[Purpose] To clarify the three-dimensional nature of foot mobility and its interrelationships within the foot due to bodyweight bearing. [Participants and Methods] Data regarding left foot mobility due to body weight bearing were collected from 31 healthy adults. Foot shape differences while sitting and standing, and their interrelationship were examined. The same examiner reapplied the landmark stickers when misaligned during measurement position changes. [Results] The foot length, heel width, forefoot width, hallux valgus angle, and calcaneus eversion angle were significantly larger in the standing than in sitting position. The digitus minimus varus angle was significantly smaller in the standing than in sitting position. The medial and lateral malleoli, navicular, and dorsum of the foot were displaced medially and inferiorly; the other indices, except for the midfoot, were displaced anteriorly. The interrelationships within the foot showed a positive correlation between the calcaneus eversion angle and the medial displacement of the medial and lateral malleoli, navicular, and dorsum of the foot points. There was a negative correlation between the calcaneus eversion angle and inferior displacement of the medial malleolus, navicular, and dorsum of the foot. [Conclusion] The intra-foot coordination relationship in response to bodyweight bearing was clarified.
Background Learning and memory deficits and pathologic changes in the hippocampus caused by toothlessness and soft diet feeding are related to reduced masseter muscle (MM) function. Objective Myosin heavy chain (MyHC) isoform expression in the MM also changes under different chewing conditions. The neurotransmitter calcitonin gene‐related peptide (CGRP) and vascular endothelial growth factor A (VEGF‐A) are involved in MM formation. However, the relationship between CGRP, VEGF‐A and MyHC isoforms in the MM in the senescence‐accelerated mouse prone 8 (SAMP8) strain, a model of learning and memory deficits, remains unclear. Methods Changes in CGRP, VEGF‐A, vasculogenesis marker and MyHC isoform mRNA expression in the MMs of ageing SAMP8 and senescence‐accelerated mouse resistant 1 (SAMR1) mice was investigated through quantitative real‐time polymerase chain reaction (qRT–PCR) and in situ hybridization. Results qRT–PCR revealed obviously high CGRP levels in the SAMP8 mouse MM (p < .001). MyHC‐IId/x mRNA expression in the MM was higher in 24‐week‐old SAMP8 mice than 24‐week‐old SAMR1 mice (p < .001) but lower in slow‐MyHC SAMP8 mice than SAMR1 mice (p < .001). CGRP mRNA was observed on the muscle fibres of the SAMP8 mouse MM but not the SAMR1 mouse MM through in situ hybridization. Principal component analysis (PCA) revealed strong positive contributions of SAMP8‐MyHC‐IId/x, SAMP8‐CGRP, SAMR1‐MyHC‐emb, SAMR1‐CGRP, SAMR1‐VEGF‐A, SAMR1‐CD31, SAMP8‐VEGF‐A, and SAMP8‐CD31 in the MM at 12 and 24 weeks. Conclusion Calcitonin gene‐related peptide is also key for the MyHC‐IId/x and slow‐MyHC patterns in the MMs of SAMP8 mice.
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