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Prurigo nodularis (PN) is a chronic dermatological condition characterized by intensely pruritic nodules resulting from repeated scratching. Its pathogenesis involves neuroimmune dysregulation, inflammatory cytokines, and neural proliferation. Conventional treatments often provide limited relief, necessitating novel therapeutic approaches. This narrative review explores emerging biologics and small molecules for PN treatment, assessing their mechanisms, efficacy, and safety. A comprehensive literature search was conducted using PubMed, Google Scholar, and Web of Science for relevant studies up to February 2025. Additionally, ongoing clinical trials were identified through a verified international website. The search terms included “prurigo nodularis”, “biologic treatments”, “monoclonal antibodies”, “small molecules”, and “JAK inhibitors”. Among new treatment options, dupilumab, an IL-4 receptor antagonist, and nemolizumab, an IL-31 receptor inhibitor, demonstrated significant efficacy in reducing pruritus and lesion severity in PN patients. Other promising monoclonal antibodies include vixarelimab (OSMRβ inhibitor) and barzolvolimab (KIT inhibitor). Small molecules such as JAK inhibitors (upadacitinib, povorcitinib) also show potential by modulating inflammatory pathways. Clinical trials highlight their efficacy, safety, and long-term benefits. Emerging biologics and small molecules represent a transformative approach for PN management, offering targeted therapies that address underlying immunological and neurological mechanisms. Ongoing research and long-term studies are crucial to optimizing treatment strategies and improving patient outcomes.

Introduction There are no strong data regarding the treatment with biologics (especially for the most recent anti-IL-17 and anti-IL-23 drugs) of patients with psoriasis and concomitant viral hepatitis. We assessed the safety of biologic drugs in patients with psoriasis who are seropositive for hepatitis B or C and did not receive antiviral prophylaxis. Methods We conducted a retrospective single-center study. The efficacy of biologic treatments was evaluated by assessing the Psoriasis Area and Severity Index (PASI) score during all visits, for a minimum follow-up of 52 weeks. All patients were evaluated by a hepatologist before starting the treatment. They were monitored for reactivation of viral hepatitis. Results Twenty patients had positive markers of hepatitis B virus (HBV) or hepatitis C virus (HCV). Seventeen patients had positive markers of HBV infection, and four patients had antibodies for HCV (one patient had serologic evidence of both infections). Anti-IL-23 biologics were the most used in our population, with risankizumab being the most prescribed drug. No patient had evidence of viral reactivation during our study. Study limitations include its retrospective nature and our inclusion of patients with different serological status receiving different biologic drugs. Conclusion Biologic therapies (including anti-IL-23 drugs) appear to be safe in patients seropositive for HCV or HBV core antibody who did not receive antiviral prophylaxis.

Introduction Risankizumab is a humanized monoclonal antibody that selectively targets interleukin-23. It is approved for treatment of moderate-to-severe plaque psoriasis. We conducted a 52-week monocentric retrospective study to evaluate the effectiveness and safety of risankizumab in a real-life setting. Methods Our study included 131 adults with moderate-to-severe plaque psoriasis all treated with risankizumab for at least 52 weeks. Patient characteristics and PASI (Psoriasis Area and Severity Index) at each visit were recorded. The percentages of patients achieving 75%/90%/100% (PASI 75/90/100) improvement in PASI with respect to baseline were registered. Results At week 52, 93.9%, 78.6%, and 61.1% of patients achieved PASI 75/90/100, respectively. An absolute PASI ≤ 2 was reached by 90.8% at week 52. The higher body mass index and the presence of cardio-metabolic comorbidities did not interfere with the odds of reaching PASI 75/90/100 at each time-point. At week 52, comparable percentages of patients achieved PASI 100, regardless of the involvement of difficult-to-treat-areas. No significant safety findings were recorded and none of the patients had to interrupt the treatment because of adverse events. Conclusions Our findings confirmed that risankizumab is a safe and effective therapeutic option for the treatment of a wide “real-life” cohort of patients with psoriasis.

