Ocean State Research Institute, Inc.

YZWJABL7PW69

4UUW4

2025-10-28

2024-10-29

2007-08-23

050440574

2023

70

4014573066

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2022

43

4014573066

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2021

31

4014573066

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2020

24

4014573066

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2019

22

4012737100

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VA630D15036

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AWARD

PO

5000.00

5000.00

5000.00

Department of Veterans Affairs

2011-09-23

TESTING

541712: RESEARCH AND DEVELOPMENT IN THE PHYSICAL, ENGINEERING, AND LIFE SCIENCES (EXCEPT BIOTECHNOLOGY)

Q301: LABORATORY TESTING SERVICES

2025-04-08

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Department of Defense

EXPLOITING ABSENCE OF TP53 MUTATIONS IN EPITHELIAL OVARIAN CANCER WITH NEXT-GENERATION P53-STABILIZING AGENTS CORRECTS THE PROGRAM ANNOUNCEMENT DESCRIPTION TO: FY24 OVARIAN CANCER RESEARCH PROGRAM - OVARIAN CANCER ACADEMY-EARLY-CAREER INVESTIGATOR AWARD

96241.00

0.00

0.00

2024-06-26

View on USAspending

Department of Health and Human Services

ROLE OF MITOCHONDRIAL C-SRC IN RIGHT VENTRICULAR DYSFUNCTION IN PULMONARY HYPERTENSION - PROJECT SUMMARY/ABSTRACT PULMONARY HYPERTENSION (PH) IS ASSOCIATED WITH POOR PROGNOSIS. RIGHT VENTRICULAR (RV) DYSFUNCTION/FAILURE CONSEQUENT TO HIGH RV AFTERLOAD IS THE PRIMARY CAUSE OF MORBIDITY AND MORTALITY IN PH, YET NO RV TARGETED THERAPIES ARE AVAILABLE. THIS CONTRASTS WITH SEVERAL DRUG CLASSES THAT ARE BENEFICIAL IN LV DYSFUNCTION. THEREFORE, THERE REMAINS AN UNMET NEED TO THERAPEUTICALLY TARGET THE MECHANISMS UNDERLYING RV DYSFUNCTION TO IMPROVE LONG-TERM OUTCOMES IN PH. CARDIOMYOCYTES DETERMINE RV FUNCTION IN PH. MITOCHONDRIA THROUGH OXIDATIVE PHOSPHORYLATION (OXPHOS) ARE THE MAJOR SOURCE OF ENERGY IN THE HEART. TARGETING RV MITOCHONDRIAL BIOENERGETICS AND FUNCTION IN SETTINGS OF PH MAY PROVIDE NOVEL THERAPEUTIC STRATEGIES TO IMPROVE RV FUNCTION IN PH. RESPIRATORY COMPLEXES IN THE MITOCHONDRIAL ELECTRON TRANSPORT CHAIN PLAY A CRITICAL ROLE IN OXIDATIVE PHOSPHORYLATION (OXPHOS) AND GENERATION OF REACTIVE OXYGEN SPECIES. OXPHOS MACHINERY SUBUNITS HAVE BEEN FOUND TO BE HIGHLY PHOSPHORYLATED, IMPLICATING PHOSPHORYLATION AS A MEANS WHEREBY OXPHOS IS REGULATED. TO DATE, TYROSINE PHOSPHORYLATION (P-TYR) IS RECOGNIZED AS A CRITICAL REGULATORY MECHANISM IN MITOCHONDRIA AND C-SRC IS THE MAJOR TYROSINE KINASE LOCALIZED IN MITOCHONDRIA. THE OVERALL GOAL OF THIS PROPOSAL IS TO DELINEATE THE MECHANISMS UNDERLYING IMPAIRED RV MITOCHONDRIAL ENERGETICS AND FUNCTION IN PH. OUR PRELIMINARY FINDINGS STRONGLY SUPPORT A NOVEL MECHANISM GOVERNING RV COMPLEX I ASSEMBLY AND FUNCTION IN PH THAT IS MEDIATED BY P-TYR OF COMPLEX PROTEINS. COMPLETION OF THIS STUDY IS EXPECTED TO IDENTIFY A NEW TARGETED STRATEGY TO PRESERVE/RESTORE ELECTRON TRANSFER CHAIN FUNCTION IN RV CARDIOMYOCYTES IN VIVO IN SETTINGS OF PH.

