Grant List
Represents Grant table in the DB
GET /v1/grants?sort=-funder
{ "links": { "first": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=1&sort=-funder", "last": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=1392&sort=-funder", "next": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=2&sort=-funder", "prev": null }, "data": [ { "type": "Grant", "id": "5337", "attributes": { "award_id": "1R21AI163548-01A1", "title": "Host response-based diagnostics for identifying bacterial versus viral causes of lower respiratory infection in resource-limited settings", "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": 18731, "first_name": "Erik J.", "last_name": "Stemmy", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2022-05-01", "end_date": "2024-04-30", "award_amount": 283617, "principal_investigator": { "id": 18732, "first_name": "GAYANI", "last_name": "TILLEKERATNE", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 246, "ror": "https://ror.org/00py81415", "name": "Duke University", "address": "", "city": "", "state": "NC", "zip": "", "country": "United States", "approved": true }, "abstract": "Project Summary/ Abstract Lower respiratory tract infection (LRTI) is a common reason for antibacterial use and misuse globally. Limitations associated with current LRTI diagnostics are a major driver of antibacterial overuse. Pathogen- based diagnostics have limited sensitivity and do not distinguish infection from colonization. In low- or middle- income countries (LMICs), LRTI diagnosis is further hindered by limited laboratory infrastructure. Host-based diagnostics that leverage the host’s response to infection and broadly classify infection as viral or bacterial in etiology could greatly reduce inappropriate antibacterial use for LRTI. Previously, we showed that novel, peripheral blood-based gene expression classifiers accurately identified bacterial versus viral febrile respiratory illness in a South Asian population. While promising, these classifiers require the collection of a blood sample, which may be challenging in pediatric populations or in LMIC settings with limited resources. Emerging data suggest that the host response in the nasopharynx may also help identify class of infection. Nasopharyngeal sampling offers the possibility of an integrated diagnostic that combines both pathogen and host response detection in a single sample, which would be especially attractive in LMIC settings. The objective of this application is to determine the performance characteristics of NP-based gene expression classifiers at differentiating viral versus bacterial LRTI in a South Asian population. The following aims are proposed 1) to derive NP-based gene expression classifiers to discriminate viral versus bacterial LRTI, and 2) to transfer the NP-based classifier to a real-time polymerase chain reaction (RT-PCR) assay that has potential to be translated to a clinical platform. Comprehensive microbiological and molecular testing for respiratory viral and bacterial pathogens will be completed. Subjects will be adjudicated as having viral versus bacterial LRTI, and RNA sequencing will be performed using NP samples. Machine-learning approaches will identify host gene expression classifiers that discriminate viral versus bacterial LRTI. The genes identified in the NP-based classifier will be migrated onto customized, TaqMan Low-Density Array (TLDA) cards and RT-PCR will be performed. Gene expression will be quantified and logistic regression performed to identify viral versus bacterial LRTI. The expected outcome of this proposal is a significant improvement in our knowledge of how novel NP-based gene expression classifiers perform at identifying viral versus bacterial LRTI in a South Asian population. Following successful completion of these aims, we plan to translate the NP-based classifier to a point-of-care, clinical diagnostic platform. The long-term goal of this work is to develop strategies for improving antibacterial use in LMICs and to help combat the global crisis of antimicrobial resistance.", "keywords": [ "Adult", "Anti-Bacterial Agents", "Antimicrobial Resistance", "Area", "Bacterial Infections", "Biological", "Biological Assay", "Biological Markers", "Blood", "Blood specimen", "COVID-19", "COVID-19 pandemic", "COVID-19 patient", "Characteristics", "Childhood", "Clinical", "Collection", "Consensus", "Country", "Custom", "Data", "Detection", "Diagnosis", "Diagnostic", "Enrollment", "Epithelial Cells", "Etiology", "Fever", "Funding", "Gene Expression", "Genes", "Genomic medicine", "Goals", "Immune response", "Income", "Infection", "Infrastructure", "Knowledge", "Laboratories", "Leukocytes", "Logistic Regressions", "Lower Respiratory Tract Infection", "Machine Learning", "Microbiology", "Molecular", "Nasal Epithelium", "Nasopharynx", "Outcome", "Patients", "Performance", "Polymerase Chain Reaction", "Population", "Research", "Research Infrastructure", "Resource-limited setting", "Resources", "Sampling", "South Asian", "Sputum", "Sri Lanka", "Testing", "Time", "Translating", "Viral", "Virus Diseases", "Work", "adjudicate", "adjudication", "base", "biobank", "clinical diagnostics", "cohort", "combat", "density", "diagnostic platform", "improved", "migration", "minority patient", "novel", "pathogen", "pathogenic bacteria", "pathogenic virus", "peripheral blood", "point of care", "precision medicine", "procalcitonin", "prospective", "respiratory", "transcriptome sequencing" ], "approved": true } }, { "type": "Grant", "id": "5272", "attributes": { "award_id": "1K01AI168579-01", "title": "Social and policy determinants and impacts on COVID-19 and influenza disparities", "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": 18573, "first_name": "Erik J.", "last_name": "Stemmy", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2022-02-10", "end_date": "2027-01-31", "award_amount": 127764, "principal_investigator": { "id": 18574, "first_name": "Alina", "last_name": "Schnake-Mahl", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 377, "ror": "https://ror.org/04bdffz58", "name": "Drexel