Grant List
Represents Grant table in the DB
GET /v1/grants?page%5Bnumber%5D=1385&sort=end_date
{ "links": { "first": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=1&sort=end_date", "last": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=1419&sort=end_date", "next": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=1386&sort=end_date", "prev": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=1384&sort=end_date" }, "data": [ { "type": "Grant", "id": "15567", "attributes": { "award_id": "5K24HL168225-02", "title": "Mentoring and Patient-Oriented Research in Clinical Informatics and Data Science", "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": 31247, "first_name": "MADELYN", "last_name": "Reyes", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2023-12-01", "end_date": "2028-11-30", "award_amount": 125901, "principal_investigator": { "id": 8404, "first_name": "Tellen", "last_name": "Bennett", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [ { "id": 784, "ror": "https://ror.org/02hh7en24", "name": "University of Colorado Denver", "address": "", "city": "", "state": "CO", "zip": "", "country": "United States", "approved": true } ] }, "other_investigators": [], "awardee_organization": { "id": 784, "ror": "https://ror.org/02hh7en24", "name": "University of Colorado Denver", "address": "", "city": "", "state": "CO", "zip": "", "country": "United States", "approved": true }, "abstract": "This K24 mid-career investigator award in patient-oriented research is to support the mentoring, research, and career development activities of Dr. Tell Bennett. Dr. Bennett is an Associate Professor in the University of Colorado School of Medicine and a practicing pediatric ICU physician and informaticist/data scientist with research concentrations in predictive analytics, electronic health record (EHR) data, and clinical decision support (CDS) tool implementation. He is the Informatics Director for the Colorado Clinical and Translational Sciences Institute (CCTSI) and Vice Chair of Clinical Informatics in the Department of Biomedical Informatics. His combined leadership roles have enabled him to build a rich mentoring environment for patient-oriented informatics research. This K24 application proposes to sustain and grow that mentorship program. He currently mentors clinician-scientists in a variety of clinical fields including intensive care, pharmacy, surgery, endocrinology, malignant hematology, and clinical psychology. The K24 Mentoring Plan aligns with Dr. Bennett’s mission to grow patient-oriented research using informatics and data science methods and tools. The mentoring plan leverages educational, career development, and research support programs available through the CCTSI and the new Department. The K24 Research Plan is to develop and implement machine learning and computational physiology models deployable as EHR-based CDS tools. Dr. Bennett currently leads and mentors projects developing CDS tools in both outpatient and inpatient care settings and in a variety of clinical domains include heart failure, traumatic brain injury, serious bacterial infection and sepsis, COVID- 19, thyroid cancer, and postpartum depression. In this K24, developing CDS tools to improve decision-making and outcomes in children with acute respiratory failure (ARF) is a natural next step in this work. ARF is a common, important, and NIH-relevant condition that causes significant pediatric morbidity and mortality. The aims of the project are to 1) develop and validate a dynamic machine learning-based real-time prediction model for intubation in children with ARF and 2) phenotype current lung injury state in mechanically ventilated children using computational physiology models. These models can be deployed as CDS tools and tested as interventions in future clinical trials to improve patient outcomes. The K24 Career Development Plan includes formal mentorship training and coursework in signal processing and dynamical systems models. This group of skills will make Dr. Bennett a more successful mentor.", "keywords": [ "Acceleration", "Acute respiratory failure", "Address", "Adult", "Ambulatory Care", "Bacteremia", "Bacterial Infections", "Biological Models", "Blood", "Breathing", "COVID-19", "Carbon Dioxide", "Caring", "Cause of Death", "Child", "Childhood", "Childhood Injury", "Clinical", "Clinical Data", "Clinical Informatics", "Clinical Psychology", "Clinical Sciences", "Clinical Trials", "Collaborations", "Colorado", "Critically ill children", "Data", "Data Science", "Data Scientist", "Decision Making", "Development", "Development Plans", "Education", "Electronic Health Record", "Endocrinology", "Environment", "Etiology", "Evaluation", "Excision", "Future", "Goals", "Grant", "Heart failure", "Hematology", "Individual", "Informatics", "Intensive Care", "Intervention", "Intubation", "Lead", "Leadership", "Link", "Machine Learning", "Malignant - descriptor", "Malignant neoplasm of thyroid", "Mechanical ventilation", "Medicine", "Mentors", "Mentorship", "Methods", "Mid-Career Clinical Scientist Award (K24)", "Midcareer Investigator Award in Patient-Oriented Research", "Mission", "Modeling", "Monitor", "Morbidity - disease rate", "National Heart Lung and Blood Institute", "Operative Surgical Procedures", "Outcome", "Patient-Focused Outcomes", "Patients", "Pharmacy facility", "Phenotype", "Physicians", "Physiology", "Postpartum Depression", "Predictive Analytics", "Procedures", "Prospective cohort study", "Registries", "Research", "Research Personnel", "Research Support", "Research Training", "Resources", "Respiratory System", "Risk", "Role", "Scientist", "Sedation procedure", "Sepsis", "Structure", "Testing", "Time", "Training", "Training Programs", "Translating", "Translational Research", "Translations", "Traumatic Brain Injury", "Tube", "United States National Institutes of Health", "Universities", "Ventilator", "Ventilator-induced lung injury", "Work", "biomedical informatics", "career", "career development", "clinical decision support", "design", "dynamic system", "experience", "implementation tool", "improved", "improved outcome", "inpatient service", "investigator training", "lung injury", "machine learning model", "mathematical model", "medical schools", "mid-career