Old Dominion University Research Foundation

INVESTING IN INNOVATION - SCALE UP

TO PROVIDE SUPPORT FOR "FAMILY PLANNING AND REPRODUCTIVE HEALTH METHODS TO ADDRESS UNMET NEEDS"

FROM QUARKS TO NUCLEI

THE PRIMARY PURPOSE OF THE PROPOSED PROGRAM IS TO TRANSFER FUNDS TO ACCOMPLISH A PUBLIC PURPOSE OF SUPPORT OR STIMULATION OF THE HIV PREVENTION PRODUCTS TARGETED FOR ADOLESCENT GIRLS AND YOUNG WOMEN IN LOW AND MIDDLE INCOME COUNTRIES.

PROJECT HORIZON: HYDROGEL INJECTABLE DEPOT SYSTEM FOR NEXT-GENERATION LONG-ACTING HIV PREVENTION AND CONTRACEPTION - PROJECT SUMMARY/ABSTRACT THERE IS A NEED TO DEVELOP NEXT-GENERATION MULTIPURPOSE PREVENTION TECHNOLOGIES (MPTS) THAT PROVIDE LONG-ACTING (LA), SIMULTANEOUS SYSTEMIC DELIVERY OF PRODUCTS FOR THE PREVENTION OF HIV ACQUISITION AND UNINTENDED PREGNANCY. WE PROPOSE TO DEVELOP A NOVEL SILICA HYDROGEL-BASED LA INJECTABLE DEPOT SYSTEM DELIVERING DOLUTEGRAVIR (DTG), A PROVEN AND POTENT HIV INTEGRASE STRAND-TRANSFER INHIBITOR (INSTI), AND LEVONORGESTREL (LNG), A LICENSED CONTRACEPTIVE AGENT. IN THE FIRST (R61) PHASE OF THE PROJECT (SPECIFIC AIMS 1-3), THE MAIN OBJECTIVE IS TO ACHIEVE MILESTONES DEMONSTRATING FEASIBILITY OF DEVELOPING A PARTICLE-BASED HYDROGEL DEPOT SYSTEM CAPABLE OF PROVIDING AT LEAST 3 MONTHS DURATION FOR BOTH DRUGS, SHORTER TAIL PHARMACOKINETIC (PK) PROFILES, AND NO DRUG-DRUG INTERACTION (DDI). IN SPECIFIC AIM 1, WE WILL CONDUCT ITERATIVE FORMULATION DEVELOPMENT TO PRODUCE AND SCREEN PROTOTYPE COMBINATIONS FOR INITIAL FEASIBILITY, WHICH WILL THEN BE EVALUATED PRECLINICALLY IN SPECIFIC AIM 2 IN RAT AND NON-HUMAN PRIMATE MODELS TO DETERMINE OPTIMAL PK/PHARMACODYNAMICS (PD) PROFILES AND CHARACTERIZE SAFETY AND DDI, TO SUPPORT SELECTION OF A LEAD MPT FORMULATION. IN SPECIFIC AIM 3, WE WILL ENGAGE WITH POTENTIAL END-USERS IN A US REGION WITH HIGH HIV INCIDENCE TO GAIN A MORE IN-DEPTH UNDERSTANDING OF USER PREFERENCES OF PRODUCT ATTRIBUTES. IN THE SECOND (R33) PHASE (SPECIFIC AIMS 4-6), THE MAIN OBJECTIVES WILL BE TO EXPAND PRODUCT DEVELOPMENT EFFORTS TO CHARACTERIZE THE LEAD FORMULATION AND OBTAIN IND-ENABLING FEEDBACK FROM THE FDA IN A PRE-IND MEETING, CONDUCT POC CONTRACEPTIVE EFFICACY AND HIV PROPHYLACTIC EFFICACY IN ANIMAL STUDIES, AND DEFINE THE OPTIMAL DOSING REGIMEN AND TARGET PRODUCT PROFILE (TPP) BASED ON END-USER INPUT. IN SPECIFIC AIM 4, FORMULATION OPTIMIZATION ACTIVITIES WILL BE PERFORMED TO IMPROVE THE HARMONIZED PK PROFILE AND DURATION FOR EACH DRUG AND TO BETTER MEET THE PRODUCT ATTRIBUTE PREFERENCES PRIORITIZED BY END USERS. PRECLINICAL PROOF-OF-CONCEPT DATA WILL BE GENERATED USING A RAT CONTRACEPTIVE EFFICACY MODEL AND THE WELL-ESTABLISHED REPEATED, LOW DOSE SHIV CHALLENGE MODELS USING PIGTAIL (INTRAVAGINAL) AND RHESUS (INTRARECTAL) MACAQUES AT CDC. UPON IDENTIFICATION OF THE LEAD FORMULATION, WE WILL ALSO DRAFT A TOXICOLOGY TESTING PLAN, CLINICAL STUDY DESIGN AND CLINICAL DEVELOPMENT PLAN TO SUPPORT A PRE-IND MEETING WITH THE FDA (SPECIFIC AIM 5). FINALLY, IN SPECIFIC AIM 6, WE WILL BUILD UPON THE FORMATIVE WORK OF SA3 WITH A DISCRETE CHOICE EXPERIMENT TO UNDERSTAND USER AND PROVIDER PREFERRED PRODUCT ATTRIBUTES FOR THE LA MPT INJECTABLE, IN ORDER TO REFINE THE TPP AND GUIDE ON-GOING PRODUCT DEVELOPMENT EFFORTS. IN SUMMARY, THIS PROJECT PROPOSES TO DEVELOP, THROUGH PRECLINICAL PROOF-OF-CONCEPT, A LA MPT INJECTABLE WITH A STRONG REGULATORY PATH FOR FUTURE CLINICAL ADVANCEMENT, PROVIDING A SIGNIFICANT ADVANCEMENT OF A NEXT-GENERATION HIV PREVENTION AND CONTRACEPTIVE PRODUCT THAT MAY FIT INTO THE LIFESTYLES OF AT-RISK WOMEN MOST IN NEED.