University", "address": "", "city": "", "state": "PA", "zip": "", "country": "United States", "approved": true }, "abstract": "The purpose of this K01 proposal is to provide Alina Schnake-Mahl, ScD MPH with the protected time and resources to pursue the additional training needed to reach her long-term goal of an independent academic career in health policy and social epidemiology, focused on generating evidence to inform law and policies that reduce health inequities in infectious diseases. This proposal builds on Dr. Schnake-Mahl’s background as a social epidemiologist with expertise in health policy. It also leverages her experience with applied health care research and evaluation, and a cohesive mentorship team, to improve our understanding of the social determinants of COVID-19 and influenza disparities. Over 878,000 people have been hospitalized for COVID- 19 over the last year, and between 140,000 to 710,000 people are hospitalized for flu annually. Studies have found wide disparities in COVID-19 and influenza, but gaps remain with respect to the interactions between the social determinants of these disparities. This project uses diverse and multi-disciplinary approaches to examine the determinants of disparities and effects of policy exposures on disparities. The specific aims are to: 1) use multilevel analysis to describe the social determinants of racial and geographic disparities in influenza and COVID-19 outcomes in US cities; 2) use non-experimental causal inference methods to estimate the effect of PSL and rent control laws on rates and disparities of influenza and COVID-19 outcomes in US cities; 3) use agent based modeling to understand mechanisms linking two key social determinants, occupational exposures and housing overcrowding, and influenza disparities. The training goals are designed to expand skills and knowledge through training in infectious disease epidemiology, casual inference methods for policy analysis, and systems approaches including agent-based modeling. Training in this set of complementary approaches will position the candidate to pursue innovative research in the area of infectious disease disparities as part of a future R01. The proposed work has substantial potential to make a significant public health impact as these aims will advance our understanding of the social determinants of COVID-19 and influenza disparities and provide a strong evidence-base for policies and interventions that may address these inequities and reduce the overall burden of COVID-19 and influenza. Furthermore, this K01 develops specific topic area (infectious disease) and methods (advanced causal inference for policy analysis and systems dynamics) expertise whose extension to other infectious disease indicates applicability beyond the scope of this proposal. The proposed work is feasible and realistic within the award period and will allow Dr. Schnake-Mahl to continue to build research skills, extend professional networks, generate numerous publications, and compete for other NIH funding. In summary, this K01 award will support and stimulate the career development activities of Dr. Schnake Mahl and allow her to successfully move into the next phase of her career as an independent investigator.", "keywords": [ "Address", "Affect", "Area", "Award", "COVID-19", "Chronic Disease", "Cities", "City Government", "Collection", "Communicable Diseases", "Complex", "Crowding", "Data", "Decision Making", "Disease", "Disease Outcome", "Emergency department visit", "Epidemiologist", "Epidemiology", "Evaluation", "Exposure to", "Funding", "Future", "Goals", "Grant", "Health Care Research", "Health Policy", "Healthcare", "Heterogeneity", "Home", "Hospitalization", "Household", "Housing", "Infectious Disease Epidemiology", "Influenza", "Intervention", "Knowledge", "Laws", "Link", "Measures", "Mentored Research Scientist Development Award", "Mentorship", "Methods", "Minority Groups", "Modeling", "Neighborhoods", "Occupational Exposure", "Outcome", "Persons", "Phase", "Policies", "Policy Analysis", "Population", "Positioning Attribute", "Poverty", "Public Health", "Publications", "Research", "Research Personnel", "Resources", "Respiratory Disease", "Risk Factors", "Science", "Sick Leave", "Social Policies", "Social Processes", "State Government", "Structure", "System", "Techniques", "Time", "Training", "United States", "United States National Institutes of Health", "Vaccination", "Variant", "Work", "Workplace", "acute care", "base", "behavior change", "burden of illness", "career", "career development", "career networking", "cohesion", "design", "disease disparity", "evidence base", "experience", "flu", "geographic disparity", "health equity", "health inequalities", "improved", "innovation", "insight", "interdisciplinary approach", "knowledge base", "metropolitan", "models and simulation", "multilevel analysis", "novel", "pandemic disease", "preempt", "prevent", "racial disparity", "respiratory", "skills", "social", "social determinants", "social epidemiology", "social factors", "social health determinants", "sociodemographics", "socioeconomics", "surveillance data", "tool", "transmission process" ], "approved": true } }, { "type": "Grant", "id": "10217", "attributes": { "award_id": "75N91019D00024-0-759102200007-1", "title": "Phase 2 COVID-19 Vaccine Variant Clinical Trial", "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": [], "start_date": "2022-03-07", "end_date": "2024-03-06", "award_amount": 36854529, "principal_investigator": { "id": 26171, "first_name": "THERESA", "last_name": "ENGEL", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 1610, "ror": "", "name": "LEIDOS BIOMEDICAL RESEARCH, INC.", "address": "", "city": "", "state": "MD", "zip": "", "country": "United States", "approved": true }, "abstract": "To support a Phase 2 clinical trial evaluating various additional COVID-19 booster shots, the COVID-19 Variant Immunologic Landscape (COVAIL) clinical trial.", "keywords": [ "2019-nCoV", "COVID-19", "COVID-19 booster", "COVID-19 vaccine", "Clinical Trials", "Immunologics", "Phase", "Phase II Clinical Trials", "SARS-CoV-2 variant", "Vaccine Research", "Variant", "booster