faculty", "mortality", "novel strategies", "patient oriented", "patient oriented research", "physiologic model", "predictive modeling", "programs", "prospective", "research and development", "resp" ], "approved": true } }, { "type": "Grant", "id": "15570", "attributes": { "award_id": "5R01AG079230-02", "title": "The Effects of COVID-19 on the Well-being, Cognition and Mortality of Persons Living With Dementia", "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": 9749, "first_name": "PRISCILLA JOY", "last_name": "Novak", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2023-12-01", "end_date": "2028-11-30", "award_amount": 857986, "principal_investigator": { "id": 31463, "first_name": "MICHAEL D", "last_name": "HURD", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 515, "ror": "https://ror.org/00f2z7n96", "name": "RAND Corporation", "address": "", "city": "", "state": "CA", "zip": "", "country": "United States", "approved": true }, "abstract": "Although the prevalence of Alzheimer’s disease and related dementias (ADRD) has been decreasing, the COVID-19 pandemic may have halted or reversed that trend. This project will quantify the effects of the pandemic and of attendant public health and social measures on the cognitive status, mortality, and well-being of persons living with ADRD and of the older population in general. Persons living with dementia were especially vulnerable to COVID-19 because many were living in nursing homes, and even those residing in the community were disproportionately vulnerable because of caregivers coming to their homes. Further, those initially not living with dementia may have experienced accelerated cognitive decline because of COVID-19 infections, as well as due to disruption of daily routines, social isolation and stress. Subpopulations by race, ethnicity and socioeconomic status were impacted unequally. This project has three specific aims. The first is to use a new and updated model of cognition to estimate trends in ADRD prevalence, incidence, and mortality prior to the pandemic. We will use data from the Health and Retirement Study (HRS), a large, nationally representative, longitudinal survey of the U.S. population over age 50. The HRS has a wide range of information on cognitive abilities, mortality, dementia risks, and physical and mental health, but only a subsample of the HRS from the Aging, Demographic, and Memory Study (ADAMS) has a clinical assessment of dementia. In prior research, we used ADAMS to develop a model of the probability of dementia to estimate the cognitive status of the entire HRS sample. In this work, we will expand this model to estimate dementia incidence and mortality as well, and incorporate recently released data from the Harmonized Cognitive Assessment Protocol, further increasing precision so as to permit the study of changes in ADRD resulting from the pandemic in subpopulations, such as race and ethnicity, marital status, and socioeconomic status. Second, we will document changes associated with the pandemic in mortality, well-being, use of formal and informal care, and other outcomes. We will incorporate variation in state policies to assess their effect on individual outcomes. We will compare these effects among those who were living with dementia prior to the pandemic to those whose cognitive function was normal. We will use innovative models and data from various HRS supplements focusing on COVID-19 to estimate these effects with precision. Third, we will estimate the incidence of dementia and dementia mortality after the pandemic through 2026 and find the extent to which COVID-19 altered pre-pandemic trends. We will assess whether ADRD incidence differed by individual characteristics, such as geographic location, race, socioeconomic status, and living arrangements. The developed cognition measures will be made publicly available to enhance future research.", "keywords": [ "Acceleration", "Affect", "Age", "Aging", "Alzheimer&apos", "s disease model", "Alzheimer&apos", "s disease related dementia", "Anger", "COVID-19", "COVID-19 burden", "COVID-19 impact", "COVID-19 pandemic", "COVID-19 pandemic effects", "COVID-19 susceptibility", "Caregivers", "Characteristics", "Classification", "Clinical assessments", "Cognition", "Cognitive", "Communities", "Data", "Data Collection", "Death Rate", "Dementia", "Disease", "Ethnic Origin", "Future", "General Population", "Geographic Locations", "Happiness", "Health", "Health Expenditures", "Health and Retirement Study", "Home", "Impaired cognition", "Incidence", "Individual", "Infection", "Interview", "Life", "Living Arrangement", "Long COVID", "Long-Term Care", "Longitudinal Surveys", "Marital Status", "Masks", "Measures", "Memory", "Mental Depression", "Mental Health", "Modeling", "Nature", "Neuropsychological Tests", "Nursing Homes", "Older Population", "Outcome", "Outcome Study", "Personal Satisfaction", "Persons", "Policies", "Population", "Prevalence", "Probability", "Protocols documentation", "Public Health", "Race", "Reporting", "Research", "Resources", "Respondent", "SARS-CoV-2 infection", "Sampling", "Sampling Studies", "Social isolation", "Socioeconomic Status", "Spouses", "Statistical Models", "Stress", "Unmarried person", "Update", "Vaccination", "Variant", "Work", "cognitive ability", "cognitive function", "cognitive testing", "data harmonization", "dementia risk", "demographics", "experience", "health data", "human old age (65+)", "infection rate", "informal care", "informant", "innovation", "insight", "interest", "mortality", "negative affect", "older adult", "outcome disparities", "pandemic disease", "pandemic impact", "physical conditioning", "pre-pandemic", "response", "satisfaction", "sex", "social", "social stress", "trend" ], "approved": true } }, { "type": "Grant", "id": "15574", "attributes": { "award_id": "5R01DC020980-02", "title": "Mechanisms of anosmia and brain infection in a genetic mouse model of COVID-19", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute on Deafness and Other Communication Disorders (NIDCD)" ], "program_reference_codes": [], "program_officials": [ { "id": 6520, "first_name": "SUSAN L.", "last_name": "SULLIVAN", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2023-12-05", "end_date": "2028-11-30", "award_amount": 