EXPERIMENTAL NUCLEAR PHYSICS

VIRGINIA SPACE GRANT CONSORTIUM

PIRE: CENTENNIAL GENETIC AND SPECIES TRANSFORMATIONS IN THE EPICENTER OF MARINE BIODIVERSITY

VIRGINIA SPACE GRANT CONSORTIUM FY2020-2024

FY 2009 TEACHER QUALITY PARTNERSHIPS GRANTS

"A THEORETICALLY DRIVEN INVESTIGATION OF THE EFFICACY OF AN IMMERSIVE INTERACTIVE AVATAR"

CYBERCORPS SCHOLARSHIP FOR SERVICE: PREPARING FUTURE CYBERSECURITY LEADERS THROUGH APPLIED LEARNING EXPERIENCES

ADVANCING RURAL COMPUTER SCIENCE (ARCS)

NURSE EDUCATION, PRACTICE, QUALITY AND RETENTION

PREPARING LEADERSHIP IN ADAPTED PHYSICAL EDUCATION THROUGH AN INTERUNIVERSITY COLLABORATORY

VSGC ALIGNS WITH THE NATIONAL SPACE GRANT PROGRAM OBJECTIVES OF: (1) PROMOTING A STRONG STEM EDUCATION BASE FROM ELEMENTARY THROUGH SECONDARY LEVELS

MISSION STATEMENT: THE VIRGINIA SPACE GRANT CONSORTIUM ACTS AS AN UMBRELLA ORGANIZATION COORDINATING AND DEVELOPING QUALITY AEROSPACE-RELATED HIGH

VIRGINIA-UCLA-TORONTO BIOMARKER CHARACTERIZATION CENTER - PROJECT SUMMARY THE CRITICAL CHALLENGE IN THE CLINICAL MANAGEMENT OF NEWLY-DIAGNOSED LOCALIZED PROSTATE CANCER REMAINS DISTINGUISHING INDOLENT FROM AGGRESSIVE AND LIFE-THREATENING CANCERS. BIOMARKERS ARE URGENTLY NEEDED TO IDENTIFY THOSE PATIENTS WHO HARBOR AGGRESSIVE DISEASE AND WILL DERIVE BENEFIT FROM DEFINITIVE TREATMENT. WE THEREFORE, PROPOSE TO APPLY COMPLIMENTARY PROTEOGENOMIC-BASED DISCOVERY APPROACHES TO IDENTIFY AND THEN VALIDATE MOLECULAR FEATURES IN PROSTATE PROXIMAL FLUIDS AND TUMOR TISSUES THAT WILL BE UTILIZED IN ACCURATE EARLY DETECTION OF AGGRESSIVE FORMS OF PROSTATE CANCER AND IMPROVE DISEASE RISK STRATIFICATION. THE INTENDED USE OF THESE BIOMARKERS WILL BE THE EARLY IDENTIFICATION OF MEN AT RISK FOR GRADE PROGRESSION AND IMPROVED RISK- STRATIFICATION FOR THEM. WE HAVE THREE BIOMARKER DEVELOPMENT LABORATORY AIMS: 1) VALIDATE OUR EXISTING URINE-BASED BIOMARKERS FOR GRADE PROGRESSION IN A PROBE-COMPLIANT STUDY SELECTED FROM OUR OWN COHORTS AND THE EDRN GU UPGRADING STUDY. 2) DEVELOP AND VALIDATE URINE AND TISSUE-BASED BIOMARKERS FOR THE RISK-STRATIFICATION OF MRI “INVISIBLE” HIGH-GRADE LESIONS. 3) DEVELOP AND VALIDATE BIOMARKERS TO SUB-STRATIFY RISK ASSOCIATED WITH DELETERIOUS GERMLINE BRCA2 VARIANTS. OUR BIOMARKER REFERENCE LABORATORY WILL DEVELOP AND VALIDATE TARGETED CLINICALLY ROBUST ASSAYS FOR MULTI-PROTEIN BIOMARKERS PANELS. WE WILL ALSO DEVELOP DECISION ALGORITHMS THAT ARE CROSS-REFERENCED FOR STATISTICAL RIGOR AND BENCHMARKED FOR OPTIMAL CLINICAL PERFORMANCE. IN ADDITION TO THESE BCC ACTIVITIES, WE WILL DEVELOP ROBUST PRM-MS ASSAYS AND STATISTICALLY RIGOROUS DECISION TOOLS FOR OTHER EDRN BCCS AND CVCS. TAKEN TOGETHER, OUR EDRN BIOMARKER CHARACTERIZATION CENTER WILL BE A CORE PART OF THE THE EDRN ECOSYSTEM. WE WILL CONTINUE TO ACTIVELY PARTICIPATE IN TRANS-NETWORK ACTIVITIES, AND TO SHARE PATIENT COHORTS, PROTOCOLS, DATASETS AND ANALYSIS APPROACHES AND EXPERTISE. WE WILL SUPPLEMENT THESE ACTIVITIES BY FOCUSING ON PROMOTING THE GROWTH OF NEW AND DIVERSE TALENT IN BIOMARKER DEVELOPMENT THROUGH FOSTERING JUNIOR INVESTIGATOR INVOLVEMENT ACROSS THE FULL SPECTRUM OF BIOMARKER DEVELOPMENT.

QUANTITATIVE IMAGE MODELING FOR BRAIN TUMOR ANALYSIS AND TRACKING

MULTI-RESOLUTION DOCKING METHODS FOR ELECTRON MICROSCOPY

TAS::89 0222::TAS; NEW; DEVELOPMENT OF A SUITE OF ENGINEERED MULTI-SPOKE SUPERCONDUCTING CAVITIES FOR NUCLEAR PHYSICS, LIGHT SOURCES AND DRIVEN SYSTE

INVESTIGATION OF NEW SUPERCONDUCTING MATERIALS FOR THE NEXT GENERATION HIGH-GRADIENT TRF CATITIVES FOR PARTICLE ACCELEARATORS

DESTRUCTIVE BLOOMS OF THE ICHTHYOTOXIC HARMFUL ALGAL BLOOM (HAB) SPECIES MARGALEFIDINIUM POLYKRIKOIDES, HAVE OCCURRED NEARLY ANNUALLY IN LATE SUMMER IN THE LOWER CHESAPEAKE BAY AND MID-ATLANTIC COASTAL WATERS FOR DECADES. SINCE 2007, M. POLYKRIKOIDES BLOOMS HAVE BEEN SUCCEEDED BY BLOOMS OF ALEXANDRIUM MONILATUM. BLOOMS HAVE BEEN LINKED TO EUTROPHICATION AND WARMING TEMPERATURES AND CONTRIBUTE TO REGIONAL HYPOXIA/ANOXIA, AND FINFISH AND SHELLFISH MORTALITY. THROUGH PREVIOUS RESEARCH, BLOOM INITIATION HOTSPOTS WERE IDENTIFIED, TRANSPORT PATHWAYS FROM INITIATION SITES ESTABLISHED, AND MODELS FOR BLOOM DEVELOPMENT AND TRANSPORT IMPLEMENTED. NETWORKS FOR BLOOM DETECTION AND MONITORING THAT INCLUDE FIXED STATION SAMPLING, UNDERWAY "DATAFLOW" SAMPLING FROM BOATS, AND SATELLITE SURVEILLANCE ARE IN PLACE AND WILL BE ENHANCED BY THE PROPOSED DEPLOYMENT OF LOW-COST, HIGH THROUGHPUT, PHYTOPLANKTON IMAGING PLANKTOSCOPES. AVAILABLE RESEARCH, STATE-OF-THE-ART ESTUARINE FORECAST MO

