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Susan I. Anderson

Researcher at University of Nottingham

Publications -  26
Citations -  798

Susan I. Anderson is an academic researcher from University of Nottingham. The author has contributed to research in topics: Osteocalcin & Biomaterial. The author has an hindex of 14, co-authored 26 publications receiving 673 citations.

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Silicon: the evolution of its use in biomaterials.

TL;DR: This review discusses the current data obtained from original research in biochemistry and biomaterials science supporting the role of silicon in bone, comparing both the biological function of the element and analysing the evolution of silicon-containing biommaterials.
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Pathogenesis of adolescent idiopathic scoliosis in girls - a double neuro-osseous theory involving disharmony between two nervous systems, somatic and autonomic expressed in the spine and trunk: possible dependency on sympathetic nervous system and hormones with implications for medical therapy

TL;DR: A speculative pathogenetic theory is formulated that AIS in girls results from developmental disharmony expressed in spine and trunk between autonomic and somatic nervous systems, and implications are discussed for neuroendocrine dysfunctions, osteopontin, sympathoactivation, medical therapy, Rett and Prader-Willi syndromes, infantile idiopathic scoliosis, and human evolution.
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Endocannabinoids modulate human blood–brain barrier permeability in vitro

TL;DR: The role of endocannabinoids in modulating blood–brain barrier permeability in normal conditions and in an ischaemia/reperfusion model is explored.
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Innervation of gonadotropin-releasing hormone neurons by peptidergic neurons conveying circadian or energy balance information in the mouse.

TL;DR: It is concluded that GnRH neurons in the mouse receive a high frequency of direct modulatory inputs from multiple hypothalamic peptide systems known to be important in conveying circadian information and signalling energy balance.
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A mitochondrial location for haemoglobins--dynamic distribution in ageing and Parkinson's disease.

TL;DR: It is demonstrated that both Hba and Hbb are co-localised with the mitochondrion in mammalian brain, and the door is opened to an examination of the role of Hb function, within the context of the mitochondRion—in health and disease.