Grant List
Represents Grant table in the DB
GET /v1/grants?page%5Bnumber%5D=4&sort=-awardee_organization
{ "links": { "first": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=1&sort=-awardee_organization", "last": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=1419&sort=-awardee_organization", "next": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=5&sort=-awardee_organization", "prev": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=3&sort=-awardee_organization" }, "data": [ { "type": "Grant", "id": "15856", "attributes": { "award_id": "1R43AG094486-01", "title": "Characterizing neurocognitive deficits in post-acute sequelae of COVID-19", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [ { "id": 44278, "first_name": "DAVID WITT", "last_name": "FRANKOWSKI", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-09-16", "end_date": "2027-05-31", "award_amount": 325672, "principal_investigator": { "id": 44279, "first_name": "Jennifer", "last_name": "Graves", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [ { "id": 44280, "first_name": "Amir Hossein", "last_name": "Meghdadi", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "awardee_organization": { "id": 3381, "ror": "", "name": "ADVANCED BRAIN MONITORING, INC.", "address": "", "city": "", "state": "CA", "zip": "", "country": "United States", "approved": true }, "abstract": "Post-acute sequelae of COVID-19 (PASC), or Long COVID, is an emerging global health crisis with an urgent need for objective assessment tools to quantify neurocognitive deficits. This proposal aims to validate and leverage a novel mobile electroencephalography (EEG) platform to provide accessible, cost-effective cognitive assessments for individuals suffering from neurological manifestations of PASC (nPASC). Our preliminary data suggests that EEG/event-related potential (ERP) biosignatures, including delayed neural responses during auditory and memory tasks, are sensitive to cognitive impairments in nPASC. However, the trajectory and specificity of these deficits remain unclear. This study will validate these preliminary findings in a larger cohort (n=52) and longitudinally monitor changes over one year to map recovery or detect early signs of persistent cognitive decline. The innovative approach integrates resting-state EEG with multiple task-based ERP protocols, enabling comprehensive profiling of neural dysfunction associated with nPASC. Leveraging Advanced Brain Monitoring's FDA-cleared mobile EEG platform and validated analysis pipelines will provide a scalable solution for widespread clinical use and remote assessments. If successful, this study will deliver a quantitative EEG/ERP biomarker profile specific to neuro-PASC, enabling objective evaluation of cognitive deficits. Longitudinal monitoring will elucidate the natural trajectory, identify potential risk factors for persistent impairment, and provide outcome measures for future therapeutic interventions. This innovative diagnostic tool will empower patients and clinicians by providing objective evidence of nPASC severity and treatment efficacy.", "keywords": [ "2019-nCoV", "Acute", "Address", "Age", "Algorithms", "Alzheimer's Disease", "Anxiety", "Assessment tool", "Attention", "Auditory", "Brain", "COVID-19", "COVID-19 patient", "COVID-19 severity", "COVID-19 treatment", "Central Nervous System", "Clinical", "Cognition", "Cognitive", "Cognitive deficits", "Control Groups", "Data", "Diagnosis", "Early Diagnosis", "Electroencephalography", "Empirical Research", "Evaluation", "Event-Related Potentials", "Exhibits", "Fatigue", "Future", "Health Professional", "Heterogeneity", "High Prevalence", "Impaired cognition", "Impairment", "Individual", "Infection", "Long COVID", "Maps", "Memory", "Mental Depression", "Methods", "Modality", "Monitor", "Nature", "Neurocognitive Deficit", "Neurologic", "Neurologic Symptoms", "Neuronal Dysfunction", "Outcome", "Outcome Measure", "Participant", "Pathway interactions", "Patient Self-Report", "Patients", "Phase", "Pilot Projects", "Post-Acute Sequelae of SARS-CoV-2 Infection", "Process", "Protocols documentation", "Public Health", "Quality of life", "Random Allocation", "Recovery", "Reporting", "Reproducibility", "Research", "Rest", "Risk", "Risk Factors", "Sample Size", "Self Assessment", "Severities", "Specificity", "Statistical Models", "Symptoms", "Techniques", "Technology", "Therapeutic Intervention", "Time", "Treatment Efficacy", "Validation", "Visit", "analysis pipeline", "auditory processing", "biomarker identification", "biosignature", "case control", "cognitive task", "cognitive testing", "cohort", "cost effective", "cost efficient", "data acquisition", "design", "diagnostic tool", "effective intervention", "empowerment", "epidemiology study", "executive function", "experience", "follow-up", "global health", "innovation", "machine learning model", "mild cognitive impairment", "neural", "neural correlate", "neurologic sequelae of COVID-19", "neuropathology", "neurophysiology", "neuropsychiatry", "novel", "post-COVID-19", "potential biomarker", "primary endpoint", "remote assessment", "response", "specific biomarkers", "symptomatology", "therapy development", "trend", "visual memory" ], "approved": true } }, { "type": "Grant", "id": "15853", "attributes": { "award_id": "1F31NS143332-01", "title": "Early life influenza infection and glial dysregulation", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Neurological Disorders and Stroke (NINDS)" ], "program_reference_codes": [], "program_officials": [ { "id": 44273, "first_name": "JENNY LILY", "last_name": "KIM", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-09-01", "end_date": "2028-08-31", "award_amount": 49538, "principal_investigator": { "id": 44274, "first_name": "Karen Elizabeth", "last_name": "Malacon", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 3380, "ror": "", "name": "STANFORD UNIVERSITY", "address": "", "city": "", "state": "CA", "zip": "", "country": "United States", "approved": true }, "abstract": "Millions of children in the United States contract respiratory infections such as influenza, RSV, and COVID-19 every year, with those under the