829884.00

0.00

0.00

2023-08-14

View on USAspending

Department of Defense

LONG-TERM OUTCOMES OF ANTIPSYCHOTIC MEDICATION USE IN VETERANS WITH PTSD

1632091.00

0.00

0.00

2024-05-20

View on USAspending

Department of Health and Human Services

METABOLIC MECHANISMS UNDERLYING BRONCHOPULMONARY DYSPLASIA-ASSOCIATED PULMONARY HYPERTENSION - SUMMARY BRONCHOPULMONARY DYSPLASIA (BPD) IS A CHRONIC LUNG DISEASE IN PREMATURE INFANTS, CAUSED BY MECHANICAL VENTILATION AND HYPEROXIA AMONGST OTHER FACTORS. THIRTY PERCENT OF INFANTS WITH MODERATE TO SEVERE BPD DEVELOP PULMONARY HYPERTENSION (PH), CHARACTERIZED BY PULMONARY VASCULAR REMODELING. THERE ARE NO CURATIVE THERAPIES FOR THIS DISEASE. CURRENT MANAGEMENT IS LIMITED TO RELIEVING SYMPTOMS USING PULMONARY VASODILATORS, AND MINIMIZING FURTHER LUNG VASCULAR AND ALVEOLAR INSULTS. MY LONG-TERM GOAL IS TO DEVELOP NOVEL TARGETED THERAPIES TO PREVENT AND/OR TREAT BPD ASSOCIATED PULMONARY HYPERTENSION (BPD-PH). PULMONARY VASCULAR REMODELING IS CHARACTERIZED BY INCREASED SMOOTH MUSCLE CELL-SPECIFIC MARKERS. THIS RESULTS FROM PROLIFERATION AND MIGRATION OF VASCULAR SMOOTH MUSCLE CELLS, OR TRANSDIFFERENTIATION FROM ENDOTHELIAL CELLS (ECS) TO SMOOTH MUSCLE CELLS (I.E., ENDOTHELIAL-MESENCHYMAL TRANSITION, ENDOMT). WE AND OTHERS HAVE SHOWN THAT HYPEROXIA TO NEWBORN MICE AND MECHANICAL VENTILATION IN PRETERM LAMBS CAUSE PULMONARY VASCULAR REMODELING RESULTING IN PH. THIS IS ASSOCIATED WITH INCREASED ENDOMT, AS SHOWN IN OUR RECENT PUBLICATION AND IN PRELIMINARY DATA. WE PRELIMINARILY SHOW THAT ENDOMT IS ALSO OBSERVED IN THE LUNG OF PREMATURE INFANTS REQUIRING MECHANICAL VENTILATION, SUGGESTING THAT THIS MAY BE CAUSATIVE IN PULMONARY VASCULAR REMODELING AND PH. IN MICE, WE HAVE REPORTED THAT NEONATAL HYPEROXIA CAUSES A PERSISTENT REDUCTION OF ENDOTHELIAL CARNITINE PALMITOYLTRANSFERASE 1A (CPT1A), THE RATE-LIMITING ENZYME OF THE CARNITINE SHUTTLE SYSTEM RESPONSIBLE FOR TRANSPORTING LONG-CHAIN FATTY ACIDS INTO MITOCHONDRIA FOR Β-OXIDATION DURING FATTY ACID OXIDATION. OUR PRELIMINARY DATA SHOW THAT LUNG CPT1A GENE EXPRESSION IS ALSO REDUCED IN MECHANICALLY VENTILATED PRETERM LAMBS AND PREMATURE HUMAN INFANTS. ADDITIONALLY, ENDOTHELIAL DELETION OF CPT1A INCREASED ENDOMT AND PULMONARY VASCULAR REMODELING IN NEONATAL MICE AFTER EXPOSURE TO HYPEROXIA. FURTHERMORE, PHARMACOLOGICAL UPREGULATION OF CPT1A ATTENUATED HYPEROXIA-INDUCED ENDOMT IN CULTURED LUNG ECS. WHETHER NEONATAL HYPEROXIA AND MECHANICAL VENTILATION REDUCE ENDOTHELIAL CPT1A, LEADING TO PH IS YET TO BE DETERMINED. THE CENTRAL HYPOTHESIS IS THAT NEONATAL HYPEROXIA AND MECHANICAL VENTILATION CAUSE ENDOMT BY DOWNREGULATING ENDOTHELIAL CPT1A, THEREBY RESULTING IN PULMONARY VASCULAR REMODELING AND PH. WE WILL TEST THIS HYPOTHESIS IN THREE SPECIFIC AIMS. AIM 1 WILL DETERMINE THE MOLECULAR MECHANISMS BY WHICH CPT1A REGULATES HYPEROXIA-INDUCED ENDOMT. IN AIM 2, WE WILL DEFINE THE ROLE OF ENDOTHELIAL CPT1A IN NEONATAL HYPEROXIA-INDUCED PH AND ENDOMT. IN AIM 3, WE WILL EVALUATE ENDOTHELIAL CPT1A AND ENDOMT AS THERAPEUTIC TARGETS FOR BPD-PH USING BOTH LAMB AND MOUSE MODELS. THE COMBINATION OF CLINICALLY RELEVANT LAMB AND MOUSE MODELS WITH OUR NEWLY GENERATED EC-SPECIFIC CPT1A KO MICE AND NEWLY DEVELOPED NANOPARTICLE DELIVERY SYSTEM PROVIDES AN INNOVATIVE APPROACH TO UNCOVER THE MECHANISMS BY WHICH CPT1A REDUCTION MEDIATES ENDOMT AND THEIR SIGNIFICANT ROLES IN BPD-PH. THIS CONTRIBUTION IS SIGNIFICANT BECAUSE IT IS LIKELY TO RESULT IN NEW THERAPIES SPECIFICALLY TARGETING ENDOTHELIAL CPT1A OR ENDOMT IN NEONATES TO PREVENT OR CURE BPD-PH.

