| 1. |
- Beal, Jacob, et al.
(författare)
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Robust estimation of bacterial cell count from optical density
- 2020
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Ingår i: Communications Biology. - : Springer Science and Business Media LLC. - 2399-3642. ; 3:1
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Tidskriftsartikel (refereegranskat)abstract
- Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals <1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data.
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| 2. |
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| 3. |
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| 4. |
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- 2019
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Tidskriftsartikel (refereegranskat)
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| 5. |
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| 6. |
- Sampson, Joshua N., et al.
(författare)
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Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types
- 2015
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Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 107:12
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Tidskriftsartikel (refereegranskat)abstract
- Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites. Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers. Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, h(l)(2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (rho = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (rho = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (rho = 0.51, SE = 0.18), and bladder and lung (rho = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures. Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.
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| 7. |
- Ablikim, M., et al.
(författare)
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Observation of the Semileptonic Decay D-0 -> a(0)(980)(-)e(+)nu(e) and Evidence for D+ -> a(0)(980)(0)e(+)nu(e)
- 2018
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Ingår i: Physical Review Letters. - : AMER PHYSICAL SOC. - 0031-9007 .- 1079-7114. ; 121:8
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Tidskriftsartikel (refereegranskat)abstract
- Using an e(+)e(-) collision data sample of 2.93 fb(-1) collected at a center-of-mass energy of 3.773 GeV by the BESIII detector at BEPCII, we report the observation of D-0 -> a(0)(980)(-)e(+)nu(e) and evidence for D+ -> a(0)(980)(0)e(+)nu(e) with significances of 6.4 sigma and 2.9 sigma, respectively. The absolute branching fractions are determined to be B(D-0 -> a(0)(980)(-)e(+)nu(e)) x B(a(0)(980)(-) -> eta pi(-)) = [1.33(-0.29)(+0.33)(stat) +/- 0.09(syst)] x 10(-4) and B(D+ -> a(0)(980)(0)e(+)nu(e)) x B(a(0)(980)(0) -> eta pi(0)) = [1.66(-0.66)(+0.81)(stat) +/- 0.11(syst) x 10(-4). This is the first time the a(0)(980) meson has been measured in a D-0 semileptonic decay, which would open one more interesting page in the investigation of the nature of the puzzling a(0)(980) states.
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| 8. |
- Ablikim, M., et al.
(författare)
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Search for invisible decays of omega and phi with J/psi data at BESIII
- 2018
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Ingår i: Physical Review D. - : American Physical Society. - 2470-0010 .- 2470-0029. ; 98:3
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Tidskriftsartikel (refereegranskat)abstract
- Using a data sample of (1310.6 +/- 7.0) x 10(6) J/psi events collected with the BESIII detector operating at the BEPCII collider, we perform the first experimental search for invisible decays of a light vector meson (V = omega, phi) via J/psi -> V-eta decays. The decay of eta -> pi(+)pi(-)pi(0) is utilized to tag the V meson decaying into the invisible final state. No evidence for a significant invisible signal is observed, and the upper limits on the ratio of branching fractions at the 90% confidence level are determined to be B(omega -> invisible)/B(omega -> pi(+)pi(-)pi(0)) < 8.1 x 10(-5) and B(phi -> invisible)/B(phi -> K+K-) < 3.4 x 10(-4). By using the world average values of B(omega -> pi(+)pi(-)pi(0) and B(phi -> K+K-,) the upper limits on the decay branching fractions at the 90% confidence level are set as B(omega -> invisible) < 7.3 x 10(-5) and B(phi -> invisible) < 1.7 x 10(-4), respectively.
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| 9. |
- Campbell, PJ, et al.
(författare)
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Pan-cancer analysis of whole genomes
- 2020
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 1476-4687 .- 0028-0836. ; 578:7793, s. 82-
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Tidskriftsartikel (refereegranskat)abstract
- Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale1–3. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4–5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter4; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation5,6; analyses timings and patterns of tumour evolution7; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity8,9; and evaluates a range of more-specialized features of cancer genomes8,10–18.
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| 10. |
- Aad, G, et al.
(författare)
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- 2015
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swepub:Mat__t
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