EDUCATIONAL OPPORTUNITY CENTERS PROGRAM

ADVANCED NURSING EDUCATION WORKFORCE

PIRE: ORIGINS OF HIGH MARINE BIODIVERSITY IN THE INDO-MALAY-PHILIPPINE ARCHIPELAGO: TRANSFORMING A BIODIVERSITY HOTSPOT INTO A RESEARCH AND EDUCATION

CYBERAI SFS: PREPARING FUTURE CYBERAI LEADERS THROUGH AI-INTEGRATED TRAINING AND APPLIED LEARNING EXPERIENCES -THIS PROJECT PROVIDES SCHOLARSHIPS FOR UNDERGRADUATE AND GRADUATE STUDENTS ENROLLED IN ARTIFICIAL INTELLIGENCE (AI) AND CYBERSECURITY (CYBERAI) PROGRAMS AT OLD DOMINION UNIVERSITY (ODU) IN EXCHANGE FOR THEIR SERVICE SUPPORTING CYBERAI MISSION OF GOVERNMENT ORGANIZATIONS. THE PROJECT SUPPORTS AN EDUCATIONAL INTERDISCIPLINARY PROGRAM THAT RELIES ON A NUMBER OF HIGH-QUALITY COURSES IN CYBERSECURITY AND AI, HANDS-ON EXPERIENCE BOTH AT ODU AND DURING SUMMER INTERNSHIPS AT GOVERNMENT ORGANIZATIONS, PARTICIPATION IN RESEARCH PROJECTS SUPERVISED BY CYBERAI FACULTY, PARTICIPATION IN EXTRACURRICULAR ACTIVITIES INCLUDING COMPETITIONS AND OUTREACH ACTIVITIES TO PREPARE STUDENTS FOR A VARIETY OF PROFESSIONS IN CYBERAI FIELD. IN ADDITION TO FULFILLING REQUIRED COURSEWORK, THIS PROJECT PLACES A STRONG EMPHASIS ON EXPERIENTIAL LEARNING OPPORTUNITIES, RESEARCH PROJECTS, AND LEADERSHIP DEVELOPMENT THROUGH TEAMWORK DEPENDING ON THE STUDENT'S PREPARATION AND ASPIRATION. WITH A STRONG INSTITUTIONAL TRACK RECORD IN THEIR SCHOLARSHIP FOR SERVICE (SFS) PROGRAM FOR PREPARING STUDENTS FOR PUBLIC SERVICE CAREERS IN CYBERAI, ODU AND ITS SCHOOL OF CYBERSECURITY ARE UNIQUELY POSITIONED TO SUCCESSFULLY RUN THIS PROJECT. ODU IS THE FIRST UNIVERSITY IN THE NATION TO HAVE ITS CYBERAI PROGRAMS VALIDATED BY THE NATIONAL SECURITY AGENCY (NSA). IN ADDITION, ODU IS DESIGNATED BY THE NSA AS A NATIONAL CENTER OF ACADEMIC EXCELLENCE IN CYBER DEFENSE RESEARCH (CAE-R) A NATIONAL CENTER OF ACADEMIC EXCELLENCE IN CYBER OPERATIONS (CAE-CO), AND NATIONAL CENTER OF ACADEMIC EXCELLENCE IN CYBER DEFENSE (CAE-CD). STUDENTS SELECTED FOR THE PROGRAM WILL RECEIVE SCHOLARSHIPS WHILE COMPLETING THE REQUIRED ACADEMIC PROGRAMS. THE GRADUATES WILL CONTRIBUTE TO NATIONAL AND GLOBAL STEM WORKFORCE COMPETITIVENESS AND NATIONAL SECURITY AS GOVERNMENT EXPERTS IN THE USE OF AI IN CYBERSECURITY OPERATIONS AND THE SECURITY AND RESILIENCE OF AI SYSTEMS THEMSELVES. THIS PROJECT IS SUPPORTED BY THE CYBERAICORPS SCHOLARSHIP FOR SERVICE (CYBERAI SFS) PROGRAM WHICH FUNDS PROPOSALS TO INCREASE NATIONAL CAPACITY TO EDUCATE AND TRAIN PROFESSIONALS IN ARTIFICIAL INTELLIGENCE (AI) OR CYBERSECURITY, AND TO SUPPORT THEIR PLACEMENT AND RETENTION IN THE CYBERAI MISSION OF GOVERNMENT ORGANIZATIONS. THE SCHOLARSHIP TRACK FUNDS ACADEMIC INSTITUTIONS TO AWARD SCHOLARSHIPS TO STUDENTS IN EXCHANGE FOR THEIR GOVERNMENT SERVICE. THE INNOVATION TRACK SEEKS TRANSFORMATIVE EDUCATION PROPOSALS IN THE AREAS OF AI, CYBERSECURITY, OR THE INTEGRATION OF AI AND CYBERSECURITY. THIS AWARD REFLECTS NSF'S STATUTORY MISSION AND HAS BEEN DEEMED WORTHY OF SUPPORT THROUGH EVALUATION USING THE FOUNDATION'S INTELLECTUAL MERIT AND BROADER IMPACTS REVIEW CRITERIA.- SUBAWARDS ARE NOT PLANNED FOR THIS AWARD.