age of five affected the most severely1,2. Respiratory infections can have long- term effects on the central nervous system in both adults and children3–11. In fact, currently, 6 million children are suffering from long COVID, and up to 44% of these children experience cognitive impairment3. Childhood is a critical period for synaptic formation and myelination, making the brain particularly vulnerable to insults that can lead to permanent and long-lasting neurocognitive changes12. In rodents, postnatal day (P)14 is a crucial period of peak synaptogenesis and myelination12–14. As a result, during this time, a respiratory immune challenge such as influenza can result in persistent neurodevelopmental dysfunction. While many studies have investigated the neurological effects of systemic immune challenges during the prenatal and adult periods15–18, the impact of influenza infection during early postnatal life remains understudied. The proposed study aims to investigate the effect of influenza infection at P14 on glial dysregulation in mice. The overarching hypothesis is that influenza infection results in multicellular dysfunction driven by aberrant microglia. My preliminary data show that influenza infection at P14 leads to an increase in reactive microglia one-week post-infection in the cingulum and dentate gyrus, along with elevated expression of inflammatory genes in microglia as revealed by single-nuclei RNA sequencing. I will employ advanced transcriptomic analysis to examine changes in glial sub-states, and to identify alterations in synapse/pruning-associated genes (Aim 1A). Additionally, changes in microglia-mediated synaptic pruning will be assessed using Imaris 3D reconstructions to quantify microglial engulfment of synapses following infection. My preliminary findings indicate that influenza infection results in a decrease in OPCs and oligodendrocytes in the cingulum and dentate gyrus one-week post-infection. I will use an established optogenetics paradigm19,20 to stimulate excitatory dentate gyrus neurons and test for changes in activity- dependent myelination following infection (Aim 2). Finally, based on the hypothesis that reactive microglia dysregulate oligodendroglial dynamics, microglia will be depleted between P7-P21 to determine if this rescues the observed loss of oligodendroglial cells (Aim 3). Given my experiences investigating the impact of prenatal environmental immune challenges on microglia and behavior, I am well-prepared to execute these experiments. This work will be conducted under the sponsorship of Michelle Monje, MD/PhD, a leading expert in glial-neuron interactions and myelin plasticity. The co-sponsorship of Catherine Blish, MD/PhD, will ensure comprehensive guidance on virologic aspects, and collaborations with Karl Deisseroth, MD/PhD, Akiko Iwasaki, PhD, and Beth Stevens, PhD, will provide the necessary support to successfully achieve the aims of this project. Stanford's rigorous training environment and the collective support from these experts will ensure the project's success and my growth into an innovative physician-scientist capable of developing therapies for neuroimmune diseases.", "keywords": [ "3-Dimensional", "Adult", "Affect", "Age", "Axon", "Behavior", "Brain", "COVID-19", "COVID-19 pandemic", "CSF1R gene", "Cd68", "Cell Lineage", "Cells", "Central Nervous System", "Child", "Childhood", "Cognitive", "Collaborations", "Contracts", "Data", "Data Set", "Development", "Doctor of Philosophy", "Ensure", "Environment", "Functional disorder", "Future", "Genes", "Goals", "Growth", "Homeostasis", "Hospitalization", "Immune", "Immunohistochemistry", "Impaired cognition", "Infection", "Inflammatory", "Influenza", "Institution", "Intraperitoneal Injections", "Life", "Light", "Long COVID", "Long-Term Effects", "MHC Class I Genes", "Mediating", "Microglia", "Mus", "Myelin", "Neurobiology", "Neurocognitive", "Neuroimmune", "Neurologic Effect", "Neurons", "Oligodendroglia", "Parahippocampal Gyrus", "Physicians", "Physiologic pulse", "Play", "Process", "Proliferating", "Research", "Respiratory System", "Respiratory Tract Infections", "Rodent", "Role", "Scientist", "Synapses", "Testing", "Time", "Training", "Transmission Electron Microscopy", "United States", "Virus", "Work", "age group", "chemokine", "confocal imaging", "critical period", "cytokine", "density", "dentate gyrus", "experience", "experimental study", "influenza infection", "inhibitor", "innovation", "myelination", "neural circuit", "neurodevelopment", "neurogenesis", "neuroimmunologic disease", "neuroimmunology", "oligodendrocyte differentiation", "oligodendrocyte progenitor", "optogenetics", "postnatal", "prenatal", "reconstruction", "respiratory", "single nucleus RNA-sequencing", "skills", "success", "synaptic pruning", "synaptogenesis", "therapy development", "transcriptomics" ], "approved": true } }, { "type": "Grant", "id": "15852", "attributes": { "award_id": "4R00AA031315-02", "title": "Characterization of acetaldehyde-protein adducts in alcohol-associated liver disease", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute on Alcohol Abuse and Alcoholism (NIAAA)" ], "program_reference_codes": [], "program_officials": [ { "id": 44271, "first_name": "LI", "last_name": "LIN", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-09-23", "end_date": "2028-08-31", "award_amount": 249000, "principal_investigator": { "id": 44272, "first_name": "Bryan R.", "last_name": "Mackowiak", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 3379, "ror": "", "name": "EAST TENNESSEE STATE UNIVERSITY", "address": "", "city": "", "state": "TN", "zip": "", "country": "United States", "approved": true }, "abstract": "Ethanol consumption has been on the rise throughout the COVID-19 pandemic and one of the major consequences has been a surge in alcohol-associated liver disease (ALD), especially severe alcoholic hepatitis (sAH). sAH is a life-threatening condition with 30-day patient mortality greater than 30%, limited treatment options, and often requires a liver transplant. There is an urgent need to identify novel mechanisms of ALD progression that are potential targets for treatment. The