1718377.00

0.00

0.00

2023-09-04

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Department of Health and Human Services

CARDIOPULMONARY VASCULAR BIOLOGY COBRE - CARDIOPULMONARY VASCULAR BIOLOGY COBRE TEAM SCIENCE SUPPLEMENT PROJECT SUMMARY: GOAL OF THE PARENT AWARD: THE VISION OF THE CARDIOPULMONARY VASCULAR BIOLOGY (CPVB) COBRE PROGRAM IS TO DEVELOP EFFECTIVE APPROACHES TO PREVENT AND TREAT VASCULAR DISEASES AFFECTING THE PULMONARY AND CARDIOVASCULAR SYSTEMS THROUGH BETTER UNDERSTANDING OF DISEASE MECHANISMS. THIS IS ACCOMPLISHED BY SERVING AS AN INTERDISCIPLINARY CENTER WHICH PROMOTES COLLABORATIVE RESEARCH AND PROVIDES EXCELLENT TECHNICAL SUPPORT AND RESOURCES TO INVESTIGATORS. THE OVERALL MISSION OF THE CPVB COBRE PROGRAM HAS BEEN TO BUILD THE HUMAN AND TECHNICAL INFRASTRUCTURE AND SERVICES THAT SERVE AS CATALYSTS TO INCREASE CPVB RESEARCH IN THE STATE. CARDIOVASCULAR AND PULMONARY DISEASES ARE AMONG THE LEADING CAUSES OF MORBIDITY AND MORTALITY IN THE US AND IN THE WORLD. THUS, THERE IS AN IMPORTANT NEED TO UNDERSTAND THE PATHOGENESIS OF CARDIOPULMONARY VASCULAR DISEASES IN ORDER TO DEVELOP MORE EFFECTIVE TREATMENTS AND PREVENTION. THE OVERALL GOAL OF THE CPVB COBRE PROGRAM IS TO FACILITATE HIGH IMPACT VASCULAR BIOLOGY RESEARCH. THE CPVB COBRE PROGRAM PROVIDES INFRASTRUCTURE WITH ADMINISTRATIVE, PILOT PROJECT, AND TWO TECHNICAL CORES, THUS PROVIDING OPPORTUNITIES TO EXPAND AREAS OF INVESTIGATION, EXPERIMENTAL AND TECHNICAL APPROACHES, AND SCIENTIFIC COLLABORATIONS. THE SPECIFIC AIMS OF PHASE III CPVB COBRE ARE TO: I) AWARD HIGH-IMPACT RESEARCH PROJECTS IN THE AREA OF CARDIOPULMONARY VASCULAR BIOLOGY; II) PROVIDE EFFECTIVE AND HIGH-QUALITY SERVICES IN CELL ISOLATION AND EX VIVO ORGAN FUNCTION (CIOF), MITOCHONDRIAL FUNCTION, AND IN VIVO IMAGING (MF-II); III) COLLABORATE WITH IDEA PROGRAMS IN RHODE ISLAND (RI) AND OTHER STATES TO FOSTER SCIENTIFIC NETWORKS BY PROVIDING PROGRAMMING, FUNDING, TECHNICAL SERVICES, AND RESOURCES TO ENHANCE RESEARCH PRODUCTIVITY; AND IV) MAINTAIN A ROBUST LINE OF INVESTIGATION IN VASCULAR BIOLOGY THAT MEETS THE NEEDS OF THE SCIENTIFIC COMMUNITY AND FURTHERS RESEARCH IN PREVENTION AND TREATMENT OF CARDIOPULMONARY VASCULAR DISEASES. WE WILL EXPAND AND ENRICH THE VASCULAR BIOLOGY RESEARCH COMMUNITY BY PROMOTING NEW COLLABORATIONS AND ENGAGING SCIENTISTS NEW TO THE FIELD FROM A VARIETY OF DISCIPLINES. AT THE END OF PHASE III, WE EXPECT TO TRANSITION TO A SUSTAINABLE CPVB CENTER SERVING AS A HOME TO THE CVPB RESEARCH COMMUNITY WITH HIGH QUALITY CORE