622679, "principal_investigator": { "id": 26334, "first_name": "Sarah E.", "last_name": "Millar", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 625, "ror": "https://ror.org/04a9tmd77", "name": "Icahn School of Medicine at Mount Sinai", "address": "", "city": "", "state": "NY", "zip": "", "country": "United States", "approved": true }, "abstract": "Infection of the olfactory epithelium in COVID-19 patients is thought to underlie loss of smell (anosmia), a pathognomonic symptom that can be long-term in some patients, significantly affecting quality of life. The olfactory epithelium is also believed to be a major entry point for systemic SARS-CoV-2 infection, which can result in neurological as well as respiratory symptoms. Wild-type SARS-CoV-2 cannot bind the mouse ACE2 receptor, and existing human ACE2 (hACE2)-expressing mouse models either do not permit conditional analysis or do not confer severe illness after infection. Due to the lack of genetically manipulable models that display severe disease, the infected cell types responsible for acute and long-term anosmia, and the route(s) by which the virus penetrates the brain, have not been definitively identified. To address these gaps in knowledge and test cell type-specific requirements for COVID-19-related pathologies we generated conditional hACE2fl knockin mice that express hACE2 in similar cell types to humans. hACE2fl mice nasally inoculated with a high dose of wild-type SARS-CoV-2 display initial infection of olfactory epithelium and rapidly develop anosmia. This is followed by infection of neurons in the olfactory bulb and brain, which is associated with lethality and requires neuronal hACE2 expression. Importantly, specific destruction of olfactory epithelium via methimazole treatment prevents olfactory bulb and brain infection and lethality, identifying the olfactory epithelium as an essential gateway to CNS infection. hACE2fl mice inoculated with a low dose of wild-type SARS-CoV-2 show reversible disease and survive, but a subset displays a long-term decrease in odor sensitivity (hyposmia) like that observed in humans. We propose to use hACE2fl mice to provide definitive genetic evidence for cellular mechanisms of short- and long-term loss of smell and identify the pathways for brain infection during COVID-19. These studies are expected to complement existing descriptive human studies to identify causal pathogenic mechanisms and preventative and therapeutic targets. Three specific aims will be pursued: (i) define the cellular requirements for acute loss of smell; (ii) determine the mechanisms of long-term hyposmia; and (iii) uncover the cellular mechanisms of olfactory bulb and brain infection.", "keywords": [ "2019-nCoV", "ACE2", "ACTL6B gene", "ATAC-seq", "Ablation", "Acute", "Address", "Affect", "Anosmia", "Autopsy", "Binding", "Biological Assay", "Brain", "COVID-19", "COVID-19 patient", "COVID-19 susceptibility", "Cells", "Central Nervous System Infections", "Cerebrospinal Fluid", "Chromatin", "Complement", "Cranial Nerves", "Data", "Defect", "Dexamethasone", "Diffuse", "Disease", "Dose", "Functional disorder", "Gene Expression Profile", "Genetic", "Hamsters", "Human", "Impairment", "Infection", "Infiltration", "Inflammation", "Inflammatory", "Invaded", "K-18 conjugate", "Knock-in Mouse", "Knowledge", "Lineage Tracing", "Maintenance", "Methimazole", "Modeling", "Mus", "Natural regeneration", "Neurologic", "Neurologic Symptoms", "Neurons", "Nose", "Odors", "Olfactory Epithelium", "Pathogenicity", "Pathology", "Patients", "Pattern", "Penetration", "Phenotype", "Population", "Publishing", "Quality of life", "Respiratory Signs and Symptoms", "Route", "SARS-CoV-2 B.1.1.529", "SARS-CoV-2 infection", "Symptoms", "Testing", "Time", "Travel", "Viral", "Virus", "Visualization", "brain pathway", "cell type", "cribriform plate", "human data", "hyposmia", "interest", "lymphatic vessel", "mouse model", "neural", "olfactory bulb", "prevent", "receptor", "secondary infection", "single-cell RNA sequencing", "sustentacular cell", "therapeutic target" ], "approved": true } }, { "type": "Grant", "id": "15619", "attributes": { "award_id": "1R01HL171220-01A1", "title": "Mitochondrial deubiquitinase USP30 regulates cell metabolism-mediated miRNA biogenesis and microvascular inflammation", "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": 20693, "first_name": "Roya", "last_name": "Kalantari", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-02-01", "end_date": "2028-11-30", "award_amount": 678803, "principal_investigator": { "id": 32117, "first_name": "Yutong", "last_name": "Zhao", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 778, "ror": "", "name": "OHIO STATE UNIVERSITY", "address": "", "city": "", "state": "OH", "zip": "", "country": "United States", "approved": true }, "abstract": "Acute inflammatory diseases are life-threatening health conditions that are most often caused by bacterial or viral infection such as Pseudomonas aeruginosa- or SARS-CoV-2-induced acute respiratory distress syndrome (ARDS) and sepsis. ARDS and sepsis-related mortality remains at unexpectedly high levels due to lack of effective pharmacotherapies. Hence, a new therapeutic strategy for ARDS and sepsis is needed. Microvascular inflammation and barrier disruption play critical roles in the pathogenesis of acute inflammatory diseases. A mitochondrial de-ubiquitinating enzyme, USP30, plays a vital role in regulation of mitochondrial outer membrane protein homeostasis. USP30 has been considered as a potential target for treating Parkinson’s disease and cancers; however, the role of USP30 in microvascular endothelial cells (ECs) and acute inflammatory diseases has not been reported. In our preliminary data, we discovered that inhibiting USP30 diminished EC dysfunction and reduced the severity of experimental lung injury. Mechanistically, we discovered a non-canonical pathway of USP30 that links MAT2A stability, the S- adenosylmethionine (SAM) cycle, DNA methylation, miRNA-30a-5p synthesis. Based on our comprehensive preliminary data, we hypothesize that inhibiting USP30 preserves EC function by modulating intracellular signaling cascades implicated in MAT2A stability, SAM production, DNA methylation, and miR-30a-5p expression. We propose