This work investigates how toxin-mediated interactions and directed movements shape the emergence of coherent structures in plant–herbivore systems. The analysis focuses on a two-compartment model enclosing a toxin-dependent functional response and a cross-diffusion term that represents ecologically plausible herbivores’ movement towards, or away from, vegetation. Two distinct dynamical regimes arise depending on toxicity strength. Under weak toxicity, the system admits at most one biologically feasible coexistence equilibrium, which may lose stability through a Hopf bifurcation generating small-amplitude temporal oscillations. Under strong toxicity, the nonlinear functional response becomes non-monotonic, allowing for multiple coexistence equilibria and abrupt regime shifts. The influence of cross-diffusion on stability is also examined, identifying the conditions under which Turing instabilities and mixed spatiotemporal patterns occur. Near the corresponding bifurcation thresholds, Stuart-Landau amplitude equations are derived via weakly nonlinear analysis, providing a unified framework for the modulation of oscillatory, stationary, and combined Turing–Hopf modes. Numerical simulations corroborate the theoretical predictions, illustrating transitions from spatially uniform states to oscillations, spatial patterns, and mixed behavior. Overall, this manuscript highlights how chemical defences, nonlinear feedbacks, and movement strategies jointly determine the emergence, selection, and robustness of coherent structures in plant–herbivore systems.
Diabetes mellitus (DM) and cancer are major global health challenges that increasingly coexist due to shared risk factors including aging, obesity, sedentary behavior, and chronic low-grade inflammation. Beyond being a common comorbidity, DM—particularly type 2 diabetes—has emerged as an important modifier of cancer risk, progression, treatment tolerance, and survival. Epidemiological studies consistently associate DM with a higher incidence of several malignancies, including pancreatic, liver, colorectal, breast, and endometrial cancers, as well as increased cancer-specific and overall mortality. The biological link between dysglycemia and cancer is complex and multifactorial. Chronic hyperglycemia, hyperinsulinemia, and insulin resistance promote tumor development and progression through altered cellular metabolism (Warburg effect), activation of insulin and insulin-like growth factor pathways, systemic inflammation, oxidative stress, immune dysfunction, and changes in the tumor microenvironment and gut microbiota. This review summarizes current evidence on the interplay between dysglycemia and cancer and explores how integrating continuous glucose monitoring (CGM)-based strategies into multidisciplinary oncology care may improve both metabolic and oncologic outcomes. A comprehensive search of online databases, including PubMed, ISI Web of Science, and Scopus, was conducted to identify studies assessing the impact of glycemic disturbances and glycemic control on cancer outcomes. Poor glycemic control and increased glucose variability are associated with worse oncologic outcomes, higher rates of treatment-related complications, reduced adherence to therapy, and diminished efficacy of chemotherapy, targeted agents, and immune checkpoint inhibitors. Severe hypoglycemia has also emerged as an independent predictor of poor prognosis. Although HbA1c has long been the cornerstone of glycemic assessment, it incompletely captures the dynamic glucose fluctuations commonly observed during cancer therapy. CGM provides a more comprehensive and clinically meaningful assessment of glycemic control, with the potential to reduce hypoglycemia, improve glycemic stability, and enhance tolerance and adherence to anticancer treatments. Current evidence indicates that diabetes and dysglycemia are key modifiers of cancer risk, progression, treatment tolerance, and survival. Optimizing glycemic control may therefore contribute to improved cancer outcomes. CGM represents a promising tool for personalizing diabetes management in oncology settings.