ethanol metabolite acetaldehyde (AcH) is known to form adducts on lysine residues within proteins, which affect protein function. Many proteins are known to bind to AcH, but no one has characterized the overall composition or downstream effects of these protein modifications on the pathogenesis of ALD. Albumin is one of the major proteins known to bind to AcH, and these AcH adducts mostly occur on the many exposed lysine residues throughout the albumin molecule. The fact that a single albumin can bind many AcH molecules combined with albumin being the most abundant protein in the liver and circulation means that albumin may act as a “sponge” for excess AcH. Therefore, any decrease in albumin levels may lead to increased modification of other proteins, having deleterious effects on ethanol-induced organ injury. My preliminary data shows that plasma albumin levels are decreased in heavy drinkers compared to control subjects in the absence of liver dysfunction. In albumin-deficient mice, ethanol feeding leads to decreased lymphocyte accumulation in the liver, but the mechanism is unknown. This project is designed to test the overarching hypothesis that albumin alters the distribution of AcH-protein adducts after ethanol consumption, modulating lymphocyte function in ALD. In Aim 1 (K99 phase) I will receive training from my mentor, Dr. Bin Gao, to determine how AcH and albumin regulate lymphocyte function. In Aim 2 (K99 phase), I will receive training in proteomic methods and analysis from my committee member Dr. Fritz to characterize the AcH-protein adductome in immune cells and albumin-deficient mice. In Aim 3 (R00 phase), I will use the training from the K99 phase to analyze public proteomic datasets and identify specific AcH-protein adducts that are present in patients with ALD. I will utilize cellular models to determine how these modifications impact immune cell and hepatocyte functions in the context of ALD. This project will provide a framework for how AcH-protein adducts modulate ALD using albumin as a model protein. The training provided by this grant will provide the PI with a strong foundation to achieve his long-term goal of identifying systemic mediators of ethanol-induced liver injury to develop therapeutics that protect against alcohol-induced injury in multiple ways. The NIAAA will provide an ideal environment for cross-disciplinary training and the necessary resources to transition to independence.", "keywords": [ "Acetaldehyde", "Address", "Affect", "Albumins", "Alcohol consumption", "Alcohol-Induced Disorders", "Alcoholic Hepatitis", "Alcoholic Liver Diseases", "Alcoholic beverage heavy drinker", "Amino Acids", "Binding", "CD3 Antigens", "COVID-19 pandemic", "Cell Physiology", "Cell model", "Cells", "Chronic", "Circulation", "Coculture Techniques", "Committee Members", "Cytoskeleton", "Data", "Data Analyses", "Data Set", "Defect", "Development", "Disease Progression", "Environment", "Ethanol", "Ethanol Metabolism", "Event", "Exhibits", "Foundations", "Goals", "Grant", "Hepatocyte", "Human", "Immune", "Impairment", "Infiltration", "Inflammation", "Life", "Liver", "Liver Dysfunction", "Liver diseases", "Lymphocyte", "Lymphocyte Count", "Lymphocyte Function", "Lysine", "Mediating", "Mediator", "Mentors", "Methods", "Modeling", "Modification", "Mus", "National Institute on Alcohol Abuse and Alcoholism", "Pathogenesis", "Patients", "Persons", "Phase", "Plasma", "Plasma Albumin", "Play", "Population", "Porifera", "Post-Translational Protein Processing", "Pre-Clinical Model", "Proliferating", "Proteins", "Proteomics", "Resources", "Role", "Sampling", "Splenocyte", "T-Lymphocyte", "Testing", "Therapeutic", "Training", "Work", "adduct", "alcohol use disorder", "comparison control", "design", "feeding", "immunoregulation", "liver injury", "liver metabolism", "liver transplantation", "mortality", "mouse model", "novel", "organ injury", "protein function" ], "approved": true } }, { "type": "Grant", "id": "15851", "attributes": { "award_id": "1F32AI194439-01", "title": "What does it really mean to be broad? Uncovering underlying biology behind broadly neutralizing antibodies", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [ { "id": 32556, "first_name": "TIMOTHY A", "last_name": "GONDRE-LEWIS", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-09-15", "end_date": "2028-09-14", "award_amount": 78040, "principal_investigator": { "id": 44270, "first_name": "Zoe", "last_name": "Lyski", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 3378, "ror": "", "name": "UNIVERSITY OF ARIZONA", "address": "", "city": "", "state": "AZ", "zip": "", "country": "United States", "approved": true }, "abstract": "The importance of antibodies in preventing and controlling human disease cannot be underestimated. Many vaccines depend on neutralizing antibodies for protection. In addition, neutralizing antibodies are highly useful when administered therapeutically. The ongoing pandemic has brought to light that few therapeutic antibodies can stand the test of time as new viral variants emerge. The promise of broadly neutralizing antibodies, which recognize conserved epitopes shared across entire groups of related pathogens, is that they are evolution-proof and remain protective in the face of pathogen evolution. Yet, as evidenced by clinical data, there are few examples where such antibodies cannot be escaped. This led me to wonder, what properties truly define what it is to be broadly neutralizing? Irrespective of the pathogen, broadly neutralizing antibodies are almost always very rare. In any given study, one might screen thousands of antigen-specific B cells to find a single broadly neutralizing antibody. Therefore, this rarity may explain some crucial underlying biology. Perhaps, these neutralizing antibodies are only broad because they are rare. In other words, pathogens are under little selective pressure to escape antibodies that are infrequently made. This leads to my central hypothesis that most broadly neutralizing antibodies are broad because they are rare, not because they target conserved epitopes that cannot mutate without a fitness cost to the pathogen. Using SARS-CoV-2 