BROMODOMAIN-CONTAINING PROTEIN 4 IN PROFIBROTIC GENE EXPRESSION AND LUNG FIBROSIS - PROJECT SUMMARY IDIOPATHIC PULMONARY FIBROSIS (IPF) IS A FATAL LUNG DISORDER OF UNKNOWN ETIOLOGY. IPF IS CHARACTERIZED BY ALTERED EPIGENETIC STATE. EPIGENETIC ALTERATIONS ARE POTENTIALLY REVERSIBLE, THUS ARE ATTRACTIVE THERAPEUTIC TARGETS. CHROMATIN STRUCTURAL REMODELING THROUGH HISTONE POST- TRANSLATIONAL-MODIFICATIONS CONTROL TRANSCRIPTIONAL RESPONSES. ACETYLATED HISTONE MARKS AS WELL AS SOME TRANSCRIPTIONAL FACTORS ARE RECOGNIZED BY BROMODOMAINS (READERS). BROMODOMAIN- CONTAINING PROTEIN (BRD) 4 IS A MEMBER OF THE BROMODOMAIN AND EXTRATERMINAL (BET) FAMILY, WHICH BINDS TO CELL TYPE-SPECIFIC ENHANCERS AND PROMOTERS. BRD4 HAS BEEN REPORTED TO BE ESSENTIAL FOR ENHANCER-MEDIATED PRO-FIBROTIC GENES EXPRESSION IN MANY ORGAN FIBROSIS. HOWEVER MECHANISMS OF HOW BRD4 REGULATES GENOME-WIDE PRO-FIBROTIC RESPONSES AND ITS INTERACTION WITH OTHER HIS ACETYLTRANSFERASE, SUCH AS P300, IS NOT CLEAR. FIBROTIC RESPONSES INVOLVE MANY CELLULAR PROCESSES, INCLUDING EPIGENETIC ALTERATIONS. OUR PRELIMINARY DATA SHOW THAT BY BLOCKING BRD4, MULTIPLE PROFIBROTIC GENES CAN BE DOWNREGULATED; INHIBITION OF BRD4 CAN DISRUPT THE ASSOCIATION OF P300 AND H3K27AC WITH PROFIBROTIC GENES PROMOTER REGION. WE HYPOTHESIS THAT BRD4 AFFECTS CHROMATIN ACCESSIBILITY, MEDIATES THE UP-REGULATION OF PROFIBROTIC GENES THROUGH INTERACTION WITH P300 BY ACETYLATING ACTIVE ENHANCER MARK H3K27AC DURING LUNG INJURY AND REPAIR PROCESS. OUR AIMS ARE: 1. DETERMINE THE EFFECTS OF BRD4 INHIBITION ON PROFIBROTIC RESPONSES IN LUNG FIBROBLASTS; 2. DETERMINE IF BRD4 THROUGH P300 MEDIATES HISTONE ACETYLATION TO REGULATE PROFIBROTIC GENES EXPRESSION, 3. DETERMINE THE IN VIVO TARGETING OF BRD4 INHIBITION IN PRE-CLINICAL MODELS OF LUNG FIBROSIS. RESULTS FROM THIS RESEARCH WILL MAKE A SIGNIFICANT IMPACT ON OUR UNDERSTANDING OF THE ROLE OF BRD4 IN EPIGENETIC REGULATION IN THE PATHOBIOLOGY OF IPF.

ED+GINEERING: AN INTERDISCIPLINARY PARTNERSHIP INTEGRATING ENGINEERING INTO ELEMENTARY TEACHER PREPARATION PROGRAMS

ADVANCING MULTI-BNABS MICRONEEDLE PATCH TECHNOLOGY FOR HIV-1 PREVENTION IN BREASTFEEDING INFANTS. - PROJECT SUMMARY / ABSTRACT DESPITE SIGNIFICANT PROGRESS MADE IN PREVENTING PERINATAL MOTHER-TO-CHILD-TRANSMISSION OF HIV, 2022 SAW ABOUT 130,000 NEW HIV INFECTIONS IN CHILDREN GLOBALLY, A VULNERABLE GROUP THAT ALSO ACCOUNTS FOR 13% OF AIDS-RELATED DEATHS. POSTNATAL INFECTION THROUGH BREASTFEEDING REMAINS A SIGNIFICANT CONTRIBUTING FACTOR FOR MOTHER-TO-CHILD TRANSMISSION OF HIV, AND OFTEN DERIVES FROM UNTREATED/UNDIAGNOSED MOTHERS LIVING WITH HIV OR POOR ADHERENCE TO ANTIRETROVIRALS (ARVS). CURRENTLY AVAILABLE PROPHYLAXIS OPTIONS FOR NEWBORNS WITH THE POTENTIAL FOR PERINATAL EXPOSURE TO HIV IS ARV THERAPY. HOWEVER, ARV FORMULATIONS (ORAL AND INJECTABLE) AND REGIMENS MEANT FOR PEDIATRIC USE ARE LIMITED, DIFFICULT TO ADHERE TO, AND POTENTIALLY ACCOMPANIED BY MULTIPLE UNDESIRABLE SIDE EFFECTS. BROADLY NEUTRALIZING ANTIBODIES (BNABS), CURRENTLY UNDER INVESTIGATION IN CLINICAL TRIALS, REPRESENT AN INNOVATIVE AND SAFER WAY TO DELIVER PERINATAL HIV PROPHYLAXIS BY DIRECTLY ENGAGING AND REINFORCING HOST IMMUNITY. DESPITE THE PROMISE, THESE HIGHLY POTENT ABS HAVE DEMONSTRATED IN ADULTS AND CHILDREN, IN THEIR CURRENT FORM, THEY OFTEN REQUIRE MULTIPLE INJECTIONS AND COLD CHAIN STORAGE AND TRANSPORTATION, WHICH IS BURDENSOME TO HEALTH CARE SYSTEMS AND A CONSIDERABLE EXPENSE IN LOW-RESOURCE SETTINGS. A USER-FRIENDLY TRANSDERMAL MICRONEEDLE (MN) PATCH CONTAINING THERMALLY STABILIZED BNABS WOULD CIRCUMVENT THESE PROBLEMS THROUGH THE SAFE AND EASY DELIVERY OF THESE POTENT ABS FOR PROTECTION AGAINST HIV-1, EVEN OUTSIDE OF A CLINIC SETTING. THE MN PATCH DESIGN PROPOSED HERE IS AIMED TO ACCOMPLISH CO-DELIVERY OF A COCKTAIL OF LONG-ACTING BNABS OFFERING LONG-LASTING PROTECTION WITHOUT THE BURDEN OF FREQUENT AND ADVERSE-EFFECT LADEN PEDIATRIC ARV FORMULATIONS OR POTENTIALLY PAINFUL AND CUMBERSOME ANTIBODY INFUSIONS FOR NEWBORNS. IN THIS PROPOSAL, WE WILL TEST THIS INNOVATIVE DELIVERY PLATFORM FOR THE CO-DELIVERY OF THREE DIFFERENT BNABS CURRENTLY IN ADVANCED CLINICAL DEVELOPMENT (VRC07-523LS, PDGM1400LS AND PGT-121LS). RIGOROUS DESIGN AND FABRICATION OF MN PATCHES WITH IN VITRO AND EX VIVO CHARACTERIZATION OF FORMULATED BNABS WILL PRECEDE THEIR IN VIVO PRECLINICAL ASSESSMENT OF SAFETY IN YOUNG RABBITS, PHARMACOKINETICS (PK) IN RATS, AND SUBSEQUENT TESTING IN NEONATE RHESUS MACAQUES TO CHARACTERIZE THE PK PROFILE AND EFFICACY AGAINST ORAL CHALLENGES WITH SHIVSF162P3. TOGETHER, THESE FINDINGS WILL INFORM THE CHARACTERISTICS AND VIABILITY OF AN INNOVATIVE BNAB DELIVERY PLATFORM THAT COULD SIGNIFICANTLY CURTAIL THE PERSISTENT HEALTH CRISIS OF PEDIATRIC HIV INFECTIONS.

