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734 results on '"WILLIAMS, PETE"'

5. NMNAT2 is a druggable target to drive neuronal NAD production

Author

Tribble, James R., Jöe, Melissa, Varricchio, Carmine, Otmani, Amin, Canovai, Alessio, Habchi, Baninia, Daskalakis, Evangelia, Chaleckis, Romanas, Loreto, Andrea, Gilley, Jonathan, Wheelock, Craig E., Jóhannesson, Gauti, Wong, Raymond C. B., Coleman, Michael P., Brancale, Andrea, and Williams, Pete A.

Published
2024
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12. The press and the Persian Gulf War

Author

Williams, Pete

Subjects
REPORTERS AND REPORTING, IRAQ-KUWAIT CRISIS, 1990-1991 - Publicity, MASS MEDIA
Abstract

illus

Published
1991

20. Inhibition of monocyte-like cell extravasation protects from neurodegeneration in DBA/2J glaucoma

Author

Williams, Pete A, Braine, Catherine E, Kizhatil, Krishnakumar, Foxworth, Nicole E, Tolman, Nicholas G, Harder, Jeffrey M, Scott, Rebecca A, Sousa, Gregory L, Panitch, Alyssa, Howell, Gareth R, and John, Simon WM

Subjects
Biomedical and Clinical Sciences, Ophthalmology and Optometry, Aging, Neurosciences, Eye Disease and Disorders of Vision, Neurodegenerative, Genetics, Aetiology, 2.1 Biological and endogenous factors, Eye, Animals, Chemotaxis, Leukocyte, Glaucoma, Mice, Monocytes, Nerve Degeneration, Optic Nerve, Retinal ganglion cell, Optic nerve, Monocyte, Vascular leakage, Extravasation, Platelet, Neuroinflammation, RNA-sequencing, Clinical Sciences, Neurology & Neurosurgery, Biochemistry and cell biology
Abstract

BackgroundGlaucoma is characterized by the progressive dysfunction and loss of retinal ganglion cells. Recent work in animal models suggests that a critical neuroinflammatory event damages retinal ganglion cell axons in the optic nerve head during ocular hypertensive injury. We previously demonstrated that monocyte-like cells enter the optic nerve head in an ocular hypertensive mouse model of glaucoma (DBA/2 J), but their roles, if any, in mediating axon damage remain unclear.MethodsTo understand the function of these infiltrating monocyte-like cells, we used RNA-sequencing to profile their transcriptomes. Based on their pro-inflammatory molecular signatures, we hypothesized and confirmed that monocyte-platelet interactions occur in glaucomatous tissue. Furthermore, to test monocyte function we used two approaches to inhibit their entry into the optic nerve head: (1) treatment with DS-SILY, a peptidoglycan that acts as a barrier to platelet adhesion to the vessel wall and to monocytes, and (2) genetic targeting of Itgam (CD11b, an immune cell receptor that enables immune cell extravasation).ResultsMonocyte specific RNA-sequencing identified novel neuroinflammatory pathways early in glaucoma pathogenesis. Targeting these processes pharmacologically (DS-SILY) or genetically (Itgam / CD11b knockout) reduced monocyte entry and provided neuroprotection in DBA/2 J eyes.ConclusionsThese data demonstrate a key role of monocyte-like cell extravasation in glaucoma and demonstrate that modulating neuroinflammatory processes can significantly lessen optic nerve injury.

Published
2019

22. A multiethnic genome-wide association study of primary open-angle glaucoma identifies novel risk loci.

Author

Choquet, Hélène, Paylakhi, Seyyedhassan, Kneeland, Stephen C, Thai, Khanh K, Hoffmann, Thomas J, Yin, Jie, Kvale, Mark N, Banda, Yambazi, Tolman, Nicholas G, Williams, Pete A, Schaefer, Catherine, Melles, Ronald B, Risch, Neil, John, Simon WM, Nair, K Saidas, and Jorgenson, Eric

Subjects
Retinal Ganglion Cells, Animals, Mice, Inbred C57BL, Humans, Mice, Mice, Mutant Strains, Glaucoma, Open-Angle, Genetic Predisposition to Disease, Proteins, Transcription Factors, Risk Factors, Cohort Studies, Gene Expression, Intraocular Pressure, Mutation, Polymorphism, Single Nucleotide, Aged, Aged, 80 and over, Middle Aged, Ethnic Groups, Female, Male, Genome-Wide Association Study, Gene Knockdown Techniques, Genetic Loci, LIM-Homeodomain Proteins, United Kingdom, Formins, Inbred C57BL, Mutant Strains, Glaucoma, Open-Angle, Polymorphism, Single Nucleotide, and over
Abstract

Primary open-angle glaucoma (POAG) is a leading cause of irreversible vision loss, yet much of the genetic risk remains unaccounted for, especially in African-Americans who have a higher risk for developing POAG. We conduct a multiethnic genome-wide association study (GWAS) of POAG in the GERA cohort, with replication in the UK Biobank (UKB), and vice versa, GWAS in UKB with replication in GERA. We identify 24 loci (P

Published
2018

28. Nicotinamide provides neuroprotection in glaucoma by protecting against mitochondrial and metabolic dysfunction

Author

Tribble, James R., Otmani, Amin, Sun, Shanshan, Ellis, Sevannah A., Cimaglia, Gloria, Vohra, Rupali, Jöe, Melissa, Lardner, Emma, Venkataraman, Abinaya P., Domínguez-Vicent, Alberto, Kokkali, Eirini, Rho, Seungsoo, Jóhannesson, Gauti, Burgess, Robert W., Fuerst, Peter G., Brautaset, Rune, Kolko, Miriam, Morgan, James E., Crowston, Jonathan G., Votruba, Marcela, and Williams, Pete A.