as a model pathogen, I will test these concepts. In Aim 1, I will determine whether infrequency is a defining feature of broadly neutralizing antibodies. In Aim 2, I will determine whether some epitopes, are more difficult to evolve away from than others. The results of this work will provide a deeper understanding of the relationship between antibody epitopes and resistance to viral escape. The methods developed in this project have applications far beyond SARS-CoV-2. In addition, this approach may provide a more efficient way for researchers to screen large amounts of sequencing data to identify potentially broadly neutralizing antibodies.", "keywords": [ "2019-nCoV", "ACE2", "Amino Acids", "Antibodies", "Antibody-mediated protection", "Antigens", "B-Lymphocytes", "Binding", "Biology", "Clinical Data", "Common Cold", "Data", "Epitopes", "Evolution", "Frequencies", "Human", "Immune Evasion", "Libraries", "Methods", "Modeling", "Monoclonal Antibodies", "Mutate", "Mutation", "Nucleotides", "Phenotype", "Process", "Property", "Recombinants", "Research Personnel", "Resistance", "Route", "SARS-CoV-2 variant", "Specificity", "Surface", "Testing", "Therapeutic", "Therapeutic antibodies", "Time", "Vaccines", "Variant", "Viral", "Work", "acute infection", "betacoronavirus", "cost", "fitness", "human disease", "loss of function", "mutant", "neutralizing antibody", "neutralizing monoclonal antibodies", "pandemic disease", "pathogen", "pressure", "prevent", "screening", "thermostability" ], "approved": true } }, { "type": "Grant", "id": "15893", "attributes": { "award_id": "1U18FD008634-01", "title": "Increased Extraction Capacity for Molecular Section", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [], "program_reference_codes": [], "program_officials": [ { "id": 44330, "first_name": "MEGAN", "last_name": "MILLER", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-09-20", "end_date": "2026-08-31", "award_amount": 31722, "principal_investigator": { "id": 44331, "first_name": "YAN", "last_name": "ZHANG", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 3378, "ror": "", "name": "UNIVERSITY OF ARIZONA", "address": "", "city": "", "state": "AZ", "zip": "", "country": "United States", "approved": true }, "abstract": "Vet-LIRN Network Capacity-Building Project and Equipment Grants (U18) PAR-23-202 Increased Extraction Capacity for Arizona Veterinary Diagnostic Laboratory Molecular Section Project Summary/Abstract- The Arizona Veterinary Diagnostic Laboratory (AZVDL) is seeking funding to purchase an Indical IndiMag2 to enhance its nucleic acid extraction capability and capacity, thereby strengthening its emergency surge testing for significant animal food/feed emergency events. Veterinary diagnostic laboratories play a critical role in protecting both animal and public health, especially during large-scale foodborne disease outbreaks or contamination incidents. Funding through the Vet-LIRN Network Capacity-Building Project and Equipment Grants (U18) is essential to expand AZVDL’s ability to respond effectively to such emergencies. This support will enable AZVDL to improve its diagnostic capabilities by acquiring advanced equipment. The COVID-19 pandemic has demonstrated that veterinary laboratories are uniquely positioned to provide high-throughput testing during public health crises, as they routinely handle large- scale diagnostic procedures for zoonotic and animal diseases. By enhancing its capacity, AZVDL will be better equipped to provide real-time detection of pathogens or contaminants in animal food and feed, helping to prevent outbreaks that threaten food safety, public health, and economic stability. This funding initiative also aligns with the goals of the Food Safety Modernization Act (FSMA), which emphasizes proactive measures to detect and prevent foodborne illnesses. Upgrading AZVDL’s infrastructure will not only improve its response to emerging threats but also contribute to the broader national network of veterinary laboratories dedicated to safeguarding both animal and human populations.", "keywords": [], "approved": true } }, { "type": "Grant", "id": "15850", "attributes": { "award_id": "1R01HL181348-01", "title": "Emulated Target Trials and Phenotyping in Patients with Acute Respiratory Distress Syndrome", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Heart Lung and Blood Institute (NHLBI)" ], "program_reference_codes": [], "program_officials": [ { "id": 44269, "first_name": "GUOFEI", "last_name": "ZHOU", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-09-23", "end_date": "2027-08-31", "award_amount": 1479335, "principal_investigator": { "id": 27913, "first_name": "Elias", "last_name": "Baedorf Kassis", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [ { "id": 32134, "first_name": "Li-Wei H", "last_name": "Lehman", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, { "id": 32135, "first_name": "Zachary", "last_name": "Shahn", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "awardee_organization": { "id": 3377, "ror": "", "name": "MASSACHUSETTS INSTITUTE OF TECHNOLOGY", "address": "", "city": "", "state": "MA", "zip": "", "country": "United States", "approved": true }, "abstract": "Acute respiratory distress syndrome (ARDS) is a severe form of lung injury with significant public health implications due to severe morbidity and mortality. The need to utilize existing data to inform prospective research and clinical decision making was emphasized during the COVID pandemic, when ARDS became a leading cause of death, and clinicians were forced to operate outside of existing evidence. Many commonly applied interventions including use of neuromuscular blockade (NMB), steroids, driving pressure and mechanical power are used despite negative data, without high quality prospective studies or with equivocal evidence and with the potential for both benefit or harm. Additionally, phenotypes of ARDS may have different prognosis and response to treatment, but thus far have not been well differentiated using routinely available dynamic clinical data, nor have they been incorporated into prospective trials. ‘Dynamic treatment regimes’ (DTRs) are rules