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Elizabeth A. Stoll

Researcher at Newcastle University

Publications -  26
Citations -  1729

Elizabeth A. Stoll is an academic researcher from Newcastle University. The author has contributed to research in topics: Computer science & Biology. The author has an hindex of 15, co-authored 20 publications receiving 1454 citations. Previous affiliations of Elizabeth A. Stoll include University of Washington.

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Differential Regulation of KiSS-1 mRNA Expression by Sex Steroids in the Brain of the Male Mouse

TL;DR: Kisspeptins are products of the Kiss1 gene, which bind to GPR54, a G protein-coupled receptor, and the effects of T are mediated by both ERalpha and AR pathways, suggesting that both estrogen receptor (ER) and androgen receptor (AR) play a role in T-mediated regulation of KiSS-1.
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Metabolic Reprogramming in Glioma

TL;DR: The current state of knowledge regarding the metabolic strategies employed by malignant glioma cells, including aerobic glycolysis; the pentose phosphate pathway; one-carbon metabolism; the tricarboxylic acid cycle, which is central to amino acid metabolism; oxidative phosphorylation; and fatty acid metabolism are presented.
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Cre recombinase-mediated restoration of nigrostriatal dopamine in dopamine-deficient mice reverses hypophagia and bradykinesia

TL;DR: The results highlight the critical role for dopamine signaling in the dorsal striatum for most dopamine-dependent behaviors but suggest that dopamine signaled in other brain regions is important to fine-tune these behaviors.
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Fatty acid oxidation is required for the respiration and proliferation of malignant glioma cells.

TL;DR: It is demonstrated that this metabolic pathway is a major contributor to aerobic respiration in primary-cultured cells isolated from human glioma and grown under serum-free conditions and inhibiting fatty acid oxidation reduces proliferative activity in these primary- Cultured cells and prolongs survival in a syngeneic mouse model of malignant gliomas.
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Neural stem cells in the adult subventricular zone oxidize fatty acids to produce energy and support neurogenic activity.

TL;DR: Higher levels of neurogenesis can be achieved in aged mice by ectopically expressing proliferator‐activated receptor gamma coactivator 1 alpha (PGC1α), a factor that increases cellular aerobic capacity by promoting mitochondrial biogenesis and metabolic gene transcription.