The development and application of an optimization tool in industrial design

AbstractDesigners are identified, in industry 4.0, as the professional figures that have to design well performing new object. In order to do this, it is necessary to take into account a series of properties called design objectives. Often the structural problem of new design is underestimated or even not considered. This can be a real problem because this objective is in competitive and in contrast with other design objectives. So, this can bring to substantial change in a design in the final phase and sometimes to the complete change. In this paper is presented an optimization workflow that adopt a Multi Objective Optimization engine so called "Octopus" and Karamba3D, that is a Finite Elements (FE) plug-in, typically used in structural simulations, these extensions run in a software: Grassopper3D, that is a parametric design tool. The workflow allows designers to explore a large range of solutions and at the same time permits to filter and sort the optimized models in order to analyze the tradeoff of the resultant solution space, both qualitatively and quantitatively. In such way designers can obtain easily a lot of information of the generate design and identify potential solution for immediate use or for further optimization. In this paper is analyzed a design problem of an ergonomic chair in order to provide the efficiency of the workflow. The design criteria and the structural problem for this type of design object are identified as the main optimization objectives in order to iteratively improve the design solutions

A social robot connected with chatGPT to improve cognitive functioning in ASD subjects

Neurodevelopmental Disorders (NDDs) represent a significant healthcare and economic burden for families and society. Technology, including AI and digital technologies, offers potential solutions for the assessment, monitoring, and treatment of NDDs. However, further research is needed to determine the effectiveness, feasibility, and acceptability of these technologies in NDDs, and to address the challenges associated with their implementation. In this work, we present the application of social robotics using a Pepper robot connected to the OpenAI system (Chat-GPT) for real-time dialogue initiation with the robot. After describing the general architecture of the system, we present two possible simulated interaction scenarios of a subject with Autism Spectrum Disorder in two different situations. Limitations and future implementations are also provided to provide an overview of the potential developments of interconnected systems that could greatly contribute to technological advancements for Neurodevelopmental Disorders (NDD)

Digital manipulation versus real one: learning and motivation in a case study on Storytelling

Abstract In this work, a Storytelling FabLab has been designed for the realization of virtual performances on a Shakesperian play in an elementary school. In this FabLab, many elements have been digitally manipulated: text, audio files, virtual actors on a 3D stage, and 3D Greek masks. Learning of contents and motivation have been assessed and compared to those of a traditional class working on the construction of real masks as artefacts. Regarding learning effectiveness, data show that there is no great difference between the score gained by the experimental group and the control one; however, results emphasize a high intrinsic motivation for both experimental and control groups. Moreover, qualitative results of both groups highlight the positive feeling of doing things reflecting user's own interest: pupils want to invent their own stories and realize them (physically or digitally)

Digital interaction: where are we going?

In the framework of the AVI 2018 Conference, the interuniversity center ECONA has organized a thematic workshop on "Digital Interaction: where are we going?". Six contributions from the ECONA members investigate different perspectives around this thematic

An interaction study in mammalian cells demonstrates weak binding of HSPB2 to BAG3, which is regulated by HSPB3 and abrogated by HSPB8

The ten mammalian small heat shock proteins (sHSPs/HSPBs) show a different expression profile, although the majority of them are abundant in skeletal and cardiac muscles. HSPBs form hetero-oligomers and homo-oligomers by interacting together and complexes containing, e.g., HSPB2/HSPB3 or HSPB1/HSPB5 have been documented in mammalian cells and muscles. Moreover, HSPB8 associates with the Hsc70/Hsp70 co-chaperone BAG3, in mammalian, skeletal, and cardiac muscle cells. Interaction of HSPB8 with BAG3 regulates its stability and function. Weak association of HSPB5 and HSPB6 with BAG3 has been also reported upon overexpression in cells, supporting the idea that BAG3 might indirectly modulate the function of several HSPBs. However, it is yet unknown whether other HSPBs highly expressed in muscles such as HSPB2 and HSPB3 also bind to BAG3. Here, we report that in mammalian cells, upon overexpression, HSPB2 binds to BAG3 with an affinity weaker than HSPB8. HSPB2 competes with HSPB8 for binding to BAG3. In contrast, HSPB3 negatively regulates HSPB2 association with BAG3. In human myoblasts that express HSPB2, HSPB3, HSPB8, and BAG3, the latter interacts selectively with HSPB8. Combining these data, it supports the interpretation that HSPB8-BAG3 is the preferred interaction

9A.07: CARDIOVASCULAR TARGET ORGAN DAMAGE IN PREMENOPAUSAL SYSTEMIC LUPUS ERYTHEMATOSUS PATIENTS AND IN CONTROLS. ARE THERE ANY DIFFERENCES?

