This paper investigates whether legality certification is associated with improved firm performance in environments exposed to organized crime. We study the Italian White List (WL) program, a public registry certifying firms as free from mafia connections, which substitutes traditional anti-mafia documentation and serves as a publicly verifiable signal of legal reliability. Using comprehensive firm-level data for 2011–2020, we implement a Difference-in-Differences design on a propensity-score common-support sample, with a switch-on and switch-off specification to examine the relationship between WL certification and firm performance. Results show that certification is associated with positive but modest changes in Total Factor Productivity (TFP) during the period of active certification, with no evidence of additional post-certification changes. By contrast, profitability differentials are larger and tend to increase further after certification lapses. The effects are strongest for micro and small enterprises and for firms operating in high-risk sectors such as construction and transport. They also vary by firm age: productivity effects are concentrated among younger firms, while profitability effects are more pronounced among young and mature firms. These patterns are consistent with a role for legality certification in strengthening firms’ credibility and facilitating market interactions in weak-governance environments.

PurposeThe purpose of this study is to examine the relationship between wages and health, with the objective of identifying the conditions under which an optimal treatment strategy can minimize financial resource waste.Design/methodology/approachThe study employs a foundational labor economics model that integrates wages, leisure, and health. This theoretical approach is supported by a panel threshold econometric analysis using data from 20 OECD countries over the period 2003 to 2022.FindingsThe analysis reveals that the effect of wages on health status is heterogeneous, with both positive and negative impacts depending on the wage level. A specific range of wage rates is identified in which disease prevention is more efficient than treatment. The econometric results indicate a threshold wage rate of $28.517, which corroborates the theoretical model.Research limitations/implicationsThe analysis is constrained by data availability, limiting the sample to 20 OECD countries.Practical implicationsThe findings offer policy-relevant insights for public health authorities, emphasizing the importance of choosing appropriate treatment strategies to reduce negative externalities. The results also underscore the necessity of designing income-sensitive interventions to enhance public health outcomes.Originality/valueThis study is the first to provide a unified theoretical and empirical explanation of the dual effects, both beneficial and adverse, that higher wage rates can have on health.

In Italy, creditworthy firms not involved in corruption, accounting frauds, and connections with organized crime benefit of cheaper loan interest rates thanks to the Legality Rating. We provide evidence that, upon receiving this public certification, firms increase their tangible capital expenditure by about 3-5% of the median capital-to-total asset ratio. The effect is stronger in provinces where it is more difficult for the banks to assess firms’ creditworthiness. This latter finding brings out the potential role of public signal for local development. JEL Classification: G14, G21, H40, H81, R38

This paper aims to explore the correlation between individual income and tax evasion. We develop a novel theoretical model based on the argument that the level of public goods provision and the perceived fairness of public services significantly influence an individual's attitude towards taxation. The model reveals a concave pattern, indicating the presence of an income threshold. Initially, as an individual's income increases, tax evasion decreases due to the perceived fairness of their contributions relative to the benefits received from public services. However, beyond this threshold, the tax burden is perceived as unfair, leading to an increase in tax evasion as income levels rise. We also proof that this income threshold is influenced by the tax rate and enforcement system. We also conduct a panel data analysis on a sample of 35 OECD countries from 2007 to 2020 to support the theoretical findings. The empirical investigation confirms a U-shaped relationship between income and the underground economy. Our findings suggest that policymakers should introduce measures to improve the quality of public goods provision, considering the potential adverse effect of higher income on economic growth. This study is the first to theoretically investigate the non-linear relationship between income and tax evasion while also providing empirical evidence.

Background and Aims: The COVID-19 pandemic, caused by the novel coronavirus SARS-CoV-2, has fundamentally reshaped the landscape of global public health, with some people suffering more adverse clinical outcomes than others. The aim of this study is to deepen our understanding of the specific impact of acute kidney injury (AKI) on the in-hospital mortality in octogenarian patients with COVID-19. Methods: This is a prospective observational cohort study, which involved 23 COVID-19 hospital units in the Campania Region, Italy. Exposure variables were collected during hospital admission and at discharge. Only patients aged ≥80 years were deemed eligible for the study. Results: 197 patients were included in the study (median age 83.0 [82.0–87.0] years; 51.5% men), with a median duration of hospitalization of 15.0 [8.0–25.0] days. From the multivariable Cox regression analysis, after the application of Šidák correction, only the respiratory rate (HR 1.09, 95% CI: 1.04 to 1.14; p < 0.001) and AKI development (HR: 3.40, 95% CI: 1.80 to 6.40; p < 0.001) were independently associated with the primary outcome. Moreover, the Kaplan–Meier analysis showed a significantly different risk of in-hospital mortality between patients with and without AKI (log-rank: <0.0001). Conclusions: In our investigation, we identified a significant association between AKI and mortality rates among octogenarian patients admitted for COVID-19. These findings raise notable concerns and emphasize the imperative for vigilant monitoring of this demographic cohort.