testing the hypothesis with the following Specific Aims: Aim 1 is to determine if USP30 in the endothelium is a potential target for treatment of acute lung injury. We will determine if inhibiting EC USP30 diminishes leukocyte cell adhesion to EC and transendothelial migration and preserves EC barrier integrity. Further, we will determine if depletion of USP30 in endothelial cells reduces severity of pseudomonas aeruginosa- or sepsis-induced experimental lung injury. Aim 2 is to determine the molecular mechanisms by which inhibiting USP30 destabilizes MAT2A, decreases the SAM production, and increases miR-30a-5p. We will determine if inhibiting USP30- induced miR-30a-5p occurs through modulation of MAT2A stability in the SAM cycle, reduction of SAM production and pri-miR-30 promoter methylation. Further, we will determine if miR-30a-5p regulates USP30 inhibition-mediated MDM2, MLC, and NFAT5 downregulation. Aim 3 is to determine if the protective effect of USP30 inhibition occurs through modulating miR-30a-5p expression. We will determine if USP30 inhibition preserves EC function by modulating miR-30a-5p expression in HLMVECs. Further, we will determine if EC USP30 depletion reduces severity of experimental lung injury through modulating miR- 30a-5p expression by using a cutting-edge RNA nanoparticle technology. Comprehensive understanding of mitochondrial de-ubiquitinating enzyme inhibition-induced changes of cell metabolisms and EC function is important for development of new therapeutic targets for treatment of acute inflammatory diseases.", "keywords": [ "Acute", "Acute Lung Injury", "Attenuated", "Azacitidine", "Bacterial Infections", "Biogenesis", "COVID-19/ARDS", "Cell Adhesion", "Cell Physiology", "Cellular Metabolic Process", "DNA Methylation", "Data", "Deubiquitinating Enzyme", "Development", "Disease", "Down-Regulation", "Endothelial Cells", "Endothelium", "Enzyme Inhibition", "Enzymes", "Extravasation", "Functional disorder", "Genes", "Health", "Human", "Inflammation", "Inflammatory", "Leukocytes", "Life", "Link", "Lipopolysaccharides", "Liquid substance", "MDM2 gene", "Malignant Neoplasms", "Mediating", "Methylation", "MicroRNAs", "Microvascular Dysfunction", "Mitochondria", "Molecular", "Multiple Organ Failure", "Mus", "Myosin Light Chains", "Outer Mitochondrial Membrane", "Parkinson Disease", "Pathogenesis", "Pathway interactions", "Pharmacotherapy", "Plasma", "Play", "Production", "Proteins", "Pseudomonas aeruginosa", "Pulmonary Inflammation", "RNA", "Regulation", "Reporting", "Role", "S-Adenosylhomocysteine", "S-Adenosylmethionine", "Scheme", "Sepsis", "Severities", "Signal Transduction", "System", "Technology", "Testing", "Tissues", "Transfection", "Vascular Cell Adhesion Molecule-1", "Vascular Endothelial Cell", "Virus Diseases", "inhibitor", "interstitial", "knock-down", "lung injury", "lung microvascular endothelial cells", "methionine adenosyltransferase", "migration", "mortality", "nanoparticle", "new therapeutic target", "novel therapeutic intervention", "preservation", "promoter", "protective effect", "proteostasis", "sepsis induced ARDS", "targeted treatment", "ubiquitin isopeptidase", "vascular inflammation" ], "approved": true } }, { "type": "Grant", "id": "15624", "attributes": { "award_id": "1R01MH135862-01A1", "title": "The neuroimmune mechanism of SARS-CoV-2 on synaptic transmission and plasticity", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Mental Health (NIMH)" ], "program_reference_codes": [], "program_officials": [ { "id": 31795, "first_name": "Leonardo H", "last_name": "Tonelli", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-01-10", "end_date": "2028-11-30", "award_amount": 384772, "principal_investigator": { "id": 32123, "first_name": "Jianyang", "last_name": "Du", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 847, "ror": "", "name": "UNIVERSITY OF TENNESSEE HEALTH SCI CTR", "address": "", "city": "", "state": "TN", "zip": "", "country": "United States", "approved": true }, "abstract": "Given the current global COVID-19 pandemic, as well as documented challenges in long-COVID health burdens among people of lower socioeconomic backgrounds, understanding the cellular and molecular mechanisms responsible for SARS-CoV-2-induced neurological disorders is of fundamental importance. We recently developed a mouse SARS-CoV-2 infection model (SARS2-N501YMA30) showing alteration in mice behaviors fourteen days post-infection, allowing us to study long-term behavioral changes caused by SARS-CoV-2. Four days after the virus infection, we detected SARS-CoV-2 genomic RNA in brain tissues. In addition, SARS-CoV-2 dsRNA was detected exclusively within neurons, along with vigorous microglia activation. These data together with previous works might implicate the involvement of brain immune cells, such as microglia. Also, these preliminary data suggest a novel mechanism of SARS-CoV-2 infection- induced behavioral changes in mice. Thus, the goal of this proposal is to elucidate the mechanisms by which SARS-CoV-2 modulates neuronal activity in mice. This proposal describes three distinct aims to reach this goal. The first aim focuses on determining whether SARS2-N501YMA30 infection induces neuronal hyperactivity in mice. The second aim will determine how SARS2-N501YMA30 activates microglia via microglia-neuron interaction. The third aim will determine how microglia activation excites surrounding excitatory neurons in response to SARS2-N501YMA30 infection. Uncovering the cellular and molecular mechanisms by which SARS-CoV-2 alters neuronal activity through regulating neuron-microglia interaction will facilitate the development of therapeutic strategies to minimize long-COVID suffering, health disparity, and mortality from the COVID-19 pandemic.", "keywords": [ "2019-nCoV", "ACE2", "Affect", "American", "Animal Model", "Animals", "Anxiety", "Astrocytes", "Behavior", "Behavioral", "Biological Assay", "Brain", "C57BL/6 Mouse", "COVID-19", "COVID-19 burden", "COVID-19 detection", "COVID-19 mortality", "COVID-19 pandemic", "Cells", "Central Nervous System", "Data", "Death Rate", "Double-Stranded RNA", "Electrophysiology (science)", "Excitatory Postsynaptic Potentials", "Exhibits", "Foundations", "Goals", "Health Care