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Garth J. S. Cooper

Researcher at University of Auckland

Publications -  309
Citations -  17579

Garth J. S. Cooper is an academic researcher from University of Auckland. The author has contributed to research in topics: Amylin & Insulin. The author has an hindex of 63, co-authored 299 publications receiving 16490 citations. Previous affiliations of Garth J. S. Cooper include Manchester Academic Health Science Centre & University of Manchester.

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Fibrillogenic Amylin Evokes Islet β-Cell Apoptosis through Linked Activation of a Caspase Cascade and JNK1

TL;DR: It is shown that fibrillogenic amylin can evoke a JNK1-mediated apoptotic pathway, which is partially dependent and partially independent of caspase-8, and in which caspases-3 acts as a common downstream effector, and casp enzyme-8 may partially act upstream of the JNK pathway.
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Systemic administration of amylin increases bone mass, linear growth, and adiposity in adult male mice

TL;DR: It is concluded that systemic administration of amylin increases skeletal mass and linear bone growth and has potential as a therapy for osteoporosis if its bone effects can be dissociated from those on soft tissue mass.
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A proteomic approach identifies early pregnancy biomarkers for preeclampsia: Novel linkages between a predisposition to preeclampsia and cardiovascular disease

TL;DR: The proteins identified are involved in lipid metabolism, coagulation, complement regulation, extracellular matrix remodeling, protease inhibitor activity and acute‐phase responses, indicating novel synergy between pathways involved in the pathogenesis of PE.
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Amyloid-like inclusions in Huntington’s disease

TL;DR: It is shown that some inclusions in Huntington's disease brain tissue possess an amyloids-like structure, suggesting parallels with other amyloid-associated diseases such as Alzheimer's and prion diseases.
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Is the failing heart out of fuel or a worn engine running rich? A study of mitochondria in old spontaneously hypertensive rats

TL;DR: Compared cardiac mitochondrial proteomes of 20‐month‐old SHR and Wistar‐Kyoto controls by iTRAQ™‐labelling combined with multidimensional LC/MS/MS, 79 differed between groups, suggesting elevated protein expression may be compensatory in the face of pathological stress.