Background & aimsSARS-Cov-2 infection manifests as a wide spectrum of clinical presentation and even now, despite the global spread of the vaccine, contagiousness is still elevated. The aim of the study was the evaluation of the impact of liver fibrosis assessed by FIB-4 and liver impairment, assessed by cytolysis indices, on intrahospital mortality in COVID-19 subjects.MethodsThis is a retrospective observational cohort study, which involved 23 COVID Hospital Units in Campania Region, Italy. Exposure variables were collected during hospital admission and at discharge. According to FIB-4 values, we subdivided the overall population in three groups (FIB-4<1.45; 1.453.25), respectively group 1,2,3.ResultsAt the end of the study, 938 individuals had complete discharged/dead data. At admission, 428 patients were in group 1 (45.6%), 387 in group 2 (41.3%) and 123 in group 3 (13.1%). Among them, 758 (81%) subjects were discharged, while the remaining 180 (19%) individuals died. Multivariable Cox's regression model showed a significant association between mortality risk and severity of FIB-4 stages (group 3 vs group 1, HR 2.12, 95%CI 1.38-3.28, p<0.001). Moreover, Kaplan-Meier analysis described a progressive and statistically significant difference (p<0.001 Log-rank test) in mortality according to FIB-4 groups. Among discharged subjects, 507 showed a FIB-4<1.45 (66.9%, group 1), 182 a value 1.453.25 (9.0%, group 3). Among dead subjects, 42 showed a FIB-4<1.45 (23.3%, group 1), 62 a value 1.453.25 (42.3%, group 3).ConclusionsFIB-4 value is significantly associated with intrahospital mortality of COVID-19 patients. During hospitalization, particularly in patients with worse outcomes, COVID-19 seems to increase the risk of acute progression of liver damage.

This paper studies the effect of different ballot structures in proportional representation systems on the educational attainment of elected politicians as a proxy for their “ability”. By exploiting the Italian electoral reform that switched from open to blocked lists of candidates, the difference-in-differences analysis shows that the reform lowered the educational attainment of national politicians compared to the counterfactual (regional politicians). The dynamic impact of the reform is persistent over time, and it is robust to several concerns. The estimates account for the changes in the party system due to the “Clean hands” judicial inquiry against political corruption that began in 1992. The voters’ choice of better politicians than political parties seems to be the most likely mechanism behind the results.

Since the first identification in December of 2019 and the fast spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, it has represented a dramatic global public health concern. Though affecting mainly the respiratory system, SARS-CoV-2 disease, defined as coronavirus disease 2019 (COVID-19), may have a systemic involvement leading to multiple organ dysfunction. Experimental evidence about the SARS-CoV-2 tropism for the liver and the increasing of hepatic cytolysis enzymes during infection support the presence of a pathophysiological relationship between liver and SARS-CoV-2. On the other side, patients with chronic liver disease have been demonstrated to have a poor prognosis with COVID-19. In particular, patients with liver cirrhosis appear extremely vulnerable to infection. Moreover, the etiology of liver disease and the vaccination status could affect the COVID-19 outcomes. This review analyzes the impact of the disease stage and the related causes on morbidity and mortality, clinical outcomes during SARS-CoV-2 infection, as well as the efficacy of vaccination in patients with chronic liver disease.

Hepatitis B virus (HBV) is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Despite the advent of vaccines and potent antiviral agents able to suppress viral replication, recovery from chronic HBV infection is still an extremely difficult goal to achieve. Complex interactions between virus and host are responsible for HBV persistence and the risk of oncogenesis. Through multiple pathways, HBV is able to silence both innate and adaptive immunological responses and become out of control. Furthermore, the integration of the viral genome into that of the host and the production of covalently closed circular DNA (cccDNA) represent reservoirs of viral persistence and account for the difficult eradication of the infection. An adequate knowledge of the virus–host interaction mechanisms responsible for viral persistence and the risk of hepatocarcinogenesis is necessary for the development of functional cures for chronic HBV infection. The purpose of this review is, therefore, to analyze how interactions between HBV and host concur in the mechanisms of infection, persistence, and oncogenesis and what are the implications and the therapeutic perspectives that follow.