SERVICES, SIGNIFICANT INSTITUTIONAL SUPPORT, AND COMMITMENT TO CONTINUE THE DEVELOPMENT OF EFFECTIVE APPROACHES TO COMBAT OR RESOLVE CARDIOPULMONARY VASCULAR DISEASES. RESEARCH QUESTION TO BE ADDRESSED BY THE SUPPLEMENT AWARD: RIGHT VENTRICULAR (RV) DYSFUNCTION IN SETTINGS OF PULMONARY HYPERTENSION (PH) IS ASSOCIATED WITH POOR OUTCOMES IRRESPECTIVE OF ASSOCIATED COMORBIDITIES AND UNDERLYING CONDITIONS. PH IS COMMON AND AFFLICTS ~ 1 % OF WORLD POPULATION, IS COMMONLY ASSOCIATED WITH CARDIOPULMONARY DISEASES, AND IN MANY CASES IS ASSOCIATED WITH PULMONARY VASCULAR REMODELING. DESPITE THE KNOWN POOR PROGNOSIS ASSOCIATED WITH RV DYSFUNCTION, TO DATE, NO RV TARGETED THERAPIES ARE AVAILABLE, AND THE UNDERLYING MECHANISMS OF RV DYSFUNCTION REMAIN UNCLEAR. THEREFORE, THERE IS AN UNMET NEED FOR A BETTER UNDERSTANDING OF CELLULAR AND MOLECULAR MECHANISMS ASSOCIATED WITH RV DYSFUNCTION AND TO CONVERT THIS KNOWLEDGE INTO THERAPIES. PATHOPHYSIOLOGICAL MECHANISMS ASSOCIATED WITH RV DYSFUNCTION INCLUDE CHANGES IN CELLULAR COMPOSITION OF THE MYOCARDIUM, MATRIX REMODELING (E.G., FIBROSIS), METABOLIC DYSFUNCTION RESULTING IN HEART FAILURE AND VENTRICULAR AND ATRIAL ARRHYTHMIAS. WHILE REDUCTIONIST APPROACHES HAVE RESULTED IN IMPORTANT INSIGHTS INTO ROLE OF SPECIFIC CELL TYPES AND SIGNALING PATHWAYS, A COMPREHENSIVE EVALUATION USING MULTI-SCALE AND MULTI- OMICS EVALUATION AND USE OF NOVEL DATA-SCIENCE ANALYTICAL TECHNIQUES TO IDENTIFY THE NETWORKS AND PATHWAYS THAT UNDERLIE MALADAPTIVE RV AND RV DYSFUNCTION HAS NOT BEEN PERFORMED AND IS THE OVERALL OBJECTIVE OF THIS PROPOSAL. WHY NEED FOR TEAM SCIENCE EFFORT? CONSIDERING THE MULTIPLE PATHOPHYSIOLOGICAL MECHANISMS, CELL TYPES AND PHENOTYPES (ARRHYTHMIA, ENERGETIC AND MECHANICAL FAILURE) ASSOCIATED WITH RV DYSFUNCTION, THERE IS NEED TO BRING TOGETHER EXPERTS IN MYOCARDIAL BIOLOGY, MITOCHONDRIAL BIOLOGY, AND ARRHYTHMIA BIOLOGY. FURTHERMORE, USE OF LARGE UNBIASED DATASETS TO UNRAVEL NOVEL NETWORKS AND PATHWAYS UNDERLYING RV DYSFUNCTION REQUIRES ANALYTICAL AND METHODOLOGICAL EXPERTISE IN REDUCING THE DIMENSIONALITY OF DATA AND IDENTIFICATION OF IMPORTANT MULTI-OMIC NETWORK FEATURES USING NOVEL ARTIFICIAL INTELLIGENCE BASED METHODOLOGY THAT RELATE WITH THE MALADAPTIVE PHENOTYPES IN SETTINGS OF RV DYSFUNCTION. THESE DATA, APPROACHES AND COLLABORATIONS ARE EXPECTED TO RESULT IN MULTI-PI AND PROGRAM PROJECT GRANT APPLICATIONS THAT WILL LEAD TO SUSTAINABLE TEAMS TO PERFORM IMPACTFUL SCIENTIFIC INVESTIGATION IN CARDIOPULMONARY VASCULAR DISEASES SUCH AS RV DYSFUNCTION AND FAILURE.

