THE HOSPITAL FOR SPECIAL SURGERY FUND, INC.

Headquarter of

F20000002254

FLORIDA

THE HOSPITAL FOR SPECIAL SURGERY FUND, INC. (FL)

LGHBJMLVD8H3

1YZN4

2025-08-29

HSS FOUNDATION

http://www.hss.edu

THE HOSPITAL FOR SPECIAL SURGERY FUND, INC.

2024-09-02

2002-06-19

1YZN4

Active

Non-Manufacturer

2024-09-02

2029-09-02

2025-08-29

DEONARINE ARJUNE

http://www.hss.edu

W912PQ15P0247

View Award on USAspending website

AWARD

PURCHASE ORDER

90000.00

90000.00

90000.00

Department of Defense

2015-09-17

IGF::CT::IGF HUMAN PERFORMANCE OPTIMIZATION

541690: OTHER SCIENTIFIC AND TECHNICAL CONSULTING SERVICES

Q518: MEDICAL- PHYSICAL MEDICINE/REHABILITATION

NNA15BC03P

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AWARD

PO

16300.00

16300.00

16300.00

National Aeronautics and Space Administration

2015-09-03

IGF::OT::IGF BONE HISTOMORPHOMETRY TO DETERMINE EFFECTS OF RADIATION AND DISUSE ON BONE

541711: RESEARCH AND DEVELOPMENT IN BIOTECHNOLOGY

AB91: R&D- COMMUNITY SERVICE/DEVELOPMENT: OTHER (BASIC RESEARCH)

HHSN264201500101PC

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AWARD

PO

3750.00

3750.00

3750.00

Department of Health and Human Services

2015-07-13

IGF::CL::IGF

811212: COMPUTER AND OFFICE MACHINE REPAIR AND MAINTENANCE

Q301: MEDICAL- LABORATORY TESTING

2025-05-07

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Department of Defense

ENDOTHELIAL CELL S1PR1 SHAPES THE AUTOIMMUNE RESPONSE AND MAY ATTENUATE INJURY IN EXPERIMENTAL LUPUS NEPHRITIS.

296093.00

0.00

0.00

2024-11-22

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Department of Health and Human Services