vaccine" ], "approved": true } }, { "type": "Grant", "id": "5258", "attributes": { "award_id": "3U19AI110483-09S1", "title": "Molecular Regulation of B cells and T cells in Human SLE", "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": 18547, "first_name": "David R.", "last_name": "Johnson", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2014-05-01", "end_date": "2024-04-30", "award_amount": 46256, "principal_investigator": { "id": 18548, "first_name": "Ignacio E.", "last_name": "Sanz", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 265, "ror": "https://ror.org/03czfpz43", "name": "Emory University", "address": "", "city": "", "state": "GA", "zip": "", "country": "United States", "approved": true }, "abstract": "The overarching objective of the Emory Autoimmunity Center of Excellence (ACE) U19 is to decipher the molecular programs responsible for the aberrant effector immune responses that lead to autoimmune disease. Specifically, based on the work performed by the Emory ACE during the current funding cycle, we postulate that epigenetic regulation of effector B cell differentiation and function is a critical pathogenic component of Systemic Lupus Erythematosus (SLE). Further, we contend that disease-related epigenetic imprinting is first established at early stages of B cell development and then maintained throughout the differentiation of naïve cells into their effector progeny upon activation by antigens and co- stimulatory pathways. Finally, we propose that SLE will also be characterized by abnormal regulation of other critical effector immune responses, namely CD8 T cells and in particular, the stem-like population responsible for the maintenance of antigen-specific responses in chronic viral infections and anti-tumor responses in patients treated with checkpoint inhibitors. The fundamental goals of the Emory ACE are: 1) to understand B cells and CD8 T cells dysregulation in human SLE; and 2) to assemble a scientific and technological platform that engages other ACE U19 and UM1 Centers to perform similar studies in other immune cells and autoimmune disorders. The specific aims of the Emory ACE U19 are: Aim 1: To establish an Administrative Core (I. Sanz, Core Director) for the successful operation of the ACE U19 Scientific Program and its interaction with the ACE Network; Aim 2: To develop a highly integrated Emory ACE U19 Scientific Program comprised of the following components: Principal Project (Sanz, PI): Mechanisms of B cell dysregulation in human SLE; Collaborative Project (Boss, PI): Epigenetic regulation of autoimmune responses; Pilot Project (Ahmed, PI): Characterization of stem-like CD8 T cells in SLE. The expected results will unravel disease pathogenesis; segment patients; design personalized therapies; and develop biomarkers of disease onset, evolution, and outcome. Our efforts will naturally dovetail with the mission of the UM1 ACEs centers and contribute greatly to the charter mission of the ACE network.", "keywords": [ "Antigens", "Antitumor Response", "Autoantigens", "Autoimmune", "Autoimmune Diseases", "Autoimmune Responses", "Autoimmunity", "B cell differentiation", "B-Cell Development", "B-Lymphocytes", "Biological Markers", "CD8-Positive T-Lymphocytes", "Cancer Patient", "Categories", "Cell physiology", "Cells", "Chronic", "Clinical", "Clinical Protocols", "Clinical Research", "Collaborations", "Committee Members", "Comparative Study", "Development", "Diagnosis", "Disease", "Effector Cell", "Epigenetic Process", "Evolution", "Funding", "Genetic Predisposition to Disease", "Goals", "Heterogeneity", "Human", "Immune", "Immune checkpoint inhibitor", "Immune response", "Immunologics", "Individual", "Knowledge", "Lead", "Leadership", "Location", "Lupus", "Maintenance", "Mission", "Molecular", "Onset of illness", "Outcome", "PD-1 blockade", "Pathogenesis", "Pathogenicity", "Pathway interactions", "Patients", "Physicians", "Pilot Projects", "Population", "Process", "Regulation", "Resources", "Scientist", "Systemic Lupus Erythematosus", "T-Lymphocyte", "Translating", "Universities", "Virus Diseases", "Work", "arm", "autoreactive B cell", "base", "clinical development", "design", "epigenetic regulation", "epigenome", "exhaustion", "experience", "immunogenic", "imprint", "innovation", "novel", "operation", "personalized medicine", "programs", "response", "self-renewal", "stem", "stem-like cell" ], "approved": true } }, { "type": "Grant", "id": "5386", "attributes": { "award_id": "3U01AG009740-33S1", "title": "Health and Retirement Study: Years 29-34", "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": 18863, "first_name": "John", "last_name": "Phillips", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "1990-09-25", "end_date": "2023-12-31", "award_amount": 990154, "principal_investigator": { "id": 18864, "first_name": "DAVID R.", "last_name": "WEIR", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 770, "ror": "", "name": "UNIVERSITY OF MICHIGAN AT ANN ARBOR", "address": "", "city": "", "state": "MI", "zip": "", "country": "United States", "approved": true }, "abstract": "This competing continuation proposal for Years 29-34 of the Health and Retirement Study (HRS) cooperative agreement is in response to NIA RFA #AG-18-005. The primary aim of the HRS is to design, collect and distribute longitudinal multi-disciplinary data to support research on aging and the health and well- being of the older population. This proposal seeks to collect three additional waves of panel data, continue collection of venous blood specimens, implement the next scheduled refreshment by adding the first Gen-X cohort in 2022, continue to conduct off-year mail surveys, and implement cost-saving innovations, including an internet mode for Core data collection. It will continue the same expanded minority oversample design for the Gen-X cohort as was implemented in 2010 and 2016 for the baby boom cohorts in which half the sample consists of traditionally underrepresented minorities. The new Gen-X cohort will be fully integrated into the HRS design, including collection of biomarkers, DNA, and linkage consents