Despite well-documented barriers to ophthalmic services, ophthalmic care delivery among incarcerated populations remains understudied. This prospective observational study aimed to characterize ophthalmic referral patterns, triage timelines, and follow-up attendance among incarcerated individuals referred to a tertiary eye care center (July 1, 2024 to July 1, 2025). On-call ophthalmology residents assigned referrals to standardized triage categories based on urgency. Referral and clinical data were extracted to evaluate wait times, triage delays, and follow-up attendance. Of 56 referrals, 48 patients (65 eyes) completed an initial visit. Trauma was the most common indication (37.5%). Most referrals were assigned high-priority triage (≤24 hours: 27.1%; ≤48 hours: 33.3%). Median wait time increased with decreasing triage priority (p < 0.001), with longer delays for lower-priority triages (p = 0.002). Follow-up was more frequently requested for trauma (66.7%) versus nontrauma (26.7%; p = 0.002). Among those scheduled for repeat appointments, 44.4% were lost to follow-up, more commonly among trauma (33.3%) versus nontrauma (6.7%; p = 0.040). Despite appropriate triage, lower-priority cases experienced delays beyond triage targets. The high rate of loss to follow-up among patients with ocular trauma, who may require complex ongoing care, highlights the need for improved continuous ophthalmic care access.

Major depressive disorder (MDD) involves network-level abnormalities that may reflect dysfunction in catecholaminergic nuclei, particularly the substantia nigra (SN) and locus coeruleus (LC), which regulate cortical gain and signal-to-noise ratio. However, whether MRI-derived SN/LC phenotypes are linked to depressive symptom severity through functional connectivity pathways in young individuals with MDD remains unclear. We studied 84 young participants (MDD, n = 46; controls, n = 38). MRI measures were extracted from the bilateral SN and LC using neuromelanin-sensitive magnetization transfer contrast (MTC) imaging and iron-sensitive quantitative susceptibility mapping (QSM). Seed-to-voxel analyses assessed associations between these phenotypes and resting-state functional connectivity. Graph-theoretical analyses extended functional connectivity findings to global network topology. Mediation analyses tested whether functional connectivity linked SN/LC MRI phenotypes to Hamilton Depression Rating Scale scores within the MDD group. Multiple comparisons were controlled using false discovery rate (FDR) at q < 0.05. Compared with controls, the MDD group exhibited reduced bilateral SN volume on QSM and decreased LC signal intensity on MTC. Neuromelanin- and iron-sensitive phenotypes showed distributed functional connectivity associations involving frontal, sensorimotor, precuneus, and cerebellar regions. Bilateral SN susceptibility showed diagnosis-dependent associations with global efficiency. Mediation analyses identified four candidate right LC functional connectivity pathways linking SN/LC qMRI phenotypes to HAMD scores, mainly involving right LC connectivity with the left precuneus, right paracentral lobule, and cerebellum.SN/LC catecholaminergic MRI phenotypes are associated with depressive severity and right LC-centered functional connectivity, supporting candidate circuit-level associations linking brainstem neuromodulatory phenotypes to clinical expression in MDD.

The endoscopic endonasal approach to the orbit or the lateral recess of the sphenoid may require passing instruments through a transfixing trans-septal corridor to obtain an adequate working angle. However, this maneuver incurs non-negligible morbidity, with septal perforation, synechia and olfactory disorder. The "sliding windows" technique aims to reconcile optimal exposure with mucosal preservation. It is a safe alternative to wide septectomy, while preserving septal trophicity and olfactory function. It is based on asymmetric mucoperichondrial flaps and a central osteocartilaginous window, providing trans-septal access, without direct mucosal incision. By reducing denuded areas and ensuring double mucosal coverage, it can decrease the incidence of perforation and of the functional sequelae reported after conventional transfixing approaches. Three variants are described, depending on the needs for reconstruction and the extent of the approach: (1) unilateral septal flap; (2) asymmetric bilateral septal flaps; (3) asymmetric bilateral flaps, using the ipsilateral flap for reconstruction of the operative site at the end of the procedure. The "sliding windows" technique thus meets the aims of endoscopic endonasal surgery, in which functional preservation is a priority.

Chronic stress exposure causes neurobiological and behavioral changes that resemble those reported in psychiatric conditions such as major depressive disorder (MDD). Preclinical stress models and studies using postmortem tissue from MDD patients have shown that DNA Damage-Inducible Transcript 4 (Ddit4) is increased in the prefrontal cortex (PFC). This is important because DDIT4 negatively regulates the mammalian target of rapamycin (mTOR) pathway, which may lead to behavioral deficits through diminished neuroplasticity and PFC function. Our prior studies indicate that coordinated neuron-microglia interactions contribute to synaptic remodeling in the PFC. The present studies aimed to test the hypothesis that increased neuronal Ddit4 expression is sufficient to drive structural remodeling of PFC neurons, in part by provoking microglia activation, and this leads to behavioral and cognitive deficits. To this end, we bilaterally infused AAV5-hSyn1-Ddit4-tdTomato or a control vector into the PFC of male Thy1-GFP and C57BL/6 mice and examined molecular, cellular, and behavioral endpoints. Mice with Ddit4 overexpression (Ddit4-OV) showed no change in passive stress coping yet exhibited a deficit in temporal order memory. Immunohistology analyses showed a decrease in dendritic spine density of Ddit4-OV mice. However, we found no changes in microglia count, microglia size, or nearest neighbor distance. Bulk RNA sequencing of Ddit4-OV PFC revealed increases in transcripts involved with dendrite and synapse function and decreases in transcripts involved with mitochondrial function, implicating mTOR dysregulation. Altogether, these results indicate that Ddit4 overexpression recapitulates some of the broad molecular, cellular, and behavioral adaptations observed following chronic stress exposure through a cell-autonomous mechanism.Significance Statement This work provides more context for the neurobiological effects of neuronal DNA Damage-Inducible Transcript 4 (Ddit4). Ddit4, an inhibitor of the mammalian target of rapamycin (mTOR) pathway, exhibits increased expression in the prefrontal cortex (PFC) of both rats exposed to pre-clinical chronic stress models and humans diagnosed with major depressive disorder (MDD). Our findings demonstrate that Ddit4 overexpression specifically in neurons is sufficient to reduce spine density in the PFC, impair temporal order memory, and induce transcriptional changes associated with stress and depression. These results indicate that neuronal Ddit4 can disrupt PFC function and cognitive performance in a cell-autonomous manner.

There is a notable lack of therapeutic alternatives for what is fast becoming a global epidemic of traumatic brain injury (TBI). Photobiomodulation (PBM) employs red or near-infrared (NIR) light (600-1300 nm) from lasers or LEDs to stimulate healing, protect tissue from dying, increase mitochondrial function, improve blood flow and tissue oxygenation. PBM can also act to reduce swelling, increase antioxidants, decrease inflammation, protect against apoptosis, and modulate microglial activation state. All these mechanisms of action strongly suggest that PBM delivered to the head should be beneficial in cases of both acute and chronic TBI. Many studies in small animal models of acute TBI have found positive effects on neurological function, learning and memory, and reduced inflammation and cell death in the brain. There is evidence that PBM can help the brain to repair itself by stimulating neurogenesis, upregulating BDNF synthesis, and encouraging synaptogenesis. Clinical studies have been conducted in patients suffering from acute TBI and the chronic effects of TBI. There have been reports of improvements in executive function, working memory, and improved sleep. Functional magnetic resonance imaging has shown modulation of the activation in intrinsic brain networks likely to be damaged in TBI (default mode network and salience network).