for making treatment decisions sequentially at multiple time-points based on a patient’s evolving history. Most relevant treatment strategies for ARDS are DTRs. DTRs may be evaluated in randomized trials, however it is infeasible to conduct randomized trials testing all DTRs of interest. This grant proposes ‘target trial emulation’ from observational data using ‘g-methods’ for confounding adjustment to address multiple gaps in our knowledge about ARDS care. We will address important methodological gaps in ARDS phenotyping and develop advanced machine learning (ML) methods for dynamic phenotyping for prognostication and personalized DTRs to determine for whom and when specific ARDS treatments are beneficial. The investigation will utilize three large datasets—including the Medical Information Mart for Intensive Care (MIMIC) IV database, the eICU collaborative research database, and the Dutch AmsterdamUMCdb database—representing a wide geographic and demographic spectrum, and the ability to assess stability of findings across geography and centers. To address these knowledge gaps regarding use of NMB, steroids, driving pressure and mechanical power, as well as identify phenotypes of patients most responsive to treatment, we propose two overarching aims for this grant. Specific Aim 1) Using target trial emulations and g-methods, we will estimate clinical outcomes that would result under a range of treatment strategies for NMB, steroids as well as driving pressure and mechanical power thresholds. Specific Aim 2) We will develop machine learning methods to derive dynamic markers for ARDS phenotyping and formulate personalized DTRs for ARDS treatment. The project represents a collaborative effort between experts in critical care medicine (with a specialty in mechanical ventilation), machine learning, and causal inference. Our results will address important gaps in clinical knowledge about treatment of ARDS and inform the design of future randomized trials. Our study designs, code, and constructed cohorts will also provide valuable templates for other researchers to use in future observational studies, which we foresee will broadly improve the quality of evidence from observational data in critical care.", "keywords": [ "Acute Respiratory Distress Syndrome", "Address", "Attenuated", "Automobile Driving", "COVID-19 pandemic", "Caring", "Cause of Death", "Cessation of life", "Clinical", "Clinical Data", "Clinical Trials", "Code", "Critical Care", "Data", "Data Science", "Data Set", "Databases", "Death Rate", "Decision Making", "Disease Marker", "Dose", "Effectiveness", "Enrollment", "Future", "Geography", "Grant", "Heterogeneity", "Hospital Mortality", "Induction of neuromuscular blockade", "Inflammation", "Intensive Care", "International", "Intervention", "Investigation", "Joints", "Knowledge", "Learning", "Light", "Machine Learning", "Mechanical ventilation", "Mechanics", "Mediating", "Medical", "Medicine", "Meta-Analysis", "Methodology", "Methods", "Modeling", "Morbidity - disease rate", "Observational Study", "Outcome", "Output", "Patient Monitoring", "Patients", "Phenotype", "Physicians", "Physiological", "Prognosis", "Prospective Studies", "Public Health", "Recording of previous events", "Research", "Research Design", "Research Personnel", "Resources", "Sedation procedure", "Sequential Treatment", "Severity of illness", "Steroids", "Syndrome", "Testing", "Therapeutic Intervention", "Tidal Volume", "Time", "Ventilator", "base", "clinical decision-making", "cohort", "common treatment", "continuous monitoring", "design", "effective intervention", "effective therapy", "improved", "improved outcome", "interest", "large datasets", "lung injury", "machine learning method", "medical specialties", "mortality", "pressure", "prognostication", "prospective", "randomized trial", "respiratory", "response", "risk stratification", "statistical and machine learning", "treatment effect", "treatment response", "treatment strategy", "ventilation" ], "approved": true } }, { "type": "Grant", "id": "15844", "attributes": { "award_id": "1R43PS005313-01", "title": "Development of an ultrasensitive, rapid and portable nucleic acid based test for detection of acute Hepatitis C Virus infection at the point-of-care.", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Center for Emerging and Zoonotic Infectious Diseases (NCEZID)" ], "program_reference_codes": [], "program_officials": [], "start_date": "2025-09-30", "end_date": "2026-09-29", "award_amount": 306992, "principal_investigator": { "id": 44259, "first_name": "Sujit", "last_name": "Jangam", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 3376, "ror": "", "name": "ARETE BIOSCIENCES", "address": "", "city": "", "state": "IL", "zip": "", "country": "United States", "approved": true }, "abstract": "Hepatitis C Virus (HCV) infections are on the rise in the US and the world. Nearly 4 million people in the United States have HCV infection, half of which will progress to chronic HCV infection. HCV infections often go undiagnosed and untreated due to limited screening, lack of accessible testing options for primary care settings and loss to follow-up. Undiagnosed and untreated HCV infections can lead to adverse health outcomes and result in extremely high direct medical costs. Chronic infections when untreated can cause liver damage, cirrhosis, liver cancer and in some cases death. HCV RNA is detectable in whole and capillary blood specimens and infections are effectively treatable with antiviral drugs. The USPTF now recommends HCV screening for all adults between the ages of 18 and 79 years. Despite the seriousness of the health outcomes mentioned above, testing levels remain low and loss to follow-up rates remain high even amongst those that get the initial screen due to the need for a confirmatory test. In order to stem the growing rate of infections and resulting adverse outcomes, testing rates need to increase followed by reduction in loss to follow-up. The COVID-19 pandemic has enabled primary care in less traditional settings such as retail and promoted the use of telemedicine. This healthcare delivery model is particularly relevant to HCV