to Social Security and other records as appropriate. This parent project will provide sample, data, and coordinate fully with the separate proposal to repeat the Harmonized Cognitive Assessment Protocol dementia study. HRS provides a uniquely rich, nationally representative longitudinal dataset for the community of scientific and policy researchers who study the health and demography of aging. It provides a research data base that can simultaneously support cross-sectional descriptions of the U.S. population age 50+, longitudinal studies of a given cohort over a substantial period of time and research on cross-cohort trends. The HRS project creates a data system extending beyond the core survey data. One component of this extended data system consists of linkages to administrative data, including Social Security earnings and benefit records, Medicare utilization and diagnostic records, including Minimum Data Set and Medicaid records, employer pension records, Veterans Health Administration data and the National Death Index. We plan to expand access to these secure data through secure enclaves. Another component is genome-wide genotyping data from consenting respondents distributed through dbGaP and a new repository of blood samples including cryopreserved cells. HRS provides public use data designed to allow the full power and creativity of America's scientific community to address the challenges of an aging population. HRS is making a significant impact on research on aging through investigator-initiated research which uses the HRS as an input without charge to researchers or granting agencies. Over 2,000 peer-reviewed journal publications have appeared, nearly 1,000 in the past six years. HRS also supports training of new scientists as over 400 doctoral dissertations have used HRS data.", "keywords": [ "Address", "Age", "Aging", "Americas", "Baby Booms", "Bibliography", "Biological Assay", "Biological Markers", "Biological Specimen Banks", "Blood", "Blood specimen", "Brazil", "Cessation of life", "Charge", "China", "Collaborations", "Collection", "Communities", "Complex", "Consent", "Consumption", "Cost Savings", "Country", "Creativeness", "Cryopreserved Cell", "DNA", "Data", "Data Collection", "Data Set", "Databases", "Decision Making", "Dementia", "Development", "Devices", "Diagnostic", "Documentation", "Elements", "England", "Enrollment", "Europe", "Exhibits", "Future", "Genetic", "Genotype", "Geography", "Grant", "Health", "Health and Retirement Study", "Income", "India", "Indonesia", "Information Systems", "International", "Internet", "Interview", "Investigator-Initiated Research", "Japan", "Journals", "Life Experience", "Longitudinal Studies", "Measurement", "Measures", "Medicaid", "Medicare", "Methods", "Mexico", "Minority", "Older Population", "Online Systems", "Peer Review", "Pensions", "Personal Satisfaction", "Persons", "Physical activity", "Policies", "Population", "Population Study", "Prevalence Study", "Protocols documentation", "Public Health", "Publications", "Records", "Research", "Research Design", "Research Personnel", "Research Support", "Respondent", "Rotation", "Sampling", "Schedule", "Scientist", "Secure", "Security", "Services", "Social Security", "Source", "South Africa", "Structure", "Surveys", "Time", "Training Support", "U-Series Cooperative Agreements", "Underrepresented Minority", "Update", "Venous", "Veterans Health Administration", "aging demography", "aging population", "cognitive ability", "cognitive function", "cognitive testing", "cohort", "cost", "cost effective", "data access", "data quality", "data resource", "database of Genotypes and Phenotypes", "design", "distributed data", "genome-wide", "improved", "indexing", "innovation", "longitudinal dataset", "member", "multidisciplinary", "neuroimaging", "parent project", "prospective", "psychosocial", "recruit", "repository", "research and development", "response", "screening", "sustained attention", "symposium", "trend", "web site" ], "approved": true } }, { "type": "Grant", "id": "5312", "attributes": { "award_id": "1R21AI171827-01", "title": "Small molecule inhibitors targeting the SARS-CoV-2 pathogenicity factor Nsp1", "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": 18663, "first_name": "DIPANWITA", "last_name": "Basu", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2022-06-07", "end_date": "2024-05-31", "award_amount": 257283, "principal_investigator": { "id": 18664, "first_name": "Morkos Adel Ibrahim", "last_name": "Henen", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [ { "id": 18665, "first_name": "Anna-Lena", "last_name": "Steckelberg", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "awardee_organization": { "id": 781, "ror": "", "name": "COLUMBIA UNIVERSITY HEALTH SCIENCES", "address": "", "city": "", "state": "NY", "zip": "", "country": "United States", "approved": true }, "abstract": "The COVID-19 pandemic has caused great harm to human life and the worldwide economy. Almost 2 years after the emergence of its etiological agent SARS-CoV-2, there are still very few available antiviral drugs. The situation is further aggravated by the emergence of new viral variants that might render available antiviral therapeutics and vaccines less effective in the future. This calls for the development of diverse antiviral strategies, aimed at targeting as many different viral pathways as possible. Here we explore for the first time the possibility to create inhibitors of the viral protein Nsp1 to fight SARS-CoV-2 infection. Nsp1 is a major virulence factor that functions by restricting host gene expression to inhibit antiviral signaling. We have recently identified nine putative inhibitors of Nsp1 function by quantitative high throughput screening. We propose an in-depth structural and functional characterization of the identified compounds to explore their capability to be developed into potent antiviral drugs. In aim 1 we will use NMR spectroscopy to identify the pharmacophore and binding site(s) of the small molecule inhibitors on Nsp1. It is the goal of aim 1 to determine the minimal ligand structural features necessary for