We revisit the problem of the stress distribution in a frictional sandpile with both normal and tangential (frictional) inter-granular forces, under gravity, equipped with a new numerical method of generating such assemblies. Numerical simulations allow a determination of the spatial dependence of all the components of the stress field, principle stress axis, angle of repose, as a function of systems size, the coefficient of static friction and the frictional interaction with the bottom surface. We compare these results with the predictions of a theory based on continuum equilibrium mechanics. Basic to the theory of sandpiles are assumptions about the form of scaling solutions and constitutive relations for cohesive-less hard grains for which no typical scale is available. We find that these constitutive relations must be modified; moreover for smaller friction coefficients and smaller piles these scaling assumptions break down in the bulk of the sandpile due to the presence of length scales that must be carefully identified. Fortunately, for larger friction coefficient and for larger piles the breaking of scaling is weak in the bulk, allowing an approximate analytic theory which agrees well with the observations. After identifying the crucial scale, triggering the breaking of scaling, we provide a predictive theory to when scaling solutions are expected to break down. At the bottom of the pile the scaling assumption breaks always, due to the different interactions with the bottom surface. The consequences for measurable quantities like the pressure distribution and shear stress at the bottom of the pile are discussed. For example one can have a transition from no dip in the base-pressure to a dip at the center of the pile as friction increases.
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JBMR Plus
February 2025
Radiology and Imaging Sciences, National Institutes of Health Clinical Center, National Institutes of Health, Bethesda, MD 20892, United States.
Jansen metaphyseal chondrodysplasia (JMC) is an ultra-rare disorder caused by constitutive activation of parathyroid hormone type 1 receptor (PTH1R). We sought to characterize the craniofacial phenotype of patients with the disease. Six patients with genetically confirmed JMC underwent comprehensive craniofacial phenotyping revealing a distinct facial appearance that prompted a cephalometric analysis demonstrating a pattern of mandibular retrognathia.
View Article and Find Full Text PDFKidney Int
January 2025
Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA, 46202; Department of Medicine/Division of Nephrology, Indiana University School of Medicine, Indianapolis, IN, USA, 46202. Electronic address:
Fibroblast growth factor 23 (FGF23) via its coreceptor αKlotho (KL) provides critical control of phosphate metabolism, which is altered in both rare and very common syndromes. However, the spatial-temporal mechanisms dictating kidney FGF23 functions remain poorly understood. Thus, developing approaches to modify specific FGF23-dictated pathways has proven problematic.
View Article and Find Full Text PDFCell Mol Gastroenterol Hepatol
January 2025
Center for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, NJ, USA. Electronic address:
Background & Aims: Erythropoietic protoporphyria (EPP) is caused by mutations in ferrochelatase which inserts iron into protoporphyrin-IX (PP-IX) to generate heme. EPP is characterized by PP-IX accumulation, skin photosensitivity, cholestasis, and end-stage liver disease. Despite available drugs that address photosensitivity, treatment of EPP-related liver disease remains an unmet need.
View Article and Find Full Text PDFJ Nurs Care Qual
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Author Affiliations: School of Nursing (Dr Fontenele Lima de Carvalho), Ceara State University, Fortaleza, Ceará, Brazil; Division of General Internal Medicine (Drs Fontenele Lima de Carvalho and Bates), Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.; and Department of Health Policy and Management (Dr Bates), Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
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Mol Biol Rep
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Department of Structural and Molecular Biology, University College London, London, WC1E 6BT, UK.
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