EDUCATIONAL OPPORTUNITY CENTERS PROGRAM

THE MECHANISMS OF CARDIAC THIN FILAMENT REGULATION IN HEALTH AND DISEASE. - PROJECT SUMMARY CARDIOMYOPATHIES ARE THE MOST COMMON GENETIC CARDIOVASCULAR DISEASE WORLDWIDE. THE PRESENCE OF CARDIAC TROPONIN VARIANTS ACCOUNTS FOR AT LEAST 15% OF ALL FAMILIAL CARDIOMYOPATHY CASES. CARDIAC MUSCLE CONTRACTION IS REGULATED BY FREE INTRACELLULAR CA2+ CONCENTRATION VIA TWO THIN FILAMENT REGULATORY PROTEINS – TROPOMYOSIN AND TROPONIN COMPLEX. CA2+ BINDING TO TROPONIN DISPLACES TROPOMYOSIN FROM MYOSIN-BINDING SITES AND ALLOWS FORMATION OF MYOSIN CROSS-BRIDGES, WHICH ON THEIR OWN CONTRIBUTE TO THIN FILAMENT ACTIVATION. TROPONIN COMPLEX IS COMPOSED OF CA2+ SENSING TROPONIN C, ACTIN-BINDING TROPONIN I, AND TM-BOUND TROPONIN T. FOR DECADES, THE HELICAL APPROACH TO ELECTRON MICROSCOPY RECONSTRUCTION OF THE THIN FILAMENT ELIMINATED INFORMATION ON THE STRUCTURE OF THE TN COMPLEX. HENCE, THE COMPLEX INTERACTIONS AMONG COMPONENTS OF THE THIN FILAMENT REMAINED UNKNOWN. WE DEVELOPED CRYO-EM NON-HELICAL ALGORITHM TO THE RECONSTRUCTION OF NATIVE CARDIAC THIN FILAMENTS TO REVEAL THE STRUCTURE OF THE WHOLE TROPONIN COMPLEX AT PHYSIOLOGICAL CA2+ LEVELS. WE SHOW THAT THE THIN FILAMENT IS COMPRISED OF AN ARRAY OF CA2+-FREE AND CA2+-BOUND NON-EQUIVALENT TROPONIN COMPLEXES WITH SHORT-RANGE COOPERATIVITY BETWEEN ADJACENT UNITS. TROPONIN VARIANTS ASSOCIATED WITH INHERITED CARDIOMYOPATHIES AFFECT THIN FILAMENT CA2+- DEPENDENT ACTIVATION. WE HYPOTHESIZE THAT: (1) DILATED (DCM) OR HYPERTROPHIC (HCM) CARDIOMYOPATHY VARIANTS IN TROPONIN AFFECT THIN FILAMENT REGULATION BY: (A) ALTERING THE EQUILIBRIUM BETWEEN CA2+-FREE AND CA2+-BOUND TROPONIN COMPLEXES VIA CONFORMATIONAL CHANGES IN CA2+-SENSING TROPONIN C UNIT; AND/OR (B) ALTERING THE DISTRIBUTION OF CA2+-FREE AND CA2+-BOUND TROPONIN COMPLEXES BY CHANGING COMMUNICATION BETWEEN THE ADJACENT TROPONINS ALONG AND ACROSS THE THIN FILAMENT. TO TEST OUR HYPOTHESIS WE CHOSE 4 STRATEGICALLY LOCATED MUTATIONS. IN AIM 1 WE WILL UTILIZE PATHOGENIC VARIANTS IN TROPONIN C LOCATED IN DISTAL PARTS OF CA2+-SENSING TROPONIN N-LOBE TO EVALUATE HOW THEY AFFECT THE EQUILIBRIUM BETWEEN CA2+-FREE AND CA2+-BOUND TROPONIN COMPLEXES, AND IF THEY AFFECT COMMUNICATION BETWEEN TROPONIN UNITS THAT MAY CURB ACTIVATING EFFECT OF RIGOR MYOSIN-S1. IN AIM 2 WE WILL FOCUS ON HIGHLY PENETRANT PATHOGENIC VARIANTS IN TROPONIN T LOCATED IN N-TERMINUS OF TROPONIN T, WHICH STABILIZES THE INTERACTION BETWEEN TROPOMYOSIN CABLES BELONGING TO ADJACENT TROPONIN UNITS. WE WILL EVALUATE HOW THESE MUTATIONS AFFECT THE COMMUNICATION BETWEEN NEIGHBORING TROPONINS AND ACTIVATION BY MYOSIN-S1. TO REVEAL HOW DISTAL PARTS OF THE TROPONIN COMPLEX (CA2+ SENSING TROPONIN C AND N-TERMINUS OF TROPONIN T) COMMUNICATE, WE WILL USE A CA2+ SENSITIZER, WHICH BINDS TO TROPONIN C TO REVERT EFFECTS OF A TROPONIN T VARIANT. OUR MULTIDISCIPLINARY, MULTI-PI APPROACH WITH COLLECTIVE EXPERTISE IN STRUCTURAL, FUNCTIONAL AND COMPUTATIONAL METHODS WILL REVEAL HOW THE COMPLEX INTERACTIONS BETWEEN COMPONENTS OF THE THIN FILAMENT MAKE HEARTBEATS POSSIBLE. SUCCESSFUL EXECUTION OF THE AIMS MAY SET THE GROUND FOR THE DEVELOPMENT OF TAILORED THERAPIES THAT COULD POTENTIALLY MODULATE THE STRUCTURE OF THE THIN FILAMENT TO TREAT VARIOUS FORMS OF HEART DISEASE.