MECHANISMS OF INFLAMMATORY OSTEOBLASTOGENESIS AND BONE FORMATION - THE INTEGRITY OF THE ADULT SKELETON IS MAINTAINED BY BALANCED REMODELING BETWEEN OSTEOCLAST-MEDIATED BONE RESORPTION AND OSTEOBLAST/OSTEOCYTE-MEDIATED BONE FORMATION. HOWEVER, EXCESSIVE BONE LOSS BUT LIMITED BONE FORMATION OFTEN OCCUR IN MANY CHRONIC INFLAMMATORY SETTINGS, SUCH AS RHEUMATOID ARTHRITIS (RA) AND PERIODONTITIS. IN CONTRAST TO THE EXTENSIVE STUDIES ON OSTEOCLASTIC BONE RESORPTION, THE DEREGULATED OSTEOBLASTOGENESIS AND DAMAGED BONE FORMATION, ESPECIALLY IN INFLAMMATORY CONDITIONS, ARE MUCH LESS UNDERSTOOD. THERE ARE NO KNOWN EFFECTIVE THERAPIES TO IMPROVE BONE FORMATION IN RA CURRENTLY. WE RECENTLY IDENTIFIED CONSTITUTIVE TYPE-I INTERFERON (IFN-I) RESPONSE ACTIVITY IN OSTEOBLASTS, EVIDENCED BY THE CONSTITUTIVE EXPRESSION OF TYPE I IFN-STIMULATED/RESPONSE GENES (ISGS), WHICH IS A NEWLY RECOGNIZED CELLULAR SIGNATURE OF OSTEOBLASTS. IT IS INTRIGUING THAT OSTEOBLASTS, A NON-TYPICAL IMMUNE CELL TYPE, PRESENT IFN-I RESPONSE SIGNATURE IN THE ABSENCE OF INFECTION. WE FOUND THAT THE CONSTITUTIVE IFN-I RESPONSE PLAYS AN INHIBITORY ROLE IN OSTEOBLAST DIFFERENTIATION AND BONE FORMATION WITH GENETIC EVIDENCE, WHICH UNDERSCORES ITS BIOLOGICAL SIGNIFICANCE IN OSTEOBLASTOGENESIS AND BONE HOMEOSTASIS. ISGS ARE USUALLY THE INDICATORS AND EFFECTORS OF IFN-I PATHWAY/RESPONSE. AMONG THE ISGS, WE IDENTIFIED EIF2AK2 (ENCODING EUKARYOTIC TRANSLATION INITIATION FACTOR 2- ALPHA KINASE 2) AS AN IMPORTANT INHIBITOR OF OSTEOGENESIS. IMPORTANTLY, EIF2AK2 IS A CENTRAL REGULATOR OF IFN-I RESPONSE IN OSTEOBLASTIC INHIBITION. EIF2AK2-/- MICE EXHIBIT SIGNIFICANTLY HIGH BONE MASS WITH PROMINENTLY INCREASED OSTEOBLASTIC BONE FORMATION IN VIVO. OUR DATA INCLUDING RNASEQ RESULTS FURTHER REVEAL A NOVEL PATHWAY MEDIATED BY IFN-I-EIF2AK2-Β-CATENIN IN THE REGULATION OF OSTEOBLASTOGENESIS. MOREOVER, INFLAMMATORY CYTOKINE TNFΑ SIGNIFICANTLY ENHANCES THE CONSTITUTIVE IFN-I RESPONSE IN OSTEOBLASTS, INDICATING A NOVEL MOLECULAR MECHANISM BY WHICH TNFΑ RESTRAINS BONE FORMATION. WE ALSO FOUND A DRASTIC AGING EFFECT OF THE CONSTITUTIVE IFN-I RESPONSE ON BONE MASS. BASED ON OUR PRELIMINARY RESULTS, IN THIS APPLICATION, WE WILL FURTHER 1) INVESTIGATE THE MECHANISMS BY WHICH THE CONSTITUTIVE IFN-I RESPONSE SUPPRESSES OSTEOBLASTOGENESIS; 2) INVESTIGATE HOW THE EFFECTS OF CONSTITUTIVE IFN-I RESPONSE IN OSTEOBLASTS/OSTEOCYTES ON BONE HOMEOSTASIS ARE INFLUENCED BY AGING IN BOTH MALES AND FEMALES; AND 3) INVESTIGATE THE FUNCTIONAL IMPORTANCE OF CONSTITUTIVE IFN-I RESPONSE IN OSTEOBLASTS/OSTEOCYTES IN INFLAMMATORY ARTHRITIC ANIMAL MODELS WITH OSTEOGENIC DEFECTS. SUCCESSFUL COMPLETION OF THIS PROPOSAL WILL SHIFT THE CURRENTLY ESTABLISHED PARADIGM IN IMMUNOLOGY FOR IFN-I RESPONSE TO A NEW PARADIGM IN BONE WITH DISTINCT FUNCTION AND MECHANISMS. IDENTIFICATION OF PREVIOUSLY UNRECOGNIZED MECHANISMS IN OSTEOGENIC INHIBITION WILL PROVIDE A RATIONAL FRAMEWORK FOR DEVELOPING NEW THERAPEUTIC APPROACHES TO ENHANCING OSTEOBLAST/OSTEOCYTE-MEDIATED BONE FORMATION/REPAIR IN SKELETAL DISEASES.