Systems", "Human", "Hyperactivity", "Immune", "Infection", "Inflammatory", "Long COVID", "Long-Term Effects", "Longitudinal Studies", "Mental Depression", "Microglia", "Modeling", "Molecular", "Mus", "Natural Resistance", "Nervous System Disorder", "Neuroimmune system", "Neuroimmunomodulation", "Neurons", "Neurotropism", "Outcome", "Perfusion", "Persons", "Play", "Post-Acute Sequelae of SARS-CoV-2 Infection", "Process", "Production", "Proteins", "Recombinants", "Recovery", "SARS-CoV-2 infection", "SARS-CoV-2 spike protein", "Scientist", "Serial Passage", "Slice", "Symptoms", "Synaptic Transmission", "Synaptic plasticity", "Syndrome", "Tail Suspension", "Time", "Virulent", "Virus Diseases", "Work", "behavior test", "brain tissue", "current pandemic", "cytokine", "excitatory neuron", "forced swim test", "genomic RNA", "glial activation", "health disparity", "improved", "in vivo", "mortality", "mouse model", "novel", "novel therapeutic intervention", "overexpression", "patch clamp", "response", "socioeconomics", "therapeutic development", "therapeutic target" ], "approved": true } }, { "type": "Grant", "id": "15626", "attributes": { "award_id": "1R01HL171013-01A1", "title": "Modulation of Acute Lung Injury by Type I Interferon Signaling", "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": 22653, "first_name": "EMMANUEL FRANCK", "last_name": "Mongodin", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-01-01", "end_date": "2028-11-30", "award_amount": 690626, "principal_investigator": { "id": 32126, "first_name": "Brian T", "last_name": "Emmer", "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": "The proliferation of type 2 alveolar (AT2) cells is a critical step in the regeneration of the alveolar epithelium after acute lung injury, but the molecular pathways that regulate this process are unclear. Our preliminary findings strongly suggest that a specific host defense response, type I interferon (IFN-I) signaling, inhibits the proliferation of AT2 cells. We performed a high-throughput CRISPR screen, unexpectedly finding that despite its canonical antiviral properties, IFN-I signaling actually reduced the fitness of SARS-CoV-2- infected respiratory epithelial cells by restricting their proliferation after the initial peak of viral replication and cytopathic effect. We furthermore found that IFN-I signaling was not only necessary but sufficient for this antiproliferative response, and that it was also present in AT2 cells derived from induced pluripotent stem cells. Although IFN-I signaling has been implicated in driving lung pathology during SARS-CoV-2 infection in vivo, the underlying basis for this effect is unknown. Our in vitro data forms the foundation of our central hypothesis that IFN-I signaling promotes acute lung injury of diverse causes by inhibiting AT2 cellular proliferation during alveolar regeneration. In Aim 1, we will identify the molecular effectors that link IFN-I signaling activation to cell cycle arrest in respiratory epithelial cells. In Aim 2, we will determine whether inhibition of AT2 proliferation and alveolar regeneration is responsible for the pathogenic effect of IFN-I signaling in a mouse model of SARS- CoV-2 infection. In Aim 3, we will determine the potential of IFN-I signaling in AT2 cells to modulate alveolar regeneration after noninfectious acute lung injury. Together, these studies will clarify the fundamental biology of IFN-I signaling in the alveolar epithelium and facilitate our long-term objective of developing new disease- modifying treatments for acute lung injury and the acute respiratory distress syndrome.", "keywords": [ "2019-nCoV", "Acute Lung Injury", "Acute Respiratory Distress Syndrome", "Affect", "Alveolar", "Alveolar Cell", "Attenuated", "Automobile Driving", "Biology", "CDKN1A gene", "COVID-19", "COVID-19 treatment", "CRISPR screen", "Cell Cycle", "Cell Cycle Arrest", "Cell Death", "Cell Proliferation", "Cells", "Clinical", "Complex", "Data", "Development", "Disease", "Epithelial Cells", "Exhibits", "Foundations", "Genetic Predisposition to Disease", "Genetic Screening", "Goals", "Host Defense", "Human", "IFNAR1 gene", "IFNAR2 gene", "Immune response", "Impairment", "In Vitro", "Infection", "Interferon Type I", "JAK1 gene", "Link", "Lung Diseases", "Mediating", "Mediator", "Modeling", "Molecular", "Mus", "Natural regeneration", "Outcome", "Pathogenicity", "Pathway interactions", "Patients", "Pharmaceutical Preparations", "Process", "Proliferating", "Property", "Pulmonary Pathology", "Recovery", "Role", "SARS-CoV-2 infection", "Severities", "Signal Induction", "Signal Transduction", "Sterility", "TYK2", "Testing", "Treatment Efficacy", "Viral", "Virus Diseases", "Virus Receptors", "Virus Replication", "Work", "airway epithelium", "alveolar epithelium", "arm", "cell type", "defense response", "fitness", "improved", "in vivo", "in vivo regeneration", "induced pluripotent stem cell", "inhibitor", "insight", "mouse model", "pathogenic virus", "pre-clinical", "receptor", "receptor expression", "response", "severe COVID-19", "targeted treatment", "therapeutic target" ], "approved": true } }, { "type": "Grant", "id": "15641", "attributes": { "award_id": "1R01HL172844-01A1", "title": "Mechanisms of Thrombosis in SARS CoV-2 Infection", "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": 24630, "first_name": "Ronald Q", "last_name": "Warren", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-01-15", "end_date": "2028-11-30", "award_amount": 503637, "principal_investigator": { "id": 32145, "first_name": "Jeremy P", "last_name": "Wood", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 1162, "ror": "https://ror.org/02k3smh20", "name": "University of Kentucky", "address": "", "city": "", "state": "KY", "zip": "", "country": "United States", "approved": true }, "abstract": "More than 100 million individuals in the United States have experienced Coronavirus Disease 2019 (COVID- 19), caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). Life-threatening thrombotic events are well-described in these patients and occur in 2-3% of hospitalized patients. However, it is clear that a much greater number of patients experience microclots, small thrombotic events capable of causing localized tissue damage, and that microclots associate with the development