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See detailThe K2-ESPRINT Project I: Discovery of the Disintegrating Rocky Planet with a Cometary Head and Tail EPIC 201637175b
Sanchis-Ojeda, R.; Rappaport, S.; Pallé, E. et al

E-print/Working paper (2015)

We present the discovery of a transiting exoplanet candidate in the K2 Field-1 with an orbital period of 9.1457 hours: EPIC 201637175b. The highly variable transit depths, ranging from $\sim$0\% to 1.3 ... [more ▼]

We present the discovery of a transiting exoplanet candidate in the K2 Field-1 with an orbital period of 9.1457 hours: EPIC 201637175b. The highly variable transit depths, ranging from $\sim$0\% to 1.3\%, are suggestive of a planet that is disintegrating via the emission of dusty effluents. We characterize the host star as an M-dwarf with $T_{\rm eff} \simeq 3800$. We have obtained ground-based transit measurements with several 1-m class telescopes and with the GTC. These observations (1) improve the transit ephemeris; (2) confirm the variable nature of the transit depths; (3) indicate variations in the transit shapes; and (4) demonstrate clearly that at least on one occasion the transit depths were significantly wavelength dependent. The latter three effects tend to indicate extinction of starlight by dust rather than by any combination of solid bodies. The K2 observations yield a folded light curve with lower time resolution but with substantially better statistical precision compared with the ground-based observations. We detect a significant ``bump' just after the transit egress, and a less significant bump just prior to transit ingress. We interpret these bumps in the context of a planet that is not only likely streaming a dust tail behind it, but also has a more prominent leading dust trail that precedes it. This effect is modeled in terms of dust grains that can escape to beyond the planet's Hill sphere and effectively undergo `Roche lobe overflow', even though the planet's surface is likely underfilling its Roche lobe by a factor of 2. [less ▲]

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See detailNFKBIA Deletion in Glioblastomas.
Bredel, M.; Scholtens, D. M.; Yadav, A. K. et al

in New England Journal of Medicine [=NEJM] (2011)

Background Amplification and activating mutations of the epidermal growth factor receptor (EGFR) oncogene are molecular hallmarks of glioblastomas. We hypothesized that deletion of NFKBIA (encoding ... [more ▼]

Background Amplification and activating mutations of the epidermal growth factor receptor (EGFR) oncogene are molecular hallmarks of glioblastomas. We hypothesized that deletion of NFKBIA (encoding nuclear factor of kappa-light polypeptide gene enhancer in B-cells inhibitor-alpha), an inhibitor of the EGFR-signaling pathway, promotes tumorigenesis in glioblastomas that do not have alterations of EGFR. Methods We analyzed 790 human glioblastomas for deletions, mutations, or expression of NFKBIA and EGFR. We studied the tumor-suppressor activity of NFKBIA in tumor-cell culture. We compared the molecular results with the outcome of glioblastoma in 570 affected persons. Results NFKBIA is often deleted but not mutated in glioblastomas; most deletions occur in nonclassical subtypes of the disease. Deletion of NFKBIA and amplification of EGFR show a pattern of mutual exclusivity. Restoration of the expression of NFKBIA attenuated the malignant phenotype and increased the vulnerability to chemotherapy of cells cultured from tumors with NFKBIA deletion; it also reduced the viability of cells with EGFR amplification but not of cells with normal gene dosages of both NFKBIA and EGFR. Deletion and low expression of NFKBIA were associated with unfavorable outcomes. Patients who had tumors with NFKBIA deletion had outcomes that were similar to those in patients with tumors harboring EGFR amplification. These outcomes were poor as compared with the outcomes in patients with tumors that had normal gene dosages of NFKBIA and EGFR. A two-gene model that was based on expression of NFKBIA and O(6)-methylguanine DNA methyltransferase was strongly associated with the clinical course of the disease. Conclusions Deletion of NFKBIA has an effect that is similar to the effect of EGFR amplification in the pathogenesis of glioblastoma and is associated with comparatively short survival. [less ▲]

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