In recent years, the frequency of extreme events such as floods, droughts, and heat waves has been increasing due to climate change. To mitigate and reduce the devastating effects of these phenomena, finding a common solution that directly involves citizens in the energy transition process is crucial. In this context, the European Union, through the Green Deal, has set the ambitious goal of achieving carbon neutrality by 2050, and, through the REPowerEU plan, covering at least 42.5% of total energy consumption with renewable energy sources by 2030. The renewable energy communities, introduced by the EU Directive 2018/2001, represent a key tool for achieving these European targets. Renewable energy communities are based on a bottom-up business model as they directly engage citizens and facilitate the expansion of renewable energy generation. Moreover, in several countries, including Italy, economic support schemes have been introduced to incentivize the development of these energy-sharing configurations. This paper analyzes a specific fair revenue distribution model among community members, taking the renewable energy community in Benevento (Southern Italy) province as a case study. The analysis highlights how variations in user types and energy consumption impact individual contributions. This underscores the need for an economic distribution model with a dynamic and flexible structure, allowing adaptation to different configurations. Therefore, the used algorithm should incorporate specific parameters that account for the different operating conditions, such as the presence of third-party producers, prosumers, and high-energy consumers, as well as solidarity-based objectives, such as addressing energy poverty. All these factors are crucial, as the implementation of an inaccurate economic distribution model could favor some users at the expense of others and, at the same time, promote environmentally and energetically unsustainable behaviors.

Energy communities (ECs), intended as collective action initiatives in the energy field involving citizens’ participation, have been gaining relevance for the past decades as an alternative way to organize the energy chain to challenge the incumbent system. With Europe’s recently adopted Clean Energy Package, ECs found a formal recognition by the European Union as potential actors of the transition of the energy system towards a wider and more decentralized use of renewable sources. Although the potential role of ECs in the transition is therefore hardly questionable, a thorough comprehension of the enabling factors that might foster their diffusion and scaling up is still lacking. Through a comparative analysis of the evolutionary trajectories in six EU countries regarding their energy systems, their regulatory frameworks and their historical evolution of ECs, namely through the example of cooperative models, this paper aims at providing some preliminary evidence about the factors and dynamics that seem to have played, and may play, a role in hampering or facilitating EC model diffusion. Attention is therefore specifically paid to three dimensions of analysis referring to: the energy mix and market structure; the institutional and policy landscape; the wider social attitudes towards environmental issues and cooperation among citizens. In addition to providing a wide comparison of different EU countries, the paper shows that the historical evolution pathways have to be carefully taken into account to understand what might trigger ECs exploitation in the EU.

Obesity disease results from a dysfunctional modulation of the energy balance whose master regulator is the central nervous system. The neural circuitries involved in such function complete their maturation during early postnatal periods, when the brain is highly plastic and profoundly influenced by the environment. This phenomenon is considered as an evolutionary strategy, whereby metabolic functions are adjusted to environmental cues, such as food availability and maternal care. In this timeframe, adverse stimuli may program the body metabolism to maximize energy storage abilities to cope with hostile conditions. Consistently, the prevalence of obesity is higher among individuals who experienced early life stress (ELS). Oxytocin, a hypothalamic neurohormone, regulates the energy balance and modulates social, emotional, and eating behaviors, exerting both central and peripheral actions. Oxytocin closely cooperates with leptin in regulating energy homeostasis. Both oxytocin and leptin impact the neurodevelopment during critical periods and are affected by ELS and obesity. In this review article, we report evidence from the literature describing the effect of postnatal ELS (specifically, disorganized/inconstant maternal care) on the vulnerability to obesity with a focus on the role of oxytocin. We emphasize the existing research gaps and highlight promising directions worthy of exploration. Based on the available data, alterations in the oxytocin system may in part mediate the ELS-induced susceptibility to obesity.

