Cilioretinal artery occlusion is an uncommon retinal vascular emergency that can cause acute monocular visual loss, particularly when the macular region is involved. Non-arteritic anterior ischemic optic neuropathy is another ischemic disorder involving the optic nerve head and is usually associated with optic disc edema and sudden painless visual impairment. Although both conditions involve vascular territories related to the posterior ciliary circulation, the temporal and pathophysiological relationship between cilioretinal artery occlusion and optic nerve head ischemia remains incompletely defined. This case describes a 62-year-old woman with poorly controlled type 2 diabetes mellitus who presented with acute painless visual loss in the right eye. Initial fundus examination showed optic disc pallor and edema, grayish-white retinal edema extending from the optic disc to the macular region, macular involvement, and arterial attenuation. Multimodal ophthalmic evaluation, including fundus photography, Humphrey visual field testing, optical coherence tomography, visual evoked potential testing, and fundus fluorescein angiography, supported a diagnosis of cilioretinal artery occlusion with concurrent and progressive optic nerve head ischemic involvement, clinically consistent with suspected non-arteritic anterior ischemic optic neuropathy. Because the time window for thrombolysis had passed, conservative management for retinal arterial occlusion was initiated. After progression of optic disc edema and angiographic evidence of optic nerve head leakage, parabulbar triamcinolone was administered after consideration of systemic steroid-related risks. Partial reduction of optic disc edema and limited visual improvement were observed during follow-up; however, the single-case design and concurrent treatments preclude any conclusion regarding treatment efficacy. This case emphasizes that optic disc changes in cilioretinal artery occlusion should be monitored dynamically and interpreted using multimodal imaging rather than assumed to represent a fixed sequential diagnostic pattern.

Intracerebral hemorrhage (ICH) is a neurological disorder associated with high mortality and disability rates and can lead to severe neurological injury. This study investigated the role and underlying mechanism of FGD5-AS1 in ICH. In vitro and in vivo models of ICH were established. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure FGD5-AS1 and miR-93-5p expression. Neurological deficits were assessed using the modified Neurological Severity Score (mNSS), and cerebral edema was evaluated using the dry-wet weight method. Enzyme-linked immunosorbent assay (ELISA) was used to measure inflammatory cytokines and oxidative stress markers. Cell viability was evaluated using a cell viability and proliferation assay kit. The interaction between FGD5-AS1 and miR-93-5p was examined using dual-luciferase reporter assays and Pearson correlation analysis. Experimental ICH was accompanied by elevated FGD5-AS1 expression in both animal and cellular models. Suppression of FGD5-AS1 alleviated brain swelling, improved neurological performance, reduced inflammatory and oxidative injury, and enhanced endothelial cell survival. Inhibition of miR-93-5p diminished these protective effects, supporting a regulatory interaction between the two molecules. FGD5-AS1 negatively regulated miR-93-5p expression, and inhibition of miR-93-5p attenuated the effects observed following FGD5-AS1 knockdown. These results indicate that FGD5-AS1 may contribute to ICH-associated brain injury through regulation of miR-93-5p and that the FGD5-AS1/miR-93-5p axis may represent a potential target for further investigation in experimental ICH.

To develop a "nutrition-volume-electrolyte" Trinity nursing protocol for elderly patients with diabetic nephropathy (DN), centered on precise nutritional protein regulation, and to evaluate its clinical and economic value. This single-center retrospective cohort study included 66 elderly patients with DN admitted between January 2022 and November 2025. Based on the implementation of the updated nursing protocol in January 2024, 31 patients who received routine nursing care were assigned to the historical control group, and 35 patients who received Trinity integrated nursing based on stratified nutritional protein management combined with volume and electrolyte regulation were assigned to the observation group. Interventions were delivered during hospitalization and continued for three months after discharge. Outcomes included nutritional indicators, volume load, electrolyte target attainment, renal function, adverse events, quality of life, and health economic measures. After three months, albumin, prealbumin, hemoglobin, and transferrin were significantly higher in the observation group than in the control group (all P < 0.01). At all assessed time points, the 24-h intake-output difference, B-type natriuretic peptide (BNP) level, and edema severity score were lower in the observation group (all P < 0.001). Target attainment rates for serum potassium, sodium, calcium, and phosphorus were higher (all P < 0.05), and changes in eGFR, serum creatinine, and 24-h urinary total protein were more favorable (all P < 0.05). Adverse events were less frequent in the observation group than in the control group (25.71% vs. 51.61%, P = 0.030). 36-Item Short Form Health Survey (SF-36) scores were higher, whereas hospital stay, total medical cost per capita, and cost per unit effect were lower (all P. < 0.001). In conclusion, the Trinity integrated nursing protocol improved nutritional status, volume, and electrolyte balance, renal outcomes, quality of life, and economic performance in elderly patients with DN, supporting its value in clinical nursing management.

