ADRD AND CONTRIBUTE TO EVIDENCE-BASED CARE AND SUPPORT FOR AFFECTED INDIVIDUALS AND THEIR COMMUNITIES.

801130.00

0.00

0.00

2025-04-16

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Department of Health and Human Services

DECIPHERING PANCREATITIS MICROENVIRONMENT THROUGH INTRAVITAL IMAGING - PROJECT SUMMARY ACUTE PANCREATITIS (AP) IS A PREVALENT GASTROINTESTINAL CONDITION THAT LEADS TO A SIGNIFICANT NUMBER OF HOSPITALIZATIONS AND HIGH HEALTHCARE COSTS. WITH NO EFFECTIVE THERAPY CURRENTLY AVAILABLE, THERE IS AN URGENT NEED FOR RESEARCH TO DEVELOP SUCCESSFUL TREATMENTS. THIS PROPOSAL AIMS TO INVESTIGATE THE ROLES OF TRYPSIN AND COAGULATION IN THE DEVELOPMENT OF ACUTE PANCREATITIS AND EXPLORE THE HYPOTHESIS THAT THROMBIN PLAYS A CRUCIAL ROLE IN THE DISEASE. PREVIOUS STUDIES HAVE SHOWN THAT THROMBIN, A DUAL THROMBIN AND TRYPSIN INHIBITOR, HAS SUPERIOR EFFECTS IN PREVENTING AND TREATING ACUTE PANCREATITIS COMPARED TO SELECTIVE TRYPSIN INHIBITORS. THIS SUGGESTS THAT ANTI- TRYPSIN AND ANTI-COAGULATION MECHANISMS WORK TOGETHER TO COMBAT THE DISEASE. TO INVESTIGATE THIS FURTHER, GENETIC APPROACHES WILL BE USED, INCLUDING A NEWLY ENGINEERED TRYPSIN KNOCKOUT MOUSE MODEL (T2457) AND A CONDITIONAL THROMBIN KNOCKOUT MOUSE MODEL. THE RESEARCH WILL FOCUS ON DISSECTING THE ROLES OF TRYPSIN AND COAGULATION IN ACUTE PANCREATITIS INITIATION AND PROGRESSION. ADDITIONALLY, THE IMPACT OF THROMBIN ON THE PANCREATIC MICROENVIRONMENT WILL BE EXAMINED USING A MULTI-PHOTON INTRAVITAL IMAGING SYSTEM. THROMBIN INHIBITORS, PAR RECEPTOR INHIBITORS, AND PAR1 KNOCKOUT MICE WILL BE UTILIZED TO GAIN A BETTER UNDERSTANDING OF THE COAGULATION PATHWAY'S INFLUENCE ON ACUTE PANCREATITIS. IN THE FINAL AIM, THE PROJECT WILL CONCENTRATE ON ENHANCING DRUG DELIVERY TO THE INFLAMED PANCREAS, ADDRESSING THE ISSUE OF LOW DRUG CONCENTRATIONS IN THE AFFECTED TISSUE. DABIGATRAN WILL BE USED AS A MODEL DRUG, AND PROOF-OF-PRINCIPLE STUDIES WILL BE CONDUCTED TO DEVELOP PANCREATITIS-SPECIFIC DRUGS THAT IMPROVE DRUG DELIVERY. AN INTRAVENOUS FORMULATION OF DABIGATRAN WILL BE FORMULATED AND TESTED FOR THERAPEUTIC EFFICACY, ALONG WITH TWO PRODRUGS DESIGNED TO ACTIVATE LOCALLY IN THE PANCREAS. THE COMPLETION OF THIS PROJECT WILL SIGNIFICANTLY ADVANCE THE UNDERSTANDING OF ACUTE PANCREATITIS PATHOPHYSIOLOGY AND CONTRIBUTE TO THE DEVELOPMENT OF TARGETED THERAPIES. THE KNOWLEDGE GAINED WILL PROVIDE A SOLID FOUNDATION FOR FUTURE CLINICAL TRIALS AIMED AT PREVENTING AND TREATING ACUTE PANCREATITIS. ULTIMATELY, THIS RESEARCH HAS THE POTENTIAL TO IMPACT PATIENT OUTCOMES AND IMPROVE THE MANAGEMENT OF THIS CHALLENGING CONDITION.

1157318.00

0.00

0.00

2025-04-15

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Department of Health and Human Services

PROTEIN KINASE D1 AS A SWITCH FROM ACUTE TO CHRONIC PANCREATITIS - PROJECT SUMMARY/ABSTRACT ACUTE PANCREATITIS, IF IT DOESN’T RESOLVE, CAN FURTHER DEVELOP INTO A CHRONIC CONDITION. RESULTING CHRONIC PANCREATITIS IS CHARACTERIZED BY PRESENCE OF INFLAMMATORY MACROPHAGES, FIBROSIS, AND LOSS OF ACINAR CELLS. MOREOVER, IT REPRESENTS A RISK FACTOR FOR PANCREATIC CANCER. THE CELLULAR AND MOLECULAR MECHANISMS THAT MEDIATE THE TRANSITION FROM ACUTE TO CHRONIC PANCREATITIS ARE ILL-DEFINED, AND EFFICIENT THERAPEUTIC TREATMENT METHODS FOR CHRONIC PANCREATITIS ARE LACKING. IN THIS PROPOSAL, IT IS OUR HYPOTHESIS THAT PROTEIN KINASE D1 PRIMES ACINAR CELLS TO PRODUCE FACTORS THAT PREVENT ACUTE PANCREATITIS FROM RESOLVING AND GENERATES A CHRONIC CONDITION. WE FURTHER HYPOTHESIZE THAT THE RESULTING CHRONIC PANCREATITIS CAN BE TARGETED WITH PKD INHIBITORS. TO TEST THIS WE WILL: DETERMINE HOW PKD1 EXPRESSION IN ACINAR CELLS CAN GENERATE AN ENVIRONMENT THAT IS FAVORABLE FOR DEVELOPING CHRONIC PANCREATITIS (SPECIFIC AIM 1); AND UTILIZE OUR ACINAR CELL- TARGETED ANIMAL MODELS TO DETERMINE THE EFFECTS OF PKD1 ON DEVELOPMENT AND RESOLUTION OF CHRONIC PANCREATITIS (SPECIFIC AIM 2). SUCCESSFUL COMPLETION OF THIS PROJECT WILL DEFINE THE ROLE OF ACTIVATED PKD1 IN ALTERING PANCREATIC ACINAR CELLS IN A WAY THAT THEY CAN FACILITATE THE TRANSITION OF ACUTE PANCREATITIS TO A CHRONIC STATE. WE WILL DEFINE HOW THESE MOLECULAR CHANGES AFFECT CELLS IN THE PANCREATIC ENVIRONMENT AND THE IMMUNE LANDSCAPE IN THE PANCREAS. EVENTUALLY, WE WILL DETERMINE IF INHIBITION OF PKD1 IN VIVO CAN RESOLVE CHRONIC PANCREATITIS. THIS WILL LAY THE GROUNDWORK OF DEVELOPING TARGETED TREATMENT STRATEGIES FOR PANCREATITIS BASED ON INHIBITION OF PKD1 OR DOWNSTREAM SIGNALING EVENTS.

680776.00

0.00

0.00