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Nearly Zero Energy Buildings (nZEB) are a significant part of the energy efficiency strategy of the European Union. As buildings represent approximately 40% of the final energy use in Europe, the reduction of their energy demand is key for a sustainable future. This paper takes a qualitative approach and presents data about professional and market barriers, as well as the educational market in relation to the implementation of nZEB policies for new and retrofit buildings in 11 European countries. Different levels of policy enactments and market penetration are reported and are generally found to be more advanced in western and central European countries. Furthermore, gender equality is examined in the building sector in relation to nZEB and presents significant gaps, with a more balanced situation reported in southern Europe. The accreditation and targeted education of nZEB experts is still almost non-existent in the examined countries, and the need for training of building professionals is highlighted as a critical missing component of current policy. This research aims to be the first step towards the creation of educational material and programmes as a mean to accelerate the transition to nZEB.

This study aims to analyze post-mortem human cardiac specimens, to verify and evaluate the existence or extent of oxidative stress in subjects whose cause of death has been traced to sepsis, through immunohistological oxidative/nitrosative stress markers. Indeed, in the present study, i-NOS, NOX2, and nitrotyrosine markers were higher expressed in the septic death group when compared to the control group, associated with also a significant increase in 8-OHdG, highlighting the pivotal role of oxidative stress in septic etiopathogenesis. In particular, 70% of cardiomyocyte nuclei from septic death specimens showed positivity for 8-OHdG. Furthermore, intense and massive NOX2-positive myocyte immunoreaction was noticed in the septic group, as nitrotyrosine immunostaining intense reaction was found in the cardiac cells. These results demonstrated a correlation between oxidative and nitrosative stress imbalance and the pathophysiology of cardiac dysfunction documented in cases of sepsis. Therefore, subsequent studies will focus on the expression of oxidative stress markers in other organs and tissues, as well as on the involvement of the intracellular pattern of apoptosis, to better clarify the complex pathogenesis of multi-organ failure, leading to support the rationale for including therapies targeting redox abnormalities in the management of septic patients.

Phosphoinositides (PI) form just a minor portion of the total phospholipid content in cells but are significantly involved in cancer development and progression. In several cancer types, phosphatidylinositol 3,4,5-trisphosphate [PtdIns(3,4,5)P3] and phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] play significant roles in regulating survival, proliferation, invasion, and growth of cancer cells. Phosphoinositide-specific phospholipase C (PLC) catalyze the generation of the essential second messengers diacylglycerol (DAG) and inositol 1,4,5 trisphosphate (InsP3) by hydrolyzing PtdIns(4,5)P2. DAG and InsP3 regulate Protein Kinase C (PKC) activation and the release of calcium ions (Ca2+) into the cytosol, respectively. This event leads to the control of several important biological processes implicated in cancer. PLCs have been extensively studied in cancer but their regulatory roles in the oncogenic process are not fully understood. This review aims to provide up-to-date knowledge on the involvement of PLCs in cancer. We focus specifically on PLCβ, PLCγ, PLCδ, and PLCε isoforms due to the numerous evidence of their involvement in various cancer types.

Phospholipase C (PLC) enzymes represent crucial participants in the plasma membrane of mammalian cells, including the cardiac sarcolemmal (SL) membrane of cardiomyocytes. They are responsible for the hydrolysis of phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) into 1,2-diacylglycerol (DAG) and inositol (1,4,5) trisphosphate (Ins(1,4,5)P3), both essential lipid mediators. These second messengers regulate the intracellular calcium (Ca2+) concentration, which activates signal transduction cascades involved in the regulation of cardiomyocyte activity. Of note, emerging evidence suggests that changes in cardiomyocytes’ phospholipid profiles are associated with an increased occurrence of cardiovascular diseases, but the underlying mechanisms are still poorly understood. This review aims to provide a comprehensive overview of the significant impact of PLC on the cardiovascular system, encompassing both physiological and pathological conditions. Specifically, it focuses on the relevance of PLCβ isoforms as potential cardiac biomarkers, due to their implications for pathological disorders, such as cardiac hypertrophy, diabetic cardiomyopathy, and myocardial ischemia/reperfusion injury. Gaining a deeper understanding of the mechanisms underlying PLCβ activation and regulation is crucial for unraveling the complex signaling networks involved in healthy and diseased myocardium. Ultimately, this knowledge holds significant promise for advancing the development of potential therapeutic strategies that can effectively target and address cardiac disorders by focusing on the PLCβ subfamily.

Lamin B1 is an essential protein of the nuclear lamina that plays a crucial role in nuclear function and organization. It has been demonstrated that lamin B1 is essential for organogenesis and particularly brain development. The important role of lamin B1 in physiological brain development and aging has only recently been at the epicenter of attention and is yet to be fully elucidated. Regarding the development of brain, glial cells that have long been considered as supporting cells to neurons have overturned this representation and current findings have displayed their active roles in neurogenesis and cerebral development. Although lamin B1 has increased levels during the differentiation of the brain cells, during aging these levels drop leading to senescent phenotypes and inciting neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease. On the other hand, overexpression of lamin B1 leads to the adult-onset neurodegenerative disease known as Autosomal Dominant Leukodystrophy. This review aims at highlighting the importance of balancing lamin B1 levels in glial cells and neurons from brain development to aging.

