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Qin Jiang

Researcher at University of Alberta

Publications -  8
Citations -  2247

Qin Jiang is an academic researcher from University of Alberta. The author has contributed to research in topics: Helicobacter pylori & Gene. The author has an hindex of 5, co-authored 7 publications receiving 2216 citations.

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Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori

TL;DR: The overall genomic organization, gene order and predicted proteomes (sets of proteins encoded by the genomes) of the two strains are quite similar, and it is found that H. pylori was believed to exhibit a large degree of genomic and allelic diversity, but this is the first such genomic comparison.
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Variability of gene order in different Helicobacter pylori strains contributes to genome diversity

TL;DR: This study demonstrates that macrodiversity, i.e. variability in gene order, in addition to microdiversity, is a characteristic of the H. pylori genome.
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Spontaneous Mutations That Confer Antibiotic Resistance in Helicobacter pylori

TL;DR: Analysis of spontaneous Rifr, Clar, and Cipr mutants confirmed previous results indicating that mutations within therpoB gene, the 23S rRNA gene, and thegyrA gene, respectively, are responsible; also, several new mutant alleles were identified.
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Cloning and functional characterization of Helicobacter pylori fumarate reductase operon comprising three structural genes coding for subunits C, A and B.

TL;DR: H. pylori FRD contains three subunits, of which FrdA and FrdB appear to form the catalytic dimer, whereas FrdC serves as a membrane anchor, suggesting that FRD-driven metabolism plays an active but non-essential role for growth of H.pylori cells in vitro.
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Genotypic Characterization of Clarithromycin-Resistant and -Susceptible Helicobacter pylori Strains from the Same Patient Demonstrates Existence of Two Unrelated Isolates

TL;DR: Pulsed-field gel electrophoresis patterns of NruI- andNotI-digested genomic DNA from the Clas and Clar isolates demonstrated that they are genetically distinct, suggesting that the development of clarithromycin resistance is not from the mutation of the existing Clas strain but from a completely new strain.