The Southern Apennines-Northern Calabrian boundary is a region marked by lithological heterogeneity, complex geodynamics and tectonics and prone to significant seismic hazard. This sector is part of a complex geodynamic system, where Africa-Eurasia convergence, Ionian subduction and slab retreat coexist. Its structure and seismic activity derive from extensive lithospheric heterogeneity and fluid-related processes, both of which are poorly constrained. Here, we present a novel application of seismic attenuation and scattering tomography of the area at a regional scale. We estimated seismic wave attenuation and scattering for the Southern Apennines-Northern Calabria region using a data set of 1581 waveforms related to 95 M >= 3.0 earthquakes that occurred between 2004 and 2024 and were recorded at 32 stations. We constrained the heterogeneous properties and fluid saturation of the Southern Apennines-Northern Calabrian region by mapping P-wave Peak Delays and inverting coda-normalized energies for total attenuation (1/Q). Results consistently reveal different seismic energy dissipation mechanisms between the two domains, reflecting their different characteristics in terms of Peak Delay and attenuation patterns. The Southern Apennines exhibit high Peak Delay values at all depths and almost no remarkable total attenuation anomalies, consistent with weakly consolidated, fractured sedimentary sequences and limited fluid content. Nevertheless, at a depth of 5.4 km, a relatively high attenuation pattern is detectable, likely linked to the presence of less cohesive and potentially fluid-saturated units. Conversely, Northern Calabria shows low Peak Delay and high attenuation in the investigated depth range, reflecting wave propagation through coherent crystalline rocks with significant fluid circulation, likely favoured by overpressurized materials or active migration pathways. The spatial correlation between high attenuation, low-seismic velocities and thermal anomalies shows that fluids modulate seismic wave behaviour, providing new constraints on the crustal structure and seismotectonic segmentation of the region. The joint interpretation of our results with other geophysical models and responses highlights the complex interplay between lithology, tectonics and fluid dynamics across this critical segment of the central Mediterranean.
Considering the increasing Italian school drop-out rates, this study aims to analyze the phenomenon of school refusal, focusing on the main individual factors that characterize it. School refusal is a multifactorial issue involving emotional, affective and social difficulties. Given these considerations, the research is divided into two consecutive studies. Study 1 examines the factor structure of the SCREEN (Gall & eacute;-Tessonneau and Gana 2019) by comparing the original version, the 18-item three-factor version, and 12-item short form four-factor version, in order to identify the best-fitting structure for Italian adolescent students (N = 351; Mage = 15.8; SD = 0.99). Confirmatory factor analysis (CFA) suggests that the short four-factor version is the best fitting model for the Italian context. Study 2 investigated the mediating role of positive and negative affect in the relationship between resilient coping and the four dimensions of school refusal (N = 581; Mage = 16.1; SD = 1.00). A Structural Equation Model (SEM) with latent variables was used to evaluate the associations between variables. Results suggest that resilient coping is associated with positive and negative affect, which are in turn differentially associated with dimensions of school refusal. Study highlights the importance of early identification and intervention, suggesting that fostering resilient coping strategies and positive affect at school may be associated with lower risk of avoidance and better school well-being.
This study investigates the effects of fluoride exposure on tissue accumulation, behavior, oxidative stress, neurotoxicity, metabolomic, and molecular alterations in Cyprinus carpio. The effects were evaluated at four different concentrations (Control: 0.8 mg/L, Group 1: 1.52 mg/L, Group 2: 3.0 mg/L, Group 3: 4.2 mg/L) over a 30-day period. Behavioral analysis revealed progressive neurobehavioral impairments including erratic swimming, lethargy, and respiratory distress. Fluoride accumulation followed the order: bone > gill > skin > muscle, indicating both systemic absorption and organ-specific retention. Enzymatic assays showed significant elevation of antioxidant enzymes (SOD, CAT, GPx) coupled with acetylcholinesterase inhibition, signifying oxidative stress and neurotoxicity. Metabolomic profiling demonstrated marked depletion of glutathione and ATP, with elevated lactate, AMP, and succinate levels, reflecting mitochondrial dysfunction and energy crisis. Concurrently, upregulation of IL-17, TNF-α, RORγ, and FoxO3a, alongside downregulation of IL-10 and Foxp3, indicated transcriptional signatures consistent with Th17-associated pro-inflammatory signaling and reduced Treg-related gene expression. Apoptotic gene activation (JNK, Bax, PUMA, Apaf-1, Caspase-9/3) and Bcl-2 suppression confirmed intrinsic mitochondrial apoptosis. Collectively, fluoride toxicity appears to progress through an integrated oxidative stress–mitochondrial dysfunction–immune imbalance–apoptotic cascade, which suggests that oxidative stress may function as an upstream trigger. These findings demonstrate that fluoride induces behavioral impairments, tissue accumulation, oxidative stress, metabolic disruption, immune imbalance, and apoptosis in C. carpio, with effects showing a strong dose-dependent (graded) response pattern, and identify key metabolites and molecular markers as early indicators of fluoride toxicity in aquatic environments.