Anti-vascular endothelial growth factor (anti-VEGF) therapy is first-line treatment for diabetic macular edema (DME) and retinal vein occlusion (RVO), but real-world practice often differs from clinical trial findings. This single-center retrospective cohort study used hospital electronic medical records to evaluate anti-VEGF treatment patterns and associations with visual outcomes. We included 332 adults who received at least one intravitreal injection of ranibizumab, aflibercept, or conbercept between January 2022 and January 2024 and had at least one post-baseline best-corrected visual acuity (BCVA) measurement. The cohort included 180 patients with DME, 138 with RVO, and 14 with other retinal vascular diagnoses. Standard treatment required three monthly loading doses, a treat-and-extend regimen with intervals of 4-16 weeks, no interval >16 weeks, and treatment duration ≥12 months; all other patterns were classified as non-standard. The primary outcome was change in LogMAR BCVA at the last available follow-up. The standard and non-standard groups included 132 and 200 patients, respectively. Treatment interruption for ≥6 months was common in the non-standard group (68.50%). Unadjusted visual outcomes favored the standard group (median ΔBCVA, -0.23 vs. -0.07 LogMAR; improvement rate, 68.18% vs. 35.00%; P<0.001). In adjusted analyses, baseline BCVA, total number of injections, and treatment duration were positive predictors of improvement, whereas longer time to first injection was a negative predictor; standard/non-standard grouping was not significant (P=0.853). Safety events were infrequent, limiting comparison of rare events. Non-standard treatment patterns were common and associated with poorer unadjusted visual outcomes; optimizing injection exposure and treatment timing may improve real-world outcomes.

Dexamethasone is widely used to control cerebral edema and inflammation in glioblastoma, but its benefits are limited by systemic toxicities and adverse prognostic associations. We evaluated local administration of dexamethasone via convection-enhanced delivery (CED) to maximize intratumoral anti-inflammatory effects by increasing local corticosteroid exposure while minimizing systemic exposure. In two glioma mouse models, continuous intraparenchymal infusion of dexamethasone was well tolerated with no adverse effects. Pharmacokinetic analyses supported preferential intratumoral distribution and reduced systemic exposure with CED compared with systemic dosing. Single-nucleus RNA sequencing (snRNA-seq) and immunohistochemistry showed attenuation of glioma-associated inflammation with downregulation of reactive microglial/macrophage programs and reduced tumor-infiltrating myeloid cells with a morphology consistent with a less activated state. Experiments in human induced pluripotent stem cell (iPSC)-derived microglia confirmed that dexamethasone directly suppresses inflammatory gene expression, indicating a conserved mechanism across species. This inflammatory suppression was recapitulated in both immortalized microglial (HMC3) and macrophage (THP1) cell lines. These findings suggest that localized dexamethasone delivered by CED reprograms the glioma immune microenvironment and achieves control of inflammation without the systemic adverse effects associated with standard systemic dexamethasone therapy. This clinically translatable strategy may improve symptom management and provide a platform for integrating local immunomodulation with future glioblastoma therapies.

Tire wear particles (TWP) that runoff into aquatic habitats are linked to fish kills in urbanized watersheds of the Pacific Northwest. These TWP leach complex chemical mixtures, including photodynamic compounds that can become orders of magnitude more toxic under solar radiation. This enhancement is especially relevant for transparent aquatic organisms in high-solar environments, such as Gulf of Mexico (GoM) estuaries that provide critical nursery habitats for recreationally and ecologically valuable early life stage (ELS) fishes. Yet data on TWP contamination and photoinduced toxicity in these systems remain limited. Using a fully factorial design, we exposed ELS red drum (Sciaenops ocellatus) and southern flounder (Paralichthys lethostigma) to TWP leachate under ambient indoor lighting or simulated solar radiation (as UV-A). Sensitivity was species-specific and dependent on UV coexposure. Red drum mortality increased independently with dose and UV, while southern flounder were sensitive regardless of UV. Sublethal impacts were mixed: red drum showed reduced growth, altered energy utilization, and diminished development under UV, whereas southern flounder showed reduced size and significant pericardial edema regardless of UV. These results demonstrate that TWP toxicity is species-specific and mediated by both phototoxic and nonphototoxic mechanisms, highlighting the vulnerability of ELS fishes in critical nursery habitats.