screenings tests that are plagued by accessibility concerns. Point-of-care tests (POC) that detect anti-HCV antibodies are available but cannot differentiate between active and past infections and are plagued by sensitivity concerns. There is a need for rapid point-of-care confirmatory tests for active HCV infection. A POC test that can accurately detect acute viremia could enable test and treat models. Several POC molecular nucleic acid amplification tests (NAATs) are currently available, however, the majority are not sensitive, have validity issues [7] and are incompatible with complex samples due to lack of genuine sample purification. The only POC platform capable of high sensitivity (Cepheid Xpert) is expensive and is designated moderately complex. Cubit Diagnostics has developed a proprietary sample to results platform that utilizes specific target capture (STC) based sample purification followed by multiplex polymerase chain reaction (PCR). The Cubit platform consists of a disposable cartridge and a reusable dock. The platform is low cost, low footprint, extremely sensitive and can complete a test in 30 minutes. Cubit has developed a SARS- CoV-2, Flu A, Flu B test on this platform and plans to prove the feasibility of its proprietary STC extraction method using blood samples via this application. During this project, bench assays for specific target capture (STC) sample purification and fast polymerase chain reaction (PCR) will be developed for detection of HCV RNA from whole blood. Primers and probes will be designed and reagent formulations optimized to allow for PCR completion in 15 min. Target purification of HCV RNA from blood samples will be demonstrated and optimized using contrived pre-clinical specimens. Following optimization of bench assays for HCV STC and PCR, the assay will be ported to the Cubit cartridge and feasibility established with contrived whole blood specimens using the end-to-end workflow on the Cubit dock.", "keywords": [ "2019-nCoV", "5' Untranslated Regions", "Acute", "Acute Hepatitis C", "Adult", "Age", "Anti-viral Agents", "Biological Assay", "Blood", "Blood capillaries", "Blood specimen", "COVID-19 detection", "COVID-19 pandemic", "Cessation of life", "Chlamydia trachomatis", "Chronic Hepatitis C", "Cirrhosis", "Complex", "Computer software", "Detection", "Development", "Diagnosis", "Diagnostic", "Docking", "Escherichia coli", "Formulation", "Freeze Drying", "Genotype", "HCV screening", "Health", "Hepatitis C", "Hepatitis C Antibodies", "Hepatitis C Therapy", "Hepatitis C virus", "Incubated", "Individual", "Infection", "Label", "Lateral", "Lead", "Length", "Liquid substance", "Location", "Malignant Neoplasms", "Malignant neoplasm of liver", "Medical Care Costs", "Methods", "Modeling", "Molecular", "Molecular Diagnostic Testing", "Neisseria gonorrhoeae", "Nucleic Acid Amplification Tests", "Nucleic Acids", "Outcome", "Performance", "Persons", "Plasma", "Polymerase Chain Reaction", "Primary Care", "Process", "RNA", "RNA Probes", "RNA primers", "Ramp", "Reaction", "Reagent", "Recommendation", "Recovery", "Reverse Transcriptase Polymerase Chain Reaction", "Running", "Sampling", "Sepsis", "Serology", "Service delivery model", "Specimen", "Speed", "Swab", "Technology", "Telemedicine", "Temperature", "Testing", "Time", "United States", "Update", "Vagina", "Venous blood sampling", "Viremia", "Virus", "Virus Diseases", "Whole Blood", "adverse outcome", "chronic infection", "cost", "design", "detection limit", "detection test", "flu", "follow-up", "improved", "infection rate", "instrument", "internal control", "liver injury", "manufacture", "nucleic acid detection", "pathogen", "point of care", "point of care testing", "portability", "pre-clinical", "primary care setting", "screening", "stem", "success", "viral RNA" ], "approved": true } }, { "type": "Grant", "id": "15842", "attributes": { "award_id": "1R35GM160192-01", "title": "Innovative Multiscale Modeling Techniques for Membrane-Bound Proteins", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of General Medical Sciences (NIGMS)" ], "program_reference_codes": [], "program_officials": [ { "id": 44257, "first_name": "ANNE", "last_name": "GERSHENSON", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-09-01", "end_date": "2030-08-31", "award_amount": 369500, "principal_investigator": { "id": 44258, "first_name": "Yu-ming Mindy", "last_name": "Huang", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 3375, "ror": "", "name": "WAYNE STATE UNIVERSITY", "address": "", "city": "", "state": "MI", "zip": "", "country": "United States", "approved": true }, "abstract": "Innovative Multiscale Modeling Techniques for Membrane-Bound Proteins SUMMARY Our laboratory develops computer models to investigate biomolecular diffusion and interactions with a particular emphasis on membrane-bound proteins and lipid metabolism. The study of diffusion using empirical techniques faces serious obstacles in capturing the intermediate-state details of kinetic processes. Even computational tools encounter inherent tradeoffs in balancing long-timescale simulations with those that reveal precise atomistic details, particularly for lipid droplet (LD) proteins. This R35 MIRA proposal has two complementary research directions. First. we will develop computational tools to model diffusion and molecular interactions and apply them to the SARS-CoV-2 spike protein, otherwise well studied during pandemic-related research and similar to other viruses. My research offers to accelerate drug discovery, coronavirus vaccine development, and treatments for other viruses. Second, we will investigate the protein networks that regulate lipid metabolism on LDs, focusing on how the ABHD5 protein interacts with LD membranes and lipid-regulating proteins. By combining computational approaches and experimental validation, my long-term research trajectory aims to advance understanding of lipid metabolism and inform potential therapeutic strategies for diseases that include diabetes and cancer.", "keywords": [ "Acceleration", "Binding", "Binding Proteins", "Computer Models", "Computing Methodologies", "Dedications", "Development", "Diabetes