Nsp1 inhibition. We will also test commercially available analogs to interrogate which chemical moieties can increase binding and inhibition. In aim 2 we will explore which functions of Nsp1 are targeted by small molecule inhibition. By combining an array of complementary biochemical and cell-based assays, we will interrogate the effect of small molecule inhibition on ribosome binding, mRNA degradation, and mRNA translation. It is the goal of aim 2 to identify the mechanism of inhibition to aid future compound optimization. By pharmacologically targeting selective functions of Nsp1, we might also gain new biological insight into the coronaviral host-shutoff pathway. Overall, these studies should provide insight into the structure and mechanism of potential small molecule inhibitors of SARS-CoV-2 Nsp1, laying the foundation for future chemical optimization of lead compounds with the goal to develop new potent anti-coronaviral drugs.", "keywords": [ "2019-nCoV", "Affinity", "Antiviral Agents", "Attenuated", "Binding", "Binding Sites", "Biochemical", "Biological", "Biological Assay", "COVID-19", "COVID-19 pandemic", "Cells", "Cessation of life", "Chemicals", "Coronavirus", "Data", "Development", "Enzymes", "Etiology", "Foundations", "Future", "Gene Expression", "Genetic Translation", "Goals", "Human", "Infection", "Knowledge", "Lead", "Life", "Ligands", "Light", "Molecular", "NMR Spectroscopy", "Pathway interactions", "Peptide Hydrolases", "Pharmaceutical Preparations", "Pharmacology", "Production", "Proteins", "RNA-Directed RNA Polymerase", "Reporter", "Respiratory Disease", "Ribosomal Interaction", "Ribosomes", "SARS coronavirus", "SARS-CoV-2 infection", "SARS-CoV-2 inhibitor", "Signal Transduction", "Structure", "Techniques", "Testing", "Therapeutic", "Time", "Vaccines", "Variant", "Viral", "Viral Proteins", "Virulence Factors", "Virus", "Virus Inhibitors", "analog", "base", "fighting", "high throughput screening", "inhibitor/antagonist", "insight", "lead optimization", "mRNA Transcript Degradation", "mutant", "pharmacophore", "small molecule", "small molecule inhibitor", "therapeutic target" ], "approved": true } }, { "type": "Grant", "id": "15679", "attributes": { "award_id": "1R01HL176493-01", "title": "Pathogenic Mechanism and Therapeutic Approaches for Exercise Intolerance 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 Heart Lung and Blood Institute (NHLBI)" ], "program_reference_codes": [], "program_officials": [ { "id": 32514, "first_name": "EMMANUEL FRANCK", "last_name": "MONGODIN", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-04-01", "end_date": "2029-01-31", "award_amount": 633045, "principal_investigator": { "id": 32524, "first_name": "Michael G", "last_name": "Risbano", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [ { "id": 32525, "first_name": "Lianghui", "last_name": "Zhang", "orcid": "", "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "awardee_organization": { "id": 848, "ror": "", "name": "UNIVERSITY OF PITTSBURGH AT PITTSBURGH", "address": "", "city": "", "state": "PA", "zip": "", "country": "United States", "approved": true }, "abstract": "Post-acute sequelae of COVID-19 (PASC) is an emerging public health priority with up to 18% prevalence. Noteably, almost 30% patients diagnosed with PASC experence exercise intolerance. This activity limitation continues to negatively impact our workforce, and poses a persistent socialeconimic burden on our society. Our Post-Covid Recovery Clinic, a RECOVERY Vital site, has evaluated exercise intolerant PASC for nearly 4 years. We recently discovered pathophysiologic endotypes that contribute to exercise intolerance in PASC via invasive cardiopulmonary exercise testing (iCPET). Yet, the molecular drivers for this population remain elusive. Four- years after the onset of the pandemic we are left without PASC-defining biomarkers, or targeted therapeutics. Thus, it is crucial to investigate the interconnected molecular and pathophysiologic links in exercise intolerant PASC, a task uniquely within our team’s expertise. Angiotensin-converting enzyme 2 (ACE2) is not just an entry receptor for SARS-CoV-2 but also an enzyme with a protective function through regulation of the renin- angiotensin system. Studies have shown that a high level of plasma ACE2 is associated with an increased risk of SARS-CoV-2-related mortality. Our preliminary data showed that the catalytic activity of increased plasma ACE2 was significantly impaired in the exercise intolerant PASC patients, and closely correlated with reduced exercise capacity as measured by peak oxygen consumption evaluated during iCPET. Furthermore, to study the pathogenic mechanism of exercise intolerance in PASC, we established a novel PASC mouse model. In this model, we observed the persistence of the SARS-CoV-2 RNAs in lung microvascular ECs, impaired ACE2 activity, chronic pulmonary inflammation, along with a significant reduction in exercise capacity. Thus, we hypothesize that dysfunctional ACE2 shed from pulmonary ECs is a major driver for exercise intolerance in PASC and an engineered solube ACE2 with enhanced ACE2 activity will improve exercise capacity of PASC. To test our hypotheses, we will investigate the predictive value of ACE2 activity as a clinical biomarker and assess its association with exercise capacity over 12 months in PASC patients in Aim 1. We will define an engineered soluble ACE2 with enhanced ACE2 activity as an innovative therapeutic intervention to improve exercise capacity and vascular function in the PASC mouse model in Aim 2. Furthermore, we will explore the mechanism of ACE2 dysfunction shed from the pulmonary vasculature in Aim 3. If successful, we will identify a diagnostic and therapeutic paradigm urgently needed for PASC patients experiencing exercise intolerance, and remediate the deficient response to this global public health threat.", "keywords": [ "2019-nCoV", "ACE2", "Acute Lung Injury", "Adult", "Affect", "Binding", "Biological Markers", "Blood Vessels", "COVID-19", "COVID-19 mortality", "COVID-19 patient", "Cardiopulmonary", "Cell surface", "Characteristics", "Chronic", "Circulation", "Clinic", "Clinical