Recovery and Renewal of Co-Design Approaches in Health: Protocol for a Realist Synthesis.

BACKGROUND: The COVID-19 pandemic significantly transformed the landscape of work and collaboration, impacting design research methodologies and techniques. Co-design approaches have been both negatively and positively affected by the pandemic, prompting a need to investigate and understand the extent of these impacts, changes, and adaptations, specifically in the health sector. Despite the challenges that the pandemic imposed on conducting co-design and related projects, it also encouraged a re-evaluation of co-design practices, leading to innovative solutions and techniques. Designers and researchers have explored alternative ways to engage stakeholders and end users, leveraging digital workshops and participatory digital platforms. These adaptations have the potential to enhance inclusivity, allowing for a wider range of individuals to contribute their perspectives and insights through co-design and thus contribute to healthcare change. OBJECTIVE: This study aims to explore the impacts of the pandemic on co-design and related practices, focusing on co-design practices in healthcare that have been gained, adapted, or enhanced, with a specific focus on issues of equity, diversity, and inclusion. METHODS: The study uses a realist synthesis methodology to identify and analyze the effects of the pandemic on co-design approaches in health, drawing on a range of sources including first-person experiences, gray literature, and academic literature. A community of practice in co-design in health will be engaged to support this process. RESULTS: By examining the experiences and insights of professionals, practitioners, and communities who were actively involved in co-design and have navigated the challenges and opportunities of the pandemic, we can gain a deeper understanding of the strategies, tools, and techniques that have facilitated effective co-design during the pandemic, contributing to building resilience and capacity in co-design in health beyond the pandemic. CONCLUSIONS: By involving community partners, community of practice (research), and design practitioners, we expect closer proximity to practice with capacity building occurring through the realist process, thus enabling rapid adoption and refinement of new techniques or insights that emerge. Ultimately, this research will contribute to the advancement of co-design methodologies and inform the future of co-design in health. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): DERR1-10.2196/58318.

Reduced Cerebrospinal Fluid Inflow to the Optic Nerve in Glaucoma.

Purpose: To determine whether cerebrospinal fluid (CSF) entry into the optic nerve is altered in glaucoma. Methods: Fluorescent 10-kDa dextran tracer was injected into the CSF of 2-month-old (n = 9) and 10-month-old DBA/2J glaucoma mice (n = 8) and age-matched controls (C57Bl/6; n = 8 each group). Intraocular pressure (IOP) was measured in all mice before tracer injection into CSF. Tracer distribution was assessed using confocal microscopy of optic nerve cross-sections of mice killed 1 hour after injection. Paravascular tracer distribution in the optic nerve was studied in relation to isolectin-stained blood vessels. Tracer intensity and cross-sectional area in the laminar optic nerve were quantitatively assessed in all four groups and statistically compared. Aquaporin 4 (AQP4) and retinal ganglion cell axonal phosphorylated neurofilament (pNF) were evaluated using immunofluorescence and confocal microscopy. Results: IOP was elevated in 10-month-old glaucoma mice compared with age-matched controls. One hour after tracer injection, controls showed abundant CSF tracer in the optic nerve subarachnoid space and within the nerve in paravascular spaces surrounding isolectin-labeled blood vessels. CSF tracer intensity and signal distribution in the optic nerve were significantly decreased in 10-month-old glaucoma mice compared with age-matched controls (P = 0.0008 and P = 0.0033, respectively). AQP4 immunoreactivity was similar in 10-month-old DBA and age-matched control mice. Half of the 10-month-old DBA mice (n = 4/8) showed a decrease in pNF immunoreactivity compared to controls. Altered pNF staining was seen only in DBA mice lacking CSF tracer at the laminar optic nerve (n = 4/5). Conclusions: This study provides the first evidence that CSF entry into the optic nerve is impaired in glaucoma. This finding points to a novel CSF-related mechanism that may help to understand optic nerve damage in glaucoma.

Progressive loss of retinal blood vessels in a live model of retinitis pigmentosa.

OBJECTIVE: To assess retinal blood vessels in a live retinitis pigmentosa (RP) model with rd1 mutation and green fluorescent protein (GFP) expressed in vascular endothelium. METHODS: Homozygous (hm) Tie2-GFP mice with rd1 mutation and known retinal degeneration were crossed with wild-type CD1 mice to generate control heterozygous (ht) Tie2-GFP mice. The retinas of 16 live hm mice were evaluated at 2 weeks and 3, 5, and 8 months of age, and compared with age-matched control ht and CD1 mice by optical coherence tomography (OCT) and confocal scanning laser ophthalmoscopy (cSLO). Fluorescence intensity was measured and compared between strains at 3, 5, and 8 months. In vivo findings were validated by immunostaining with collagen IV and isolectin histopathology. RESULTS: All hm Tie2-GFP mice showed progressive outer retinal degeneration by OCT. Loss of small branches of blood vessels and then larger main vessels was seen by cSLO. Retinal tissue and vessels were preserved in control ht mice. At all ages, measurements of fluorescence intensity were reduced in hm compared with ht mice (p < 0.001). In all strains, intensity at 8 months was reduced compared with 3 months (p < 0.001) and 5 months (p = 0.021). Histopathological studies confirmed in vivo findings and revealed a pattern of blood vessel regression in the deep plexus, followed by intermediate and superficial retinal plexuses. CONCLUSIONS: This is the first evidence of progressive loss of retinal blood vessels in a live mouse model of RP. These findings may be highly relevant to understanding retinal degeneration in RP to prevent blindness.