Test and Validation of a Multi-Block Solution for Improved Tracking in Outdoor Scenarios: A Case Study in the Pinocchio Park

Augmented reality techniques have recently found many applications in the field of cultural heritage. When used in outdoor scenarios, however, this technology can face several issues, mainly due to unstable light conditions, jeopardizing the users’ experience. Various solutions to this problem have been proposed in the literature; however, none of them are fully effective. This paper introduces a solution based on a multi-block image target segmentation and a dedicated add-on for the Unity3D game engine. After tests in the lab, the solution was validated in a real scenario at Pinocchio Park (Collodi, Italy), using two different Augmented Reality (AR) libraries and comparing it to a standard methodology. Quantitative results show that the proposed approach provides superior performance and usability. Although the proposed solution is still open to improvement, it combines effectiveness and ease of implementation without any drawbacks

Test and Validation of a Multi-Block Solution for Improved Tracking in Outdoor Scenarios: A Case Study in the Pinocchio Park

Augmented reality techniques have recently found many applications in the field of cultural heritage. When used in outdoor scenarios, however, this technology can face several issues, mainly due to unstable light conditions, jeopardizing the users’ experience. Various solutions to this problem have been proposed in the literature; however, none of them are fully effective. This paper introduces a solution based on a multi-block image target segmentation and a dedicated add-on for the Unity3D game engine. After tests in the lab, the solution was validated in a real scenario at Pinocchio Park (Collodi, Italy), using two different Augmented Reality (AR) libraries and comparing it to a standard methodology. Quantitative results show that the proposed approach provides superior performance and usability. Although the proposed solution is still open to improvement, it combines effectiveness and ease of implementation without any drawbacks

Distinct Signaling Pathways Mediate Stimulation of Cell Cycle Progression and Prevention of Apoptotic Cell Death by Estrogen in Rat Pituitary Tumor PR1 Cells

Estrogens control cell growth and viability in target cells via an interplay of genomic and extragenomic pathways not yet elucidated. Here, we show evidence that cell proliferation and survival are differentially regulated by estrogen in rat pituitary tumor PR1 cells. Pico- to femtomolar concentrations of 17β-estradiol (E2) are sufficient to foster PR1 cell proliferation, whereas nanomolar concentrations of the same are needed to prevent cell death that occurs at a high rate in these cells in the absence of hormone. Activation of endogenous (PRL) or transfected estrogen-responsive genes occurs at the same, higher concentrations of E2 required to promote cell survival, whereas stimulation of cyclin D3 expression and DNA synthesis occur at lower E2 concentrations. Similarly, the pure antiestrogen ICI 182,780 inhibits estrogen response element-dependent trans-activation and cell death more effectively than cyclin-cdk activity, G(1)-S transition, or DNA synthesis rate. In antiestrogen-treated and/or estrogen-deprived cells, death is due predominantly to apoptosis. Estrogen-induced cell survival, but not E2-dependent cell cycle progression, can be prevented by an inhibitor of c-Src kinase or by blockade of the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling pathway. These data indicate the coexistence of two distinguishable estrogen signaling pathways in PR1 cells, characterized by different functions and sensitivity to hormones and antihormones

Oscillatory mTOR inhibition and Treg increase in kidney transplantation

Intracellular metabolic pathways dependent upon the mammalian target of rapamycin (mTOR) play a key role in immune-tolerance control. In this study, we focused on long-term mTOR-dependent immune-modulating effects in kidney transplant recipients undergoing conversion from calcineurin inhibitors (CNI) to mTOR inhibitors (everolimus) in a 1-year follow-up. The conversion to everolimus is associated with a decrease of neutrophils and of CD8(+) T cells. In addition, we observed a reduced production of interferon (IFN)-γ by CD8(+) T cells and of interleukin (IL)-17 by CD4(+) T lymphocytes. An increase in CD4(+) CD25(+) forkhead box protein 3 (FoxP3)(+) [regulatory T cell [(Treg )] numbers was also seen. Treg increase correlated with a higher proliferation rate of this regulatory subpopulation when compared with the CD4(+) FoxP3(-) effector counterpart. Basal phosphorylation level of S6 kinase, a major mTOR-dependent molecular target, was substantially maintained in patients treated with everolimus. Moreover, oscillations in serum concentration of everolimus were associated with changes in basal and activation-dependent S6 kinase phosphorylation of CD4(+) and CD8(+) T cells. Indeed, T cell receptor (TCR) triggering was observed to induce significantly higher S6 kinase phosphorylation in the presence of lower everolimus serum concentrations. These results unveil the complex mTOR-dependent immune-metabolic network leading to long-term immune-modulation and might have relevance for novel therapeutic settings in kidney transplants

Immunologia e immupatologia. Ediz. illustrata

Obiettivo di questa opera è spiegare l’immunologia in un momento storico in cui si vedono le incredibili ricadute pratiche delle conoscenze immunologiche accumulate negli ultimi decenni, affiancate dai progressi fatti dalla biologia molecolare. L’opera dà pari spazio all’immunologia di base e all’immunopatologia, dalla spiegazione dei meccanismi biologici della risposta immunitaria alla descrizione delle applicazioni pratiche date dalla possibilità di modulare questi meccanismi con farmaci biotecnologici mirati. Hanno risalto gli interventi di immunomodulazione della risposta immunitaria, che coinvolgono sia i trattamenti vaccinali classici e di nuova generazione, inclusi i vaccini ad acidi nucleici e quelli tollerogenici, sia le nuove terapie immunostimolanti recentemente introdotte per il trattamento delle patologie neoplastiche, sia le terapie immunosoppressive, che intervengono con un approccio di terapia molecolare mirata su specifici sistemi molecolari della risposta immunitaria. Inserti di clinica, approfondimenti e un capitolo dedicato alle infezioni da coronavirus (come SARS e COVID-19) analizzano aspetti specifici legati alla fisiopatologia del sistema immunitario

CD8+ T cells specific for cryptic apoptosis-associated epitopes exacerbate experimental autoimmune encephalomyelitis

The autoimmune immunopathology occurring in multiple sclerosis (MS) is sustained by myelin-specific and -nonspecific CD8+ T cells. We have previously shown that, in MS, activated T cells undergoing apoptosis induce a CD8+ T cell response directed against antigens that are unveiled during the apoptotic process, namely caspase-cleaved structural proteins such as non-muscle myosin and vimentin. Here, we have explored in vivo the development and the function of the immune responses to cryptic apoptosis-associated epitopes (AEs) in a well-established mouse model of MS, experimental autoimmune encephalomyelitis (EAE), through a combination of immunization approaches, multiparametric flow cytometry, and functional assays. First, we confirmed that this model recapitulated the main findings observed in MS patients, namely that apoptotic T cells and effector/memory AE-specific CD8+ T cells accumulate in the central nervous system of mice with EAE, positively correlating with disease severity. Interestingly, we found that AE-specific CD8+ T cells were present also in the lymphoid organs of unprimed mice, proliferated under peptide stimulation in vitro, but failed to respond to peptide immunization in vivo, suggesting a physiological control of this response. However, when mice were immunized with AEs along with EAE induction, AE-specific CD8+ T cells with an effector/memory phenotype accumulated in the central nervous system, and the disease severity was exacerbated. In conclusion, we demonstrate that AE-specific autoimmunity may contribute to immunopathology in neuroinflammation