assessments", "Data", "Diagnosis", "Diagnostic", "Disease Progression", "Disintegrins", "Endothelial Cells", "Endothelium", "Engineering", "Enzymes", "Exercise", "Exercise Test", "Fatigue", "Functional disorder", "Health", "Impairment", "Inflammation", "Knock-in", "Knockout Mice", "Left", "Link", "Long COVID", "Lung", "Measures", "Medicine", "Metalloproteases", "Modeling", "Molecular", "Outpatients", "Oxygen Consumption", "Pathogenicity", "Pathology", "Patients", "Peptides", "Plasma", "Population", "Post-Acute Sequelae of SARS-CoV-2 Infection", "Predictive Value", "Prevalence", "Proteins", "Public Health", "Pulmonary Inflammation", "Questionnaires", "RNA", "Recovery", "Regulation", "Renin-Angiotensin System", "Risk", "SARS-CoV-2 infection", "Site", "Societies", "Symptoms", "Testing", "Therapeutic", "Therapeutic Intervention", "clinical biomarkers", "clinical infrastructure", "design", "dosage", "endothelial dysfunction", "exercise capacity", "exercise intolerance", "experience", "improved", "innovation", "knock-down", "lung microvascular endothelial cells", "mortality", "mouse model", "novel", "pandemic disease", "post SARS-CoV-2 infection", "post-COVID-19", "public health priorities", "receptor", "remediation", "research clinical testing", "response", "symptom cluster", "targeted treatment", "treatment optimization" ], "approved": true } }, { "type": "Grant", "id": "5373", "attributes": { "award_id": "1R21AI169392-01", "title": "Spatiotemporal transcriptomics at the maternal-fetal interface in COVID placenta", "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": 18831, "first_name": "Erik J.", "last_name": "Stemmy", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2022-05-06", "end_date": "2024-04-30", "award_amount": 182500, "principal_investigator": { "id": 18833, "first_name": "YUPING", "last_name": "WANG", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 835, "ror": "", "name": "LOUISIANA STATE UNIV HSC SHREVEPORT", "address": "", "city": "", "state": "LA", "zip": "", "country": "United States", "approved": true }, "abstract": "COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has emerged as the greatest threat to global health and significantly impact pregnant women worldwide. COVID-19 infection during pregnancy is associated with substantial risk of increases in maternal morbidity and mortality and neonatal complications, compared with their non-infected pregnant counterparts. However, vertical transmission of the virus is uncommon, which suggest that innate immune system must function at the maternal-fetal interface to shield the developing fetus from infection. Despite fast-tracked intensive research on many aspects of SARS- CoV-2, the impact of the viral infection in the placenta and the placental defense mechanism(s) are poorly explored. Placenta is the structural and immunological barrier of pathogen transmission. To explore the innate antiviral defense mechanism(s), in our preliminary study we specifically determined expression of interferon pathway-related molecules in placental tissues. Strikingly, we found distinct patterns of stimulator of interferon genes (STING), interferon regulator factor 3 (IRF3), and Type I IFN (such as IFNb) expression at the maternal- fetal interface of the placentas from women infected with COVID-19. STING is a sensor for viral infection. STING-IRF3 pathway signaling regulates Type I IFN production, and Type I IFNs are potent antiviral cytokines. We also noticed that Toll-like receptor 7 (TLR7) is upregulated in both syncytiotrophoblasts ( STs) and extravillous trophoblasts (EVTs) in placentas from patients with COVID-19 compared to those are not. TLR7, located on the X chromosome, is a sensor for single strand RNA (ssRNA) viruses. These findings are intriguing and indicate that an innate antiviral immune system is activated at the maternal-fetal interface in patients with COVID-19 during pregnancy. The objective of the study is to identify spatiotemporal transcriptomic signatures and networks of the innate antiviral immune system at the maternal-fetal interface. We will test the hypothesis an effective and robust innate antiviral immune system is activated at the maternal-fetal interface to prevent viral transmission and shield the fetus from infection, which will be tested in two specific aims. Aim 1 will identify spatiotemporal innate immunity gene profiles and networks in villous tissue that respond to maternal SARS-CoV-2 infection. Aim 2 will identify spatiotemporal innate immunity gene profiles and networks in fetal membrane and decidual tissue that respond to maternal SARS-CoV-2 infection. A state-of-the-art novel technique of 10x Genomics Visium Gene Expression assay in placental formalin-fixed paraffin embedded (FFPE) tissues combined with RNA-seq will be employed . Placentas from women with active COVID infection, recovered from COVID infection, and received COVID vaccination, etc. will be studied. This novel ideal approach will allow us to map the whole transcriptome with morphological context in placental FFPE tissue and discover the cellular and molecular profiles and networks in different cell types and gene activity at the maternal-fetal interface without disruption of the tissue integrity. Results of the study will provide novel insights into how SARS-CoV-2 infection impacts the innate immune system at the mater-fetal interface, and how the innate immune system at the maternal-fetal interface responds to COVID vaccination during pregnancy, which may help to identify new strategies to prevent COVID-19 infection and reduce maternal and fetal complications in women with COVID-19 infection in the future.", "keywords": [ "2019-nCoV", "Antiviral Agents", "Brain", "COVID-19", "COVID-19 patient", "COVID-19 prevention", "COVID-19 vaccination", "Cells", "Cerebrum", "Clinical Management", "Decidual Cell", "Defense Mechanisms", "Embryo", "Epithelial Cells", "Fetal Development", "Fetal Membranes", "Fetus", "Formalin", "Future", "Gene Expression Profiling", "Genes", "Genomics", "Gestational Diabetes", "Homeostasis", "Immune", "Immune