Robustness Testing of Mesenchymal Stem Cell Monotherapy Following Vascularized Composite Allotransplantation.

Background:  Immunosuppression risks are a major concern with vascularized composite allotransplantation (VCA). As an emerging strategy, the antirejection role played by mesenchymal stem cells (MSCs) is receiving attention. However, the current literature reports are inconclusive regarding the robustness of the MSC monotherapy.

Depletion of Mast Cells and Macrophages Impairs Heterotopic Ossification in an Acvr1 Mouse Model of Fibrodysplasia Ossificans Progressiva.

Heterotopic ossification (HO) is a clinical condition that often reduces mobility and diminishes quality of life for affected individuals. The most severe form of progressive HO occurs in those with fibrodysplasia ossificans progressiva (FOP; OMIM #135100), a genetic disorder caused by a recurrent heterozygous gain-of-function mutation (R206H) in the bone morphogenetic protein (BMP) type I receptor ACVR1/ALK2. In individuals with FOP, episodes of HO frequently follow injury.

Musculoskeletal stiffness changes linearly in response to increasing load during walking gait.

Development of biologically inspired exoskeletons to assist soldiers in carrying load is a rapidly expanding field. Understanding how the body modulates stiffness in response to changing loads may inform the development of these exoskeletons and is the purpose of the present study. Seventeen subjects walked on a treadmill at a constant preferred walking velocity while nine different backpack loading conditions ranging from 12.

Center of mass trajectory and orientation to ankle and knee in sagittal plane is maintained with forward lean when backpack load changes during treadmill walking.

Maintaining the normal shape and amplitude of the vertical trajectory of the center of mass (COM) during stance has been shown to maximize the efficiency of unloaded gait. Kinematic adaptations to load carriage, such as forward lean have yet to be understood in relation to COM movement. The purpose of this study is to better understand how load impacts the vertical COM(TSYS) trajectory and to clarify the impact of forward lean as it relates to the dynamics of sagittal plane COM(TSYS) movement during stance with changing load.

An Acvr1 R206H knock-in mouse has fibrodysplasia ossificans progressiva.

Fibrodysplasia ossificans progressiva (FOP; MIM #135100) is a debilitating genetic disorder of dysregulated cellular differentiation characterized by malformation of the great toes during embryonic skeletal development and by progressive heterotopic endochondral ossification postnatally. Patients with these classic clinical features of FOP have the identical heterozygous single nucleotide substitution (c.617G > A; R206H) in the gene encoding ACVR1/ALK2, a bone morphogenetic protein (BMP) type I receptor.

Understanding social motor coordination.

Recently there has been much interest in social coordination of motor movements, or as it is referred to by some researchers, joint action. This paper reviews the cognitive perspective's common coding/mirror neuron theory of joint action, describes some of its limitations and then presents the behavioral dynamics perspective as an alternative way of understanding social motor coordination. In particular, behavioral dynamics' ability to explain the temporal coordination of interacting individuals is detailed.

Dysregulated BMP signaling and enhanced osteogenic differentiation of connective tissue progenitor cells from patients with fibrodysplasia ossificans progressiva (FOP).

Unlabelled: The study of FOP, a disabling genetic disorder of progressive heterotopic ossification, is hampered by the lack of readily available connective tissue progenitor cells. We isolated such cells from discarded primary teeth of patients with FOP and controls and discovered dysregulation of BMP signaling and rapid osteoblast differentiation in FOP cells compared with control cells.

Introduction: Fibrodysplasia ossificans progressiva (FOP), the most disabling condition of progressive heterotopic ossification in humans, is caused by a recurrent heterozygous missense mutation in activin receptor IA (ACVR1), a bone morphogenetic protein (BMP) type I receptor, in all classically affected individuals.

Over-expression of BMP4 and BMP5 in a child with axial skeletal malformations and heterotopic ossification: a new syndrome.

Bone morphogenetic proteins (BMPs) are a highly conserved class of signaling molecules that induce ectopic cartilage and bone formation in vivo. Dysregulated expression of bone morphogenetic protein 4 (BMP4) is found in the cells of patients who have fibrodysplasia ossificans progressiva (FOP), a genetic disorder of axial and appendicular skeletal malformation and progressive heterotopic ossification. Loss of function mutations in the bone morphogenetic protein 5 (bmp5) gene leading to under-expression of BMP5 cause the murine short ear syndrome, characterized by small malformed ears and a broad range of axial skeletal malformations.