of long-term complications from COVID-19. We hypothesize that these microclots result from a combined procoagulant and antifibrinolytic state. Through our preliminary studies we have identified two novel regulatory mechanisms that lead to the hemostatic and fibrinolytic dysfunction and microclot formation: (1) Activated endothelial cells secrete von Willebrand Factor (VWF), which binds and sequesters and inhibits protein S (PS), a critical plasma anticoagulant; and (2) dyslipidemia and elevated plasminogen activator inhibitor-1 result in sequestration and inhibition of the fibrinolytic protein tissue plasminogen activator (tPA). This combination of impaired anticoagulant and impaired fibrinolytic activity results in the formation of stable microclots, capable of blocking blood flow in microvascular beds, and causing localized hypoxia and tissue damage. We hypothesize that these dysfunctions occur during the acute phase of COVID-19 infection and persist in a sub-population of patients post-infection. As such, these mechanisms contribute to both acute and post-acute COVID- 19-associated coagulopathy. In the present study, we will test these hypotheses and extend our previous findings by following patients longitudinally from first diagnosis through 6-months post-infection, to identify the changes in the hemostatic and fibrinolytic systems, directly assess the contributions of PS and tPA to this process and their regulatory mechanisms, and determine the correlation of dysfunctions in these systems with microclot formation and recovery post-infection. Finally, we will perform similar analyses using samples from a cohort of patients with post-acute sequelae of COVID-19 (PASC), long-term complications from their initial infection. We hypothesize that these patients are individuals whose systems did not fully recover from the initial infection, and the proposed studies will allow us to compare the hemostatic and fibrinolytic systems between acute and PASC patients to evaluate this hypothesis, with particular focus on PS and tPA. The results from this study will inform on the mechanism(s) leading to COVID-19-associated coagulopathy and may determine biomarkers that can be used to identify those patients at greatest risk.", "keywords": [ "2019-nCoV", "Acute", "Alteplase", "Anticoagulants", "Antifibrinolytic Agents", "Binding", "Binding Proteins", "Biological Markers", "Blood Coagulation Disorders", "Blood Platelets", "Blood coagulation", "Blood flow", "COVID-19", "COVID-19 complications", "COVID-19 patient", "COVID-19 treatment", "Cause of Death", "Cell secretion", "Centers for Disease Control and Prevention (U.S.)", "Clinical", "Coagulation Process", "Data", "Development", "Diagnosis", "Dyslipidemias", "Endothelial Cells", "Endothelium", "Event", "Functional disorder", "Goals", "Health", "Hematologist", "Hemostatic Agents", "Hospitalization", "Hypoxia", "Immunologist", "Impairment", "Individual", "Infection", "Inflammation", "Inflammatory", "Inflammatory Response", "Lead", "Life", "Lipoprotein Binding", "Lipoproteins", "Long COVID", "Low-Density Lipoproteins", "Measurement", "Microcirculatory Bed", "Modeling", "Outcome", "Pathology", "Patients", "Persons", "Phase", "Phenotype", "Plasma", "Plasmin", "Plasminogen", "Plasminogen Activator Inhibitor 1", "Population", "Post-Acute Sequelae of SARS-CoV-2 Infection", "Predisposition", "Prevalence", "Process", "Protein S", "Protein S Deficiency", "Proteins", "Recovery", "Regulation", "Risk", "SARS-CoV-2 infection", "Sampling", "Stimulus", "Symptoms", "System", "Testing", "Thrombosis", "Time", "Tissues", "United States", "Virus", "activated Protein C", "acute COVID-19", "acute infection", "cohort", "experience", "individual patient", "insight", "mortality", "novel", "patient subsets", "response", "severe COVID-19", "therapeutic target", "thrombotic", "von Willebrand Factor" ], "approved": true } }, { "type": "Grant", "id": "15642", "attributes": { "award_id": "1R01HL176717-01", "title": "Aerocyte-mediated Alveolar Epithelial Regeneration following Lung Injury", "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": 23738, "first_name": "Sara", "last_name": "Lin", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2025-01-16", "end_date": "2028-11-30", "award_amount": 480990, "principal_investigator": { "id": 32146, "first_name": "Bisheng", "last_name": "Zhou", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 2548, "ror": "", "name": "UNIVERSITY OF ILLINOIS AT CHICAGO", "address": "", "city": "", "state": "IL", "zip": "", "country": "United States", "approved": true }, "abstract": "/ ABSTRACT Acute Respiratory Distress Syndrome (ARDS) is a life-threatening lung injury caused by various factors such as infection and trauma, currently lacking a cure. Annually, approximately 190,000 Americans are diagnosed with ARDS, a number further amplified by the COVID-19 pandemic. The primary pathology involves damage to the alveolar epithelium, necessitating innovative approaches to accelerate alveolar epithelial regeneration for treating ARDS. Alveoli, surrounded by abundant capillaries for gas exchange, remain poorly understood in their regulatory role within this intensive capillary niche. Our focus is on aerocytes, a recently identified capillary endothelial population specialized in the lungs and positioned on the outer surface of the alveolar epithelium. Given this unique location, we propose that aerocytes play a pivotal role in alveolar epithelial regeneration. Preliminary data indicate that aerocytes express the angiocrine factor R-spondin3, a Wnt signaling activator, and stem cell factor. Loss of angiocrine R-spondin3 impedes regenerative epithelial remodeling and lung repair following injury, suggesting a crucial role for aerocyte-derived signaling in lung alveolar regeneration. Our research proposal aims to establish the central role of aerocytes in regulating alveolar regeneration post lung injury, with a specific focus on the signaling molecule R-spondin3. We hypothesize that aerocytes guide regenerative alveolar remodeling through R-spondin3, enhancing Wnt signaling in alveolar epithelium, and orchestrating interstitial macrophage plasticity for the necessary regenerative niche. To rigorously test this hypothesis, we outline the following