688634.00

0.00

0.00

2025-03-24

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Department of Health and Human Services

ACTIVATION OF SYNOVIAL LINING FIBROBLASTS IN RHEUMATOID ARTHRITIS - PROJECT SUMMARY / ABSTRACT THIS PROPOSAL COMPRISES A FIVE-YEAR RESEARCH AND CAREER DEVELOPMENT PROGRAM FOR MELANIE H. SMITH, MD, PHD TO ACHIEVE INDEPENDENCE AS AN INVESTIGATOR AT THE INTERSECTION OF IMMUNOLOGY AND STROMAL BIOLOGY IN THE HUMAN SYNOVIUM. DR. SMITH IS AN ASSISTANT ATTENDING PHYSICIAN IN THE DIVISION OF RHEUMATOLOGY AT HOSPITAL FOR SPECIAL SURGERY (HSS) AND AN ASSISTANT ATTENDING PROFESSOR OF MEDICINE AT WEILL CORNELL MEDICAL COLLEGE IN NEW YORK CITY. SHE WILL CONDUCT RESEARCH UNDER THE JOINT MENTORSHIP OF DR. LAURA DONLIN (HSS) AND DR. ALEXANDER RUDENSKY (MEMORIAL SLOAN KETTERING CANCER CENTER) FOCUSED ON UNDERSTANDING THE ROLE OF SYNOVIAL FIBROBLASTS IN RHEUMATOID ARTHRITIS (RA). DR. SMITH WILL ENGAGE IN CAREER DEVELOPMENT ACTIVITIES INCLUDING DIDACTICS, WORKSHOPS IN GRANT WRITING AND LEADERSHIP, CONFERENCES, AND ACQUISITION OF TECHNICAL SKILLS AND SCIENTIFIC EXPERTISE. THESE ACTIVITIES WILL BE AUGMENTED THROUGH REGULAR INPUT FROM HER SCIENTIFIC ADVISORY TEAM. THIS TRAINING GRANT WILL GENERATE KEY SKILLS, DATA, AND PUBLICATIONS NECESSARY TO BECOME AN R01-FUNDED INDEPENDENT INVESTIGATOR. SYNOVIAL FIBROBLASTS (FLS) ARE THE MOST ABUNDANT RESIDENT CELLS IN THE SYNOVIUM AND ARE IMPLICATED IN MULTIPLE ASPECTS OF RA PATHOGENESIS. FLS SPECIFICALLY WITHIN THE SYNOVIAL LINING LAYER EXHIBIT EVIDENCE OF EXTENSIVE ACTIVATION AND ARE SELECTIVELY DEFINED BY ACCESSIBILITY OF AP-1 TRANSCRIPTION FACTOR MOTIFS. HERE WE WILL TEST THE CONTRIBUTIONS OF TOLL LIKE RECEPTOR (TLR) LIGANDS FROM THE SYNOVIAL FLUID, AND LOCAL EXPRESSION OF EPIDERMAL GROWTH FACTOR RECEPTOR (EGFR) LIGANDS IN ACTIVATING AP-1 IN FLS. THE CENTRAL HYPOTHESIS IS THAT THESE ACTIVATORS OF AP- 1, WHICH ARE PRESENT IN THE SYNOVIAL LINING MICROENVIRONMENT, PRIME LINING FLS TO MOUNT HEIGHTENED RESPONSES TO CYTOKINES DERIVED FROM INFILTRATING LEUKOCYTES, AND THAT AP-1 DRIVEN GENE EXPRESSION DRIVES FLS FUNCTIONAL SPECIALIZATION. WE WILL USE PRIMARY HUMAN SYNOVIAL FIBROBLASTS BOTH IN CULTURE AND DIRECTLY ISOLATED FROM SYNOVIAL TISSUE ALONG WITH SELECTIVE AGONISTS, TARGETED INHIBITORS AND CRISPR INTERFERENCE TO INTERROGATE THE MECHANISTIC BASIS AND FUNCTIONAL CONSEQUENCES OF THE FLS ACTIVATION OBSERVED SPECIFICALLY IN LINING FLS. THE SIGNIFICANCE OF THIS PROPOSAL LIES IN THE IDENTIFICATION OF KEY FACTORS RESPONSIBLE FOR FLS ACTIVATION THAT MAY FURTHER THE DEVELOPMENT OF FLS-TARGETED THERAPIES IN RA. THIS PROPOSAL IS INNOVATIVE IN THE INVESTIGATION OF NON-CYTOKINE DRIVEN PRIMING IN THE ESTABLISHMENT OF INFLAMMATORY MEMORY AND THE IDENTIFICATION OF THE SPECIFIC TRANSCRIPTION FACTORS INVOLVED USING ADVANCED SEQUENCING METHODS AS WELL AS CRISPR IN PRIMARY HUMAN FLS. LONG-TERM, DR. SMITH AIMS TO APPLY THE EXPERTISE GAINED IN THIS PROPOSAL TO IDENTIFY ENVIRONMENTAL AND INFLAMMATORY SIGNALS THAT MAINTAIN AND REGULATE SYNOVIAL INFLAMMATION TO IMPROVE TREATMENT OF RA.