ROLE OF THE NLRP3 INFLAMMASOME IN MEDIATING MICROGLIAL ACTIVATION AND DEVELOPMENT OF NEUROPSYCHIATRIC SYMPTOMS INDUCED BY HIV, ANTIRETROVIRALS AND COCAINE - ABSTRACT ALTHOUGH PEOPLE LIVING WITH HIV (PLWHIV) HAVE COMPARABLE LIFE-EXPECTANCY AS THE HIV-NEGATIVE POPULATION DOES, THEIR LIFE-QUALITY IS STILL DEEPLY COMPROMISED DUE TO THE PREVALENCE OF NEUROPSYCHIATRIC DISORDERS INCLUDING DEPRESSION AND ANXIETY. THE MAIN PATHOLOGICAL CHANGES IN THE BRAINS OF THOSE PEOPLE INCLUDE ABERRANT MICROGLIAL (MG) ACTIVATION AND NEURONAL INJURIES. DRUG ABUSE IS A HIGH COMORBIDITY OF HIV INFECTION AND ABUSED DRUGS COULD EXAGGERATE THE EXISTING NEUROLOGIC COMPLICATIONS IN PLWHIV. THE DETAILED MECHANISMS UNDERLYING SUCH PHENOMENON REMAIN MUCH ELUSIVE. SEVERAL CONTRIBUTING FACTORS HAVE BEEN SUGGESTED FOR SUCH NEUROLOGICAL DISORDERS INCLUDING THE CONTINUED EXPRESSION HIV PROTEINS SUCH AS TRANS-ACTIVATOR OF TRANSCRIPTION (TAT), THE LONG-TERM USE OF ANTIRETROVIRALS (ARVS), AND DRUGS OF ABUSE. OUR PRELIMINARY DATA DEMONSTRATED THAT :1) NLRP3 INFLAMMASOME SIGNALING WAS INVOLVED IN HIV-TAT-MEDIATED MG ACTIVATION; 2) COCAINE ACTIVATED MG THROUGH DYSREGULATING MIR-124/TLR4 AXIS, WHICH COULD BE REVERSED BY INHIBITION OF NLRP3 INFLAMMASOME; 3) COMBINATION ARVS USED IN CLINICAL PRACTICE (TENOFOVIR:TFV, EMTRICITABINE:FTC, AND DOLUTEGRAVIR:DTG) COULD ACTIVATE MG VIA LYSOSOMAL DYSFUNCTION; 4) CO-EXPOSURE OF MG TO THREE AGENTS (TAT, COCAINE, AND ARVS) INTRIGUINGLY RESULTED IN INCREASED ACTIVITY OF NLRP3 INFLAMMASOME IN VITRO; 5) IL1SS, THE FINAL EXECUTOR OF NLRP3 INFLAMMASOME ACTIVATION, DECREASED THE SPINE DENSITY AND INCREASE THE GLUTAMATE RECEPTOR IONOTROPIC NMDA SUBUNITS (GRINS) IN VITRO; AND 6) INCREASED NLRP3 INFLAMMASOME ACTIVITY WAS SHOWN IN THE BRAINS OF SIV-INFECTED MACAQUE. BASED ON THESE FINDINGS AND TWO DISTINCT STEPS OF NLRP3 INFLAMMASOME ACTIVATION, WE HYPOTHESIZE THAT EXACERBATED NLRP3 INFLAMMASOME ACTIVATION IN THE CONTEXT OF HIV-TAT/HIV, COCAINE, ARVS WILL LEAD TO EXAGGERATED MG ACTIVATION AND NEURONAL INJURIES, WHICH ARE RESPONSIBLE FOR THE HIGH INCIDENCE OF NEUROPSYCHIATRIC DISORDERS IN PLWHIV WITH COCAINE USE. WE WILL TEST THIS HYPOTHESIS IN THE FOLLOWING TWO SPECIFIC AIMS (SA) USING COMPLIMENTARY IN VITRO AND IN VIVO APPROACHES. SA1: INVESTIGATE THE ROLE OF NLRP3 INFLAMMASOME IN MG ACTIVATION AND NEURONAL INJURIES IN THE CONTEXT OF HIV-TAT/HIV, COCAINE, & ARVS. WE WILL SPLIT THIS SA INTO THREE SUB AIMS. SA1A WILL EXPLORE THE DETAILED MECHANISMS RESPONSIBLE FOR EXAGGERATED NLRP3 INFLAMMASOME ACTIVATION IN VITRO; SA1B WILL EXPLORE THE MECHANISMS UNDERLYING NLRP3 INFLAMMASOME-MEDIATED NEURONAL INJURIES; AND SA1C WILL INVESTIGATE THE STATUS OF NLRP3 INFLAMMASOME AND NEURONAL INJURIES IN ARCHIVED SIV- INFECTED MACAQUE BRAINS AND HIV-INFECTED INDIVIDUAS WITH OR WITHOUT COCAINE USE. SA2: EXPLORE THE POTENTIAL THERAPEUTIC EFFECTS OF NLRP3 INFLAMMASOME INHIBITION ON NEUROPSYCHIATRIC BEHAVIORS IN HIV ITAT MICE IN VIVO.

CREATING TEAMS OF EDUCATORS TO BUILD THE LITERACY SKILLS OF ENGLISH LEARNERS WITH AND WITHOUT DISABILITIES

GRADUATE TRAINEESHIPS IN ACCELERATOR ENGINEERING AND PHYSICS

NASA EDUCATION AND OUTREACH PROGRAM SUPPORT: THE GCCE PROJECT IS DESIGNED TO IMPROVE THE QUALITY OF GLOBAL CLIMATE CHANGE AND EARTH SYSTEM SCIENCE E

ONE OF NASA'S BIGGEST CONCERNS ABOUT THE LONG-TERM HEALTH OF ASTRONAUTS WHO GO ON DEEP SPACE MISSIONS IS THE IMPACT THAT HIGH Z, HIGH ENERGY (HZE) PA

TOPICS IN THEORETICAL NUCLEAR PHYSICS

FEDERAL TRIO UPWARD BOUND PROJECT

ADVANCED NURSING EDUCATION GRANTS

NASA STRATEGIC GOAL 4: ENHANCE CAPABILITIES AND OPERATIONS TO CATALYZE CURRENT AND FUTURE MISSION SUCCESS. NASA INVESTMENTS IN STEM ENGAGEMENT ARE FOCUSED ON BUILDING A FUTURE STEM WORKFORCE THROUGH PROGRAM ELEMENTS DESIGNED TO BOLSTER CAPACITY AND TO ATTRACT ENGAGE AND ENABLE STUDENTS TO MOVE TOWARD STEM CAREERS THROUGH NASA-UNIQUE OPPORTUNITIES.

