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David A. Pearce

Researcher at Northumbria University

Publications -  405
Citations -  20297

David A. Pearce is an academic researcher from Northumbria University. The author has contributed to research in topics: Batten disease & CLN3. The author has an hindex of 72, co-authored 396 publications receiving 18416 citations. Previous affiliations of David A. Pearce include University of Zurich & University of York.

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Review of the MEPAG Report on Mars Special Regions

TL;DR: The Mars Exploration Program Analysis Group (MEPAG) established the special regions science analysis group (SR-SAG2) to examine the quantitative definition of a special region and proposed modifications to it, as necessary, based upon the latest scientific results.

Low-latency mac-layer handoff for a high-altitude platform delivering broadband communications

TL;DR: In this paper, a low-latency handoff algorithm that exploits the unique characteristics of a high-altitude platform (HAP) multi-cell system payload to significantly reduce the need for payload stabilization is presented.
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A novel c.776_777insA mutation in CLN1 leads to infantile neuronal ceroid lipofuscinosis.

TL;DR: A patient with infantile neuronal ceroid lipofuscinosis with a novel c.776_777insA mutation in CLN1 is described, which induces a frameshift and a premature stop codon late within the CLn1 messenger RNA (mRNA) transcript which is likely recognized by nonsense-mediated translation repression, decreasing PPT1 abundance.
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De novo assembly of complete genome sequence of Planococcus kocurii ATCC 43650T, a potential plant growth-promoting bacterium

TL;DR: The first complete genome and annotation of P. kocurii ATCC 43650(T) is presented, identifying its potential as a plant growth promoting bacterium and its capability in the biosynthesis of butanol.
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Lack of serum- and glucocorticoid-inducible kinase 3 leads to podocyte dysfunction.

TL;DR: It is demonstrated that SGK3 contributes to the maintenance of podocyte integrity by controlling the expression and activity of GSK3 in mice treated with puromycin aminonucleoside and aSGK3 target protein, glycogen synthase kinase‐3 (GSK3), was discovered to be dramatically activated in PAN and SGk3 shRNA‐treated MPCs and in SGK 3 KO mice.