Augmented Reality to Engage Visitors of Science Museums through Interactive Experiences

In the last years, interactive exhibitions based on digital technologies have become widely common, thanks to their flexibility and effectiveness in engaging visitors and creating memorable experiences. One of the topics in which digital technologies can be particularly effective is the communication of abstract concepts that are difficult for the human mind to imagine. An emblematic example is the astronomy discipline, which requires us to imagine and understand phenomena far away from our everyday life. In this paper, the authors present a research project, MARSS, in which digital technologies are used effectively to enhance the Users' Experience of the Museo Astronomico di Brera located in Milan. Specifically, the MARSS project aims at designing and developing a new digital journey inside the museum to allow different categories of visitors to enjoy the exhibition in an engaging and interactive way. The paper presents the design and development phases of the experience and its evaluation with users. The results of the evaluation indicate that the digital interactive experience is appreciated by users and is successful in translating the content of high scientific value into more engaging and easily understandable elements

Muscle molecular signature in sporadic ALS patients

Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease leading to muscular atrophy. 5\u201310% of total ALS cases are familial, the 20% of them having a mutation in the SOD1 gene, but most cases are sporadic; moreover the onset could be both spinal and bulbar. Retraction of motor axons from the synaptic connections with muscle is one of the earliest presymptomatic events. Understanding the role of muscle in ALS could have implications for the disease treatment, since, despite the broader etiology of human ALS, muscle impairment represents the common endpoint of the disease, indicating that results provided by studies conducted on animal models could be translated to patients. A proteomic and signalling study performed in a transgenic SOD1G93A mouse model showed that differential changes in muscle proteome can act as signalling events inducing progressive damage both at the muscular and motoneuronal levels [1]. The same differential proteomics approach was conducted in ALS patients. We examined the proteomic profiles of vastus lateralis muscles from 8 sporadic and a SOD1-mutated (L144F) patients by two-dimensional difference in gel electrophoresis (2-D DIGE) and mass spectrometry. Healthy age-matched subjects were considered as controls. According to the animal model proteomic study, variations were observed in mitochondrial structure, respiratory chain and TCA cycle, in anaerobic metabolism and in contractile/structural proteins. Signalling molecules were also monitored, providing a set of putative markers for validation in a larger patients\u2019 cohort. Validation of these changes will represent an important step forward for diagnosis and monitoring of the disease progression in ALS patients

Effects of degeneration-regeneration induced by nerve crush in rat flexor digitorum sublimis

Peripheral nerve lesions occur as a consequence of a variety of traumas and diseases inducing a dramatic muscle atrophy. Although transected peripheral nerves can spontaneously regenerate leading to functional recovery, axon regeneration requires a longer time during which the denervated muscles undergo atrophy. The required time hinder the functional muscle recovery after reinnervation. To monitor these events, 2-D DIGE and mass spectrometry were applied to profile the qualitative and quantitative differences in the proteome of rat flexor digitorum sublimis muscle during the process of denervation-reinnervation after median nerve crush. The changes in protein expression levels were analysed at days: 1, 3, 7, 15, 30 after nerve crush, respectively, using non-crushed samples as controls. Results revealed 240 differentially expressed spots matched among the 6 groups. Statistical multivariate analysis highlighted 9 main spot clusters with a time-course expression pattern compatible with the degenerative-regenerative process. The major alterations were shown at time point 3 and 7, after which protein levels were progressively renormalized. After mass spectrometry identification, proteins were grouped in 11 functional classes, the majority of them were involved in energy transduction (8 spots), glycolysis (20 spots), transport (19 spots), stress response (13 spots). Furthermore, 19 spots were identified as structural components of the muscle cell. Next goal will be to define the contribution of these quantitative protein variations after merging data from mRNA arrays on the same samples defining targets for the degeneration-reinnervation process

Extracellular matrix alterations in hypertension : effects of emilin1deficiency in mouse aorta

Objective Emilin1, an extracellular matrix glycoprotein, regulates blood pressure by inhibiting transforming growth factor (TGF)-\u3b21 processing. Emilin1 knockout mice are hypertensive. A proteomic approach was performed to characterize transgenic mouse models in order to understand molecular mechanisms involved in hypertension pathogenesis. Design and method We examined the proteomic profiles of aorta in two animal models, constitutive Emilin1 knockout mouse and tamoxifen-inducible vascular smooth muscle cells specific knockout mice (Emilin1flox/flox;Smmhc-Cre-ERT2). Wild-type mice and Smmhc-Cre-ERT2 mice treated by tamoxifen respectively were used as controls. Qualitative and quantitative differences in the proteome were obtained by the combination of two proteomics techniques, 2D-DIGE and ICPL, and the differentially expressed proteins were identified by MALDI-ToF/ToF or LC-ESI-MS/MS mass spectrometry. A comparative analysis of the two different experimental datasets was performed by DeCyder and Warp-LC (Proteinscape) softwares in order to cluster samples according to protein expression levels. Results Both techniques showed similar functional groups of proteins involved in hypertension pathogenesis, but complementary proteins were identified. Variations were observed in metabolism, stress response, cell adhesion and in contractile/structural proteins. These classes resulted over-expressed in Emilin1 knockout model and down-expressed in Emilin1flox/flox;Smmhc-Cre-ERT2 mouse. Conclusions This study shows the most important alterations due to Emilin1 deficiency in mouse aorta. In Emilin1 knockout mouse there is a general down-regulation of aorta proteins. In this model Emilin1 gene is expressed neither in smooth muscle nor in endothelial cells and blood vessels are constitutively smaller than controls. These results indicate that the KO model reflects the adaptation to a congenital hypertension condition. Emilin1flox/flox;Smmhc-Cre-ERT2 mice show an up-regulation in the majority of cellular proteins involved in hypertension pathogenesis. In this model, the conditional silencing of Emilin1 gene is restricted to smooth muscle cells of blood vessels which are normal in size. The observed molecular alterations can be considered as putative biomarkers to monitor the onset of the disease