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Abstract Humans can stably hold and skillfully manipulate an object by coordinated control of a complex, redundant musculoskeletal system. However, how the human central nervous system actually accomplishes precision grip tasks by coordinated control of fingertip forces remains unclear. In the present study, we aimed to construct a hypothetical neural network model that can spontaneously generate humanlike precision grip. The nervous system was modeled as a recurrent neural network model prescribing kinematic and kinetic constraints that must be satisfied in precision grip tasks in the form of energy functions. The recurrent neural network autonomously behaves so as to decrease the energy functions; therefore, given the estimated mass and center-of-mass location of the target object, the nervous system model can spontaneously generate muscle activation signals that achieve stable precision grips due to dynamic relaxation of the energy functions embedded in the nervous system. Fingertip forces are modulated by sensory information about slip between the object and fingertips. A two-dimensional musculoskeletal model of the human hand with a thumb and an index finger was constructed. Forward dynamic simulation of the precision grip was performed using the proposed neural network model. Our results demonstrated that the proposed neural network model could stably pinch and successfully hold up the object in various conditions, including changes in friction, object shape, object mass, and center-of-mass location. The proposed hypothetical neuro-computational model may possibly explain some aspects of the control strategy humans use for precision grip. [ABSTRACT FROM AUTHOR]

Objective P. gingivalis is a gram-negative anaerobic bacterium and a major periodontal pathogen. LPS produced by P. gingivalis promotes osteoclast formation. TECK is a CC chemokine whose expression is increased in gingival epithelial cells exposed to P. gingivalis LPS. In this study, we investigated the effect of TECK in osteoclastogenesis induced by P. gingivalis LPS. Designs Real time reverse transcriptase polymerase chain reaction (RTPCR) analysis and western blotting were performed to confirm TECK in MG63, human osteoblast cell line and primary murine osteoblasts and CCR9 in RAW 264.7 cells and murine bone marrow macrophages (BMMs) as osteoclast precursors. P. gingivalis LPS-treated BMMs and Raw 264.7 cells were cultured with or without TECK or TECK antibody to examine the effect of TECK on osteoclast formation. Cocultures with murine osteoblasts and bone marrow cells were also treated with or without TECK or TECK antibody. Luciferase assay and western blotting were used to determine whether TECK-CCR9 induced osteoclastogenesis was mediated through NFATc1 or NF-kB signaling. Results TECK was shown to be expressed by osteoblasts, and its receptor, CCR9, by osteoclast precursors. TECK increased P. gingivalis LPS-induced osteoclast numbers in an in vitro osteoclast formation assay using osteoclast precursors. The enhanced osteoclast formation by TECK was mediated by NFATc1, but not by NF-kB signaling. Conclusion TECK may be a novel regulator of osteoclast formation induced by P. gingivalis LPS in periodontitis. [ABSTRACT FROM AUTHOR]