The cellular basis of cartilage morphogenesis in embryonic chick limbs.

Cartilagineous long bone rudiments, of the chick embryo, were used as a model for the mammalian epiphyseal growth plate. Both contain 3 zones of chondrocytes which, therefore allows the cartilege rudiment to be considered as an expanded growth plate. The involvement of each zone in the growth of the rudiment was determined at the cellular level, by counting cell numbers in histological sections of the ulna. Studies in the cell kinetics of the rudiments, in vitro, demonstrated that cell division was confined, mainly to the zone of rounded cells, with little or no division observed in the zones of cell flattening and hypertrophy. It is proposed that the morphogenesis of the early cartilage long bone rudiment is influenced by the structure of it's surrounding perichondrium, rather than by propert intrinsic to the constituent chondrocytes. The perichondrium is thought to exert its influence though a process termed 'directed dilation', whereby circumferential expansion is resisted and longtitudinal growth is favoured. Ultrastructural examinations show that the perichondrium of a long bone rudiment has a variable structure: distinct at the diaphysis and loose at the epiphysis. By contrast, the perichondrium surrounding heckel's cartilage, which has only one type of chondrocyte, appears to have a uniform structure. Evidence for the lack of intrinsic property determining morphogenesis comes from the observation that chondrocytes, from various cartilage elements, behave identically in vitro, underappropriate conditions. In addition, contrary to reports that that the expression of a cartilage phenotype is dependant on high cell densities and histogenic interactions, it is proposed that the maintenance of a rounded cell configuration is sufficient to elicit phenotypic expression. Experimental evidence suggests that the 3 zones of cells are set up by combination of interactions with the perichondrium and by a signal specific to the cartilage matrix

Pose, posture, formation and contortion in kinematic systems

The concepts of pose, posture, formation and contortion are defined for serial, parallel and hybrid kinematic systems. Workspace and jointspace structure is examined in terms of these concepts. The inter-relationships of pose, posture, formation and contortion are explored for a range of robot workspace and jointspace types

Suppression of Kelvon-induced decay of quantized vortices in oblate Bose-Einstein Condensates

We study the Kelvin mode excitations on a vortex line in a three-dimensional trapped Bose-Einstein condensate at finite temperature. Our stochastic Gross-Pitaevskii simulations show that the activation of these modes can be suppressed by tightening the confinement along the direction of the vortex line, leading to a strong suppression in the vortex decay rate as the system enters a regime of two-dimensional vortex dynamics. As the system approaches the condensation transition temperature we find that the vortex decay rate is strongly sensitive to dimensionality and temperature, observing a large enhancement for quasi-two-dimensional traps. Three-dimensional simulations of the recent vortex dipole decay experiment of Neely et al. [Phys. Rev. Lett. 104, 160401 (2010)] confirm two-dimensional vortex dynamics, and predict a dipole lifetime consistent with experimental observations and suppression of Kelvon-induced vortex decay in highly oblate condensates.Comment: 8 pages, 8 figure

Persistent current formation in a high-temperature Bose-Einstein condensate: an experimental test for c-field theory

Experimental stirring of a toroidally trapped Bose-Einstein condensate at high temperature generates a disordered array of quantum vortices that decays via thermal dissipation to form a macroscopic persistent current [T. W. Neely em et al. arXiv:1204.1102 (2012)]. We perform 3D numerical simulations of the experimental sequence within the Stochastic Projected Gross-Pitaevskii equation using ab initio determined reservoir parameters. We find that both damping and noise are essential for describing the dynamics of the high-temperature Bose field. The theory gives a quantitative account of the formation of a persistent current, with no fitted parameters.Comment: v2: 7 pages, 3 figures, new experimental data and numerical simulation

Are You the O\u27Reilly? / Susan Van Doozen / The Irish Lullaby

https://digitalcommons.library.umaine.edu/mmb-vp/5705/thumbnail.jp

The role of the microbiome in driving RA-related autoimmunity

Once referred to as “normal commensal flora” the human microbiome plays an integral role between health and disease. The host mucosal surface replete with a multitude of immune cells is a vast arena constantly sensing and responding to antigen presentation and microbial by-products. It is this key role that may allow the microbiome to prime or protect the host from autoimmune disease. Rheumatoid arthritis (RA) is a chronic, disabling inflammatory condition characterized by a complex multifactorial etiology. The presence of certain genetic markers has been proven to increase susceptibility to RA however it does not guarantee disease development. Given low concordance rates demonstrated in monozygotic twin studies there is a clear implication for the involvement of external players in RA pathogenesis. Since the historical description of rheumatoid factor, numerous additional autoantibodies have been described in the sera of RA patients. The presence of anti-cyclic citrullinated protein antibody is now a standard test, and is associated with a more severe disease course. Interestingly these antibodies are detectable in patient’s sera long before the clinical signs of RA occur. The production of autoantibodies is driven by the lack of tolerance of the immune system, and how tolerance is broken is a crucial question for understanding RA development. Here we review current literature on the role of the microbiome in RA development including periodontal, gut and lung mucosa, with particular focus on proposed mechanisms of host microbiome interactions. We discuss the use of Mendelian randomization to assign causality to the microbiome and present considerations for future studies