specific aims: Aim 1: Investigate the role of aerocyte-derived R-spondin3 in lung growth and recovery using loss-of- function and gain-of-function animal studies within disease-related lung injury models. Aim 2: Define the mechanisms of regenerative alveolar remodeling guided by aerocyte-derived signaling, focusing on AT2 cell renewal, transition into TSCs, and differentiation into AT1 cells using advanced techniques such as alveolar organoids. Aim 3: Examine the impact of aerocytes on interstitial macrophage plasticity in establishing a regenerative alveolar niche. By unveiling the role and mechanisms of aerocytes in alveolar epithelial regeneration, this research potentially leads to innovative therapeutic strategies for treating ARDS by targeting aerocyte-derived signaling to regenerate the alveoli, ultimately improving the health and quality of life for individuals affected by severe respiratory complications associated with COVID-19 and ARDS.", "keywords": [ "AGTR2 gene", "Acceleration", "Acute Lung Injury", "Acute Respiratory Distress Syndrome", "Address", "Affect", "Alveolar", "Alveolus", "American", "Animals", "Blood capillaries", "COVID-19 pandemic", "COVID-19/ARDS", "Cells", "Critical Illness", "Data", "Diagnosis", "Disease", "Endothelium", "Epithelium", "Gases", "Growth", "Health", "Individual", "Infection", "Injury", "Life", "Location", "Lung", "Macrophage", "Mediating", "Modeling", "Natural regeneration", "Organoids", "Pathology", "Play", "Population", "Positioning Attribute", "Quality of life", "Recovery", "Research", "Research Proposals", "Role", "Sepsis", "Signal Transduction", "Signaling Molecule", "Stem Cell Factor", "Surface", "Techniques", "Testing", "Therapeutic", "Trauma", "WNT Signaling Pathway", "alveolar epithelium", "effective intervention", "epithelium regeneration", "gain of function", "improved", "innovation", "interstitial", "loss of function", "lung injury", "lung repair", "new therapeutic target", "regenerative", "respiratory", "severe COVID-19" ], "approved": true } }, { "type": "Grant", "id": "14718", "attributes": { "award_id": "1R01MH132551-01A1", "title": "State Telehealth Policies and Mental Care for Children in Underserved Areas", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Mental Health (NIMH)" ], "program_reference_codes": [], "program_officials": [ { "id": 6350, "first_name": "Jennifer", "last_name": "Humensky", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2024-03-01", "end_date": "2028-12-31", "award_amount": 754470, "principal_investigator": { "id": 27082, "first_name": "HAO", "last_name": "YU", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 1912, "ror": "", "name": "HARVARD PILGRIM HEALTH CARE, INC.", "address": "", "city": "", "state": "MA", "zip": "", "country": "United States", "approved": true }, "abstract": "Unmet need for child mental health services is a persistent and pressing public health problem in the US. One of the key drivers of the unmet need is health workforce shortage, which has been exacerbated during the COVID-19 pandemic. This exacerbation has occurred against the backdrop of rising mental disorders among children, leading to the national emergency in child mental health declared by multiple specialty organizations. At the same time, the pandemic has also stimulated innovations, including the widespread adoption of telehealth, which has been promoted by recent government policies. Although telehealth has long been advocated for improving health care access for vulnerable populations, such as children living in mental health professional shortage areas (MHPSAs), no study to date has examined how the recent dramatic growth of telehealth affects mental health care availability and utilization for children in MHPSAs. Furthermore, amid the rapid transition to telehealth during the pandemic, some experts have been concerned with disparities in telehealth access and utilization and called for further research on the equitable development of telehealth. In response to that call, this proposed project aims to draw lessons about telehealth adoption during the pandemic to inform future telehealth policies. As a comprehensive evaluation of state telehealth policies on licensure, insurance coverage, and reimbursement, the proposed project has three aims: (1) mental health treatment facility (MHTF) level analyses to assess how changes in state telehealth policies affect disparities in mental health service availability for children from before to during the pandemic, (2) child level analyses to evaluate how changes in state telehealth policies affect disparities in mental care access, utilization, and spending among children from before to during the pandemic, and (3) qualitative interviews with medical directors at MHTFs to understand their experiences using telehealth to serve children as well as facilitators and barriers that they have identified for expanding telehealth in MHPSAs. For each aim, we will analyze two types of disparities—by area of residence (e.g., MHPSAs vs. non- shortage areas), and by child socio-demographic characteristic (e.g., race/ethnicity). Examining these disparities is crucial given the concern about digital health equity during the pandemic. To examine the aims, we will analyze quantitative data from both primary and secondary sources, including our unique longitudinal survey of nearly all MHTFs in the US. We will also collect complementary qualitative data through interviews with medical directors at MHTFs. The proposed study is both timely and important, as state policymakers are considering actions to revise their telehealth policies. The study findings will help them identify policies that have (or haven’t) been successful in expanding telehealth services for children with mental disorders—especially those who live in MHPSAs—to inform subsequent policy decisions.", "keywords": [ "Address", "Adoption", "Adult", "Advocate", "Affect", "Area", "COVID-19", "COVID-19 pandemic", "Categories", "Characteristics", "Child", "Child Care", "Child Health", "Child Health Services", "Child Mental Health", "Child health care", "Complement", "Country", "Data", "Data Files", "Development", "Disparity", "Drug usage", "Emergency Situation", "Employee", "Equity", "Ethnic