The journal retracts the article titled "EGF-Enhanced GnRH-II Regulation in Decidual Stromal Cell Motility through Twist and N-Cadherin Signaling" [...].

In the original publication [...].

The journal's Editorial Office and Editorial Board are jointly issuing a resolution and removal of the Journal Notice linked to this article [...].

Error in Figure 4 [...].

The following reference [69] has been retracted and should be removed from the original publication [...].

In the original publication [...].

In the original publication [...].

The following references [181] have been retracted and should be removed from the original publication [...].

Metal dyshomeostasis contributes to Alzheimer's disease (AD) by influencing amyloid aggregation, oxidative imbalance, and impaired clearance mechanisms. Safranal, a bioactive constituent of Crocus sativus, exhibits antioxidant properties, but its metal-modulating actions remain insufficiently understood. This study investigated whether safranal modulates metal (Fe, Cu, Zn) levels in an AD rat model while evaluating its cytoprotective rescue capacity against Aβ1-42 induced neurotoxicity in differentiated SH-SY5Y cells. AD was induced in male rats via intracerebroventricular streptozotocin, followed by a four-week safranal administration (0.5 mg/kg/day, ip). Behavioral performance, plasma metal levels (ICP-MS), and cerebral total antioxidant capacity (FRAP) were evaluated alongside histological assessment. Post-treatment protocols were employed to evaluate the effects of safranal on cell viability and apoptosis in differentiated SH-SY5Y cells exposed to Aβ1-42. Longitudinal analyses revealed that safranal attenuated exploratory deficits and recognition memory impairments in AD rats. Decreased plasma iron levels in the AD group were restored by safranal, accompanied by a return of cerebral antioxidant capacity to normal. Although overt hippocampal histological alterations were absent in this early phase, post-treatment with safranal successfully offered a therapeutic rescue window, preserving cell viability and attenuating Aβ1-42-induced apoptotic features in vitro. Safranal demonstrates beneficial neuroprotective effects in AD models by improving behavioral outcomes, partially correcting plasma iron levels, and mediating cytoprotective rescue windows against Aβ1-42-induced cellular toxicity. These findings suggest that safranal represents a promising natural candidate for reducing behavioral deficits, supporting peripheral iron status, and offering functional cell survival in AD models.

Vascular calcification and atherosclerotic arterial disease are complex processes involving multiple inhibitory and pro-calcific mechanisms. Matrix Gla protein (MGP) is an important inhibitor of vascular calcification, and its inactive dephosphorylated-uncarboxylated form (dp-ucMGP) has been proposed as a biomarker of cardiovascular risk. The present study aimed to evaluate the association of circulating dp-ucMGP, total MGP (tMGP), and Fetuin-A concentrations as markers for calcification associated with the presence of fibrocalcific plaques and/or arterial stenosis. A total of 160 patients were included in this observational study. Patients were classified according to the presence of fibrocalcific plaques and/or arterial stenosis. The study group included 136 patients, whereas 24 patients without fibrocalcific plaques or stenosis served as the control group. dp-ucMGP concentrations were significantly higher in the study group [1.29 vs. 1.07, p = 0.047]. In contrast, no significant differences were observed for tMGP [15.79 vs. 12.67, p = 0.532] or Fetuin-A [388.50 vs. 403.05, p = 0.894]. Glucose concentrations were significantly higher in the study group (p < 0.001), together with significant differences in fibrinogen, urea, creatinine, LDL cholesterol, and uric acid. Spearman correlation analysis showed weak positive correlations between dp-ucMGP and urea (ρ = 0.175, p = 0.034), creatinine (ρ = 0.183, p = 0.026), and triglycerides (ρ = 0.197, p = 0.017). Higher circulating dp-ucMGP concentrations were associated with the presence of fibrocalcific plaques and/or arterial stenosis, whereas tMGP and Fetuin-A did not differ significantly between groups. These findings support the potential relevance of dp-ucMGP as a biomarker associated with fibrocalcific and stenotic arterial disease. Further studies are required to determine its independent predictive value and clinical utility.

The molecular features shared by non-alcoholic fatty liver disease (NAFLD) and myocardial infarction (MI) remain incompletely understood. We analyzed six microarray cohorts from the GEO database to identify shared disease-associated transcriptomic features across independent NAFLD and MI populations. Weighted gene co-expression network analysis, differential expression analysis, and fuzzy c-means clustering across ordered cross-sectional NAFLD groups were used to define candidate genes. LASSO regression, random forest, and SVM-RFE identified consensus computational candidates, which were examined using exploratory classification, receiver operating characteristic curves, calibration curves, decision curve analysis, and SHapley Additive exPlanations. IDI1 was selected for exploratory expression assessment by qPCR in patients with established MI and in a mouse model of acute ischemic myocardial injury. Fifty-three shared candidate genes were identified, and five genes were retained by all three feature-selection methods. Single-gene ROC analyses showed SULF2, GADD45A, LIN7A, and IDI1 within the analyzed case-control datasets. IDI1 expression was higher in patients with MI than in healthy controls (p = 0.004), as well as in mice blood (p = 0.034) and infarcted myocardium (p = 0.0072) following LAD ligation. These findings indicate shared transcriptomic links between NAFLD and MI, supporting an association between IDI1 and myocardial injury.

