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Stephen E. Hamby

Researcher at Nottingham Trent University

Publications -  5
Citations -  212

Stephen E. Hamby is an academic researcher from Nottingham Trent University. The author has contributed to research in topics: Gene & Germline. The author has an hindex of 5, co-authored 5 publications receiving 194 citations.

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Comparative Analysis of Genome Sequences Covering the Seven Cronobacter Species

TL;DR: C. sakazakii is unique in the Cronobacter genus in encoding genes enabling the utilization of exogenous sialic acid which may have clinical significance, and also suggested various degrees of divergence.
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A meta-analysis of single base-pair substitutions in translational termination codons ('nonstop' mutations) that cause human inherited disease

TL;DR: It is speculated that recruitment of an alternative stop codon at greater distance from the mutated stop codons may trigger nonstop mRNA decay, thereby decreasing the amount of protein product and yielding a readily discernible clinical phenotype.
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In Silico identification of pathogenic strains of Cronobacter from Biochemical data reveals association of inositol fermentation with pathogenicity

TL;DR: The use of Expectation Maximization clustering was used to categorise 98 strains of Cronobacter as pathogenic or non-pathogenic based on biochemical test results from standard diagnostic test kits, demonstrating a computational approach allowing existing diagnostic kits to be used to identify pathogenic strains ofronobacter.
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Exploring the somatic NF1 mutational spectrum associated with NF1 cutaneous neurofibromas.

TL;DR: 109 cutaneous neurofibromas, excised from 46 unrelated NF1 patients, are screened for somatic NF1 mutations and no association was noted between the type of germline and somaticNF1 lesion within the same individual.
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Comparative analysis of germline and somatic microlesion mutational spectra in 17 human tumor suppressor genes

TL;DR: A comparison of somatic, germline, shared and somatic recurrent mutational spectra for 17 human tumor suppressor genes concluded that ∼50% of these somatic missense mutations possess features consistent with their being either shared or recurrent, suggesting that a disproportionate number of such lesions are likely to be drivers of tumorigenesis.