MultiMedica

To describe a novel optical coherence tomography finding called "scolex sign" in cases of central serous chorioretinopathy. This retrospective multicenter study included patients with central serous chorioretinopathy with serous pigment epithelial detachments (PEDs) greater than 100 µ m, with or without subretinal fluid. Eyes showing a distinct hyperreflective focus on the PED wall (scolex sign) were analyzed. An equal number of age-matched controls with PEDs but without the scolex sign were included. Multimodal imaging data were reviewed. A subgroup analysis based on subretinal fluid status was also performed. Of 291 eyes with large serous PEDs, 52 eyes exhibited the "scolex sign" and were compared with 52 age-matched controls. Baseline characteristics including sex, systemic comorbidities, best-recorded visual acuity and optical coherence tomography parameters were similar in both the groups. However, eyes with the "scolex" sign exhibited a greater number of central PEDs and shorter distance from the foveal center. On follow-up, eyes with the "scolex" sign showed a higher rate of PED flattening and subretinal fluid resolution trended to be higher compared with controls. The "scolex" sign represents a novel, benign optical coherence tomography feature seen in a subset of central serous chorioretinopathy cases. While not associated with poorer outcomes or adverse sequelae, it may reflect ongoing reparative changes, indicating a resolving stage of the disease.

Emerging evidence implicates neuroinflammation in progressive supranuclear palsy (PSP) pathophysiology, with elevated cyto-chemokines suggesting natural killer (NK) cell involvement. We characterized peripheral NK in PSP (N = 11) versus Parkinson's disease (PD, N = 10) and healthy controls (HC, N = 8) at both immunophenotypic and transcriptional levels. PSP patients showed significantly reduced CD3-CD56 + NK frequency (1.35% ± 0.98%) compared with HC (2.96% ± 1.14%) and PD (2.03% ± 0.86%), specifically affecting the immunoregulatory CD56brightCD16-/dim subset. PSP NK cells exhibited elevated CX3CR1 expression, suggesting enhanced migratory capacity toward inflamed tissues. Transcriptomic analysis of primary NK cells revealed 208 DEG with significant enrichment in angiogenesis pathways, particularly vascular endothelial growth factor-A (VEGF-A). Plasma VEGF-A measurements demonstrated a disease-specific pattern: inverse correlation with severity in PSP versus direct correlation in PD. These findings identify a potentially disease-specific transcriptional signature with repercussions on the cyto-chemokine plasma profile. Further investigation of the NK cell-mediated immune response in PSP may provide new insights into disease mechanisms and open avenues for immunomodulatory therapeutic strategies. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

L19IL2 is a clinical-stage antibody-cytokine fusion protein that has been investigated for the treatment of various cancer types. Despite its promising antitumor activity, the precise mechanism of action is still not fully understood. In this work, we employed a myc-driven B-cell lymphoma murine model to demonstrate that systemic administration of L19IL2 induced a robust CD8⁺ T cell-dependent tumor regression across multiple organs without expansion of regulatory T cells. Following L19IL2 administration, intratumoral CD8+ T cells proliferated and acquired effector and memory phenotypes, associated with private clonal expansion and enhanced killing. Moreover, the spatial behavior of peritumoral CD8+ T cells studied by intravital microscopy demonstrated a rapid increase in tumor-directed motility and infiltration following L19IL2 administration. These findings described the detailed mechanism of action of L19IL2 against B cell lymphoma and revealed for the first time the dynamic responses of peritumoral CD8+ T cells to targeted IL2 stimulation, supporting the use of L19IL2 for patients with aggressive B cell lymphoma.

Background: Intravenous fluids modify acid-base balance by changing plasma strong ion difference (SIDPL) and total non-volatile weak acids. Experimental data suggest that pre-infusion plasma bicarbonate (HCO3-) may further modulate these effects. We tested this hypothesis in a large cohort of postoperative ICU patients receiving intravenous fluids. Methods: We retrospectively analyzed all-consecutive post-operative ICU admissions over a 21-month period who received fluid therapy. Fluid inputs/outputs, plasma electrolytes, and arterial blood gases were collected from admission to 9:00 A.M. of postoperative day one. Average SID of infused fluids (SIDINF) was calculated, and SIDPL and standard base excess variations (ΔSBE) were assessed. Patients were stratified by SIDINF tertiles (low, <41.0 mEq/L; medium, 41.2-54.6 mEq/L; high, ≥55.0 mEq/L), median pre-infusion HCO3- (24.3 [22.4-26.3] mmol/L), and tertiles of SIDINF-HCO3- difference. Results: Among 650 admissions, 641 were included (83% elective surgery). Pre-infusion acid-base was, as average, within normal ranges. Total infused volume averaged 2327 ± 1111 mL. Across SIDINF tertiles, ΔSBE increased from 1.2 ± 3.4 to 3.0 ± 3.0 and 3.4 ± 3.0 mmol/L (p < 0.001), paralleled by ΔSIDPL rise (0.6 ± 2.3, 1.3 ± 2.4 and 1.4 ± 2.3 mEq/L, respectively; p = 0.004). For any given SIDINF, patients with lower pre-infusion HCO3- showed greater ΔSBE and ΔSIDPL (p < 0.001). When analyzed by tertiles of SIDINF-HCO3- difference, ΔSBE rose from 1.0 ± 3.2 to 2.7 ± 2.9 and 4.0 ± 3.0 mmol/L (p < 0.001), with amplified effects at higher infused volume (>2500 mL). Conclusions: In postoperative ICU patients, fluid-induced acid-base changes are largely driven by SIDINF-HCO3- difference, supporting individualized fluid selection based on baseline HCO3-.

Necrotising fasciitis is a rare and rapidly progressive infection that demands early diagnosis and aggressive management to prevent fatal outcomes. We present a case of a woman in her 70s who developed a necrotising fasciitis of the hand and forearm after a minor thumb injury while cleaning artichokes.The initially underestimated wound progressed rapidly, requiring multiple surgical debridement. After clinical stabilisation, a complex full-thickness defect remained, exposing critical structures. Reconstruction was performed using scapular and parascapular free flap, ensuring excellent functional recovery. This case highlights the importance of early recognition and aggressive management of necrotising fasciitis. It also underlines the role of the reconstructive surgeon in restoring both form and function, balancing adequate excision of non-viable tissue with the risk of over-debridement. We find it potentially beneficial to discuss our management of this case because practical difficulties often arise due to the rarity and complexity of these conditions.

Microplastics are emerging as mediators in the interaction between environmental pollutants and cardiovascular health. Micro- and nanoplastics (MNPs) can enter the human body through ingestion, inhalation, or skin exposure, disrupting biological processes such as autophagy, inflammation, oxidative stress, immune activation, and vascular dysfunction. Therefore, MNPs might promote the development of cardiovascular diseases. The link between MNPs and cardiovascular diseases remains unclear, with no consistent data confirming a correlation between their concentration in tissues and disease onset. Continuously evolving analytical techniques to detect MNPs within human organs and tissues will help the design of prospective studies detailing the possible harm provided by different microplastics as well as their effects according to their physical properties and associated chemicals. In this review, we provide an update on the existing techniques for MNP detection and characterization to summarize the mechanisms linking these pollutants to human health, focusing on their effects on the cardiovascular system.