Origin", "Evaluation", "Expenditure", "Future", "Goals", "Government", "Growth", "Health", "Health Personnel", "Health Policy", "Health Services", "Health Services Accessibility", "Healthcare Systems", "Insurance Coverage", "Interview", "Licensure", "Location", "Longitudinal Surveys", "Medial", "Mental Health", "Mental Health Services", "Mental disorders", "Physician Executives", "Policies", "Policy Maker", "Prevalence", "Provider", "Psyche structure", "Public Health", "Race", "Reporting", "Research", "Source", "Surveys", "Time", "Vulnerable Populations", "child mental health service", "digital health", "disparity reduction", "experience", "health care availability", "health care service utilization", "health equity", "health professional shortage areas", "improved", "innovation", "longitudinal analysis", "medical specialties", "minority children", "pandemic disease", "residence", "response", "sociodemographics", "telehealth", "underserved area" ], "approved": true } }, { "type": "Grant", "id": "14727", "attributes": { "award_id": "1R01AI178125-01A1", "title": "Immunogenicity of lipid nanoparticles", "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": 12151, "first_name": "AARON MICHAEL", "last_name": "Joffe", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2024-02-16", "end_date": "2028-12-31", "award_amount": 616143, "principal_investigator": { "id": 31416, "first_name": "SHAOYI", "last_name": "JIANG", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 279, "ror": "https://ror.org/05bnh6r87", "name": "Cornell University", "address": "", "city": "", "state": "NY", "zip": "", "country": "United States", "approved": true }, "abstract": "The immunogenicity of nanomaterials is directly related to their performance and toxicity. However, there is still a lack of systematic studies of how nanomaterials interact with the immune system. In this work, we will focus on the immunogenicity of lipid nanoparticles (LNPs). Various studies have raised concerns about the adverse event of LNPs from PEG lipids, ionizable lipids, and even helper phospholipids, such as anti-polyethylene glycol (PEG) antibodies found in BioNTech/Pfizer and Moderna COVID vaccines. During our recent studies of LNP- based mRNA cancer vaccines, the side effects, including ulcerative dermatitis, were also found on vaccinated mice after subcutaneous administrations. Most studies of LNPs via screening or design today have mainly focused on LNP efficacy while few on LNP immunogenicity. Very limited human data on very limited formulations in the context of COVID-19 vaccines following intramuscular administration have very limited scope in immunogenicity such as accessing the overall outcome of immunogenicity only. The investigations have not extensively delved into the underlying causes of the widely reported adverse effects associated with LNP-based mRNA vaccines, the specific immunological pathways of immunogenicity, and the underlying relationship between immunogenicity and components of LNPs. Currently, the mechanism of how LNPs induce adverse events is yet to be fully understood. Here we will formulate three libraries of LNPs covering widely used lipids and vary chemical properties of each component. We will perform immunological assays on primary murine cells to evaluate cytokine secretion and profile inducible gene expression. Similar tests will be performed in human peripheral blood mononuclear cells (hPBMCs). Toll-like receptor (TLR) and NOD-like receptor (NLR)-dependent immune response will be evaluated by reporter assays and validated in deficient mouse primary cells. Furthermore, the immunogenicity of LNPs will be profiled in the setting of intramuscular injections by assessing local inflammatory responses at the injection sites, and intravenous injections by evaluating the systemic response including accelerated blood clearance effects. Through these studies, we will identify key components that are responsible for LNP immunogenicity, understand how the chemistry of each LNP component alters the level of immune activation, and discover any synergistic effects on the immunogenicity among the components. The success of this work will advance current LNP technologies and provide clinical benefits for applications from vaccines to therapeutics.", "keywords": [ "Acceleration", "Adverse effects", "Adverse event", "Amines", "Antibodies", "B-Lymphocytes", "Biological Assay", "Blood", "Bone Marrow", "COVID-19 vaccine", "Cancer Vaccines", "Cell Maturation", "Cells", "Charge", "Chemistry", "Clinical", "Collaborations", "Dendritic Cells", "Dermatitis", "Drug Kinetics", "Ensure", "Evaluation", "Formulation", "Gene Expression Profiling", "Genetic Medicine", "Guidelines", "Hepatotoxicity", "Human", "Hydration status", "Immune", "Immune response", "Immune system", "Immunologics", "Immunology", "Immunology procedure", "In Vitro", "Individual", "Inflammatory Response", "Injections", "Intramuscular", "Intramuscular Injections", "Investigation", "Knock-out", "Knockout Mice", "Libraries", "Lipids", "Longevity", "Macrophage", "Maps", "Measures", "Mediating", "Medicine", "Messenger RNA", "Microbiology", "Moderna COVID-19 vaccine", "Mononuclear", "Mus", "Outcome", "Pathway interactions", "Performance", "Peripheral", "Peripheral Blood Mononuclear Cell", "Phenotype", "Phospholipids", "Polyethylene Glycols", "Polymers", "Population", "Proteins", "Proteomics", "RNA vaccine", "Receptor Activation", "Reporter", "Reporting", "Safety", "Site", "Structure", "Structure of germinal center of lymph node", "Technology", "Testing", "Therapeutic", "Toll-like receptors", "Toxic effect", "Transfection", "Vaccinated", "Vaccines", "Veterinary Medicine", "Wild Type Mouse", "Work", "chemical property", "clinical translation", "clinically relevant", "college", "cytokine", "design", "human data", "immune activation", "immune cell infiltrate", "immunogenicity", "in vivo evaluation", "inducible gene expression", "inorganic phosphate", "intravenous injection", "lipid nanoparticle", "nanocarrier", "nanomaterials", "professor", "receptor", "response", "screening", "side effect", "subcutaneous", "success", "systemic toxicity", "tertiary amine", "transcriptome sequencing" ], "approved": true } } ], "meta": { "pagination": { "page": 1385, "pages": 1419, "count": 14184 } } }