West Nile Virus (WNV) is a significant global health threat, and the molecular mechanisms of its pathogenic activity in human hosts remain partially understood. This study applies an extensive proteomic approach combining "top-down" (2DE/MS) and "bottom-up" (LC-MS/MS) technologies to investigate protein changes in the Huh7 human hepatoma cellular model at 48 h post-infection with WNV. Our results demonstrate that WNV infection induces a massive downregulation of host proteins, particularly those involved in cell-cell adhesion and extracellular matrix (ECM) integrity (FN1, VTN, desmosome proteins and tight junctional proteins), which supports theories of blood-brain barrier disruption. Moreover, we highlighted a modulation of iron homeostasis (FTH1, IRP1, and IREB2) reflecting a "nutritional immunity" host response aimed at limiting host enzyme functions essential for virus replication. In particular, the top-down approach demonstrated a significant protein species modulation related to the unfolded protein response (UPR) (HSP90, HSPA8), as well as the hijacking of translation initiation factors (EIF1, eIF3 complex, and EIF4A1), which suggests viral strategies for immune evasion and efficient replication. Taken together, these findings offer a comprehensive overview of WNV-induced perturbations, revealing the quantitative modulation of proteins and potential post-translational signatures, thereby providing a robust foundation for identifying new antiviral drug targets and therapeutic strategies.

Temporomandibular joint osteoarthritis (TMJ-OA) involves inflammation and degeneration of mandibular condylar cartilage and subchondral bone. Dedifferentiated fat cells (DFATs) were established from buccal fat pad tissue obtained from a single human donor. We examined the effects of DFAT-derived extracellular vesicle preparations (DFAT-EVs) on inflammatory macrophage responses in vitro and disease-related outcomes in TMJ-OA in vivo. DFAT-EVs were applied to lipopolysaccharide- and interferon-γ-stimulated RAW264.7 macrophages and administered intra-articularly in rats with monosodium iodoacetate-induced TMJ-OA. Fluorescence signals from labeled DFAT-EVs were observed in RAW264.7 cells. DFAT-EVs reduced nitric oxide production and modulated nitric oxide synthase 2, interleukin (IL)-1β, IL-6, IL-10, IL-4, and tumor necrosis factor-α responses, although effects varied among inflammatory mediators. Head withdrawal threshold was significantly higher in the DFAT-EVs group than in the OA group at several time points in the 6-week cohort, but not in the 4-week cohort. Administration of DFAT-EVs attenuated the reduction in mandibular condylar bone volume fraction and was associated with preservation of cartilage architecture and matrix. Osteoarthritis Research Society International scores were significantly lower in the DFAT-EVs group than in the OA group at 4 weeks but not at 6 weeks. These in vitro and in vivo findings support further evaluation of DFAT-EVs for TMJ-OA.

Carbapenem-resistant Klebsiella pneumoniae (CRKP) causes serious infections in intensive care units (ICUs), but the relationship between carbapenemase gene profiles and mortality remains uncertain. This prospective two-center cohort included 94 adult ICU patients with clinical CRKP infection from April to September 2026. The first clinical isolate from each patient was included. blaKPC, blaNDM, blaVIM, blaIMP, blaOXA-48, and blaCTX-M genes were investigated by polymerase chain reaction. The primary outcome was 28-day ICU mortality; 14-day and final ICU mortality were secondary outcomes. blaOXA-48, blaNDM, blaKPC, and blaCTX-M were detected in 65 (69.1%), 49 (52.1%), 19 (20.2%), and 73 (77.7%) of isolates, respectively; blaNDM and blaOXA-48 co-occurred in 39 (41.5%). Fourteen-day, 28-day, and final ICU mortality rates occured in 38 (40.4%), 48 (51.1%), and 53 (56.4%), respectively. No statistically significant associations were observed between individual genes, the presence of two carbapenemase genes, or carbapenemase profiles and any mortality endpoint; adjusted analyses of 28-day ICU mortality yielded similar findings. In the exploratory Firth model, the profile effect was not significant (p = 0.198), whereas a higher age-adjusted Charlson Comorbidity Index and bloodstream infection or ventilator-associated pneumonia, compared with urinary tract infection, were associated with higher odds of 28-day ICU mortality. Frequent gene co-occurrence was observed; however, clinically meaningful gene-mortality associations cannot be excluded because of imprecise estimates.

A novel lytic bacteriophage, designated vB_ValS-L9, infecting the potentially pathogenic bacterium Vibrio alginolyticus L4, was isolated from a coastal aquaculture area in Beihai, China. Transmission electron microscopy revealed that vB_ValS-L9 possesses an icosahedral head (56.50 ± 4.19 nm in diameter) and a long tail (143.03 ± 5.32 nm in length), exhibiting a typical siphovirus-like morphology within the class Caudoviricetes. The phage demonstrated stability across various temperatures, pH levels, and salinities. Genomic sequencing showed that vB_ValS-L9 has a circular double-stranded DNA genome of 44,025 bp with a G + C content of 43.56% and 61 predicted ORFs. No tRNA, virulence, or antibiotic resistance genes were identified. Genomic and phylogenetic analyses, including ANI, VICTOR, VIRIDIC, and conserved protein phylogenies, identified vB_ValS-L9 as a novel species that, together with Vibrio phages Artemius and VapS30, forms a new genus in the class Caudoviricetes, for which the name Artemiovirus is proposed. Furthermore, in vivo trials using juvenile pearl oysters (Pinctada martensii) revealed that vB_ValS-L9 provides substantial prophylactic and therapeutic protection against V. alginolyticus L4 infection, especially when the phage was administered before bacterial challenge. Collectively, these findings suggest that vB_ValS-L9 shows potential as a safe, environmentally robust, and promising biocontrol candidate for managing vibriosis in aquaculture.