Mellitus", "Diffusion", "Disease", "Face", "Foundations", "Kinetics", "Laboratories", "Ligands", "Lipids", "Malignant Neoplasms", "Mediating", "Membrane", "Methodological Studies", "Modeling", "Molecular", "Polysaccharides", "Process", "Proteins", "Research", "SARS-CoV-2 spike protein", "System", "Techniques", "Therapeutic", "Validation", "Viral", "Virus", "computerized tools", "coronavirus vaccine", "drug discovery", "glycosylation", "innovation", "insight", "lipid metabolism", "multi-scale modeling", "new therapeutic target", "pandemic disease", "protein function", "protein metabolism", "refractory cancer", "simulation", "targeted treatment", "vaccine development" ], "approved": true } }, { "type": "Grant", "id": "15935", "attributes": { "award_id": "1K99AG086538-01A1", "title": "Molecular profiles for mortality risk and longevity: a multiomics approach", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute on Aging (NIA)" ], "program_reference_codes": [], "program_officials": [ { "id": 44380, "first_name": "CHRISTY", "last_name": "CARTER", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-06-16", "end_date": "2027-03-31", "award_amount": 122858, "principal_investigator": { "id": 44381, "first_name": "Fenglei", "last_name": "Wang", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 3374, "ror": "", "name": "HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH", "address": "", "city": "", "state": "MA", "zip": "", "country": "United States", "approved": true }, "abstract": "The US life expectancy experienced a generally upward trend over the past few decades; however, in recent years, it has seen a decline. This decline cannot be solely attributed to the excess mortality caused by COVID- 19 but also to an increased death rate from other leading causes (e.g., heart disease, cancer, and stroke). The biological mechanisms that underlie aging process and mortality in humans are multifactorial and remain poorly understood. Although multiple genetic variants have been linked to lifespan in model organisms, many of these genes do not exhibit significant variation in human populations. The heritability of human lifespan also appears to be relatively low. One possible explanation for lack of significant loci and low heritability is the complexity of survival as a phenotype, which involves multiple biological processes, environmental influences, and chance. The stochastic component of survival may dilute the genetic influence on the time-to-death phenotype. Consequently, a substantial mechanistic gap exists between genotype and mortality. The proposed K99/R00 project aims to utilize plasma metabolomic and proteomics profile to bridge this gap and comprehensively investigate the relationship between genes, proteins, metabolites, and mortality risk. To achieve this goal, Dr. Fenglei Wang will incorporate data from multiple sources, including the Nurses’ Health Study (NSH), NHSII, Health Professionals Follow-up Study (HPFS), Hispanic Community Health Study/Study of Latinos (HCHS/ SOL), VITamin D Omega3 TriAL (VITAL), UK Biobank (UKB), and eQTLGen. In Aim 1 (K99), Dr. Wang will determine genetic factors that influence a plasma metabolomic signature, previously developed by him, which has the potential to predict all-cause mortality. He will also evaluate the causal relationship between the metabolomic signature and four diseases that are major causes of death. In Aim 2 (R00), Dr. Wang will construct a plasma proteomic signature capable of predicting all-cause mortality and identify genetic factors influencing the proteomic signature. Then he will compare the influential genetic factors identified for the proteomic signature to those for the metabolomic signature. In Aim 3 (R00), Dr. Wang will conduct plasma proteomic profiling in a nested case-control study to examine the relationship between longitudinal changes in plasma metabolomic and proteomic profiles and healthy longevity. Findings from this project may improve our understanding of the molecular profiles associated with the aging process and mortality, and inform potential interventions for improving health outcomes and extending human lifespan. Dr. Wang has assembled a strong mentoring team to provide expertise in aging research and training in genetics, proteomics, and multi-omics integration. The new skills will complement his current expertise in nutritional epidemiology and metabolomic research. His outlined training plan will provide the necessary knowledge and skills for Dr. Wang to advance towards his career goal of becoming an independent researcher who specializes in the application of multi-omics approach to study nutrition and healthy aging.", "keywords": [ "Affect", "Age", "Aging", "Biological", "Biological Process", "COVID-19", "COVID-19 mortality", "Cardiovascular Diseases", "Cause of Death", "Cessation of life", "Chronic Disease", "Colorectal Cancer", "Complement", "Coronary heart disease", "Data", "Data Set", "Databases", "Death Rate", "Diet", "Dietary Factors", "Disease", "Etiology", "Excess Mortality", "Follow-Up Studies", "Future", "Gene Expression", "Genes", "Genetic", "Genomics", "Genotype", "Goals", "Health", "Health Professional", "Heart Diseases", "Heritability", "Hispanic Community Health Study/Study of Latinos", "Human", "Influentials", "Intervention", "Investigation", "Knowledge", "Life Expectancy", "Link", "Longevity", "Malignant Neoplasms", "Mendelian randomization", "Mentors", "Molecular", "Molecular Profiling", "Multiomic Data", "National Institute on Aging", "Nested Case-Control Study", "Non-Insulin-Dependent Diabetes Mellitus", "Nurses' Health Study", "Nutrition", "Omega-3 Fatty Acids", "Outcome", "Participant", "Pattern", "Phenotype", "Pilot Projects", "Plasma", "Population", "Population Study", "Prospective cohort study", "Proteins", "Proteome", "Proteomics", "Publishing", "Recommendation", "Research", "Research Personnel", "Risk", "Stroke", "Technology", "Time", "Training", "Variant", "Vitamin D", "Work", "aging process", "aging related", "biobank", "career", "endophenotype", "experience", "genetic variant", "genome wide association study", "genome-wide", "healthy aging", "improved", "life