Hepatocellular carcinoma (HCC) is the most frequent liver neoplasm, and its incidence rates are constantly increasing. Despite the availability of potentially curative treatments (liver transplantation, surgical resection, thermal ablation), long-term outcomes are affected by a high recurrence rate (up to 70% of cases 5 years after treatment). HCC recurrence within 2 years of treatment is defined as "early" and is generally caused by the occult intrahepatic spread of the primary neoplasm and related to the tumor burden. A recurrence that occurs after 2 years of treatment is defined as "late" and is related to de novo HCC, independent of the primary neoplasm. Early HCC recurrence has a significantly poorer prognosis and outcome than late recurrence. Different pathogenesis corresponds to different predictors of the risk of early or late recurrence. An adequate knowledge of predictive factors and recurrence risk stratification guides the therapeutic strategy and post-treatment surveillance. Patients at high risk of HCC recurrence should be referred to treatments with the lowest recurrence rate and when standardized to combined or adjuvant therapy regimens. This review aimed to expose the recurrence predictors and examine the differences between predictors of early and late recurrence.

Despite maximizing techniques and patient selection, liver resection and ablation for HCC are still associated with high rates of recurrence. To date, HCC is the only cancer with no proven adjuvant or neoadjuvant therapy used in association to potentially curative treatment. Perioperative combination treatments are urgently needed to reduce recurrence rates and improve overall survival. Immunotherapy has demonstrated encouraging results in the setting of adjuvant and neoadjuvant treatments for non-hepatic malignancies. Conclusive data are not yet available in the context of liver neoplasms. However, growing evidence suggests that immunotherapy, and in particular immune checkpoint inhibitors, could represent the cornerstone of an epochal change in the treatment of HCC, improving recurrence rates and overall survival through combination treatments. Furthermore, the identification of predictive biomarkers of treatment response could drive the management of HCC into the era of a precision medicine. The purpose of this review is to analyze the state of the art in the setting of adjuvant and neoadjuvant therapies for HCC in association with loco-regional treatments in patients not eligible for liver transplantation and to hypothesize future scenarios.

Several chronic liver diseases are characterized by a clear gender disparity. Among them, hepatocellular carcinoma (HCC) shows significantly higher incidence rates in men than in women. The different epidemiological distribution of risk factors for liver disease and HCC only partially accounts for these gender differences. In fact, the liver is an organ with recognized sexual dysmorphism and is extremely sensitive to the action of androgens and estrogens. Sex hormones act by modulating the risk of developing HCC and influencing its aggressiveness, response to treatments, and prognosis. Furthermore, androgens and estrogens are able to modulate the action of other factors and cofactors of liver damage (e.g., chronic HBV infection, obesity), significantly influencing their carcinogenic power. The purpose of this review is to examine the factors related to the different gender distribution in the incidence of HCC as well as the pathophysiological mechanisms involved, with particular reference to the central role played by sex hormones.

The bioeconomy is an essential part of the transition from a linear to a circular production model, which repositions production systems to favour sustainability and innovation. There are two main contributors to the development of this process: the choices made by public decision-makers (national and European), and the strategies adopted by companies and the recent increased diffusion of new business networks and clusters in Europe, which favour industrial and technological transformation processes. We move from analysis of the international context and how Italy's positioning in the new circular bioeconomy is evolving to focus on the diffusion of business clusters and networks in Europe linked to the circular bioeconomy to propose a preliminary empirical study of corporate behaviour. For this we use survey data on Italian bio-industries that are part of the cluster SPRING (Sustainable Processes and Resources for Innovation and National Growth). The results show how SPRING cluster firms are pushed to improve their positioning in numerous fields characterizing the most innovative business models.

Diabetic neuropathy (DN) is one of the main microvascular complications of both type 1 and type 2 diabetes mellitus. Sometimes, this could already be present at the time of diagnosis for type 2 diabetes mellitus (T2DM), while it appears in subjects with type 1 diabetes mellitus (T1DM) almost 10 years after the onset of the disease. The impairment can involve both somatic fibers of the peripheral nervous system, with sensory-motor manifestations, as well as the autonomic system, with neurovegetative multiorgan manifestations through an impairment of sympathetic/parasympathetic conduction. It seems that, both indirectly and directly, the hyperglycemic state and oxygen delivery reduction through the vasa nervorum can determine inflammatory damage, which in turn is responsible for the alteration of the activity of the nerves. The symptoms and signs are therefore various, although symmetrical painful somatic neuropathy at the level of the lower limbs seems the most frequent manifestation. The pathophysiological aspects underlying the onset and progression of DN are not entirely clear. The purpose of this review is to shed light on the most recent discoveries in the pathophysiological and diagnostic fields concerning this complex and frequent complication of diabetes mellitus.

