Carol Morris
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Also affiliated: University of Technology Sydney (2009); United States Department of Veterans Affairs (1988); The University of Queensland (2011); Wayne State University (2002); University of Arkansas Medical Center (2024); Veterans Health Administration (1988–1989); Brien Holden Vision Institute (2009); UNSW Sydney (1996–2009); Yale University (1988–1990); University of Florida (1987–1988); VA Connecticut Healthcare System (1988–1989); University of Colorado Health (2000); Vision Cooperative Research Centre (2009); Saint Louis University (1975); Southern Cross University (2006–2012)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Carol Morris's research focuses on the analysis of proteins and biochemical markers in biological fluids, particularly tears, to understand physiological processes and identify potential diagnostic indicators. Her work has involved the characterization of chemokines, cytokines, and growth factors in both open- and closed-eye tear conditions, identifying constituents such as angiogenin and other components of the defense system. Morris has also investigated tear glucose dynamics, with a publication specifically addressing its role in diabetes mellitus. Her research has extended to establishing reference maps for proteins in human reflex tears using two-dimensional polyacrylamide gel electrophoresis, aiming to uncover proteins with diagnostic value.
Further investigations have explored the host-defense mechanisms of ocular surfaces and the development of models for the pre-ocular tear layer. In addition to her work on ocular fluids, Morris has contributed to studies examining immune and antioxidant status in human males through bovine lactoferrin supplementation, as well as research into the alpha-glucosidase inhibitory activity of wheat bran and germ. Her scholarship metrics include an h-index of 25, 2,048 total citations across 77 publications, and she is recognized as a highly cited researcher. She actively collaborates with researchers at the University of Arkansas for Medical Sciences, including Abdelrahman Y. Fouda, Esraa Shosha, Rami Ahmad Shahror, and Nancy J. Rusch.
Metrics
- h-index: 24
- Publications: 69
- Citations: 1,891
Selected Publications
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Temporal and Age-Dependent Regulation of Phagocytosis-Related Signatures After Ischemic Stroke: Cross-Species Transcriptomic Evidence (2026)
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Myeloid HDAC3 deletion protects against traumatic optic injury (2026)
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HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis (2025)
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The role of efferocytosis in ischemic stroke and insights from retinopathy (2025)
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Disrupting the CD47/SIRPα Axis Protects Against Traumatic Optic Neuropathy (2025)
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Disrupting the CD47/SIRPα Axis as a Novel and Translational Therapy for Stroke (Abstract ID: 161422) (2025)
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Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology (2024)
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Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury (2024)
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Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions (2024)
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The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury (2023)
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Multi-color Flow Cytometry Protocol to Characterize Myeloid Cells in Mouse Retina Research (2023)
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Herbal Extracts from Lycii Radicis Corex and Achyranthes japonica Prevent Multiple Myeloma (2021)
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An Improved Animal Model of Multiple Myeloma Bone Disease (2021)
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Animal Models of Multiple Myeloma Bone Disease (2021)
Collaboration Network
Top Collaborators
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury
- Multi-color Flow Cytometry Protocol to Characterize Myeloid Cells in Mouse Retina Research
- The role of efferocytosis in ischemic stroke and insights from retinopathy
Showing 5 of 11 shared publications
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury
- Multi-color Flow Cytometry Protocol to Characterize Myeloid Cells in Mouse Retina Research
- Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology
Showing 5 of 8 shared publications
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury
- The role of efferocytosis in ischemic stroke and insights from retinopathy
- Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology
Showing 5 of 8 shared publications
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury
- The role of efferocytosis in ischemic stroke and insights from retinopathy
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury
- Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Disrupting the CD47/SIRPα Axis Protects Against Traumatic Optic Neuropathy
- Animal Models of Multiple Myeloma Bone Disease
- An Improved Animal Model of Multiple Myeloma Bone Disease
- Herbal Extracts from Lycii Radicis Corex and Achyranthes japonica Prevent Multiple Myeloma
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Animal Models of Multiple Myeloma Bone Disease
- An Improved Animal Model of Multiple Myeloma Bone Disease
- Animal Models of Multiple Myeloma Bone Disease
- Herbal Extracts from Lycii Radicis Corex and Achyranthes japonica Prevent Multiple Myeloma
- The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury
- Multi-color Flow Cytometry Protocol to Characterize Myeloid Cells in Mouse Retina Research
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions
- Proteomic Analysis of Aqueous Humor in Central Retinal Artery Occlusion: Unveiling Novel Insights Into Disease Pathophysiology
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Myeloid HDAC3 deletion protects against traumatic optic injury
- HDAC3 mediates retinal endothelial cell metabolic reprogramming and angiogenesis
- Myeloid HDAC3 deletion protects against traumatic optic injury
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