University of Siena

Recent studies have reported that severe cases of COVID-19 are primarily characterized by endotheliitis (or endothelialitis), whose severity is related to the pre-existing or current damage to the complex structure that lines the surface of the vascular endothelium, most notably the glycocalyx. Such damage results in the loss of many endothelial cell functions. To restore these functions, the cell must repair the glycocalyx that covers it. However, this is not always possible, especially when the repair capacity of such an exo-endo-cytoplasmic cell structure is limited due to cellular senescence. If the gene repair system remains activated, the damaged glycocalyx can be reconstituted via specific transcriptional pathways in response to oxidative and reductive stresses. Despite the experimental evidence in favour of this hypothesis, many of the recently published reviews on long COVID do not mention the use of therapeutic treatments via specific 'oxidative eustress'. In fact, mild and controlled oxidative stress is able to induce an activating response to cellular damage repair processes. This perspective aims to draw the attention of researchers to these aspects in an attempt to address this gap in understanding.

Direct immunofluorescence (DIF) is the gold standard for diagnosing subepidermal blistering diseases (SBDs). However, DIF requires specialized expertise; therefore, alternative immunological methods such as enzyme-linked immunosorbent assays (ELISA) are worth exploring. The aim of this review was to evaluate the diagnostic agreement between DIF and ELISA for the diagnosis of SBD. A systematic literature review of international journals and electronic databases (MEDLINE via OVID, Scopus, and Web of Science) was conducted between their inception and December 2023. The risk of bias and overall quality of evidence were assessed using the Newcastle-Ottawa Scale and the GRADE system. Of the 1691 articles identified, 38 were included in the qualitative synthesis and 37 in the quantitative analysis. Three meta-analyses were developed and revealed the superiority of DIF over ELISA, with the following risk differences: BP180, 0.26 (95% CI: 0.19-0.33, p < 0.00001, I 2 : 96%); BP230, 0.59 (95% CI: 0.47-0.71, p < 0.00001, I 2 : 98%); and Lam332, 0.82 (95% CI: 0.70-0.94, p < 0.00001, I 2 : 89%). DIF remains the gold standard for the diagnosis of autoimmune SBDs. ELISA can serve as a complementary diagnostic tool, especially as a follow-up instrument for patients with SBD, owing to its low invasiveness.

Implantable cardioverter-defibrillators (ICDs) are the cornerstone of sudden cardiac death prevention in cardiomyopathies, but disease-specific structural and electrophysiological substrates profoundly affect device performance and outcomes. Understanding these distinctions is critical for tailoring therapy and improving patient safety. This review examines current evidence and practical experience regarding ICD implantation, programming, and management in hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), and cardiac amyloidosis (CA). We performed a structured narrative synthesis to identify phenotype-specific technical challenges, programming strategies, and complication trends. For HCM, lead placement and programming to minimize inappropriate therapies are emphasized; for ARVC, issues of lead instability, oversensing, and ATP efficacy are explored; and for CA, defibrillation thresholds, sensing difficulties, and individualized indications are discussed. ICD therapy in cardiomyopathies must be individualized, balancing arrhythmic protection against disease-specific risks and device-related complications. Tailored programming, careful system selection, and remote monitoring are key to improving outcomes. Emerging technologies such as modular and extravascular ICD systems promise safer and more phenotype-driven care.

