Model-Based Reinforcement Learning Variable Impedance Control for Human-Robot Collaboration

Industry 4.0 is taking human-robot collaboration at the center of the production environment. Collaborative robots enhance productivity and flexibility while reducing human’s fatigue and the risk of injuries, exploiting advanced control methodologies. However, there is a lack of real-time model-based controllers accounting for the complex human-robot interaction dynamics. With this aim, this paper proposes a Model-Based Reinforcement Learning (MBRL) variable impedance controller to assist human operators in collaborative tasks. More in details, an ensemble of Artificial Neural Networks (ANNs) is used to learn a human-robot interaction dynamic model, capturing uncertainties. Such a learned model is kept updated during collaborative tasks execution. In addition, the learned model is used by a Model Predictive Controller (MPC) with Cross-Entropy Method (CEM). The aim of the MPC+CEM is to online optimize the stiffness and damping impedance control parameters minimizing the human effort (i.e, minimizing the human-robot interaction forces). The proposed approach has been validated through an experimental procedure. A lifting task has been considered as the reference validation application (weight of the manipulated part: 10 kg unknown to the robot controller). A KUKA LBR iiwa 14 R820 has been used as a test platform. Qualitative performance (i.e, questionnaire on perceived collaboration) have been evaluated. Achieved results have been compared with previous developed offline model-free optimized controllers and with the robot manual guidance controller. The proposed MBRL variable impedance controller shows improved human-robot collaboration. The proposed controller is capable to actively assist the human in the target task, compensating for the unknown part weight. The human-robot interaction dynamic model has been trained with a few initial experiments (30 initial experiments). In addition, the possibility to keep the learning of the human-robot interaction dynamics active allows accounting for the adaptation of human motor system

Basement membrane components in normal, dysplastic, neoplastic laryngeal tissue and metastatic lymph nodes

9nonenoneANTONELLI A.R; P. NICOLAI; CAPPIELLO J; PERETTI G; MOLINARI-TOSATTI M.P; ROSA D; GRIGOLATO P.G; FAVRET M; MAROCCOLO DANTONELLI A., R; Nicolai, Piero; Cappiello, Johnny; Peretti, G; MOLINARI TOSATTI M., P; Rosa, D; Grigolato, Pier Giovanni; Favret, M; Maroccolo, D

Basic fibroblast growth factor-induced angiogenic phenotype in mouse endothelium. A study of aortic and microvascular endothelial cell lines.

The mouse is the most commonly used species for in vivo studies on angiogenesis related to tumor development. Yet, to the best of our knowledge, very few reports on the in vitro interaction of the angiogenic basic fibroblast growth factor (bFGF) with mouse endothelial cells are available. Three mouse endothelial cell lines originated from aorta (MAECs), brain capillaries (MBECs), and heart capillaries (MHECs) were characterized for endothelial phenotypic markers, in vivo tumorigenic activity, and the capacity to respond in vitro to bFGF. These cells express angiotensin-converting enzyme, acetylated LDL receptor, constitutive endothelial nitric oxide synthase, and vascular cell adhesion molecule-1 and bind Griffonia simplicifolia-I lectin. When injected subcutaneously in nude mice, MAECs induced the appearance of slow-growing vascular lesions reminiscent of epithelioid hemangioendothelioma, whereas MBEC xenografts grew rapidly, showing Kaposi's sarcoma-like morphological features. No lesions were induced by injection of MHECs. MAECs, MBECs, and MHECs expressed both low-affinity heparan sulfate bFGF-binding sites and high-affinity tyrosine kinase receptors (FGFRs) on their surfaces. In particular, MAECs expressed FGFR-2/bek mRNA, whereas microvascular MBECs and MHECs expressed FGFR-1/flg mRNA. Accordingly, bFGF induced a mitogenic response and the phosphorylation of extracellular signal-regulated kinase-2 in all the cell lines. In contrast, upregulation of urokinase-type plasminogen activator expression was observed in bFGF-treated microvascular MBECs and MHECs but not in MAECs. Also, bFGF-treated MBECs and MHECs but not MAECs invaded a three-dimensional fibrin gel and formed hollow, capillary-like structures. The relevance of the modifications of the fibrinolytic balance of mouse microvascular endothelium in bFGF-induced angiogenesis was validated in vivo by a gelatin-sponge assay in which the plasmin inhibitors tranexamic acid and epsilon-aminocaproic acid given to mice in the drinking water inhibited neovascularization induced by the growth factor. In conclusion, differences in response to bFGF exist between large-vessel MAECs and microvascular MBECs and MHECs. Both in vitro and in vivo data point to a role of the profibrinolytic phenotype induced by bFGF in microvascular endothelial cells during mouse angiogenesis. Our observations make these endothelial cell lines suitable for further studies on mouse endothelium during angiogenesis and in angioproliferative diseases

Growth advantage and vascularization induced by basic fibroblast growth factor overexpression in endometrial HEC-1-B cells: an export-dependent mechanism of action.

The human endometrial adenocarcinoma HEC-1-B cell line was transfected with an expression vector harboring the human basic fibroblast growth factor (bFGF) cDNA under the control of the human beta-actin gene promoter. Stable transfectants were obtained in which a constitutive, limited overexpression of M(r) 24,000, 22,000, and 18,000 bFGF isoforms was observed. When transfectants were screened for the capacity to release the growth factor, significant amounts of bFGF were present in the conditioned medium and extracellular matrix of the bFGF-B9 clone but not of the bFGF-A8 clone, even though both cell lines produced similar levels of intracellular bFGF. When compared to parental cells, bFGF-B9 cells showed down-regulation of tyrosine kinase fibroblast growth factor receptors along with up-regulation of urokinase-type plasminogen activator expression which was abolished by incubation of the cell cultures with neutralizing anti-bFGF antibody. In vivo, bFGF-B9 cells formed highly vascularized tumors growing faster than parental cells when injected s.c. in nude mice. Also, they were more potent than nontransfected cells in inducing an angiogenic response in the rabbit cornea assay. In contrast, the bFGF-A8 cell phenotype was indistinguishable from parental cells both in vitro and in vivo. In conclusion, clonal differences exist within the HEC-1-B cell line in the capacity to release bFGF. bFGF export by human endometrial adenocarcinoma cells results in autocrine and paracrine effects that confer a growth advantage in vivo associated with increased neovascularization