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Précis:The relationship between structural and hemodynamic parameters in patients with primary open angle glaucoma is strongest in the temporal region of the optic nerve. Purpose:To investigate the relationship between radial peripapillary capillary (RPC) vessel density (VD) and retinal nerve fiber layer (RNFL) thickness in quadrants and sectors of the optic nerve head (ONH) in patients with and without primary open angle glaucoma (POAG). Methods:In a cross-sectional prospective analysis, 191 subjects (80 early-stage POAG; 111 non-glaucomatous controls) were assessed for RNFL thickness and RPC VD in each quadrant [superior (S), inferior (I), nasal (N) and temporal (T)] and sector [inferior-temporal (IT), temporo-inferior (TI), temporo-superior (TS), superior-temporal (ST), inferior-nasal (IN), naso-inferior (NI), naso-superior (NS), and superior-nasal (SN) sectors] of the ONH through optical coherence tomography angiography (OCTA). Pearson correlations were used to test for associations between measurements, withP<0.05 considered statistically significant. Results:Significantly stronger positive correlations were found between RPC VD and RNFL thickness in the S, I, and T quadrants in POAG patients compared with non-glaucomatous controls (allP<0.05). The temporal quadrant in POAG patients displayed the largest difference in correlation compared with controls. A stronger positive correlation was also found between RPC VD and RNFL thickness in the temporal sectors of the ONH in POAG patients compared with controls, with the largest difference in the TS sector (allP<0.05). Conclusion:Early-stage POAG patients have a stronger relationship between RPC VD and RNFL in the temporal regions of the ONH compared with non-glaucomatous controls, with the TS sector demonstrating the largest difference between groups. Temporal sector VD loss may represent an early-stage biomarker for vascular-linked POAG disease. 

As populations worldwide show increasing levels of stress, understanding emerging links among stress, inflammation, cognition, and behavior is vital to human and planetary health. We hypothesize that inflammation is a multiscale driver connecting stressors that affect individuals to large-scale societal dysfunction and, ultimately, to planetary-scale environmental impacts. We propose a “central inflammation map” hypothesis to explain how the brain regulates inflammation and how inflammation impairs cognition, emotion, and action. According to our hypothesis, these interdependent inflammatory and neural processes, and the inter-individual transmission of environmental, infectious, and behavioral stressors—amplified via high-throughput digital global communications—can culminate in a multiscale, runaway, feed-forward process that could detrimentally affect human decision-making and behavior at scale, ultimately impairing the ability to address these same stressors. This perspective could provide non-intuitive explanations for behaviors and relationships among cells, organisms, and communities of organisms, potentially including population-level responses to stressors as diverse as global climate change, conflicts, and the COVID-19 pandemic. To illustrate our hypothesis and elucidate its mechanistic underpinnings, we present a mathematical model applicable to the individual and societal levels to test the links among stress, inflammation, control, and healing, including the implications of transmission, intervention (e.g., via lifestyle modification or medication), and resilience. Future research is needed to validate the model’s assumptions and conclusions against empirical benchmarks and to expand the factors/variables employed. Our model illustrates the need for multilayered, multiscale stress mitigation interventions, including lifestyle measures, precision therapeutics, and human ecosystem design. Our analysis shows the need for a coordinated, interdisciplinary, international research effort to understand the multiscale nature of stress. Doing so would inform the creation of interventions that improve individuals’ lives; enhance communities’ resilience to stress; and mitigate the adverse effects of stress on the world. 

Stress is a feeling of being worried, scared, or overwhelmed, caused by challenging situations or big life changes. Not all stress is bad, and some kinds of stress, like exercise, can even be good for us. However, when stress is severe or lasts a long time, it can harm our health. Severe stress causes inflammation, which is the body’s way of protecting itself. Inflammation helps the body heal, but long-lasting inflammation can lead to health problems. Stress can also affect the brain, making it hard to think clearly or make good decisions. In our work, we linked all these stress-related factors together (using math) to explain our hypothesis that stress can spread from person to person through our actions, words, and body language—and even over social media—until it affects whole societies and eventually the entire planet! This is a dangerous cycle that can lead to evenmorestress and inflammation, making problems worse. To break the cycle, we each need to focus on reducing stress in our own lives. 

Background/Objectives: To investigate macular vascular biomarkers for the detection of primary open-angle glaucoma (POAG). Methods: A total of 56 POAG patients and 94 non-glaucomatous controls underwent optical coherence tomography angiography (OCTA) assessment of macular vessel density (VD) in the superficial (SCP), and deep (DCP) capillary plexus, foveal avascular zone (FAZ) area, perimeter, VD, choriocapillaris and outer retina flow area. POAG patients were classified for severity based on the Glaucoma Staging System 2 of Brusini. ANCOVA comparisons adjusted for age, sex, race, hypertension, diabetes, and areas under the receiver operating characteristic curves (AUCs) for POAG/control differentiation were compared using the DeLong method. Results: Global, hemispheric, and quadrant SCP VD was significantly lower in POAG patients in the whole image, parafovea, and perifovea (p < 0.001). No significant differences were found between POAG and controls for DCP VD, FAZ parameters, and the retinal and choriocapillaris flow area (p > 0.05). SCP VD in the whole image and perifovea were significantly lower in POAG patients in stage 2 than stage 0 (p < 0.001). The AUCs of SCP VD in the whole image (0.86) and perifovea (0.84) were significantly higher than the AUCs of all DCP VD (p < 0.05), FAZ parameters (p < 0.001), and retinal (p < 0.001) and choriocapillaris flow areas (p < 0.05). Whole image SCP VD was similar to the AUC of the global retinal nerve fiber layer (RNFL) (AUC = 0.89, p = 0.53) and ganglion cell complex (GCC) thickness (AUC = 0.83, p = 0.42). Conclusions: SCP VD is lower with increasing functional damage in POAG patients. The AUC for SCP VD was similar to RNFL and GCC using clinical diagnosis as the reference standard. 

This study investigated the heterogeneity of ocular hemodynamic biomarkers in early open angle glaucoma (OAG) patients and healthy controls of African (AD) and European descent (ED). Sixty OAG patients (38 ED, 22 AD) and 65 healthy controls (47 ED, 18 AD) participated in a prospective, cross-sectional study assessing: intraocular pressure (IOP), blood pressure (BP), ocular perfusion pressure (OPP), visual field (VF) and vascular densities (VD) via optical coherence tomography angiography (OCTA). Comparisons between outcomes were adjusted for age, diabetes status and BP. VF, IOP, BP and OPP were not significantly different between OAG subgroups or controls. Multiple VD biomarkers were significantly lower in OAG patients of ED (p < 0.05) while central macular VD was lower in OAG patients of AD vs. OAG patients of ED (p = 0.024). Macular and parafoveal thickness were significantly lower in AD OAG patients compared to those of ED (p = 0.006–0.049). OAG patients of AD had a negative correlation between IOP and VF index (r = −0.86) while ED patients had a slightly positive relationship (r = 0.26); difference between groups (p < 0.001). Age-adjusted OCTA biomarkers exhibit significant variation in early OAG patients of AD and ED.