Abstract Myrmeleontini is a widespread antlion tribe within the lacewing family Myrmeleontidae, well known for its larvae building cone‐shaped pits in sandy soil to trap prey. The monophyly of the tribe is well supported, but the monophyly of many genera within the tribe as well as the definition of the genus Myrmeleon Linnaeus has long been questioned. Here, we present a phylogenomic analysis of Myrmeleontini with emphasis on the Eurasian fauna, using ultraconserved elements (UCE) data. Our results recovered Myrmeleon as a diverse grade, with Baliga Navás, Callistoleon Banks, Euroleon Esben‐Petersen, Hagenomyia Banks and Megistoleon Navás deeply nested within it. Based on our sampling of type species of many genera (including those synonymized with Myrmeleon ) and detailed morphological comparisons, we provide a new phylogeny‐based classification of Myrmeleontini. Accordingly, Myrmeleon s. str . only refers to the formerly recognized M. formicarius group from Palaearctic region. The status of 12 genera that were previously considered as junior synonyms of Myrmeleon is restored (i.e., Banyaleon Zheng &amp; Liu nom. n ., Bordus Navás stat. rev ., Callistoleon Banks stat. rev ., Cocius Navás stat. rev ., Enza Navás stat. rev ., Macroleon Banks stat. rev ., Moreyus Navás stat. rev ., Morter Navás stat. rev ., Neleon Navás stat. rev ., Neseurus Navás stat. rev ., Myrmeleodes Navás stat. rev . and Tafanerus Navás stat rev .), while Neohornius stat. rev ., previously treated as a subgenus of Myrmeleon, is herein elevated to genus. Additionally, based on comprehensive sampling from the Oriental region, five new genera from this region are described, that is, Ancyroleon Zheng &amp; Liu gen. n ., Baligaptes Zheng &amp; Liu gen. n . Melanobaliga Zheng &amp; Liu gen. n ., Orientaleon Zheng &amp; Liu gen. n . and Sinobaliga Zheng &amp; Liu gen. n .

Post-COVID19 pulmonary fibrosis (PCPF) has been reported in a significant proportion of patients who survive the acute SARS-CoV-2 infection. Krebs von den Lungen-6 (KL-6) emerges as a marker of disease severity and progression in COVID-19-related lung involvement. A total of 231 patients (median age (interquartile range, IQR), 65[57-74] years; 143 males) were enrolled in the study. Thirty-four had IPF, 56 sarcoidosis, 141 had been hospitalized for COVID-19. After hospital discharge (median (IQR), 7(5-17) months), a diagnosis of PCPF was made in 65/141 patients and 76/141 did not show fibrotic abnormalities. Serum KL-6 concentrations were measured by KL-6 reagent assay (AIA-CL300, Tosoh Biosciences). Most PC-nonPF patients (n=70, 92%) did not require invasive mechanical ventilation (IMV) during hospital stay, while 27 (41.5%) of PCPF patients did. KL-6 concentrations were strongly suggestive of lung fibrosis with a cutoff value of 467.8 U/mL (sensitivity 73% and specificity 66%). Model obtained though machine learning approach combined lung parameters and KL-6 values for clustering fibrotic and non-fibrotic patients with an acceptable accuracy. KL-6>765 U/mL and FVC%≤88 cluster for 67% of IPF patients, while KL-6 values ≤765U/mL and FVC >60% for 81% of PCPF patients. KL-6 levels are not significantly elevated in patients undergoing IMV, indicating that IMV per se does not alter the values of this biomarker, thereby further supporting its reliability in detecting PCPF. Our study proposed a combination of KL-6 values and clinical data may lead to a further improvement in diagnostic accuracy for pulmonary fibrosis, idiopathic and secondary to COVID19.

