| 41. |
- Fletcher, C. L., et al.
(författare)
-
Investigating the Magnetospheres of Rapidly Rotating B-type Stars
- 2017
-
Ingår i: Lives And Death-Throes Of Massive Stars. - 9781107170063 ; , s. 369-372
-
Konferensbidrag (refereegranskat)abstract
- Recent spectropolarimetric surveys of bright, hot stars have found that similar to 10% of OB-type stars contain strong (mostly dipolar) surface magnetic fields (similar to kG). The prominent paradigm describing the interaction between the stellar winds and the surface magnetic field is the magnetically confined wind shock (MCWS) model. In this model, the stellar wind plasma is forced to move along the closed field loops of the magnetic field, colliding at the magnetic equator, and creating a shock. As the shocked material cools radiatively it will emit X-rays. Therefore, X-ray spectroscopy is a key tool in detecting and characterizing the hot wind material confined by the magnetic fields of these stars. Some B-type stars are found to have very short rotational periods. The effects of the rapid rotation on the X-ray production within the magnetosphere have yet to be explored in detail. The added centrifugal force due to rapid rotation is predicted to cause faster wind outflows along the field lines, leading to higher shock temperatures and harder X-rays. However, this is not observed in all rapidly rotating magnetic B-type stars. In order to address this from a theoretical point of view, we use the X-ray Analytical Dynamical Magnetosphere (XADM) model, originally developed for slow rotators, with an implementation of new rapid rotational physics. Using X-ray spectroscopy from ESA's XMM-Newton space telescope, we observed 5 rapidly rotating B-types stars to add to the previous list of observations. Comparing the observed X-ray luminosity and hardness ratio to that predicted by the XADM allows us to determine the role the added centrifugal force plays in the magnetospheric X-ray emission of these stars.
|
|
| 42. |
- Fortner, Renée T., et al.
(författare)
-
Ovarian cancer risk factors by tumor aggressiveness : An analysis from the Ovarian Cancer Cohort Consortium
- 2019
-
Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 145:1, s. 58-69
-
Tidskriftsartikel (refereegranskat)abstract
- Ovarian cancer risk factors differ by histotype; however, within subtype, there is substantial variability in outcomes. We hypothesized that risk factor profiles may influence tumor aggressiveness, defined by time between diagnosis and death, independent of histology. Among 1.3 million women from 21 prospective cohorts, 4,584 invasive epithelial ovarian cancers were identified and classified as highly aggressive (death in <1 year, n = 864), very aggressive (death in 1 to < 3 years, n = 1,390), moderately aggressive (death in 3 to < 5 years, n = 639), and less aggressive (lived 5+ years, n = 1,691). Using competing risks Cox proportional hazards regression, we assessed heterogeneity of associations by tumor aggressiveness for all cases and among serous and endometrioid/clear cell tumors. Associations between parity (phet = 0.01), family history of ovarian cancer (phet = 0.02), body mass index (BMI; phet ≤ 0.04) and smoking (phet < 0.01) and ovarian cancer risk differed by aggressiveness. A first/single pregnancy, relative to nulliparity, was inversely associated with highly aggressive disease (HR: 0.72; 95% CI [0.58-0.88]), no association was observed for subsequent pregnancies (per pregnancy, 0.97 [0.92-1.02]). In contrast, first and subsequent pregnancies were similarly associated with less aggressive disease (0.87 for both). Family history of ovarian cancer was only associated with risk of less aggressive disease (1.94 [1.47-2.55]). High BMI (≥35 vs. 20 to < 25 kg/m2 , 1.93 [1.46-2.56] and current smoking (vs. never, 1.30 [1.07-1.57]) were associated with increased risk of highly aggressive disease. Results were similar within histotypes. Ovarian cancer risk factors may be directly associated with subtypes defined by tumor aggressiveness, rather than through differential effects on histology. Studies to assess biological pathways are warranted.
|
|
| 43. |
- Gürer, D., et al.
(författare)
-
Women in Computing
- 2009
-
Ingår i: Wiley Encyclopedia of Computer Science and Engineering. - Hoboken, NJ, USA : John Wiley & Sons. - 9780470050118 ; , s. 3099-3122
-
Bokkapitel (övrigt vetenskapligt/konstnärligt)
|
|
| 44. |
|
|
| 45. |
- Hodgins-Davis, Andrea, et al.
(författare)
-
Abundant Gene-by-Environment Interactions in Gene Expression Reaction Norms to Copper within Saccharomyces cerevisiae.