Background Despite the overall major impact of long-lasting insecticide treated nets (LLINs) in eliciting individual and collective protection to malaria infections, some sub-Saharan countries, including Burkina Faso, still carry a disproportionately high share of the global malaria burden. This study aims to analyse the possible entomological bases of LLIN limited impact, focusing on a LLIN-protected village in the Plateau Central region of Burkina Faso. Methods Human landing catches (HLCs) were carried out in 2015 for 12 nights both indoors and outdoors at different time windows during the highest biting activity phase for Anopheles gambiae ( s.l. ). Collected specimens were morphologically and molecularly identified and processed for Plasmodium detection and L1014F insecticide-resistance allele genotyping. Results Almost 2000 unfed An. gambiae ( s.l. ) (54% Anopheles coluzzii and 44% Anopheles arabiensis ) females landing on human volunteers were collected, corresponding to a median number of 23.5 females/person/hour. No significant differences were observed in median numbers of mosquitoes collected indoors and outdoors, nor between sporozoite rates in An. coluzzii (6.1%) and An. arabiensis (5.5%). The estimated median hourly entomological inoculation rate (EIR) on volunteers was 1.4 infective bites/person/hour. Results do not show evidence of the biting peak during night hours typical for An. gambiae ( s.l. ) in the absence of bednet protection. The frequency of the L1014F resistant allele ( n  = 285) was 66% in An. coluzzii and 38% in An. arabiensis . Conclusions The observed biting rate and sporozoite rates are in line with the literature data available for An. gambiae ( s.l. ) in the same geographical area before LLIN implementation and highlight high levels of malaria transmission in the study village. Homogeneous biting rate throughout the night and lack of preference for indoor-biting activity, suggest the capacity of both An. coluzzii and An. arabiensis to adjust their host-seeking behaviour to bite humans despite bednet protection, accounting for the maintenance of high rates of mosquito infectivity and malaria transmission. These results, despite being limited to a local situation in Burkina Faso, represent a paradigmatic example of how high densities and behavioural plasticity in the vector populations may contribute to explaining the limited impact of LLINs on malaria transmission in holo-endemic Sudanese savannah areas in West Africa.

Adipose tissue fibrosis is associated with metabolic alterations in patients with obesity and involves three major collagen types: fibrillar collagens I and III and non-fibrillar collagen VI. In this study, fibrosis was found to be significantly increased only in visceral adipose tissue in patients with obesity (4.7% vs. 2.5% in controls, p  < 0.001), whereas no significant difference was observed in subcutaneous adipose tissue. Transmission electron microscopy and high-resolution scanning electron microscopy suggested that hypertrophic adipocytes may contribute to the production of fibrillar collagens I and III. In vitro data were consistent with this interpretation. Expression of the COL6 gene, which encodes the non-fibrillar collagen VI, was reduced in adipose tissue from obese patients. Notably, patients carrying mutations in COL6 genes displayed increased fibrosis even in subcutaneous fat, approximately 6.5-fold higher than controls in the patient with the severe form (Ullrich) and 2.8-fold higher in two patients with the milder form (Bethlem). Approximately 15% of adipocytes in obese tissue appeared stressed or dead (perilipin-1 negative), and the associated infiltrating macrophages exhibited increased expression of CD38, an ectoenzyme implicated in systemic fibrosis. Correlations with gene expression also indicated the importance of myofibroblasts and the extracellular-matrix peptidase D. Taken together, our data suggest that obese adipocytes may contribute to fibrillar collagen production and identify collagen VI and CD38 as potential molecular contributors, consistent with the concept that adipose tissue fibrosis in humans has a multifactorial origin.

Subcutaneous adipocytes are crucial for mammary gland epithelial development during pregnancy. Our and others’ previous data have suggested that adipo-epithelial transdifferentiation could play a key role in the mammary gland alveolar development. In this study, we tested whether adipo-epithelial transdifferentiation occurs in vitro. Data show that, under appropriate co-culture conditions with mammary epithelial organoids (MEOs), mature adipocytes lose their phenotype and acquire an epithelial one. Interestingly, even in the absence of MEOs, extracellular matrix and diffusible growth factors are able to promote adipo-epithelial transdifferentiation. Gene and protein expression studies indicate that transdifferentiating adipocytes exhibit some characteristics of milk-secreting alveolar glands, including significantly higher expression of milk proteins such as whey acidic protein and β-casein. Similar data were also obtained in cultured human multipotent adipose-derived stem cell adipocytes. A miRNA sequencing experiment on the supernatant highlighted mir200c, which has a well-established role in the mesenchymal–epithelial transition, as a potential player in this phenomenon. Collectively, our data show that adipo-epithelial transdifferentiation can be reproduced in in vitro models where this phenomenon can be investigated at the molecular level.