It is known that V-set and immunoglobulin domain containing 1 (VSIG1) is a cell–cell adhesion molecule that can serve as an indicator of better survival in patients with gastric cancer. Its interaction with cytoplasmic thyroid transcription factor 1 (TTF-1) has been hypothesized to characterize gastric-type HCC, but its clinical importance is far from understood. As VSIG1 has also been supposed to be involved in the epithelial–mesenchymal transition (EMT) phenomenon, we checked for the first time in the literature the supposed interaction between VSIG1, TTF-1, and Vimentin (VIM) in HCCs. Immunohistochemical (IHC) stains were performed on 217 paraffin-embedded tissue samples that included tumor cells and normal hepatocytes, which served as positive internal controls. VSIG1 positivity was seen in 113 cases (52.07%). In 71 out of 217 HCCs (32.71%), simultaneous positivity for VSIG1 and TTF-1 was seen, being more specific for G1/G2 carcinomas with a trabecular architecture and a longer OS (p = 0.004). A negative association with VIM was revealed (p < 0.0001). Scirrhous-type HCC proved negative for all three examined markers. The present paper validates the hypothesis of the existence of a gastric-type HCC, which shows a glandular-like architecture and is characterized by double positivity for VSIG1 and TTF-1, vimentin negativity, and a significant OS.

Background: Histological signs of carotid atheromatous plaque vulnerability, such as hemorrhage, neovascularization, atherothrombosis, and ulceration, develop against an unstable biological background. Declining renal function contributes to atherosclerotic progression and worsens cardiovascular outcomes. Methods: In a single-center prospective cohort study, we studied 41 endarterectomized patients with severe carotid atherosclerosis. The histological samples were stained with H&E to assess morphology and immunohistochemically labeled with antibodies for CRP and MMP-9 proteins. Complete blood count, the presence of serum biomarkers hsCRP, oxLDL, MCP-1, and MMP-9, and the level of eGFR were determined. Results: Twenty-eight patients with complicated plaques had significantly lower eGFR values: 79.5 (24–110) vs. 94 (69–114) (p = 0.004). Patients with eGFR > 90 mL/min/1.73m² had a higher incidence of intraplaque hemorrhage and histologic complications of any cause (p = 0.012 and p = 0.003). Patients with bleeding and ulceration from the carotid plaque had a higher neutrophil/lymphocyte ratio. Significantly lower levels of MCP-1 were found in the serum of patients with massive inflammatory infiltrate of the carotid plaques, while serum levels of biomarkers like hsCRP, MMP-9, and oxLDL did not show differences in cases with plaque vulnerability. Conclusions: Signs of plaque vulnerability are associated with reduced renal function, a higher neutrophil/lymphocyte ratio, and lower serum levels of MCP-1 in advanced carotid artery stenosis disease.

Background/Objectives: Pressure overload (PO) and volume overload (VO) represent important mechanisms underlying right ventricular (RV) failure; however, long-term comparative data regarding their distinct pathophysiological consequences remain limited. This study aimed to compare the long-term effects of PO versus VO in a large animal model. Methods: Juvenile sheep were randomly assigned to either a PO group (n = 7) or a VO group (n = 8). PO was induced by pulmonary artery banding, whereas VO was induced by pulmonary leaflet perforation (n = 4) or transannular patch (TAP) reconstruction (n = 4). Both VO procedures resulted in moderate-to-severe pulmonary regurgitation with comparable acute hemodynamic profiles and were therefore analyzed as a single VO group for the long-term assessment. Six animals from each group completed the follow-up period. Animals were evaluated preoperatively and at one-year follow-up using invasive hemodynamic monitoring, blood gas analysis, and echocardiography, followed by postmortem histological analysis of the myocardium. Results: Both models resulted in significant reductions in stroke volume index, cardiac index, RV stroke work index, ScvO₂ and tricuspid annular plane systolic excursion (TAPSE). Similarly, the TAPSE/RV systolic pressure (RVSP) ratio decreased in both groups but was significantly lower in the PO group than in the VO group (p = 0.0022). Moreover, PO showed more pronounced RV diastolic dysfunction, characterized by a significant increase in right atrial pressure from baseline (p = 0.0313) and higher RV diastolic pressure compared to VO (p = 0.0065). In contrast, VO showed a greater impact on left ventricular (LV) geometry and diastolic filling, evidenced by reduced transmitral filling (p = 0.0313) and a lower indexed LV internal diameter compared to PO (p = 0.0411). Histological analysis revealed myocardial hypertrophy and fibrosis in both groups, as well as clusters of multinucleated cardiomyocyte-like cells showing preferential ventricular distribution according to overload physiology. Conclusions: Chronic PO and VO induced distinct phenotypes of RV dysfunction with differential ventricular adaptation and remodelling patterns.

Hepatocellular carcinoma (HCC) is a heterogeneous primary liver malignancy characterized by limited treatment options and low overall survival rates. Recent studies have explored the role of programmed death ligand 1 (PD-L1), tumor-associated macrophages (TAMs), and epithelial-mesenchymal transition (EMT) in modulating tumor progression and the response to immunotherapy. This study aimed to investigate the association among PD-L1 expression, TAMs, and EMT in HCC, highlighting the recently proposed immunophenotypic variant—gastric-type HCCs. A retrospective cohort of 50 surgically resected HCC patients was analyzed. Immunohistochemical staining was performed for PD-L1 (clones 28-8 and 22C3), CD68 (TAMs), and EMT markers (VSIG-1, TTF-1, and vimentin). PD-L1 expression was detected in 52% of the patients and was significantly associated with high TAM counts (p < 0.001). Compared with PD-L1-negative patients, those with gastric-type HCCs, which are characterized by VSIG-1 and TTF-1 co-expression and vimentin negativity, demonstrated improved survival outcomes (p = 0.03). Integration of immune and EMT profiling of tumor cells in routine diagnostics may guide prognosis and immunotherapeutic strategies in HCC. Further molecular validation is required to confirm the biological significance of the proposed gastric-type HCC immunophenotype.