OBJECTIVE: In patients with systemic lupus erythematosus (SLE) a greater prevalence of structural and functional cardiovascular (CV) alterations has been described, possibly explaining the higher incidence of CV events, as compared to subjects matched for age and sex.Aim of this study was to analyze the presence of target organ damage in premenopausal women with SLE and in controls matched not only for demographic characteristics but also for other cardiovascular risk factors. DESIGN AND METHOD: 34 patients with SLE clinically stable (SLEDAI Score 2.5 +/- 1.5) (mean age 32 ± 7 years, range 19-44) and 34 controls matched for sex, age, body mass index (BMI), clinic blood pressure (BP) and antihypertensive treatment (if present), underwent: 24 hours BP monitoring, echocardiography with tissue Doppler analysis (TDI) for the evaluation of left ventricular (LV) structure and of systolic and diastolic function, carotid ultrasound for intima-media thickness (IMT) and carotid distensibility measurement, and pulse wave velocity measurement for aortic stiffness (PWV). RESULTS: By definition no difference was observed for age, sex, BMI and clinic BP values and a similar Framingham risk score was observed between SLE and controls (1.3 ± 2.7 vs 1.5 ± 2.3%, p = ns). No significant differences were observed for all echocardiographic parameters except LV longitudinal systolic function (Sm), an early index of LV systolic dysfunction (see Table). Carotid IMT and distensibility, as well as PWV and the prevalence of an abnormal aortic stiffness were both similar in the two groups. At the logistic analysis, PWV was independently associated with LV mass in controls and with the steroid weekly dose in SLE patients.(Figure is included in full-text article.) CONCLUSIONS: In patients with SLE and low activity index of the disease we did not observe significant vascular alterations as compared to controls with similar cardiovascular risk. The early LV systolic impairment observed in this group of patients needs confirmation in larger cohorts

Identification of Sclerostin as a Putative New Myokine Involved in the Muscle-to-Bone Crosstalk

Bone and muscle have been recognized as endocrine organs since they produce and secrete “hormone-like factors” that can mutually influence each other and other tissues, giving rise to a “bone–muscle crosstalk”. In our study, we made use of myogenic (C2C12 cells) and osteogenic (2T3 cells) cell lines to investigate the effects of muscle cell-produced factors on the maturation process of osteoblasts. We found that the myogenic medium has inhibitory effects on bone cell differentiation and we identified sclerostin as one of the myokines produced by muscle cells. Sclerostin is a secreted glycoprotein reportedly expressed by bone/cartilage cells and is considered a negative regulator of bone growth due to its role as an antagonist of the Wnt/β-catenin pathway. Given the inhibitory role of sclerostin in bone, we analyzed its expression by muscle cells and how it affects bone formation and homeostasis. Firstly, we characterized and quantified sclerostin synthesis by a myoblast cell line (C2C12) and by murine primary muscle cells by Western blotting, real-time PCR, immunofluorescence, and ELISA assay. Next, we investigated in vivo production of sclerostin in distinct muscle groups with different metabolic and mechanical loading characteristics. This analysis was done in mice of different ages (6 weeks, 5 and 18 months after birth) and revealed that sclerostin expression is dynamically modulated in a muscle-specific way during the lifespan. Finally, we transiently expressed sclerostin in the hind limb muscles of young mice (2 weeks of age) via in vivo electro-transfer of a plasmid containing the SOST gene in order to investigate the effects of muscle-specific overproduction of the protein. Our data disclosed an inhibitory role of the muscular sclerostin on the bones adjacent to the electroporated muscles. This observation suggests that sclerostin released by skeletal muscle might synergistically interact with osseous sclerostin and potentiate negative regulation of osteogenesis possibly by acting in a paracrine/local fashion. Our data point out a role for muscle as a new source of sclerostin.Bone and muscle have been recognized as endocrine organs since they produce and secrete “hormone-like factors” that can mutually influence each other and other tissues, giving rise to a “bone–muscle crosstalk”. In our study, we made use of myogenic (C2C12 cells) and osteogenic (2T3 cells) cell lines to investigate the effects of muscle cell-produced factors on the maturation process of osteoblasts. We found that the myogenic medium has inhibitory effects on bone cell differentiation and we identified sclerostin as one of the myokines produced by muscle cells. Sclerostin is a secreted glycoprotein reportedly expressed by bone/cartilage cells and is considered a negative regulator of bone growth due to its role as an antagonist of the Wnt/β-catenin pathway. Given the inhibitory role of sclerostin in bone, we analyzed its expression by muscle cells and how it affects bone formation and homeostasis. Firstly, we characterized and quantified sclerostin synthesis by a myoblast cell line (C2C12) and by murine primary muscle cells by Western blotting, real-time PCR, immunofluorescence, and ELISA assay. Next, we investigated in vivo production of sclerostin in distinct muscle groups with different metabolic and mechanical loading characteristics. This analysis was done in mice of different ages (6 weeks, 5 and 18 months after birth) and revealed that sclerostin expression is dynamically modulated in a muscle-specific way during the lifespan. Finally, we transiently expressed sclerostin in the hind limb muscles of young mice (2 weeks of age) via in vivo electro-transfer of a plasmid containing the SOST gene in order to investigate the effects of muscle-specific overproduction of the protein. Our data disclosed an inhibitory role of the muscular sclerostin on the bones adjacent to the electroporated muscles. This observation suggests that sclerostin released by skeletal muscle might synergistically interact with osseous sclerostin and potentiate negative regulation of osteogenesis possibly by acting in a paracrine/local fashion. Our data point out a role for muscle as a new source of sclerostin

