Explore the vast range of titles available.

Low-cost RGB-D cameras are increasingly being used in several research fields, including human–machine interaction, safety, robotics, biomedical engineering and even reverse engineering applications. Among the plethora of commercial devices, the Intel RealSense cameras have proven to be among the most suitable devices, providing a good compromise between cost, ease of use, compactness and precision. Released on the market in January 2018, the new Intel model RealSense D415 has a wide acquisition range (i.e., ~160–10,000 mm) and a narrow field of view to capture objects in rapid motion. Given the unexplored potential of this new device, especially when used as a 3D scanner, the present work aims to characterize and to provide metrological considerations for the RealSense D415. In particular, tests are carried out to assess the device performance in the near range (i.e., 100–1000 mm). Characterization is performed by integrating the guidelines of the existing standard (i.e., the German VDI/VDE 2634 Part 2) with a number of literature-based strategies. Performance analysis is finally compared against the latest close-range sensors, thus providing a useful guidance for researchers and practitioners aiming to use RGB-D cameras in reverse engineering applications.

In brain tumor surgery, an appropriate and careful surgical planning process is crucial for surgeons and can determine the success or failure of the surgery. A deep comprehension of spatial relationships between tumor borders and surrounding healthy tissues enables accurate surgical planning that leads to the identification of the optimal and patient-specific surgical strategy. A physical replica of the region of interest is a valuable aid for preoperative planning and simulation, allowing the physician to directly handle the patient’s anatomy and easily study the volumes involved in the surgery. In the literature, different anatomical models, produced with 3D technologies, are reported and several methodologies were proposed. Many of them share the idea that the employment of 3D printing technologies to produce anatomical models can be introduced into standard clinical practice since 3D printing is now considered to be a mature technology. Therefore, the main aim of the paper is to take into account the literature best practices and to describe the current workflow and methodology used to standardize the pre-operative virtual and physical simulation in neurosurgery. The main aim is also to introduce these practices and standards to neurosurgeons and clinical engineers interested in learning and implementing cost-effective in-house preoperative surgical planning processes. To assess the validity of the proposed scheme, four clinical cases of preoperative planning of brain cancer surgery are reported and discussed. Our preliminary results showed that the proposed methodology can be applied effectively in the neurosurgical clinical practice both in terms of affordability and in terms of simulation realism and efficacy.

Autophagy is a fundamental cellular pathway involved in the clearance of protein aggregates, and it is particularly important in neurons. The toxic aggregates derived from the mutated Huntingtin have been shown to interfere with the physiological autophagic flux, resulting in neuronal death. Glutamate Dehydrogenase (GDH) is an evolutionary conserved enzyme that catalyses the conversion of glutamate and ammonia to α-ketoglutarate and vice versa and is also member of the Glutamate-Glutamine Cycle (GGC), a physiological process between glia and neurons that controls glutamate homeostasis. Through a genetic screen using a Drosophila model for Huntington’s disease (HD), we identified that reduction of GDH ameliorates animal motility and decreases the size of mutated Huntingtin’s (mHTT) aggregates in brains. The aim of our project is to analyze how GDH downregulation induces autophagy in neurons. We modeled HD phenotype in Drosophila by expressing mHTT with 93-CAG repetition (HTTQ93) in neurons. To investigate the effect of GDH we used motility and viability assay, while western blots and immunofluorescence analysis were used to investigate changes in mHTT aggregates. We found the reduction of GDH inhibits the accumulation of p62/Ref(2)P, an autophagic adaptor that abnormally increases in mHTT-expressing neurons. Reduction of GDH also leads to a substantial decrease in essential aminoacids in heads of adult flies. In particular we focused on Leucine and Glutamine, two major activators of TOR pathway. Leucine binds to its sensor Sestrin, while Glutamine enters the cell through specific receptors including LAT1/SCLA7/Minidisc, a Glutamine/Leucine antiporter. We are currently exploiting whether these sensors modulate TOR activity in the mechanism through which GDH downregulation induces autophagy. The goal of our work is also to design pharmacological inhibitors of GDH to be tested in vivo in flies to ameliorate HD pathology in humans.

