ELFE Group (Greece)

ABSTRACT Uveal melanoma (UM) is the most lethal primary intraocular tumour in adults: contemporary eye‐preserving treatments secure local control but frequently compromise vision and do little to prevent liver‐tropic metastases. Nanobiotechnology offers routes to change this equation by overcoming ocular barriers, concentrating therapy precisely within tumour tissue, and extending control to micrometastases. This review surveys liposomal and polymeric carriers, virus‐like drug conjugates (exemplified by belzupacap sarotalocan), nucleic‐acid and gene‐editing platforms, and nano‐enabled photo‐ and immunotherapies that can be delivered intravitreally, suprachoroidally, or systemically. We highlight theranostic designs that pair deep‐tissue imaging with on‐demand cytotoxicity, nano‐vaccines and immune‐reprogramming formulations that convert “cold” UM into treatment‐responsive disease, and strategies tuned for the hepatic niche that underlies UM mortality. Across these technologies, we distil design principles for ocular targeting, controlled release, and immune engagement, and we map the translational pipeline from preclinical validation to ongoing trials. We also delineate the outstanding hurdles such as manufacturing scale‐up, biodistribution and immunotoxicity profiling, dose optimization, and biomarker‐guided patient selection, whose resolution will determine clinical impact. Together, convergent advances in materials science, ocular oncology and tumour immunology position nanomedicine to deliver vision‐sparing, metastasis‐addressing treatments for UM and to redefine standards of care.

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Several studies found an association between COVID-19 incidence, cumulated over the first pandemic wave, and the risk of death for infected individuals. They attributed this association to hospital overload. We studied this association across the French departments using 82,467 serological samples and a hierarchical Bayesian model with spatial smoothing. In high-incidence areas, we hypothesized that hospital overload would increase infection fatality rate (IFR) without increasing infection hospitalization rate (IHR). The analyses were adjusted for intensive care beds per capita, age of the population, and diabetes prevalence (as a surrogate for obesity). We found that increasing departmental incidence from 3 to 9% rose IFR from 0.42 to 1.14% (difference 0.72%, 95% CI 0.49–1.01%), and IHR from 1.66 to 3.61% (difference 1.94%, 95% CI 1.18–2.80%). An increase in incidence from 6 to 12% in people under 60 was associated with an increased proportion of people over 60 among those infected, from 11.6 to 17.4% (difference 5.8%, 95% CI 2.9–8.8%). Higher incidence increased the risk of death for infected individuals and their risk of hospitalization by the same magnitude. These findings could be explained by a higher age among infected individuals in high-incidence areas, rather by than hospital overload.