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- Fu, SS, et al.
(författare)
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Genetic diversity of the enterohaemolysin gene (ehxA) in non-O157 Shiga toxin-producing Escherichia coli strains in China
- 2018
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Ingår i: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 8:1, s. 4233-
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Tidskriftsartikel (refereegranskat)abstract
- Non-O157 Shiga toxin-producing Escherichia coli (STEC) is increasingly recognized as an important enteric foodborne pathogen. The hallmark of the disease is the production of Shiga toxins; however, there are other virulence factors that contribute to the pathogenesis of STEC. This study aimed to investigate the prevalence and genetic diversity of the enterohaemolysin gene, ehxA, among non-O157 STEC strains from human, animal, and food sources. The ehxA gene was amplified from 138 (31.8%) of 434 non-O157 STEC strains, among which 36 unique ehxA sequences were identified. Based on ehxA sequence analysis, three phylogenetic ehxA groups (I II, and III) were determined. Correlations between ehxA groups and sources, serotypes, and virulent gene profiles were observed. The ehxA group II strains were mostly diarrhoeal patient-derived and may demonstrate higher pathogenic potential compared with the ehxA group I and group III strains. Five types of replicons (I1-Ig, FIB, K, F, and B/O) were identified in the 138 ehxA-positive strains, and 3.6%, 5.8%, and 52.2% of the strains harboured toxB, katP and espP genes, respectively, implying marked genetic diversity of ehxA containing plasmids in non-O157 STEC strains. Sequence-based ehxA genotyping might be important in modern strain typing and in epidemiological surveillance of non-O157 STEC infections.
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- van der Meer, PF, et al.
(författare)
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Aggregates in platelet concentrates
- 2015
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Ingår i: Vox sanguinis. - : Wiley. - 1423-0410 .- 0042-9007. ; 108:1, s. 96-125
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Tidskriftsartikel (refereegranskat)
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- Yuen, RKC, et al.
(författare)
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Genome-wide characteristics of de novo mutations in autism
- 2016
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Ingår i: NPJ genomic medicine. - : Springer Science and Business Media LLC. - 2056-7944. ; 1, s. 160271-1602710
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Tidskriftsartikel (refereegranskat)abstract
- De novo mutations (DNMs) are important in autism spectrum disorder (ASD), but so far analyses have mainly been on the ~1.5% of the genome encoding genes. Here, we performed whole-genome sequencing (WGS) of 200 ASD parent–child trios and characterised germline and somatic DNMs. We confirmed that the majority of germline DNMs (75.6%) originated from the father, and these increased significantly with paternal age only (P=4.2×10−10). However, when clustered DNMs (those within 20 kb) were found in ASD, not only did they mostly originate from the mother (P=7.7×10−13), but they could also be found adjacent to de novo copy number variations where the mutation rate was significantly elevated (P=2.4×10−24). By comparing with DNMs detected in controls, we found a significant enrichment of predicted damaging DNMs in ASD cases (P=8.0×10−9; odds ratio=1.84), of which 15.6% (P=4.3×10−3) and 22.5% (P=7.0×10−5) were non-coding or genic non-coding, respectively. The non-coding elements most enriched for DNM were untranslated regions of genes, regulatory sequences involved in exon-skipping and DNase I hypersensitive regions. Using microarrays and a novel outlier detection test, we also found aberrant methylation profiles in 2/185 (1.1%) of ASD cases. These same individuals carried independently identified DNMs in the ASD-risk and epigenetic genes DNMT3A and ADNP. Our data begins to characterize different genome-wide DNMs, and highlight the contribution of non-coding variants, to the aetiology of ASD.
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