RELATIVE SEA LEVEL RISE (RSLR), MORE INTENSE STORMS, AND INCREASE IN EXTREME RAINFALLS WILL EXACERBATE FLOOD RISK TO COASTAL SURFACE TRANSPORTATION NETWORKS (STNS). THUS, COASTAL REGIONS NEED TO PRIORITIZE BUILDING RESILIENCE TO RSLR IN THEIR TRANSPORTATION PLANNING AND MANAGEMENT. WITH THE SHIFT IN PREFERRED COASTAL PROTECTION MEASURES FROM TRADITIONAL COASTAL STRUCTURES TO NATURAL AND NATURE-BASED BASED FEATURES (NNBFS), IT IS IMPERATIVE TO QUANTIFY NNBFS BENEFITS IN PROTECTING TRANSPORTATION INFRASTRUCTURE ASSETS FROM FLOODING UNDER RSRL AND ASSESS HOW THIS PROTECTION TRANSLATES TO SOCIAL AND ECONOMIC BENEFITS. HOWEVER, THERE ARE CRITICAL GAPS IN THE UNDERSTANDING OF HOW FLOODING RESULTS IN STN DEGRADATION AND THUS SHORTCOMINGS IN DECISION-MAKING TOOLS. TO ADDRESS THESE GAPS, A NEW DYNAMIC AND INTEGRATED MODELING FRAMEWORK IS PROPOSED FOR PREDICTING ADVERSE RSLR EFFECTS ON AND NNBF BENEFITS FOR TRANSPORTATION SYSTEMS. THE FRAMEWORK, FIRST, EMPLOYS HYDRODYNAMIC AND MORPHODYNAMIC MODE

EPIGENETIC MODULATION OF CELLULAR SENESCENCE IN THE CYSTIC FIBROSIS LUNG - PROJECT SUMMARY CYSTIC FIBROSIS (CF) HAS BEEN A PEDIATRIC DISEASE, BUT WITH IMPROVED TREATMENT AND CARE IT HAS BECOME A CHRONIC DISEASE EXTENDING THE LIFE EXPECTANCY OF PATIENTS. THE CHARACTERISTIC CHRONIC PRO-INFLAMMATORY PROCESS IN CF ACCELERATES CELLULAR SENESCENCE AND FURTHER COMPLICATES THIS DISEASE. THEREFORE, NOVEL THERAPEUTIC STRATEGIES ARE NEEDED TO COMBAT CELLULAR SENESCENCE IN THE CF LUNG. CELLULAR SENESCENCE IS A KEY PROCESS UNDERLYING AGING, WHICH LEADS TO AN ACCUMULATION OF EPIGENETIC NOISE. SUCH NOISE DISTORTS THE EPIGENETIC LANDSCAPE AND DYSREGULATES GENE EXPRESSION, RESULTING IN DECLINED TISSUE FUNCTION AND AGE-RELATED DISEASES. WE AND OTHERS HAVE ESTABLISHED THAT EPIGENETICS ARE INVOLVED IN THE PATHOGENESIS OF AGE-RELATED DISEASES. WE HAVE SHOWN THAT ANTI-AGING METHODS IMPROVE MUCOCILIARY CLEARANCE IN THE CF BRONCHIAL EPITHELIUM. CELLULAR SENESCENCE IS REGULATED VIA GENE TRANSCRIPTION THROUGH THE INTERPLAY BETWEEN PROMOTERS, ENHANCERS, AND CIS-ACTING REGULATORY ELEMENTS BOUND BY TRANSCRIPTION FACTORS. BROMODOMAIN- CONTAINING PROTEIN 4 (BRD4) IS AN EPIGENETIC READER PROTEIN. IT BINDS TO ACETYLATED HISTONE AND RECRUITS TRANSCRIPTIONAL FACTORS FOR ACTIVELY TRANSCRIBED GENES. TRANSCRIPTION FACTOR AP-1 WAS RECENTLY REPORTED TO MARK THE SENESCENCE ENHANCER LANDSCAPE AND DRIVE THE TRANSCRIPTIONAL PROGRAM IN SENESCENT CELLS. BRD4 IS CRITICAL FOR MANY SENESCENCE-ASSOCIATED SECRETORY PHENOTYPE RELATED INFLAMMATORY GENE EXPRESSION PROFILES. HOWEVER, THE ROLE OF BRD4 AND ITS INTERACTIONS WITH AP-1 TO CONTROL THE SENESCENT RELATED GENE EXPRESSION IN THE CF BRONCHIAL EPITHELIUM HAS NOT BEEN EXPLORED. OUR PRELIMINARY DATA SHOWED THAT BLOCKING BRD4 DOWN-REGULATED MULTIPLE SENESCENT GENES, AND REDUCED THE RECRUITMENT OF AP-1 TO THOSE GENES. WE HYPOTHESIZE THAT BLOCKING BRD4 IN THE CF BRONCHIAL EPITHELIUM WILL EPIGENETICALLY REDUCE CELLULAR SENESCENCE IN THE CF LUNG ULTIMATELY PRESERVING LUNG FUNCTION. TO TEST OUR HYPOTHESIS, WE WILL FIRST DETERMINE IF BRD4 REGULATES THE CHROMATIN ACCESSIBILITY AND IS REQUIRED FOR SENESCENT-RELATED GENE EXPRESSION IN THE CF BRONCHIAL EPITHELIUM; WE WILL ALSO EXPLORE THE UNDERLYING MECHANISMS AND THE INTERACTIONS OF BRD4 AND AP-1 IN REGULATING SENESCENT RELATED GENE EXPRESSION; LASTLY, WE WILL DETERMINE THE EFFICACY OF BRD4 INHIBITION IN CFTR RESPONSIVE AND UNRESPONSIVE CF RAT MODELS. RESULTS FROM THIS STUDY WILL OFFER NEW INSIGHTS OF EPIGENETIC REGULATION IN THE CF BRONCHIAL EPITHELIUM AND PROVIDE SUPPORT FOR TARGETING SENESCENT AIRWAY CELLS IN CF LUNG DISEASE AS A NOVEL THERAPEUTIC STRATEGY.