351920.00

0.00

0.00

2024-08-29

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Department of Health and Human Services

ORIGINS AND FUNCTIONS OF INTRAMUSCULAR MACROPHAGES IN DUCHENNE MUSCULAR DYSTROPHY - PROJECT SUMMARY DUCHENNE MUSCULAR DYSTROPHY (DMD), THE MOST COMMON GENETIC MUSCLE DISEASE, IS LETHAL WITH NO CURE AT THIS POINT. MUSCLE PATHOLOGY OF DMD AND ITS MOUSE MODEL MDX5CV FEATURES CHRONIC INFLAMMATION WITH PREDOMINANT MACROPHAGE (MP) INFILTRATION. PRECLINICAL STUDIES BY OUR LAB AND OTHERS DEMONSTRATE THAT AMELIORATING MUSCLE INFLAMMATION IMPROVES MUSCULAR DYSTROPHY PHENOTYPE. IT ALSO IMPROVES LOCAL TISSUE ENVIRONMENT TO PROMOTE MUSCLE REGENERATION AND GENE AND CELL ENGRAFTMENT. TISSUE MACROPHAGES ARE FUNCTIONALLY HETEROGENEOUS WITH DIVERSE ORIGINS. THEY CAN BE PRO-INFLAMMATORY, PRO-FIBROTIC, OR PRO-REGENERATIVE DEPENDING ON THE TISSUE ENVIRONMENT AND ORIGINS. WHILE TISSUE INFLAMMATORY MPS ARE DERIVED FROM BLOOD MONOCYTES (MOS), TISSUE RESIDENT MPS CAN ORIGINATE FROM BLOOD MOS AND/OR EMBRYO. MURINE PERIPHERAL BLOOD MOS CONSIST OF TWO SUBSETS, LY6CHI AND LY6CLO CELLS, WITH CORRESPONDING SUBSETS IN HUMANS. LY6CHI CELLS (CCR2+/CX3CR1LOW) ARE INFLAMMATORY MOS, WHICH ENTER TISSUES IN RESPONSE TO INJURY VIA CC CHEMOKINE RECEPTOR 2 (CCR2) AND THEN DIFFERENTIATE INTO INFLAMMATORY MPS. WITHIN INJURED TISSUES, LY6CHI MPS CAN SWITCH INTO LY6CLO MPS. LY6CHI MOS MAY ALSO CONTRIBUTE TO TISSUE RESIDENT MPS AT THE STEADY STATE. LY6CLO MOS (CCR2-/CX3CR1HI) PATROL THE VASCULAR ENDOTHELIAL SURFACE AND MAY ENTER NORMAL TISSUE VIA CHEMOKINE RECEPTOR CX3CR1 TO REPLENISH RESIDENT MPS. EMBRYO-DERIVED TISSUE RESIDENT MPS ARE ALSO LY6CLO, AND THEY PERSIST INTO ADULT TISSUES THROUGH PROLIFERATIVE SELF-RENEWAL. OUR PRELIMINARY DATA SHOW THAT BOTH LY6CHI AND LY6CLO SUBSETS OF MPS ACCUMULATE IN MDX5CV SKELETAL MUSCLE, AND THAT CCR2 IS ESSENTIAL TO THE MUSCLE RECRUITMENT OF LY6CHI INFLAMMATORY MOS. KNOCKOUT OF CCR2 DIMINISHES INTRAMUSCULAR LY6CHI MPS AT ALL STAGES, BUT IT ONLY REDUCES LY6CLO MPS AT EARLY STAGES. THE REDUCTION OF INTRAMUSCULAR MPS AT THE EARLY STAGES IS ACCOMPANIED BY DECREASED MUSCLE DAMAGE, REDUCED MUSCLE FIBROSIS, AND IMPROVED MUSCLE FUNCTION, WHICH SUPPORTS A PATHOGENIC ROLE FOR THE INTRAMUSCULAR LY6CHI MPS. HOWEVER, THE BENEFICIAL EFFECTS ARE LOST AT THE LATE STAGE IN THE MDX5CV/CCR2-/- MICE AFTER THE EXPANSION OF INTRAMUSCULAR LY6CLO MPS. TARGETING LY6CHI MP ALONE DOES NOT PROVIDE SUSTAINED BENEFITS. WE THUS GENERATE OUR CENTRAL HYPOTHESIS THAT LY6CLO MPS ALSO PLAY A PATHOGENIC ROLE IN THE MDX5CV DIAPHRAGM DYSTROPHY, LY6CLO MPS FROM DIFFERENT ORIGINS MAY CONTRIBUTE DIFFERENTLY, AND TARGETING THE MONOCYTIC ORIGINS IS THERAPEUTICALLY USEFUL. WE WILL TEST OUR HYPOTHESIS BY THREE SPECIFIC AIMS. AIM 1 WILL STUDY THE ORIGINS OF SKELETAL MUSCLE RESIDENT MPS AT THE NORMAL STEADY STATE. AIM 2 WILL DEFINE THE ORIGINS OF INTRAMUSCULAR MPS IN THE MDX5CV DIAPHRAGM. AIM 3 WILL DETERMINE THE EFFECTOR AND REGULATORY FUNCTIONS OF INTRAMUSCULAR MPS DERIVED FROM DIFFERENT ORIGINS IN THE MDX5CV DIAPHRAGM, AND TEST THE THERAPEUTIC POTENTIAL OF TARGETING MONOCYTIC ORIGINS. THIS PROJECT WILL ADDRESS THE KEY QUESTIONS RELATED TO THE INTRAMUSCULAR MPS, AND THE KNOWLEDGE GAINED WILL BE CRITICAL TO THE FUTURE DEVELOPMENT OF NOVEL MONOCYTE/MACROPHAGE-BASED THERAPIES FOR DMD.