Background: Piperine, an alkaloid from Piper nigrum, modulates oxidative stress, proliferation, and survival pathways in several cancer models; however, its mechanistic effects in colorectal epithelial Caco-2 cells remain insufficiently defined. Objective: This study aimed to investigate the cytotoxic, antiproliferative, oxidative, autophagic, and anti-migratory effects of piperine in Caco-2 cells. Methods: Caco-2 cells were treated with piperine (0.001-0.1 mg/mL) for up to 72 h. Cell viability, proliferation, and migration were assessed using SRB and scratch assays. Oxidative stress, apoptosis, autophagy, and tight junction integrity were evaluated through ROS quantification, Western blotting, gene expression analysis, confocal microscopy, and transmission electron microscopy (TEM). NACET was used to determine the contribution of oxidative stress to piperine-induced cytotoxicity and autophagy. Results: Piperine induced a time- and dose-dependent reduction in viability, with viability decreasing to 53.0 ± 2.88% at 0.1 mg/mL after 72 h. Proliferation decreased to 51% of control levels (p < 0.001), accompanied by p21 upregulation (p < 0.05), indicating G2/M cell cycle arrest. Piperine markedly increased intracellular ROS (p < 0.001), downregulated NRF2 (p < 0.05), and suppressed GSTA1 expression (p < 0.001), while NACET co-treatment restored viability (p < 0.001). No activation of caspase-dependent apoptosis was observed. Piperine significantly enhanced autophagic flux, as shown by the increased LC3B-II/LC3B-I ratio (p < 0.01), elevated LC3B-II/LAMP-1 co-localization (p < 0.01), and chloroquine-induced accumulation of LC3B-II and p62 (p < 0.01), with preserved lysosomal function. TEM analysis confirmed a marked increase in double-membrane autophagosomes in piperine-treated cells compared with controls. NACET reduced LC3B-II/LC3B-I levels, increased p21 expression, and significantly improved cell viability, indicating that piperine-induced autophagy is cytotoxic and driven by oxidative stress. Additionally, piperine upregulated occludin (p < 0.01) and reduced cell migration independently of proliferation (p < 0.01). Conclusions: Piperine exerts antiproliferative effects in Caco-2 cells through ROS-mediated stress, p21-dependent G2/M arrest, and activation of cytotoxic autophagy. Its ability to impair migration and enhance tight junction integrity further supports its potential as a complementary therapeutic agent in colon cancer.

Background/Objectives: Breastfeeding represents a critical developmental window during which maternal biology, environmental exposures, and nutrition converge to influence infant gastrointestinal health and long-term developmental trajectories. From a One Health perspective, breastfeeding can be conceptualized not as a static nutritional act, but as a dynamic and modifiable biological system in which maternal factors shape early-life microbiota assembly and immune programming. This narrative review explores how microbiota-oriented strategies during breastfeeding may foster a favorable trajectory of infant health, potentially extending to transgenerational outcomes. Methods: This narrative review is structured around a ten-point decalogue addressing interconnected domains relevant to the maternal-milk-infant microbiota axis, including maternal diet, microbial diversity, environmental exposures, psychological stress and probiotic use. Current mechanistic and clinical evidence was examined to evaluate how these domains may modulate microbiota composition and function during breastfeeding. Attention was given to probiotic supplementation, including strain specificity, timing of administration, and clinical context, as well as to the broader implications of a One Health framework. Results: Available evidence suggests that maternal nutritional patterns, environmental and psychosocial exposures, and targeted microbiota-modulation strategies may influence the composition and functional properties of human milk and the developing infant microbiota. Probiotic use during breastfeeding appears to have strain-specific and context-dependent effects, with potential benefits in selected clinical scenarios. However, findings remain heterogeneous, and uncertainties persist regarding optimal strains, timing, and long-term outcomes. Conclusions: Breastfeeding can be understood as a dynamic biological interface shaped by maternal and environmental factors. Integrating microbiota-oriented strategies within a One Health framework may support infant gastrointestinal health and possibly contribute to longer-term developmental trajectories. Nevertheless, careful interpretation of the current evidence is warranted to avoid reductionist, supplement-centered approaches and to prevent maternal overmedicalization or blame.

This study aims to enrich the existing literature on prison officers by examining how various work-related variables influence their readiness to use force—an area that remains relatively underexplored. Specifically, it focuses on officers’ institutional delegitimization, their perception of insecurity at work, their professional orientation, the quality of their relationships with prisoners, and some indicators of what they feel during their work, namely perceived satisfaction, self-efficacy, and emotions. The study was conducted in Italy and involved 684 male and 130 female prison officers, who completed a questionnaire made up of 46 questions, grouped into seven dimensions. A Structural Equation Model (SEM) was employed to evaluate the robustness of a model describing the relationships among the seven dimensions in light of the collected data. The model tested was built on seven exogenous variables and six endogenous variables, with a total of 24 estimated parameters. Among the variables analyzed, institutional delegitimization was found to have the largest total effect—both directly and indirectly—on prison officers’ readiness to use force. This finding suggests that while interventions aimed at shaping officers’ attitudes toward the use of force should consider all the dimensions examined, particular emphasis should be placed on fostering an institutional environment that strengthens legitimacy.