ONE OF NASAS BIGGEST CONCERNS ABOUT THE LONG TERM HEALTH OF ASTRONAUTS WHO GO ON DEEP SPACE MISSIONS IS THE IMPACT THAT HADRON PARTICLES HAVE ON BRAI

INFLUENCE OF HEMODYNAMIC SHEAR STRESS ON CIRCULATING TUMOR CELLS - CIRCULATING TUMOR CELLS (CTCS) ARE EXPOSED TO VARIOUS INSULTS THOUGHT TO REDUCE THEIR SURVIVAL INCLUDING LACK OF ANCHORAGE AND TROPHIC SUPPORT FROM THE PRIMARY TUMOR MICROENVIRONMENT, IMMUNE-MEDIATED DESTRUCTION AND EXPOSURE TO HEMODYNAMIC FORCES THAT MAY MECHANICALLY DESTROY THEM. HOWEVER, THE RELATIVE CONTRIBUTION OF THESE FACTORS TO CTC SURVIVAL AND THEIR OVERALL ROLE IN METASTASIS IS UNCLEAR. IT HAS RECENTLY BEEN SHOWN THAT CANCER CELLS FROM MANY TISSUE ORIGINS ACTIVELY RESIST DESTRUCTION BY FLUID SHEAR STRESS (FSS), IMPLYING THAT VIABLE CTCS ARE NOT MECHANICALLY FRAGILE AS SUSPECTED. OUR LONG-TERM GOAL IS TO UNDERSTAND THE BIOMECHANICAL INFLUENCES ON CTCS AND HOW THIS CONTRIBUTES TO METASTASIS. THE OBJECTIVE OF THIS PROPOSAL IS TO DETERMINE THE MECHANISM OF FSS RESISTANCE IN CANCER CELLS AND ITS ROLE IN METASTATIC COLONIZATION. OUR CENTRAL HYPOTHESIS IS THAT MECHANO-ADAPTATION OF VIABLE CTCS TO FSS PROMOTES THEIR SURVIVAL IN THE CIRCULATION AND “PRIMES” THEM FOR SUBSEQUENT EVENTS IN METASTASIS. OUR HYPOTHESIS IS BASED ON OUR PREVIOUSLY PUBLISHED AND PRELIMINARY DATA PRESENTED BELOW AS WELL AS RECENTLY PUBLISHED DATA FROM OTHERS WHICH IS SUPPORTIVE OF OUR HYPOTHESIS. THE RATIONALE FOR THE PROPOSED RESEARCH IS THAT ONCE WE UNDERSTAND THE MECHANISM UNDERLYING FSS RESISTANCE; THIS WOULD REPRESENT A NOVEL THERAPEUTIC APPROACH AIMED AT DECREASING THE SURVIVAL OF CTCS BY ENHANCING THEIR DESTRUCTION DUE TO THE MECHANICAL FORCES THAT NATURALLY EXIST IN THE CIRCULATION. GUIDED BY PRELIMINARY DATA, THE CENTRAL HYPOTHESIS WILL BE TESTED BY PURSUING THE FOLLOWING SPECIFIC AIMS: 1) DEFINE MOLECULAR MECHANISMS OF FSS RESISTANCE; 2) DETERMINE THE EFFECT OF FSS EXPOSURE ON METASTATIC COLONIZATION; 3) DETERMINE THE EFFECTIVENESS OF INHIBITING FSS RESISTANCE AS AN ANTI-METASTATIC STRATEGY. TO ACCOMPLISH THESE AIMS, WE WILL EMPLOY A FORWARD GENETIC SCREEN TO IDENTIFY NOVEL GENES THAT MEDIATE FSS RESISTANCE AND DETERMINE THEIR INVOLVEMENT WITH RHOA- ACTOMYOSIN INTERACTIONS. SHORT-TERM SURVIVAL OF CTCS WILL BE ASSESSED USING A NOVEL MOUSE MODEL TO MEASURE ENTRAPMENT OF INTACT CTCS IN THE LUNG AND DESTRUCTION OF CTCS MEASURED BY A PLASMA BIOMARKER. WE WILL VALIDATE NOVEL GENES IDENTIFIED IN A FORWARD GENETIC SCREEN IN SIMILAR ASSAYS. WE WILL DETERMINE THE INVOLVEMENT OF RHOA- YAP ACTIVATION BY FSS IN SUPPORTING THE SURVIVAL AND EXTRAVASATION OF CANCER CELLS LODGED IN THE MICROCIRCULATION. FINALLY, WE WILL TEST THE POTENTIAL OF CLINICALLY ACTIONABLE DRUGS THAT SENSITIZE CELLS TO FSS AS WELL AS CONDITIONAL RHOA/YAP KNOCKDOWN TO BLOCK PRODUCTIVE METASTATIC COLONIZATION IN MOUSE MODELS. THE PROPOSED RESEARCH IS INNOVATIVE BECAUSE, IT REPRESENTS A PARADIGM SHIFT FROM THE IDEA THAT CTCS ARE MECHANICALLY FRAGILE BY ELUCIDATING A MECHANISM WHEREBY VIABLE CTCS ACTIVELY RESIST DESTRUCTION BY HEMODYNAMIC FORCES AND DRIVES FURTHER EVENTS IN METASTASIS. THE PROPOSED RESEARCH IS SIGNIFICANT BECAUSE DEFINING THE MECHANISMS AND CONSEQUENCES OF FSS RESISTANCE IN CTCS WILL OPEN ENTIRELY NEW DIAGNOSTIC AND THERAPEUTIC POSSIBILITIES IN CANCER PATIENTS.

"(MURI 02) SUBCELLULAR RESPONSES TO NARROWBAND AND WIDEBAND RADIOFREQUENCY RADIATION"

ASTRONAUTS MAY EXPERIENCE SEVERAL PHYSICAL AND PSYCHOLOGICAL CHALLENGES INCLUDING PROLONGED EXPOSURE TO MICROGRAVITY POTENTIAL SOCIAL ISOLATION (SI) AND PREDICTED EXPOSURE TO ~ 13 CGY/YR SPACE RADIATION (SR).....

INTERLEUKIN 12 DISRUPTION PROVIDES BETA CELL AND MICROVESSEL PROTECTION IN TYPE 2DIABETES

OLD DOMINION UNIVERSITY UPWARD BOUND PROGRAM

VIRGINIA AEROSPACE SCIENCE AND TECHNOLOGY SCHOLARS: VIRGINIA AEROSPACE SCIENCE AND TECHNOLOGY