Malodorous sulfur-containing volatile organic compounds (SVOCs) pose severe environmental and health risks, while existing physical or chemical abatement technologies suffer from low efficiency and poor economic viability. Herein, a low concentration ozone-assisted swelling-fixation of SVOCs (OSS) strategy is proposed using YMn2O5 mullite as a sulfur-fixing material, with CH3SH as a model pollutant. A sulfur fixation capacity of 1344.2 wt % (13.4× the YMO mass) is achieved and validated in a prototype device. Combined experimental characterizations and theoretical simulations reveal that ozone-derived reactive oxygen species synergize with Mn-Mn dimers, enable the thermodynamically and kinetically favorable conversion of CH3SH into liquid CH3SO2SCH3 and solid Mn(CH3SO3)2/SO42- products. The accumulation of these products builds a swollen surface layer on YMn2O5 that remains reactive toward CH3SH/O3 and allows continued sulfur fixation. Life-cycle assessment reveals a favorable trend in reducing carbon emissions, pollutant emissions, and eco-costs compared with conventional adsorption and oxidation routes. This room-temperature strategy enables scalable and sustainable SVOCs abatement, odor control, and sulfur resource fixation.

Urethane adhesives are critical to the structural integrity and long-term durability of automotive glazing systems, yet robust bonding of the windshield to chemically inert, cross-linked clearcoat surfaces of the vehicle body remains a persistent challenge. This study systematically investigates the molecular-level mechanisms governing the reactivity of automotive clearcoat surfaces toward isocyanate-based adhesives, focusing on the effects of aqueous pH pretreatment and solvent swelling. A model acrylosilane-melamine clearcoat was subjected to controlled hydrolysis under acidic, neutral, and basic conditions to modulate surface silanol (Si-OH) density. Phenyl isocyanate (Ph-NCO), chosen for its distinct aromatic spectroscopic signature, was employed as a model isocyanate to probe interfacial reactivity, forming the urethane bond to the clearcoat surface, both in vapor phase and in N-methyl-2-pyrrolidone (NMP) solution. Photoinduced force microscopy (PiFM) was used to probe subsurface structural changes, and vibrational sum-frequency generation (SFG) spectroscopy was used to probe the topmost surface chemistry. From these analyses, it was found that acidic and basic pretreatments significantly increase the density of reactive OH groups exposed to the topmost surface, leading to enhanced urethane formation upon exposure to isocyanate vapor. In the solution-phase reaction, the NMP solvent induces swelling and reorganization of polymer chains in the surface region, thus allowing reactions with subsurface OH groups. These findings elucidate molecular-level factors governing the reactivity of clearcoat OH groups toward isocyanates and provide mechanistic insight into interfacial reactions relevant to urethane adhesive bonding.

BackgroundThe relationship between acute myocardial injury and prognosis in acute myocarditis (AM) is unclear.PurposeTo evaluate myocardial injury characteristics by cardiovascular magnetic resonance (CMR) tissue parameters and their impact on adverse outcomes of AM patients.Material and MethodsThis retrospective study enrolled 41 patients with fulminant myocarditis (FM, including 17 FM patients without mechanical circulatory support [MCS] and 24 FM patients with MCS) and 35 patients with non-fulminant myocarditis (non-FM). Cine, mapping (native T1, T2, and post-T1), and late gadolinium enhancement (LGE) of the left ventricle were performed during CMR. Adverse clinical outcomes consisted of a primary endpoint, major adverse cardiovascular events (MACEs), and a secondary endpoint, a decline in functional status (defined as New York Heart Association [NYHA] functional classes II-IV).ResultsCompared with patients with non-FM, those in FM with MCS exhibited increased native T1 (P = 0.001), extracellular volume (ECV) (P = 0.018), and LGE (P = 0.005) values. After adjusting for the clinical variables (CRP > 67.9 mg/dL), LGE > 8.4% remained independently associated with adverse clinical outcomes and improved the predicting ability of the model (C-statistic improved from 0.74 to 0.82).ConclusionThe burden of necrosis and fibrosis was greatest in FM with MCS, while edema was similar across groups. Higher LGE% adds incremental prognostic value. A new classification using CRP and LGE improved prediction of adverse outcomes. Thus, CMR evaluation of myocardial injury extent offers variable information to improve risk stratification in FM.