The use of nanocellulose in traditional lime-based mortars is a promising solution for green buildings in the frame of limiting the CO2 emissions resulting from Portland Cement production. The influence of the fibrillated cellulose (FC) on lime pastes and lime-based mortars was studied incorporating FC at dosages of 0%, 0.1%, 0.2% and 0.3 wt% by weight of binder. The lime pastes were subjected to thermal and nitrogen gas sorption analyses to understand if FC affects the formation of hydraulic compounds and the mesoporosities volume and distribution. The setting and early hydration of the mortars were studied with isothermal calorimetry. The mechanical performances were investigated with compressive and three-point-bending tests. Furthermore, fragments resulting from the mechanical tests were microscopically studied to understand the reinforcement mechanism of the fibres. It was found that 0.3 wt% of FC enhances the flexural and compressive strengths respectively by 57% and 44% while the crack propagation after the material failure is not affected.

While it has been shown that climate change anxiety (emotional distress response to climate change) can enhance pro-environmental behaviours (PEBs) in some subjects, in others it can induce eco-paralysis, thus leading individuals to avoid any form of engagement in actions against climate change. This study aims to clarify which factors influence the relationship between climate change anxiety and the disposition to PEBs, focusing on the role of self-efficacy as a mediating factor. A cross-sectional study was conducted on 394 healthy subjects living in Italy who completed the Pro-Environmental Behaviours Scale (PEBS), the General Self-Efficacy scale (GSE), and the Climate Change Anxiety Scale (CCAS). As a result, the mediation model showed a positive direct effect of the cognitive impairment subscale of CCAS on PEBS and an indirect negative effect of the cognitive impairment subscale of CCAS on PEBS mediated by GSE. These findings show that climate change anxiety has simultaneously two different effects on individuals: it directly encourages PEBs, and indirectly may have detrimental effects on PEBs such as eco-paralysis. Consequently, therapeutic approaches to treat climate change anxiety should not be aimed at rationalising irrational thoughts but rather at helping patients develop coping strategies such as PEBs which, in turn, foster self-efficacy.

Proteinopathies are a large group of neurodegenerative diseases caused by both genetic and sporadic mutations in particular genes which can lead to alterations of the protein structure and to the formation of aggregates, especially toxic for neurons. Autophagy is a key mechanism for clearing those aggregates and its function has been strongly associated with the ubiquitin-proteasome system (UPS), hence mutations in both pathways have been associated with the onset of neurodegenerative diseases, particularly those induced by protein misfolding and accumulation of aggregates. Many crucial discoveries regarding the molecular and cellular events underlying the role of autophagy in these diseases have come from studies using Drosophila models. Indeed, despite the physiological and morphological differences between the fly and the human brain, most of the biochemical and molecular aspects regulating protein homeostasis, including autophagy, are conserved between the two species.In this review, we will provide an overview of the most common neurodegenerative proteinopathies, which include PolyQ diseases (Huntington’s disease, Spinocerebellar ataxia 1, 2, and 3), Amyotrophic Lateral Sclerosis (C9orf72, SOD1, TDP-43, FUS), Alzheimer’s disease (APP, Tau) Parkinson’s disease (a-syn, parkin and PINK1, LRRK2) and prion diseases, highlighting the studies using Drosophila that have contributed to understanding the conserved mechanisms and elucidating the role of autophagy in these diseases.

Autophagy is a fundamental physiological pathway involved in the clearance of cellular debris, exhausted organelles and protein aggregates, particularly important for neuronal health. Mutant huntingtin (mHTT) aggregates have been shown to interfere with the physiological autophagic flux, favouring neuronal death. Glutamate Dehydrogenase (GDH) is an evolutionary conserved enzyme that catalyses the conversion of glutamate to α-ketoglutarate and vice versa and it is involved in the Glutamate-Glutamine Cycle (GGC) occurring between neurons and glia to regulate glutamate homeostasis. Our genetic screening identified GDH as a mediator of autophagy in neurons and its reduction in vivo ameliorates the pathologic phenotypes of HD in a Drosophila model for this disease. The aim of our project was to understand the biochemical and genetic mechanisms by which GDH downregulation induced autophagy by exploiting a Drosophila model that expresses huntingtin exon-1 containing 93 CAG repetitions (HttQ93) in neurons. By performing motility and viability assays, western blot analysis and immunofluorescence experiments we investigated how the reduction of GDH in neurons ameliorates animal motility and reduces the size of mHTT aggregates by enhancing autophagy. Recent biochemical evidence shows how GDH downregulation (1) reduces aminoacidic levels, resulting in TOR inactivation, and (2) induces the activation of AMPK, a kinase that is active when cells are in a low-energy status. These two pathways seem to be important for the induction of cell survival and to control cellular energy, both necessary for neuronal health, highlighting venues for pharmacological inhibitors that could ameliorate HD phenotype.