Clusterin enhances migration and invasion of prostate cancer cells through an isoform-specific Akt2/miR-190/PHLPP1 circuit

During prostate cancer progression cancer cells undergo a variety of molecular alterations that lead to the acquisition of uncontrolled growth properties. One such set of molecular alterations is mediated by the PI3K/Akt signaling pathway. Here, we describe a regulatory system that modulates the phosphoinosited 3-kinase/Akt (PI3K/Akt) pathway downstream of secreted Clusterin (sCLU) in normal and cancer prostate cells. The overexpression of sCLU is very frequent in prostate cancer, and can lead to Akt-activation. This prompted us to investigate how sCLU overexpression influences PI3K/Akt signaling network in a study model represented by human epithelial prostate PNT1A cells stably transfected with sCLU or with empty vector alone. We found that CLU cells show a marked differential phosphorylation of several members of the PI3K/Akt cascade, and in particular of Akt2. Moreover, we found that the phosphatase PHLPP1, known to dephosphorylate Akt2 at S473, is severely downregulated in CLU compared to MOCK cells. We thus investigated whether sCLU alters PHLPP1 protein stability or expression. Our results indicate that sCLU indeed stimulates PHLPP1 degradation by β-TrCP. Interestingly, we further demonstrated that sCLU alters also PHLPP1 through the negative regulator miR-190. Next, because sCLU has been reported to inhibit or to stimulate the aggressive behavior of cancer cells depending on the cell model, we investigated the effects of CLU overexpression or addition of recombinant Clusterin to the medium on cell migration and invasion in PNT1A cell line, which is not expected to display an invasive phenotype, and in the cancer prostate epithelial cell lines LNCaP and PC3. The result was extremely clear: not only CLU overexpression gives PNT1A cells the same behavior of wild-type PC3 cells, but also increases the migration and invasion index of all the above cell models by two to four times, compared to controls. As a confirmation, in the same model silencing of Clusterin abrogates migration of CLU cells. Next, the effect of Akt single-isoform silencing on cell migration was explored. While silencing of Akt1 affected migration only slightly, silencing of Akt2 prevented migration of both MOCK and CLU cells completely. The same result was obtained by pharmacological inhibition of Akt2. All together our results, clearly demonstrate for the first time that Clusterin can switch the low migration phenotype of normal prostate cells towards a high migration phenotype through the modulation of the expression of the PHLPP1 and, in turn, the activity of Akt2