2903437.00

0.00

0.00

05-0440574

% V A MEDICAL CTR

Government Instrumentality, Title-Holding Corporation, Charitable Organization, Agricultural Organization, Board of Trade, Pleasure, Recreational, or Social Club, Fraternal Beneficiary Society, Order or Association, Voluntary Employees' Beneficiary Association (Non-Govt. Emps.), Domestic Fraternal Societies and Associations, Teachers Retirement Fund Assoc., Benevolent Life Insurance Assoc., Burial Association, Credit Union, Mutual Insurance Company or Assoc. Other Than Life or Marine, Corp. Financing Crop Operations, Supplemental Unemployment Compensation Trust or Plan, Employee Funded Pension Trust (Created Before 6/25/59), Post or Organization of War Veterans, Legal Service Organization, Black Lung Trust, Multiemployer Pension Plan, Veterans Assoc. Formed Prior to 1880, Trust Described in Sect. 4049 of ERISA, Title Holding Co. for Pensions, etc., State-Sponsored High Risk Health Insurance Organizations, State-Sponsored Workers' Compensation Reinsurance, ACA 1322 Qualified Nonprofit Health Insurance Issuers, Apostolic and Religious Org. (501(d)), Cooperative Hospital Service Organization (501(e)), Cooperative Service Organization of Operating Educational Organization (501(f)), Child Care Organization (501(k)), Charitable Risk Pool, Qualified State-Sponsored Tuition Program, 4947(a)(1) - Private Foundation (Form 990PF Filer)

1989-07

Type of organization and use of contribution: A public charity. Deductibility Limitation: 50% (60% for cash contributions)

2020-04-14

Paid in Full

100

272926.35

272926.35

Unanswered

Unknown/NotStated

Unanswered

Unanswered

275064.27