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To gain initial stability for cementless fixation the acetabular components of a total hip replacement are press-fit into the acetabulum. Uneven stiffness of the acetabular bone will result in irregular deformation of the shell which may hinder insertion of the liner or lead to premature loosening. To investigate this, we removed bone cores from the ilium, ischium and pubis within each acetabulum and from selected sites in corresponding femoral heads from four cadavers for mechanical testing in unconfined compression. From a stress-relaxation test over 300 s, the residual stress, its percentage of the initial stress and the stress half-life were calculated. Maximum modulus, yield stress and energy to yield (resilience) were calculated from a load-displacement test. Acetabular bone had a modulus about 10–20%, yield stress about 25% and resilience about 40% of the values for the femoral head. The stress half-life was typically between 2–4 s and the residual stress was about 60% of peak stress in both acetabulum and femur. Pubic bone was mechanically the poorest. These results may explain uneven deformation of press-fit acetabular shells as they are inserted. The measured half-life of stress-relaxation indicates that waiting a few minutes between insertion of the shell and the liner may allow seating of a poorly congruent liner. [ABSTRACT FROM AUTHOR]

The role of the core planar cell polarity (PCP) pathway protein, Vangl2, was investigated in the corneal epithelium of the mammalian eye, a paradigm anatomical model of planar cell migration. The gene was conditionally knocked out in vivo and knocked down by siRNA, followed by immunohistochemical, behavioural and morphological analysis of corneal epithelial cells. The primary defects observed in vivo were of apical‐basal organisation of the corneal epithelium, with abnormal stratification throughout life, mislocalisation of the cell membrane protein, Scribble, to the basal side of cells, and partial loss of the epithelial basement membrane. Planar defects in migration after wounding and in the presence of an applied electric field were noted. However, knockdown of Vangl2 also retarded cell migration in individual cells that had no contact with their neighbours, which precluded a classic PCP mechanism. It is concluded that some of the planar polarity phenotypes in PCP mutants may arise from disruption of apical‐basal polarity. [ABSTRACT FROM AUTHOR]