system", "Immunologics", "Infection", "Innate Immune System", "Institutes", "Interferon-beta", "Interferons", "International", "Low Birth Weight Infant", "Maps", "Maternal Mortality", "Maternal-Fetal Exchange", "Mesenchymal", "Molecular", "Molecular Profiling", "Morphology", "Natural Immunity", "Neonatal", "Nucleic Acids", "Nucleocapsid Proteins", "Organ", "Organoids", "Outcome", "Paraffin Embedding", "Pathway interactions", "Pattern", "Placenta", "Pre-Eclampsia", "Pregnancy", "Pregnant Women", "Premature Birth", "Prevent viral transmission", "Production", "Proteins", "RNA Viruses", "Research", "Risk", "SARS-CoV-2 infection", "SARS-CoV-2 spike protein", "Signal Pathway", "Signal Transduction Pathway", "Stimulator of Interferon Genes", "Stromal Cells", "Symptoms", "Syncytiotrophoblast", "System", "TLR7 gene", "Techniques", "Testing", "Tissue Embedding", "Tissues", "Vaccination", "Vertical Disease Transmission", "Villous", "Viral", "Virus Diseases", "Woman", "Women&apos", "s Group", "X Chromosome", "adverse pregnancy outcome", "cell type", "coronavirus disease", "cytokine", "cytotrophoblast", "epidemiology study", "fetal", "gene network", "global health", "insight", "maternal morbidity", "novel", "pandemic disease", "pathogen", "pregnant", "response", "sensor", "spatiotemporal", "stillbirth", "transcriptome", "transcriptome sequencing", "transcriptomics", "transmission process", "trophoblast", "viral transmission" ], "approved": true } }, { "type": "Grant", "id": "5323", "attributes": { "award_id": "3R01AG056699-05S1", "title": "Impact of Heightened UPR Activation on Inflammasome Responses to Influenza and Secondary Streptococcus pneumoniae Infection in Aged Lung", "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": 18689, "first_name": "HONGWEI", "last_name": "Gao", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2018-05-01", "end_date": "2023-04-30", "award_amount": 372900, "principal_investigator": { "id": 18690, "first_name": "HEATHER Winona", "last_name": "STOUT-DELGADO", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 825, "ror": "", "name": "WEILL MEDICAL COLL OF CORNELL UNIV", "address": "", "city": "", "state": "NY", "zip": "", "country": "United States", "approved": true }, "abstract": "With an aging population and pulmonary infections becoming an increasingly significant cause of morbidity and mortality, there is an urgent need to investigate molecular pathways underlying these impairments and devise new therapeutics that can stimulate innate immune responses within this population. Our results demonstrate aged hosts have impaired inflammasome activation, decreased gene expression of several key components of the NLRP3 signaling pathway, reduced caspase-1 activity, and diminished IL1production in response to in vitro and in vivo infection with influenza or S. pneumoniae. Using in vitro and in vivo aging murine models of primary influenza and secondary S. pneumoniae infection, we will employ cellular and molecular techniques to test our overall hypothesis that the NLRP3 inflammasome is necessary for survival and age associated impairments in ER and mitochondrial Ca2+ homeostasis result in impaired activation of the NLRP3 inflammasome in aged lung; thereby, resulting in increased pathogenesis, tissue injury, and pneumonic edema in the elderly lung. To test this hypothesis, we will examine the role of the unfolded protein response (UPR) on inflammasome activity in response to influenza (Aim 1) and the impact of overly heightened pathogenic mediated UPR on inflammasome activation in response to secondary S. pneumoniae infection (Aim 2). Summary and impact: As pulmonary pneumococcal infections remain a substantial cause of morbidity and mortality in the elderly, even in an era of routine adult vaccination, there is a pressing need to identify mechanistic pathways that regulate innate immune responses and investigate novel therapeutics and treatment strategies that reduce serious disease and improve clinical outcomes. By establishing and dissecting a pivotal mechanistic link between UPR activation and inflammasome signaling in aged lung, this research proposal has high potential to elucidate innovative regulatory pathways and expand current understanding of age associated changes in ER homeostasis. Therapeutic strategies designed to target defects in innate signaling in the aged host will aid in circumventing emergent strains of antibiotic resistant bacteria and may be utilized for treatment against a wide variety of pathogenic stimuli. Completion of the proposed aims will further define the role of the NLRP3 inflammasome as an important innate signaling pathway during influenza and secondary S. pneumoniae infections as well as yield new therapeutics that can be readily tested in primary human cells and evaluated in additional model systems.", "keywords": [ "ATF6 gene", "Adult", "Age", "Aging", "Animal Model", "Bacterial Antibiotic Resistance", "Bacterial Infections", "Biological Aging", "Biological Models", "CASP1 gene", "Cell Culture Techniques", "Cells", "Clinical", "Complex", "Data", "Defect", "Disease", "Edema", "Elderly", "Endoplasmic Reticulum", "Functional disorder", "Gene Expression", "Genetic Transcription", "Homeostasis", "Human", "IL18 gene", "Immune", "Immune response", "Impairment", "In Vitro", "Infection", "Inflammasome", "Inflammation", "Influenza", "Innate Immune Response", "Interleukin-1", "Knowledge", "Link", "Lung", "Lung infections", "Mediating", "Mediator of activation protein", "Mitochondria", "Molecular", "Morbidity - disease rate", "Outcome", "Pathogenesis", "Pathogenicity", "Pathway interactions", "Pneumococcal Infections", "Population", "Predisposition", "Process", "Production", "Proteins", "RNA Splicing", "Regulation", "Regulatory Pathway", "Research Proposals", "Role", "Secondary to", "Signal Pathway", "Signal Transduction", "Stimulus", "Streptococcus pneumoniae", "Stress", "Techniques", "Testing", "Therapeutic", "Therapeutic Intervention", "Time", "Translations", "Vaccination", "Variant", "Viral Pathogenesis", "Virulence", "Virus Diseases", "Work", "adaptive immune response", "aged", "aging