Sodium-glucose co-transporters (SGLTs) family members are involved in several vital biological functions. Except for SGLT3, they are involved in the mechanisms of active transport of sodium and glucose and several micromolecules. The discovery of functions and mechanisms of SGLT1 inhibition and, in particular, of SGLT2 has radically changed the natural history of some pathologies. SGLT2 inhibitors have revolutionized the therapeutic approach not only of type 2 diabetes mellitus but also of heart failure and chronic kidney failure. Considering the role played by the other SGLTs and the functions still unknown to date, clinical implications of the inhibition of SGLT2 could represent the prelude for a wider modulation of these cotransporters. A better understanding of the role and function of SGLTs could represent a revolution in the therapeutic approach in the hepatological, metabolic, neurological and oncological fields. The purpose of this review is to illustrate the knowledge currently available on SGLTs, its clinical implications and future perspectives.

Type 2 Diabetes Mellitus (T2DM) is associated with an elevated incidence of cardiovascular and renal diseases, responsible for mortality rates significantly higher than in the general population. The management of both cardiovascular risk and progression of kidney disease thus seem crucial in the treatment of the diabetic patient. The availability of new classes of drugs which positively affect both cardiovascular and renal risk, regardless of the glycemic control, represents a revolution in the treatment of T2DM and shifts the attention from the intensive glycemic control to a holistic management of the diabetic patient. Among these, sodium-glucose cotransporter-2 inhibitors (SGLT2i) have been associated with a remarkable reduction of cardiovascular and renal mortality, lower hospitalization rates for heart failure and lower progression of renal damage and albuminuria. Thus, their use in selected subpopulations seems mandatory. Aim of this review was the assessment of the current evidence on SGLT2i and their related impact on the cardiovascular and renal profiles.

Background. Evidence has shown a close association between COVID-19 infection and renal complications in both individuals with previously normal renal function and those with chronic kidney disease (CKD). Methods. The aim of this study is to evaluate the in-hospital mortality of SARS-CoV-2 patients according to their clinical history of CKD or estimated glomerular filtration rate (eGFR). This is a prospective multicenter observational cohort study which involved adult patients (≥18 years old) who tested positive with SARS-CoV-2 infection and completed their hospitalization in the period between November 2020 and June 2021. Results. 1246 patients were included in the study, with a mean age of 64 years (SD 14.6) and a median duration of hospitalization of 15 days (IQR 9–22 days). Cox’s multivariable regression model revealed that mortality risk was strongly associated with the stage of renal impairment and the Kaplan–Meier survival analysis showed a progressive and statistically significant difference (p < 0.0001) in mortality according to the stage of CKD. Conclusion. This study further validates the association between CKD stage at admission and mortality in patients hospitalized for COVID-19. The risk stratification based on eGFR allows clinicians to identify the subjects with the highest risk of intra-hospital mortality despite the duration of hospitalization.

This study evaluates the effectiveness of a novel cultural policy to recover the valorization function of Italian state museums by increasing managerial autonomy. The policy is part of the Franceschini reform, introduced in 2014, that concerns the governance of cultural institutions and was justified by the severe budget constraints resulting from economic crisis and a spending review. Given the staggered implementation of the reform across 32 museums that obtained special autonomy, we apply a difference-in-differences strategy that allows to properly investigate the causal effect of the policy reform on museums' outcome measures of exhibition function, as visitors and revenue from admissions. Our findings robustly support the effectiveness of the cultural policy reform in terms these outcomes. Although we provide some suggestive evidence of the efficacy of museums' management (through a number of communication and supplementary services), this study suffers of the limitations due to the lack of more appropriate measures on how successful changes in management have been. However, results aim to offer policy recommendations in favor of greater managerial and financial autonomy of state museums that, while preserving their conservation function, can promote the widespread utilization of collections ensuring museums' greater sustainability.

Cardiac hypertrophy develops in response to increased workload to reduce ventricular wall stress and maintain function and efficiency. Pathological hypertrophy can be adaptive at the beginning. However, if the stimulus persists, it may progress to ventricular chamber dilatation, contractile dysfunction, and heart failure, resulting in poorer outcome and increased social burden. The main pathophysiological mechanisms of pathological hypertrophy are cell death, fibrosis, mitochondrial dysfunction, dysregulation of Ca 2 + -handling proteins, metabolic changes, fetal gene expression reactivation, impaired protein and mitochondrial quality control, altered sarcomere structure, and inadequate angiogenesis. Diabetic cardiomyopathy is a condition in which cardiac pathological hypertrophy mainly develop due to insulin resistance and subsequent hyperglycaemia, associated with altered fatty acid metabolism, altered calcium homeostasis and inflammation. In this review, we summarize the underlying molecular mechanisms of pathological hypertrophy development and progression, which can be applied in the development of future novel therapeutic strategies in both reversal and prevention.