1837917.00

0.00

0.00

2025-01-06

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Department of Health and Human Services

DISCOVERING IMMUNE DRIVERS OF FIBROBLAST POLARIZATION ANDRECOVERY IN SYSTEMIC SCLEROSIS - PROJECT SUMMARY / ABSTRACT BACKGROUND: THIS PROPOSAL IS DESIGNED FOR DR. KIMBERLY LAKIN, MD, MS TO GROW TOWARD BECOMING AN INDEPENDENT INVESTIGATOR FOCUSED UPON CHARACTERIZING THE CLINICAL SIGNIFICANCE OF IMMUNE CELL-FIBROBLAST ASSOCIATIONS IN SYSTEMIC SCLEROSIS (SSC) SKIN. CURRENTLY, THERE ARE NO APPROVED TREATMENTS TO MANAGE BOTH SKIN AND INTERNAL ORGAN FIBROSIS CAUSED BY SYSTEMIC SCLEROSIS (SSC), A DEADLY AUTOIMMUNE DISEASE WITH A COMPLEX AND POORLY UNDERSTOOD PATHOPHYSIOLOGY INVOLVING INFLAMMATION AND EXCESS COLLAGEN PRODUCTION BY SKIN FIBROBLASTS. IN CLINICAL AND TRIAL SETTINGS, SOME PATIENTS IMPROVE, AT TIMES DRAMATICALLY, WHILE OTHERS DO NOT, POSSIBLY RELATED TO DISTINCT DISEASE PHASES WHEN CELLS ARE AMENABLE (OR NOT) TO TREATMENT. RELIABLE TOOLS ARE NEEDED TO INFORM INDIVIDUALIZED TREATMENT DECISIONS AND TRIAL ENROLLMENT. PRELIMINARY DATA BY DR. LAKIN AND HER MENTORS SUGGEST ASSESSMENTS OF FIBROBLAST ACTIVATION STATUS MAY YIELD SUCH A TOOL. PRELIMINARY DATA: USING PAIRED BIOLOGICAL (HISTOLOGY, GENE EXPRESSION) AND CLINICAL DATA FROM 24 INDIVIDUALS WITH DIFFUSE CUTANEOUS (DC)SSC, HISTOLOGIC ASSESSMENTS OF TWO, INVERSELY RELATED FIBROBLAST MARKERS (ASMA, CD34) WERE ASSOCIATED WITH CLINICAL SEVERITY AND PREDICTED THE SSC INFLAMMATORY GENE EXPRESSION SUBSET, USING MACHINE LEARNING METHODS. SAMPLES WITH INFLAMMATORY VS. NON-INFLAMMATORY FIBROBLASTS HAD INCREASED B CELLS AND TYPE I INTERFERON GENE SIGNATURE. A GENE SIGNATURE OF FIBROBLAST POLARIZATION (BY ASMA/CD34) WAS COMPUTED AND FOUND TO BE HIGHER AT BASELINE IN 52-WEEK CLINICAL IMPROVERS