- 2012
-
Ingår i: Genome Biology and Evolution. - : Oxford University Press (OUP). - 1759-6653. ; 4:11, s. 1061-79
-
Tidskriftsartikel (refereegranskat)abstract
- Genetic variation for plastic phenotypes potentially contributes phenotypic variation to populations that can be selected during adaptation to novel ecological contexts. However, the basis and extent of plastic variation that manifests in diverse environments remains elusive. Here, we characterize copper reaction norms for mRNA abundance among five Saccharomyces cerevisiae strains to 1) describe population variation across the full range of ecologically relevant copper concentrations, from starvation to toxicity, and 2) to test the hypothesis that plastic networks exhibit increased population variation for gene expression. We find that although the vast majority of the variation is small in magnitude (considerably <2-fold), not just some, but most genes demonstrate variable expression across environments, across genetic backgrounds, or both. Plastically expressed genes included both genes regulated directly by copper-binding transcription factors Mac1 and Ace1 and genes indirectly responding to the downstream metabolic consequences of the copper gradient, particularly genes involved in copper, iron, and sulfur homeostasis. Copper-regulated gene networks exhibited more similar behavior within the population in environments where those networks have a large impact on fitness. Nevertheless, expression variation in genes like Cup1, important to surviving copper stress, was linked with variation in mitotic fitness and in the breadth of differential expression across the genome. By revealing a broader and deeper range of population variation, our results provide further evidence for the interconnectedness of genome-wide mRNA levels, their dependence on environmental context and genetic background, and the abundance of variation in gene expression that can contribute to future evolution.
|
|
| 46. |
- Huang, Tianyi, et al.
(författare)
-
Reproductive and Hormonal Factors and Risk of Ovarian Cancer by Tumor Dominance : Results from the Ovarian Cancer Cohort Consortium (OC3)
- 2020
-
Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - : AMER ASSOC CANCER RESEARCH. - 1055-9965 .- 1538-7755. ; 29:1, s. 200-207
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Laterality of epithelial ovarian tumors may reflect the underlying carcinogenic pathways and origins of tumor cells.Methods: We pooled data from 9 prospective studies participating in the Ovarian Cancer Cohort Consortium. Information on measures of tumor size or tumor dominance was extracted from surgical pathology reports or obtained through cancer registries. We defined dominant tumors as those restricted to one ovary or where the dimension of one ovary was at least twice as large as the other, and nondominant tumors as those with similar dimensions across the two ovaries or peritoneal tumors. Competing risks Cox models were used to examine whether associations with reproductive and hormonal risk factors differed by ovarian tumor dominance.Results: Of 1,058 ovarian cancer cases with tumor dominance information, 401 were left-dominant, 363 were right-dominant, and 294 were nondominant. Parity was more strongly inversely associated with risk of dominant than nondominant ovarian cancer (P-heterogeneity = 0.004). Ever use of oral contraceptives (OC) was associated with lower risk of dominant tumors, but was not associated with nondominant tumors (Pheterogeneity = 0.01). Higher body mass index was associated with higher risk of left-dominant tumors, but not significantly associated with risk of right-dominant or nondominant tumors (P-heterogeneity = 0.08).Conclusions: These data suggest that reproductive and hormonal risk factors appear to have a stronger impact on dominant tumors, which may have an ovarian or endometriosis origin.Impact: Examining the associations of ovarian cancer risk factors by tumor dominance may help elucidate the mechanisms through which these factors influence ovarian cancer risk.
|
|
| 47. |
- Johannesson, Hanna, et al.
(författare)
-
Concerted evolution in the rpeats of an immunomodulating cell surface protein, SOWgp, of the human pathogenic fungi Coccidioides immitis and C. posadasii.
- 2005
-
Ingår i: Genetics.
-
Tidskriftsartikel (refereegranskat)abstract
- Genome dynamics that allow pathogens to escape host immune responses are fundamental to our understanding of host-pathogen interactions. Here we present the first population-based study of the process of concerted evolution in the repetitive domain of a protein-coding gene. This gene, SOWgp, encodes the immunodominant protein in the parasitic phase of the human pathogenic fungi Coccidioides immitis and C. posadasii. We sequenced the entire gene from strains representing the geographic ranges of the two Coccidioides species. By using phylogenetic and genetic distance analyses we discovered that the repetitive part of SOWgp evolves by concerted evolution, predominantly by the mechanism of unequal crossing over. We implemented a mathematical model originally developed for multigene families to estimate the rate of homogenization and recombination of the repetitive array, and the results indicate that the pattern of concerted evolution is a result of homogenization of repeat units proceeding at a rate close to the nucleotide point mutation rate. The release of the SOWgp molecules by the pathogen during proliferation may mislead the host: we speculate that the pathogen benefits from concerted evolution of repeated domains in SOWgp by an enhanced ability to misdirect the host’s immune system.
|
|
| 48. |
- Johannesson, Henrik, et al.