The role of metacognition in gambling disorder (GD) is underexplored. To date, only two studies have investigated the role of metacognitive functioning, but among the adolescent population. The first aim of the current research was to assess and compare adult male gamblers with healthy controls (HCs) in relation to metacognition, impulsivity and emotional dysregulation. The second aim was to identify the variables among metacognition, impulsivity and emotional dysregulation associated with the severity of GD by means of linear regression. A total of 116 adult males (58 with GD and 58 HCs) completed self-report questionnaires on gambling severity, metacognition, emotional dysregulation and impulsivity. A linear regression analysis was run to assess the variables associated with gambling severity. Patients with GD exhibited more impaired scores than HCs in all the psychopathological dimensions investigated. More interestingly, gambling severity was significantly associated with metacognitive differentiation/decentration, difficulty in controlling impulses and non-acceptance of negative emotions. According to our results, the severity of gambling is associated with impaired metacognitive differentiation, high difficulty in controlling impulses and non-acceptance of negative emotions, and these findings can lead to new treatment implications. Interventions focused on metacognition and emotion regulation could help patients with GD to avoid maladaptive strategies such as behavioural addictions and, more specifically, to manage their own emotions. This type of treatment could help gamblers to become more aware of their internal state and learn strategies for adaptively managing emotions through functional metacognitive differentiation.

Electrochemiluminescence (ECL) biosensing offers high sensitivity and low background but remains limited by the lack of simple strategies for electrode patterning, signal confinement, and multiplexed detection. Here, we report a silica nanoparticle–based coating and photopatterning approach for gold electrodes that enables spatially resolved and multiplexed ECL detection. The resulting electrode architecture confines aqueous droplets to designated locations and supports localized ECL signal generation. Compared with bare gold electrodes, the modified surfaces exhibit up to a ten‐fold increase in ECL intensity, which correlates with reduced charge‐transfer resistance and improved electron‐transfer kinetics. The patterned electrodes are compatible with magnetic bead–based immunoassays and allow parallel ECL measurements from multiple spatially separated regions on a single chip. Multiplexed detection is demonstrated using the synthetic SARS‐CoV‐2 spike protein as a model analyte. This coating and patterning strategy provides a straightforward route to spatially resolved ECL electrodes and can be applied to multiplexed electrochemical and bioanalytical measurements where signal confinement and multiplexing are required. The use of a simple silica nanoparticle surface coating and patterning process can transform ordinary gold electrodes into multiplexed ECL sensing electrodes. Through spatially confined droplet formation and local ECL emission, it is possible to perform multiple analyses simultaneously from individual locations as well as intensify the ECL signal by as much as ten times.

Pericytes are multipotent cells embedded within the vascular system, primarily surrounding capillaries and microvessels where they closely interact with endothelial cells. These cells are known for their intriguing properties due to their heterogeneity in tissue distribution, origin, and multifunctional capabilities. Specifically, pericytes are essential in regulating blood flow, promoting angiogenesis, and supporting tissue homeostasis and regeneration. These multifaceted roles draw on pericytes’ remarkable ability to respond to biochemical cues, interact with neighboring cells, and adapt to changing environmental conditions. This review aims to summarize existing knowledge on pericytes, emphasizing their versatility and involvement in vascular integrity and tissue health. In particular, a comprehensive view of the major signaling pathways, such as PDGFβ/ PDGFRβ, TGF-β, FOXO and VEGF, along with their downstream targets, which coordinate the behavior of pericytes in preserving vascular integrity and promoting tissue regeneration, will be discussed. In this light, a deeper understanding of the complex signaling networks defining the phenotype of pericytes in healthy tissues is crucial for the development of targeted therapies in vascular and degenerative diseases.

Polyphosphoinositides (PPIns) are signalling messengers representing less than five per cent of the total phospholipid concentration within the cell. Despite their low concentration, these lipids are critical regulators of various cellular processes, including cell cycle, differentiation, gene transcription, apoptosis and motility. PPIns are generated by the phosphorylation of the inositol head group of phosphatidylinositol (PtdIns). Different pools of PPIns are found at distinct subcellular compartments, which are regulated by an array of kinases, phosphatases and phospholipases. Six of the seven PPIns species have been found in the nucleus, including the nuclear envelope, the nucleoplasm and the nucleolus. The identification and characterisation of PPIns interactor and effector proteins in the nucleus have led to increasing interest in the role of PPIns in nuclear signalling. However, the regulation and functions of PPIns in the nucleus are complex and are still being elucidated. This review summarises our current understanding of the localisation, biogenesis and physiological functions of the different PPIns species in the nucleus.

Among healthy participants, the interindividual variability of brain response to facial emotions is associated with genetic variation, including common risk variants for schizophrenia, a heritable brain disorder characterized by anomalies in emotion processing. We aimed to identify genetic variants associated with heritable brain activity during processing of facial emotions among healthy participants and to explore the impact of these identified variants among patients with schizophrenia. We conducted a data-driven stepwise study including samples of healthy twins, unrelated healthy participants and patients with schizophrenia. Participants approached or avoided pictures of faces with negative emotional valence during functional magnetic resonance imaging (fMRI). We investigated 3 samples of healthy participants — including 28 healthy twin pairs, 289 unrelated healthy participants (genome-wide association study [GWAS] discovery sample) and 90 unrelated healthy participants (replication sample) — and 1 sample of 48 patients with schizophrenia. Among healthy twins, we identified the amygdala as the brain region with the highest heritability during processing of angry faces (heritability estimate 0.54, p < 0.001). Subsequent GWAS in both discovery and replication samples of healthy non-twins indicated that amygdala activity was associated with a polymorphism in the miR-137 locus (rs1198575), a micro-RNA strongly involved in risk for schizophrenia. A significant effect in the same direction was found among patients with schizophrenia (p = 0.03). The limited sample size available for GWAS analyses may require further replication of results. Our data-driven approach shows preliminary evidence that amygdala activity, as evaluated with our task, is heritable. Our genetic associations preliminarily suggest a role for miR-137 in brain activity during explicit processing of facial emotions among healthy participants and patients with schizophrenia, pointing to the amygdala as a brain region whose activity is related to miR-137.