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Numrering	Referens	Omslagsbild	Hitta
1.	Ajileye, Adebisi, et al. (författare) Some Synonymous and Nonsynonymous gyrA Mutations in Mycobacterium tuberculosis Lead to Systematic False-Positive Fluoroquinolone Resistance Results with the Hain GenoType MTBDRsl Assays 2017 Ingår i: Antimicrobial Agents and Chemotherapy. - : AMER SOC MICROBIOLOGY. - 0066-4804 .- 1098-6596. ; 61:4 Tidskriftsartikel (refereegranskat)abstract In this study, using the Hain GenoType MTBDRsl assays (versions 1 and 2), we found that some nonsynonymous and synonymous mutations in gyrA in Mycobacterium tuberculosis result in systematic false-resistance results to fluoroquinolones by preventing the binding of wild-type probes. Moreover, such mutations can prevent the binding of mutant probes designed for the identification of specific resistance mutations. Although these mutations are likely rare globally, they occur in approximately 7% of multidrug-resistant tuberculosis strains in some settings.
2.	Eyre, David W., et al. (författare) Gonorrhoea treatment failure caused by a Neisseria gonorrhoeae strain with combined ceftriaxone and high-level azithromycin resistance, England, February 2018 2018 Ingår i: Eurosurveillance. - : European Centre for Disease Prevention and Control (ECDC). - 1025-496X .- 1560-7917. ; 23:27, s. 2-7 Tidskriftsartikel (refereegranskat)
3.	Lakens, Daniel, et al. (författare) Justify your alpha 2018 Ingår i: Nature Human Behaviour. - : Nature Publishing Group. - 2397-3374. ; 2:3, s. 168-171 Tidskriftsartikel (refereegranskat)abstract In response to recommendations to redefine statistical significance to P ≤ 0.005, we propose that researchers should transparently report and justify all choices they make when designing a study, including the alpha level.
4.	Mörén, Lina, et al. (författare) Metabolomic profiling identifies distinct phenotypes for ASS1 positive and negative GBM 2018 Ingår i: BMC Cancer. - : BioMed Central. - 1471-2407. ; 18 Tidskriftsartikel (refereegranskat)abstract Background: Tumour cells have a high demand for arginine. However, a subset of glioblastomas has a defect in the arginine biosynthetic pathway due to epigenetic silencing of the rate limiting enzyme argininosuccinate synthetase (ASS1). These tumours are auxotrophic for arginine and susceptible to the arginine degrading enzyme, pegylated arginine deiminase (ADI-PEG20). Moreover, ASS1 deficient GBM have a worse prognosis compared to ASS1 positive tumours. Since altered tumour metabolism is one of the hallmarks of cancer we were interested to determine if these two subtypes exhibited different metabolic profiles that could allow for their non-invasive detection as well as unveil additional novel therapeutic opportunities.Methods: We looked for basal metabolic differences using one and two-dimensional gas chromatography-time-of-flight mass spectrometry (1D/2DGC-TOFMS) followed by targeted analysis of 29 amino acids using liquid chromatography-time-of-flight mass spectrometry (LC-TOFMS). We also looked for differences upon arginine deprivation in a single ASS1 negative and positive cell line (SNB19 and U87 respectively). The acquired data was evaluated by chemometric based bioinformatic methods.Results: Orthogonal partial least squares-discriminant analysis (OPLS-DA) of both the 1D and 2D GC-TOFMS data revealed significant systematic difference in metabolites between the two subgroups with ASS1 positive cells generally exhibiting an overall elevation of identified metabolites, including those involved in the arginine biosynthetic pathway. Pathway and network analysis of the metabolite profile show that ASS1 negative cells have altered arginine and citrulline metabolism as well as altered amino acid metabolism. As expected, we observed significant metabolite perturbations in ASS negative cells in response to ADI-PEG20 treatment.Conclusions: This study has highlighted significant differences in the metabolome of ASS1 negative and positive GBM which warrants further study to determine their diagnostic and therapeutic potential for the treatment of this devastating disease.

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Resultat 1-4 av 4

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Typ av publikation: tidskriftsartikel (4)

Typ av innehåll: refereegranskat (4)

Författare/redaktör: Peto, Tim E. A. (2); Crook, Derrick W. (2); Schön, Thomas (1); Kenny, David A. (1); Johansson, Christer (1); Albers, Casper J. (1); visa fler...; Ajileye, Adebisi (1); Alvarez, Nataly (1); Merker, Matthias (1); Walker, Timothy M. (1); Akter, Suriya (1); Brown, Kerstin (1); Moradigaravand, Dane ... (1); Andres, Soenke (1); Schleusener, Viola (1); Omar, Shaheed V. (1); Coll, Francesc (1); Huang, Hairong (1); Diel, Roland (1); Ismail, Nazir (1); Parkhill, Julian (1); de Jong, Bouke C. (1); Niemann, Stefan (1); Robledo, Jaime (1); Grace Smith, E. (1); Peacock, Sharon J. (1); Koeser, Claudio U. (1); Ingre, Michael (1); Unemo, Magnus, 1970- (1); Danielsson, Henrik (1); Grange, James A. (1); Hasselman, Fred (1); Spies, Jeffrey R. (1); van Assen, Marcel A. ... (1); Antti, Henrik (1); Golparian, Daniel, 1 ... (1); Carlsson, Rickard, 1 ... (1); Sjoerds, Zsuzsika (1); Edwards, Anne (1); Zwaan, Rolf A. (1); Mörén, Lina (1); Buchanan, Erin M. (1); Nilsonne, Gustav, 19 ... (1); Collins, Gary S. (1); Williams, Donald R. (1); Cole, Michelle J. (1); Fifer, Helen (1); De Xivry, Jean Jacqu ... (1); Holmes, Nicholas P. (1); Lukavský, Jiří (1); visa färre...

Lärosäte: Linköpings universitet (2); Umeå universitet (1); Stockholms universitet (1); Örebro universitet (1); Linnéuniversitetet (1); Karolinska Institutet (1)

Språk: Engelska (4)

Forskningsämne (UKÄ/SCB): Medicin och hälsovetenskap (4); Naturvetenskap (1); Samhällsvetenskap (1)

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