Published
2021
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29. Neuroinflammation in glaucoma: A new opportunity

Author

Williams, Pete A, Marsh-Armstrong, Nick, Howell, Gareth R, Participants, The Lasker IRRF Initiative on Astrocytes and Glaucomatous Neurodegeneration, Bosco, Alejandra, Danias, John, Simon, John, Di Polo, Adriana, Kuehn, Markus H, Przedborski, Serge, Raff, Martin, and Trounce, Ian

Subjects
Biomedical and Clinical Sciences, Ophthalmology and Optometry, Aging, Brain Disorders, Neurosciences, Acquired Cognitive Impairment, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurodegenerative, Eye Disease and Disorders of Vision, Eye, Animals, Astrocytes, Glaucoma, Humans, Inflammation, Optic Nerve, Optic Neuritis, Retinal Ganglion Cells, Astrocyte, Microglia, Monocyte, Neurodegeneration, Lasker, Lasker/IRRF Initiative on Astrocytes and Glaucomatous Neurodegeneration Participants, Medical Biochemistry and Metabolomics, Opthalmology and Optometry, Ophthalmology & Optometry, Ophthalmology and optometry
Abstract

Mounting evidence suggests neuroinflammation is a key process in glaucoma, yet the precise roles are not known. Understanding these complex processes, which may also be a key in other common neurodegenerations such as Alzheimer's disease, will lead to targeted therapeutics for a disease that affects as many as 80 million people worldwide. Here, we define neuroinflammation as any immune-relevant response by a variety of cell types including astrocytes, microglia, and peripherally derived cells occurring in the optic nerve head and/or retina. In this review article, we first discuss clinical evidence for neuroinflammation in glaucoma and define neuroinflammation in glaucoma. We then review the inflammatory pathways that have been associated with glaucoma. Finally, we set out key research directions that we believe will greatly advance our understanding of the role of neuroinflammation in glaucoma. This review arose from a discussion of neuroinflammation in glaucoma at the 2015 meeting of The Lasker/IRRF Initiative for Innovation in Vision Science. This manuscript sets out to summarize one of these sessions; "Inflammation and Glaucomatous Neurodegeneration", as well as to review the current state of the literature surrounding neuroinflammation in glaucoma.

Published
2017

31. Evaluating the effect of rapamycin treatment in Alzheimer's Disease and aging usingin vivoimaging: the ERAP phase IIa clinical study protocol

Author

Svensson, Jonas E., primary, Bolin, Martin, additional, Thor, Daniel, additional, Williams, Pete A., additional, Brautaset, Rune, additional, Carlsson, Marcus, additional, Sörensson, Peder, additional, Marlevi, David, additional, Spin-Neto, Rubens, additional, Probst, Monika, additional, Hagman, Göran, additional, Morén, Anton Forsberg, additional, Kivipelto, Miia, additional, and Plavén-Sigray, Pontus, additional

Published
2024
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32. Using genetic mouse models to gain insight into glaucoma: Past results and future possibilities

Author

Fernandes, Kimberly A, Harder, Jeffrey M, Williams, Pete A, Rausch, Rebecca L, Kiernan, Amy E, Nair, K Saidas, Anderson, Michael G, John, Simon WM, Howell, Gareth R, and Libby, Richard T

Subjects
Biomedical and Clinical Sciences, Ophthalmology and Optometry, Human Genome, Eye Disease and Disorders of Vision, Aging, Neurosciences, Neurodegenerative, Genetics, 2.6 Resources and infrastructure (aetiology), Aetiology, Eye, Animals, Disease Models, Animal, Glaucoma, Humans, Intraocular Pressure, Mice, Retinal Ganglion Cells, Neuroinflammation, IOP, Axonal degeneration, Trabecular meshwork, Mouse genetics, Genomics, Neurodegeneration, DBA/2J, Medical Biochemistry and Metabolomics, Opthalmology and Optometry, Ophthalmology & Optometry, Ophthalmology and optometry
Abstract