Objectives: Ameloblastoma is a locally aggressive odontogenic tumor of the jaws characterized by a high recurrence rate. This work aims to present our clinical experience in managing patient oral rehabilitation following an extensive mandibular ameloblastoma, with a specific focus on mandibular reconstruction using a fibula free flap, followed by dental implant placement and prosthetic rehabilitation in a female patient. Additionally, we provide a comprehensive review of the current evidence on surgical management, reconstruction techniques, and long-term outcomes in ameloblastoma treatment. Methods: A 44-year-old female patient presented with a painless swelling in the left mandible. Orthopantomography (OPG) and computed tomography (CT) demonstrated a well-defined radiolucent lesion extending from the canine to the second premolar. An incisional biopsy was performed, and histopathological examination confirmed the diagnosis of mandibular ameloblastoma. The patient underwent segmental resection of the left mandibular body, followed by immediate reconstruction using a vascularized fibular free flap. Eighteen months postoperatively, four dental implants were placed. One implant failed during the osseointegration phase and was removed. Due to residual hard and soft tissue deficiency, prosthetic rehabilitation was achieved with a metal-reinforced resin overdenture, restoring both function and aesthetics. Results: At the three-year follow-up, clinical and radiographic examinations revealed no evidence of tumor recurrence. The patient remained asymptomatic, reporting neither pain nor functional discomfort. Prosthetic rehabilitation with the metal-reinforced resin overdenture was successfully completed, achieving satisfactory masticatory function and aesthetics. Conclusions: The use of the fibula free flap for mandibular reconstruction after ameloblastoma resection provides excellent flexibility, enabling effective bone integration of dental implants.

Exosomes are promising therapeutics for tissue repair and regeneration to induce and guide appropriate immune responses in dystrophic pathologies. However, manipulating exosomes to control their biodistribution and targeting them in vivo to achieve adequate therapeutic benefits still poses a major challenge. Here we overcome this limitation by developing an externally controlled delivery system for primed annexin A1 myo-exosomes (Exo myo ). Effective nanocarriers are realized by immobilizing the Exo myo onto ferromagnetic nanotubes to achieve controlled delivery and localization of Exo myo to skeletal muscles by systemic injection using an external magnetic field. Quantitative muscle-level analyses revealed that macrophages dominate the uptake of Exo myo from these ferromagnetic nanotubes in vivo to synergistically promote beneficial muscle responses in a murine animal model of Duchenne muscular dystrophy. Our findings provide insights into the development of exosome-based therapies for muscle diseases and, in general, highlight the formulation of effective functional nanocarriers aimed at optimizing exosome biodistribution. Exosome targeting for therapeutic needs remains a challenge. Here, the authors show that ferromagnetic-nanotube-passivated exosomes promote the transition of proinflammatory macrophages to an anti-inflammatory state and myogenic maturation of dystrophic muscle progenitors in a murine model.

Understanding the effects induced by carcinogens on primary colonic epithelial cells and how to counteract them might help to prevent colon cancer, which is one of the most frequent and aggressive cancers. In this study, we exposed primary human colonic epithelial cells (HCoEpC) to Benzo[a]pyrene (B[a]P) and found that it led to an increased production of pro-inflammatory cytokines and activated ERK1/2 and mTOR. These pathways are known to be involved in inflammatory bowel disease (IBD), which represents a colon cancer risk factor. Moreover, B[a]P reduced autophagy and mitophagy, processes whose dysregulation has been clearly demonstrated to predispose to cancer either by in vitro or in vivo studies. Interestingly, all the effects induced by B[a]P could be counteracted by 3,4-Dihydroxyphenylethanol (DPE or Hydroxytyrosol, H), the most powerful anti-inflammatory and antioxidant compound contained in olive oil. This study sheds light on the mechanisms that could be involved in colon carcinogenesis induced by a chemical carcinogen and identifies a safe natural product that may help to prevent them.