span", "lifestyle factors", "machine learning model", "metabolomics", "model organism", "molecular marker", "mortality", "mortality risk", "multiple data sources", "multiple omics", "nutritional epidemiology", "prospective", "proteomic signature", "skills", "statistics", "transcriptome", "trend" ], "approved": true } }, { "type": "Grant", "id": "15841", "attributes": { "award_id": "1R01HL178888-01", "title": "Role of a Novel Hormone Complex, Fabkin, in Dyslipidemia and Inflammation in Atherosclerosis", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Heart Lung and Blood Institute (NHLBI)" ], "program_reference_codes": [], "program_officials": [ { "id": 44255, "first_name": "MARTIN P", "last_name": "PLAYFORD", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-09-05", "end_date": "2029-05-31", "award_amount": 692742, "principal_investigator": { "id": 44256, "first_name": "GOKHAN S", "last_name": "HOTAMISLIGIL", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 3374, "ror": "", "name": "HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH", "address": "", "city": "", "state": "MA", "zip": "", "country": "United States", "approved": true }, "abstract": "Project Summary: Despite effective strategies for lowering cholesterol, atherosclerosis, and related cardiovascular diseases remain the leading cause of death worldwide, even in the COVID era. Recent clinical data highlights a key benefit of targeting inflammatory processes in atherosclerosis. Thus, the discovery of novel therapeutics that can modulate both dyslipidemia and inflammation would represent a major breakthrough for atherosclerosis treatment. This proposal is focused on the fatty acid-binding protein 4 (FABP4) hormone complex we discovered, called Fabkin, as a key mediator of dyslipidemia and inflammation that contributes to atherosclerosis. In Fabkin, FABP4, adenosine kinase, and nucleoside diphosphate kinase interact to regulate extracellular ATP and ADP levels, which signal through purinergic receptors. Our long-term goal is to understand Fabkin's roles and mechanisms in physiology and cardio-metabolic pathophysiology and elucidate translational opportunities. Our objective in this proposal is to elucidate the roles and mechanisms of Fabkin in lipid metabolism and inflammation and assess its potential as a therapeutic target for atherosclerosis. We hypothesize that Fabkin is a key regulator of hepatic lipid metabolism and a pro-inflammatory factor, contributing to dyslipidemia and macrophage inflammation via purinergic signaling to promote atherosclerosis. This is based on available evidence of a role of purinergic signaling in atherosclerosis, our compelling preliminary data showing that mice lacking adipocyte FABP4 hormone, or treated with Fabkin-targeting monoclonal antibody, are protected from dyslipidemia and atherosclerosis, and our experiments supporting a role of Fabkin to induce de novo lipogenesis (DNL) and very low-density lipoprotein (VLDL) secretion in hepatocytes, and inflammation in macrophages. We will test our hypothesis in the following three specific aims: 1) Determine the effect of in vivo Fabkin deficiency on dyslipidemia and atherosclerosis. 2) Elucidate the roles and signaling mechanisms of Fabkin in hepatocyte DNL and VLDL secretion, 3) Identify the roles and signaling mechanisms of Fabkin in macrophage responses to cholesterol stress. In Aim 1 we will treat ApoE-/- mice with Fabkin-targeting antibody and employ ApoE-/-Ndpk-/- mice to examine the effects of in vivo Fabkin deficiency on atherosclerosis, dyslipidemia, and hepatic DNL and VLDL secretion. In Aim 2 we will characterize Fabkin's direct effects on hepatocyte DNL and VLDL secretion in vitro, test the efficacy of Fabkin-targeting antibody, and identify the purinergic signaling pathways induced by Fabkin. In Aim 3 we will determine Fabkin's direct effects on macrophage responses to cholesterol stress in vitro, including foam cell formation, inflammation, ER stress, and cell death. We will also test the efficacy of Fabkin-targeting antibody and identify the underlying purinergic signaling pathways. The expected outcome of these studies will be a clear understanding of the functions and mechanisms of action of Fabkin in lipid metabolism and inflammation, and its potential as a novel therapeutic target for treating atherosclerosis.", "keywords": [ "Address", "Adenosine Kinase", "Antibodies", "Apolipoprotein E", "Arterial Fatty Streak", "Atherosclerosis", "COVID-19 pandemic", "Cardiac", "Cardiovascular Diseases", "Cause of Death", "Cell Death", "Cholesterol", "Clinical Data", "Complex", "Data", "Diabetes Mellitus", "Disease", "Dyslipidemias", "Event", "FABP4 gene", "Foam Cells", "Functional disorder", "Goals", "Hepatic", "Hepatocyte", "Hormonal", "Hormone secretion", "Hormones", "Human", "Hyperlipidemia", "In Vitro", "Individual", "Inflammation", "Inflammatory", "Intervention", "LDL Cholesterol Lipoproteins", "Lesion", "Link", "Lipid A", "Lipids", "Liver", "Macrophage", "Mediating", "Mediator", "Metabolism", "Mission", "Modeling", "Molecular", "Monoclonal Antibodies", "Mus", "Myocardial Ischemia", "Nucleoside-Diphosphate Kinase", "Nucleosides", "Outcome Study", "Pathogenesis", "Pathologic", "Pathology", "Patients", "Phosphotransferases", "Physiology", "Plasma", "Process", "Public Health", "Purinoceptor", "Regulation", "Risk Factors", "Risk Reduction", "Role", "Signal Pathway", "Signal Transduction", "Stress", "Testing", "Therapeutic", "United States National Institutes of Health", "Very low density lipoprotein", "Work", "antagonist", "cardiometabolism", "cardiovascular disorder risk", "cardiovascular risk factor", "efficacy testing", "endoplasmic reticulum stress", "experimental study", "extracellular", "fatty acid-binding proteins", "in vivo", "inhibitor", "insight", "kinase inhibitor", "lipid biosynthesis", "lipid metabolism", "mortality", "mutant", "new therapeutic target", "novel", "novel therapeutic intervention", "novel therapeutics", "response", "therapeutic target", "translational potential", "western diet" ], "approved": true } } ], "meta": { "pagination": { "page": 4, "pages": 1419, "count": 14184 } } }