(författare)
-
Phase-specific gene expression underlying morphological adaptations of the dimorphic human pathogenic fungus, Coccidioides posadasii
- 2006
-
Ingår i: Fungal Genetics and Biology. - : Elsevier BV. - 1087-1845 .- 1096-0937. ; 43:8, s. 545-559
-
Tidskriftsartikel (refereegranskat)abstract
- Coccidioides posadasii is a dimorphic fungal pathogen that grows as a Wlamentous saprobe in the soil and as endosporulating spheruleswithin the host. To identify genes speciWc to the pathogenic phase of Co. posadasii, we carried out a large-scale study of gene expression intwo isolates of the species. From the sequenced Co. posadasii genome, we chose 1000 open reading frames to construct a 70-mer microarray.RNA was recovered from both isolates at three life-cycle phases: hyphae, presegmented spherules, and spherules releasing endospores.Comparative hybridizations were conducted in a circuit design, permitting comparison between both isolates at all three life-cyclephases, and among all life-cycle phases for each isolate. By using this approach, we identiWed 92 genes that were diVerentially expressedbetween pathogenic and saprobic phases in both fungal isolates, and 43 genes with consistent diVerential expression between the two parasiticdevelopmental phases. Genes with elevated expression in the pathogenic phases of both isolates included a number of genes thatwere involved in the response to environmental stress as well as in the metabolism of lipids. The latter observation is in agreement withprevious studies demonstrating that spherules contain a higher proportion of lipids than saprobic phase tissue. Intriguingly, we discoveredstatistically signiWcant and divergent levels of gene expression between the two isolates proWled for 64 genes. The results suggest thatincorporating more than one isolate in the experimental design oVers a means of categorizing the large collection of candidate genes thattranscriptional proWling typically identiWes into those that are strain-speciWc and those that characterize the entire species.
|
|
| 49. |
- Mancuso, N, et al.
(författare)
-
Author Correction: Large-scale transcriptome-wide association study identifies new prostate cancer risk regions
- 2019
-
Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 10:1, s. 171-
-
Tidskriftsartikel (refereegranskat)abstract
- The original version of this Article contained an error in the spelling of a member of the PRACTICAL Consortium, Manuela Gago-Dominguez, which was incorrectly given as Manuela Gago Dominguez. This has now been corrected in both the PDF and HTML versions of the Article. Furthermore, In the original HTML version of this Article, the order of authors within the author list was incorrect. The consortium PRACTICAL consortium was incorrectly listed after Bogdan Pasaniuc and should have been listed after Kathryn L. Penney. This error has been corrected in the HTML version of the Article; the PDF version was correct at the time of publication.
|
|
| 50. |
- Mukherjee, S, et al.
(författare)
-
Murine cytotoxic T lymphocytes recognize an epitope in an EBNA-1 fragment, but fail to lyse EBNA-1-expressing mouse cells
- 1998
-
Ingår i: The Journal of experimental medicine. - : Rockefeller University Press. - 0022-1007 .- 1540-9538. ; 187:3, s. 445-450
-
Tidskriftsartikel (refereegranskat)abstract
- Major histocompatibility complex class I–restricted cytotoxic T lymphocytes (CTLs) specific for epitopes within eight of the nine Epstein Barr Virus (EBV)-encoded latency-associated proteins have been recovered from EBV-infected human subjects by restimulation of lymphocytes in vitro. However, human class I–restricted CTL responses capable of recognizing EBNA-1 expressing cells were not detected in these studies. We have raised a murine CTL line that recognizes an epitope within EBNA-1 by immunizing mice with a vaccinia virus encoding a COOH-terminal EBNA-1 fragment. This novel CTL line was used to investigate whether the epitope (positions 509–517 in EBNA-1, presented through Kd) was presented to CTL by mouse cells expressing full-length EBNA-1 or a deletion mutant of EBNA-1, lacking the Glycine-Alanine (Gly-Ala)–rich region. Cells expressing full-length EBNA-1 are not lysed by the CTL line, whereas cells expressing the Gly-Ala deletion mutant are recognized. These results suggest that epitopes from full-length EBNA-1 are poorly presented, and that the Gly-Ala–rich region is responsible for this phenomenon. The inefficient presentation of EBNA-1–derived epitopes may explain the absence or rarity of EBNA-1–specific CTLs in vivo, a strategy that may allow EBV to maintain persistence within the immunocompetent host without being eliminated by CTLs.
|
|