While all forms of glaucoma are characterized by a specific pattern of retinal ganglion cell death, they are clinically divided into several distinct subclasses, including normal tension glaucoma, primary open angle glaucoma, congenital glaucoma, and secondary glaucoma. For each type of glaucoma there are likely numerous molecular pathways that control susceptibility to the disease. Given this complexity, a single animal model will never precisely model all aspects of all the different types of human glaucoma. Therefore, multiple animal models have been utilized to study glaucoma but more are needed. Because of the powerful genetic tools available to use in the laboratory mouse, it has proven to be a highly useful mammalian system for studying the pathophysiology of human disease. The similarity between human and mouse eyes coupled with the ability to use a combination of advanced cell biological and genetic tools in mice have led to a large increase in the number of studies using mice to model specific glaucoma phenotypes. Over the last decade, numerous new mouse models and genetic tools have emerged, providing important insight into the cell biology and genetics of glaucoma. In this review, we describe available mouse genetic models that can be used to study glaucoma-relevant disease/pathobiology. Furthermore, we discuss how these models have been used to gain insights into ocular hypertension (a major risk factor for glaucoma) and glaucomatous retinal ganglion cell death. Finally, the potential for developing new mouse models and using advanced genetic tools and resources for studying glaucoma are discussed.

Published
2015

36. Nicotinamide Prevents Retinal Vascular Dropout in a Rat Model of Ocular Hypertension and Supports Ocular Blood Supply in Glaucoma Patients

Author

Gustavsson, Simon T., primary, Enz, Tim J., additional, Tribble, James R., additional, Nilsson, Mattias, additional, Lindqvist, Anna, additional, Lindén, Christina, additional, Hagström, Anna, additional, Rutigliani, Carola, additional, Lardner, Emma, additional, Stålhammar, Gustav, additional, Williams, Pete A., additional, and Jóhannesson, Gauti, additional

Published
2023
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38. 8. Banding Encounters

Author

Hahn, Tomie, primary, Campbell, Louise, additional, Vogt, Lindsay, additional, Rose, Simon, additional, Blake, George, additional, Lee, Catherine, additional, Tucker, Sherrie, additional, Mouillot, François, additional, Milović, Jovana, additional, and Williams, Pete, additional

Published
2020
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41. THE QUESTION OF CAPACITY: As resorts experience increasingly large crowds, the concept of comfortable carrying capacity can help the broader community plan for the influx.

Author

WILLIAMS, PETE

Abstract

The article discusses the concept of comfortable carrying capacity (CCC) in mountain resorts and its importance in managing large crowds. The article highlights the Park City case in Utah, where lift upgrades were denied due to a lack of parking. CCC refers to a level of use that provides a pleasant recreational experience and ensures that capacities are balanced across various resort components. The calculation of CCC involves analyzing lift capacity, skier flow characteristics, and other factors. CCC is used by resorts to achieve balance between the capacities of different components, such as parking, restaurants, and base lodges. The text emphasizes that while CCC is a useful planning tool, it should not be the sole factor considered in discussions about resort plans and their impacts on surrounding communities. [Extracted from the article]

Published
2024

45. Nicotinamide prevents retinal vascular dropout in a rat model of ocular hypertension and supports ocular blood supply in glaucoma patients

Author

Gustavsson, Simon T., Enz, Tim J., Tribble, James R., Nilsson, Mattias, Lindqvist, Anna, Linden, Christina, Hagström, Anna, Rutigliani, Carola, Lardner, Emma, Stålhammar, Gustav, Williams, Pete A., Jóhannesson, Gauti, Gustavsson, Simon T., Enz, Tim J., Tribble, James R., Nilsson, Mattias, Lindqvist, Anna, Linden, Christina, Hagström, Anna, Rutigliani, Carola, Lardner, Emma, Stålhammar, Gustav, Williams, Pete A., and Jóhannesson, Gauti

Abstract

PURPOSE. To investigate whether nicotinamide (NAM) modulates retinal vasculature in glaucoma. METHODS. This was a prospective controlled clinical trial investigating animal and human histopathology. Participants included normotensive and ocular hypertensive rats, postmortem human ocular tissue, glaucoma patients (n = 90), and healthy controls (n = 30). The study utilized histopathology, computer-assisted retinal vasculature analysis, optical coherence tomography angiography (OCTA), and NAM treatment. The main outcome measures included retinal vascular parameters in rats as assessed by AngioTool; retinal vasculature integrity in rats and humans as assessed by histopathology, antibody-staining, and ImageJ-based measurements; and retinal perfusion density (PD) and flux index in humans as assessed by OCTA. RESULTS. A number of vessel parameters were altered in ocular hypertension/glaucoma compared to healthy controls. NAM treatment improved the retinal vasculature in ocular hypertensive rats, with an increase in mean vessel area, percentage area covered by vessels, total vessel length, total junctions, and junction density as assessed by AngioTool (all P < 0.05); vessel wall integrity as assessed by VE-cadherin antibody staining was also improved (P < 0.01). In humans, as assessed by OCTA, increases in PD in the optic nerve head and macula complete image (0.7%, P = 0.04 and 1.0%, P = 0.002, respectively) in healthy controls, and an increase in the temporal quadrant of the macula (0.7%, P = 0.02) in glaucoma patients was seen after NAM treatment. CONCLUSIONS. NAM can prevent retinal vascular damage in an animal model of glaucoma. After NAM treatment, glaucoma patients and healthy controls demonstrated a small increase in retinal vessel parameters as assessed by OCTA.

Published
2023
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