
This research note reconceptualizes tourism intensity as a structural stressor capable of undermining the social capital that sustains urban life. Drawing on a 15-year longitudinal panel data of 42 Italian cities (2009-2023) and employing a dynamic System GMM estimator, our study analyses how varying levels of tourism intensity affect social capital, operationalized through a multi-indicator civic engagement index. The results reveal a non-linear erosion process, where social capital remains stable at low and moderate levels of tourism intensity but declines sharply once cities surpass high-intensity thresholds. Our findings provide a quantifiable basis for understanding overtourism as a threshold-based social phenomenon, extending beyond resident perceptions to the structural weakening of civic cooperation, trust, and engagement. The present study advances theoretical debates by positioning tourism intensity as a civic destabilizer and highlights the need for governance models that protect social capital as a critical urban asset. Without such safeguards, cities risk transitioning from vibrant, participatory communities into socially depleted Non-places.
Abstract As the global population ages, neurodegenerative and neuroinflammatory diseases are becoming a rapidly growing public health challenge, with available interventions remaining largely symptomatic and often only modestly affecting long-term disease progression. Therapies involving mesenchymal stromal cells (MSCs) have attracted substantial attention as a potential clinical therapeutic strategy across chronic central nervous system (CNS) disorders, due to their multifaceted ability to modulate immune response and confer neuroprotection. While initially explored for their multilineage differentiation potential, MSCs are now predominantly recognized for their paracrine functions, including secretion of soluble factors and extracellular vesicles. These acellular mediators induce diverse neuroprotective effects by attenuating neuroinflammation, stabilizing the blood–brain barrier, reprogramming glial and lymphocyte activity, and delivering regulatory microRNAs that modulate neuronal apoptosis and inflammatory gene networks. In this review, we summarize molecular evidence from in vitro and in vivo preclinical models, and early clinical investigations that demonstrate how tissue source and immunobiological plasticity shape the efficacy of MSCs. We further highlight emerging trends toward acellular MSC-derived therapies, offering a mechanistically versatile platform for therapeutic interventions for common neurodegenerative and neuroinflammatory disorders of the CNS, particularly Alzheimer’s disease, Parkinson’s disease and multiple sclerosis, a primary autoimmune demyelinating disorder. Graphical abstract
Several psychobiological factors are supposed to play a role in the association between insomnia and mental disorders. The current review was aimed at providing an overview of the associations between brain-derived neurotrophic factor (BDNF), insomnia, and psychopathology. BDNF is involved in neural plasticity and supports cognitive functioning and mood regulation. In animal models, sleep deprivation produces a decrease in central (e.g., hypothalamic) BDNF. Peripheral BDNF is sensitive to sleep loss in animal and human studies, and serum BDNF concentrations are remarkably lower in individuals with persistent insomnia and patients with mental disorders compared to their respective healthy controls. Recent evidence suggests that both non-rapid-eye-movement (NREM) and REM sleep may be associated with BDNF. Theoretical models and empirical data suggest that BDNF expression is reduced in patients with stress-related mood, anxiety, and psychotic disorders. Therefore, BDNF may play a critical role in the association between insomnia and psychopathology. Putatively, persistent sleep disruption may downregulate BDNF through several factors including neuroinflammation (e.g., cytokines, migroglia) and stress-related hormones (e.g., glucocorticoids) which may, in turn, increase the risk of psychopathology. Research on the effects of standard insomnia treatment on BDNF still needs to be developed.
This study investigates the causal impact of hedge fund activism (HFA) on market liquidity. The empirical results show that HFA leads to a deterioration in stock liquidity, with the effect being more pronounced in firms characterized by greater information asymmetry and financial constraints. The decline in liquidity is also more evident in cases of high-intensity campaigns, led by funds with weaker market reputation, and that engage more frequently in activist interventions. Additional analyses reveal that price efficiency, corporate information flow, and operating complexity contribute to liquidity decline. This evidence holds using several liquidity metrics and sensitivity tests, and we rule out any potential endogeneity concern using an exogenous setting in our Difference-in-Differences regression analysis. Overall, this study underscores the disruptive influence of HFA on corporate dynamics and its wider market repercussions.
This paper explores the effect of Lean Production and Industry 4.0 technologies on the operational performance improvement. While there is a widespread consensus on the positive effect that both paradigms can produce on the operational performance improvement, it is still questionable whether their joint interaction can enhance the effectiveness of Industry 4.0 due to the human-centricity of lean organizations, which seems to be in contrast with the strong focus on the technology-centricity peculiar to Industry 4.0. Based on the analysis of survey data coming from 189 factories located in Italy, the paper reveals a positive association between Lean Production practices and the adoption of Industry 4.0 technologies. However, it also shows that their interaction weakens the impact of Industry 4.0 technologies on productivity and product quality in factories with a longer and more intense Lean Production adoption. Interviews conducted among seven plants help in identifying the main reasons for such phenomenon.