Publications by authors named "J Gloy"

Background: Wildfires are recognized as an important ecological component of larch-dominated boreal forests in eastern Siberia. However, long-term fire-vegetation dynamics in this unique environment are poorly understood. Recent paleoecological research suggests that intensifying fire regimes may induce millennial-scale shifts in forest structure and composition.

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With changing climate, the boreal forest could potentially migrate north and become threatened by droughts in the south. However, whether larches, the dominant tree species in eastern Siberia, can adapt to novel situations is largely unknown but is crucial for predicting future population dynamics. Exploring variable traits and trait adaptation through inheritance in an individual-based model can improve our understanding and help future projections.

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Introduction: Seven of 10 patients with non-dialysis chronic kidney disease (CKD) experience burdensome persistent somatic symptoms (PSS). Despite the high prevalence and relevance for quality of life, disease progression and mortality, the pathogenesis of PSS in CKD remains poorly understood. The SOMA.

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We explore a model system consisting of a particle confined to move along a toroidal helix while being exposed to a static potential as well as a driving force due to a harmonically oscillating electric field. It is shown that in the limit of a vanishing helix radius, the governing equations of motion coincide with those of the well-known Kapitza pendulum-a classical pendulum with oscillating pivot-implying that the driven toroidal helix represents a corresponding generalization. It is shown that the two dominant static fixed points present in the Kapitza pendulum are also present for a finite helix radius.

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Nesprin-2, a type II transmembrane protein of the nuclear envelope, is a component of the LINC complex that connects the nuclear lamina with the actin cytoskeleton. To elucidate its physiological role we studied wound healing in Nesprin-2 Giant deficient mice and found that a loss of the protein affected wound healing particularly at later stages during fibroblast differentiation and keratinocyte proliferation leading to delayed wound closure. We identified altered expression and localization of transcription factors as one of the underlying mechanisms.

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