population", "common salivary protein 1", "design", "endoplasmic reticulum stress", "experimental study", "improved", "in vivo", "infection rate", "influenza infection", "influenza pneumonia", "innovation", "lung injury", "macrophage", "mitochondrial dysfunction", "mortality", "mouse model", "novel therapeutics", "pathogen", "programs", "protein expression", "response", "sensor", "therapeutic evaluation", "tissue injury", "treatment strategy", "young adult" ], "approved": true } }, { "type": "Grant", "id": "5363", "attributes": { "award_id": "5R01NR019944-02", "title": "Intensifying Community Referrals for Health: The SINCERE Intervention to Address COVID-19 Health Disparities", "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": 18804, "first_name": "AMANDA ALISE", "last_name": "Price", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2021-05-14", "end_date": "2025-03-31", "award_amount": 742753, "principal_investigator": { "id": 18806, "first_name": "Andrea Schneider", "last_name": "Wallace", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 202, "ror": "https://ror.org/03r0ha626", "name": "University of Utah", "address": "", "city": "", "state": "UT", "zip": "", "country": "United States", "approved": true }, "abstract": "In an effort to slow transmission of the 2019 novel coronavirus (COVID-19, or COVID), communities worldwide have implemented strict quarantine policies. While these efforts appear to be having a positive public health impact, they are negatively impacting economies, limiting personal resources for both COVID+ and non- COVID infected patients, and exacerbating health disparities. Community service providers report steady increases in calls for resources (e.g., for food, housing, transportation) during the COVID-19 pandemic, particularly from underserved and underrepresented communities, and additional strain is being placed on health systems. There is a critical need to identify how to overcome community service access barriers during COVID-19, particularly for underserved communities. Our program of research has successfully leveraged existing, low-cost technology to conduct social needs screening during busy emergency department (ED) care, follow-up by United Way 211’s community referral service, and data exchange between systems, suggesting it may be a solution for understanding and meeting the needs of vulnerable and underserved patients during the COVID-19 pandemic. However, findings from our recent sample of approximately 5000 patients screened for social needs during ED visits and qualitative data from service providers, 211 community information specialists, ED Staff, and patients reveal that effectively addressing social needs and connecting to community service providers requires thoughtful, targeted approaches in order to develop relationships among patients and those involved in screening and outreach. Using a pragmatic trial approach in a sample of 1500 patients screened for social needs in ED and community-based and mobile COVID testing sites, the objective of this real world efficacy (NIH stage 3) study is to determine whether community service use for those with social needs improves general and COVID-related health outcomes, and whether random assignment to intensive follow-up and collaborative goal setting helps overcome barriers to community service use. We hypothesize that patients who use community services to meet social needs will experience improvement in general and COVID-specific health outcomes, and that patients randomized to a collaborative goal setting process with a 211 information specialist will have greater community service use. Given the unknown timeframe for social distancing measures needed during the months or years ahead, it is critical to broadly understand the barriers to, and facilitators of, COVID-19 prevention; and of how to address effects on social, mental, and physical wellbeing among COVID-19 vulnerable and socioeconomically disadvantaged populations.", "keywords": [ "2019-nCoV", "Accident and Emergency department", "Address", "Affect", "Age", "Anxiety", "Behavior", "COVID testing", "COVID-19", "COVID-19 health disparity", "COVID-19 pandemic", "COVID-19 prevention", "COVID-19 susceptibility", "Characteristics", "Charge", "Clinic", "Clinic Visits", "Clinical", "Communities", "Community Services", "Computer software", "Country", "Data", "Drops", "Emergency Care", "Emergency Department patient", "Emergency department visit", "Emotional", "Environment", "Ethnic Origin", "Food", "Gender", "Goals", "Health", "Health Services Accessibility", "Health Status", "Health system", "Hospitalization", "Housing", "Individual", "Information Specialists", "Intervention", "Interview", "Language", "Location", "Measures", "Mental Depression", "Methods", "Modeling", "Motivation", "Outcome", "Patients", "Personal Satisfaction", "Play", "Policies", "Population", "Preventive", "Process", "Protocols documentation", "Psyche structure", "Public Health", "Quarantine", "Race", "Randomized", "Reporting", "Research", "Resources", "Role", "Rural", "SARS-CoV-2 transmission", "Sampling", "Services", "Site", "Social Distance", "System", "Technology", "Telephone", "Testing", "Transportation", "Underserved Population", "United States National Institutes of Health", "Vaccines", "base", "behavioral economics", "community based service", "coping", "coronavirus disease", "cost", "data exchange", "disadvantaged population", "economic impact", "effectiveness evaluation", "efficacy study", "experience", "follow-up", "health care availability", "health disparity", "health disparity populations", "health information technology", "health service use", "improved", "meetings", "outreach", "patient engagement", "patient screening", "post-COVID-19", "pragmatic trial", "programs", "referral services", "response", "screening", "screening services", "service providers", "social", "social determinants", "socioeconomic disadvantage", "transmission process", "treatment arm", "treatment as usual", "underserved community" ], "approved": true } } ], "meta": { "pagination": { "page": 1, "pages": 1392, "count": 13920 } } }