VS. NON-IMPROVERS. METHODS: FINE PHENOTYPE MAPPING OF DCSSC (N=105), PRESSC (VERY EARLY ONSET OF SSC; N=12) AND HEALTHY (N=12) SKIN WILL BE PERFORMED CROSS-SECTIONALLY. IMMUNE PATHWAYS AND CELL TYPES ASSOCIATED WITH ACTIVATED FIBROBLASTS WILL BE EVALUATED BY IMAGING MASS CYTOMETRY (IMC), DIGITAL CELL DECONVOLUTION, AND HISTOLOGY. IN A LONGITUDINAL ANALYSIS, BASELINE CLINICAL AND MOLECULAR FEATURES (HISTOLOGY SCORES; IMMUNE CELL AND FIBROBLAST POLARIZATION SIGNATURES) WILL BE TESTED AS INPUTS IN A MODEL TO PREDICT 52 WEEKS CLINICAL IMPROVEMENT. CAREER DEVELOPMENT: THE STUDY GOAL IS TO UNRAVEL IMMUNE CELL-FIBROBLAST INTERACTIONS IN SSC AND TO TEST A HISTOLOGY-DERIVED MODEL FOR CLASSIFYING PATIENTS MOST LIKELY TO CLINICALLY IMPROVE AT ONE YEAR. DR. LAKIN IS AN ASSISTANT ATTENDING PHYSICIAN AT HOSPITAL FOR SPECIAL SURGERY (HSS) AND ASSISTANT ATTENDING PROFESSOR OF MEDICINE AT WEILL CORNELL MEDICAL COLLEGE WITH ACCESS TO THE OUTSTANDING CORE SERVICES AT THESE INSTITUTIONS. SHE WILL CONDUCT PATIENT-ORIENTED RESEARCH UNDER THE MENTORSHIP OF DR. ROBERT SPIERA (HSS), AN EXPERT IN SSC CLINICAL RESEARCH, AND DR. DANA ORANGE (ROCKEFELLER), AN EXPERT IN THE USE OF BIOINFORMATIC APPROACHES TO DISCOVER PATIENT SUBSETS IN RHEUMATIC DISEASES. DR. LAKIN WILL ENGAGE IN EXPERIENTIAL AND FORMAL COURSEWORK TO ADVANCE HER BIOINFORMATICS, IMMUNOLOGY, AND SKIN IMAGING MASS CYTOMETRY SKILLS. THIS CAREER DEVELOPMENT AWARD WILL POSITION DR. LAKIN FOR SUCCESS IN HER OBJECTIVE TO BECOME AN R01-FUNDED INDEPENDENT INVESTIGATOR FOCUSED UPON IMPROVING SSC PATIENT CARE WHILE UNCOVERING KEY MECHANISMS OF SSC PATHOGENESIS.

351586.00

0.00

0.00

13-6714749

% TODD GORLEWSKI

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)

1987-06

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