2,073 research outputs found
Effects of deleting cannabinoid receptor-2 on mechanical and material properties of cortical and trabecular bone
Acknowledgements We thank Dr J.S. Gregory for assistance with Image J and Mr K. Mackenzie for assistance with Micro-CT analysis. Funding ABK was funded by a University of Aberdeen, Institute of Medical Sciences studentship and the Overseas Research Students Awards Scheme.Peer reviewedPublisher PD
Mechanical and material properties of cortical and trabecular bone from cannabinoid receptor-1-null (Cnr1-/-) mice
Funding ABK was funded by a studentship from the University of Aberdeen, Institute of Medical Sciences, and the Overseas Research Students Awards Scheme Acknowledgments We are grateful to Dr J.S. Gregory for assistance with Image J and Mr K. Mackenzie for assistance with Micro-CT analysis.Peer reviewedPostprin
A comparison of cortical and trabecular bone from C57 Black 6 mice using Raman spectroscopy
Peer reviewedPostprin
Stereociliary Myosin-1c Receptors Are Sensitive to Calcium Chelation and Absent from Cadherin 23 Mutant Mice
The identities of some of the constituents of the hair-cell transduction apparatus have been elucidated only recently. The molecular motor myosin-1c (Myo1c) functions in adaptation of the hair-cell response to sustained mechanical stimuli and is therefore an integral part of the transduction complex. Recent data indicate that Myo1c interacts in vitro with two other molecules proposed to be important for transduction: cadherin 23 (Cdh23), a candidate for the stereociliary tip link, and phosphatidylinositol 4,5-bisphosphate (PIP2), which is abundant in the membranes of hair-cell stereocilia. It is not known, however, whether these interactions occur in hair cells. Using an in situ binding assay on saccular hair cells, we demonstrated previously that Myo1c interacts with molecules at stereociliary tips, the site of transduction, through sequences contained within its calmodulin (CaM)-binding neck domain, which can bind up to four CaM molecules. In the current study, we identify the second CaM-binding IQ domain as a region of Myo1c that mediates CaM-sensitive binding to stereociliary tips and to PIP2 immobilized on a solid support. Binding of Myo1c to stereociliary tips of cochlear and vestibular hair cells is disrupted by treatments that break tip links. In addition, Myo1c does not bind to stereocilia from mice whose hair cells lack Cdh23 protein despite the presence of PIP2 in the stereociliary membranes. Collectively, our data suggest that Myo1c and Cdh23 interact at the tips of hair-cell stereocilia and that this interaction is modulated by CaM
Planning the Kitchen
Provides a brief discussion of new trends in kitchen planning
Can we improve the prediction of hip fracture by assessing bone structure using shape and appearance modelling?
Copyright 2013 Elsevier B.V., All rights reserved.Peer reviewedPreprin
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Cortisol levels in response to starting school in children at increased risk for social phobia
Background: Research on depression has identified hyperactivity of the HPA axis as a
potential contributory factor to the intergenerational transmission of affective symptoms. However,
this has not yet been examined in the context of social phobia. The current study compared HPA axis
activity in response to a universal social stressor (starting school) in children of 2 groups of women:
one with social phobia and one with no history of anxiety (comparison group). To determine specificity
of effects of maternal social phobia, a third group of children were also examined whose mothers had
generalised anxiety disorder (GAD).
Method: Children provided salivary cortisol samples in the morning, afternoon and at bedtime across 3
time-blocks surrounding the school start: a month before starting school (baseline), the first week at
school (stress response), and the end of the first school term (stress recovery). Child behavioural
inhibition at 14 months was also assessed to explore the influence of early temperament on later stress
responses.
Results: All children displayed an elevation in morning and afternoon cortisol from baseline during the
first week at school, which remained elevated until the end of the first term. Children in the social
phobia group, however, also displayed an equivalent elevation in bedtime cortisol, which was not
observed for comparison children or for children of mothers with GAD. Children in the social phobia
group who were classified as 'inhibited' at 14 months displayed significantly higher afternoon cortisol
levels overall.
Summary: A persistent stress response to school in the morning and afternoon is typical for all
children, but children of mothers with social phobia also display atypical elevations in evening cortisol
levels when at school - signalling long-term disruption of the circadian rhythm in HPA axis activity.
This is the first study to report HPA axis disruption in children at risk of developing social phobia, and
future research should aim to determine whether this represents a pathway for symptom
development, taking early temperament into account
CARETS: A prototype regional environmental information system. Volume 13: Utility of CARETS products to local planners; an evaluation
There are no author-identified significant results in this report
Ultrastructural defects in stereocilia and tectorial membrane in aging mouse and human cochleae
The aging cochlea is subjected to a number of pathological changes to play a role in the onset of age-related hearing loss (ARHL). Although ARHL has often been thought of as the result of the loss of hair cells, it is in fact a disorder with a complex etiology, arising from the changes to both the organ of Corti and its supporting structures. In this study, we examine two aging pathologies that have not been studied in detail despite their apparent prevalence; the fusion, elongation, and engulfment of cochlear inner hair cell stereocilia, and the changes that occur to the tectorial membrane (TM), a structure overlying the organ of Corti that modulates its physical properties in response to sound. Our work demonstrates that similar pathological changes occur in these two structures in the aging cochleae of both mice and humans, examines the ultrastructural changes that underlie stereocilial fusion, and identifies the lost TM components that lead to changes in membrane structure. We place these changes into the context of the wider pathology of the aging cochlea, and identify how they may be important in particular for understanding the more subtle hearing pathologies that precede auditory threshold loss in ARHL
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