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- Döring, J., et al.
(författare)
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Band terminations in the valence space of 86Zr
- 2000
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Ingår i: Physical Review C - Nuclear Physics. - 0556-2813. ; 61:3, s. 343101-343106
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Tidskriftsartikel (refereegranskat)abstract
- High-spin states in 86Zr up to 30+ and 27- were observed via the 58Ni(32S,4p) reaction at 135 MeV beam energy using the combined GAMMASPHERE and MICROBALL systems. Calculations performed with the configuration-dependent shell-correction approach show that these states are built from six g9/2 neutrons and at most four protons excited from the p1/2,p3/2,f5/2 subshells to the g9/2 subshell at small deformation. The highest observed states at 27- and 30+ are interpreted as band-terminating states with the latter having the highest spin available in the valence space for 86Zr.
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| 5. |
- Jansson, Malin, et al.
(författare)
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MiR-155-mediated loss of C/EBP beta shifts the TGF-beta response from growth inhibition to epithelial-mesenchymal transition, invasion and metastasis in breast cancer
- 2013
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Ingår i: Oncogene. - : Nature Publishing Group. - 0950-9232 .- 1476-5594. ; 32:50, s. 5614-5624
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Tidskriftsartikel (refereegranskat)abstract
- During breast cancer progression, transforming growth factor-beta (TGF-beta) switches from acting as a growth inhibitor to become a major promoter of epithelial-mesenchymal transition (EMT), invasion and metastasis. However, the mechanisms involved in this switch are not clear. We found that loss of CCAAT-enhancer binding protein beta (C/EBP beta), a differentiation factor for the mammary epithelium, was associated with signs of EMT in triple-negative human breast cancer, and in invasive areas of mammary tumors in MMTV-PyMT mice. Using an established model of TGF-beta-induced EMT in mouse mammary gland epithelial cells, we discovered that C/EBP beta was repressed during EMT by miR-155, an oncomiR in breast cancer. Depletion of C/EBP beta potentiated the TGF-beta response towards EMT, and contributed to evasion of the growth inhibitory response to TGF-beta. Furthermore, loss of C/EBP beta enhanced invasion and metastatic dissemination of the mouse mammary tumor cells to the lungs after subcutaneous injection into mice. The mechanism by which loss of C/EBP beta promoted the TGF-beta response towards EMT, invasion and metastasis, was traced to a previously uncharacterized role of C/EBP beta as a transcriptional activator of genes encoding the epithelial junction proteins E-cadherin and coxsackie virus and adenovirus receptor. The results identify miR-155-mediated loss of C/EBP beta as a mechanism, which promotes breast cancer progression by shifting the TGF-beta response from growth inhibition to EMT, invasion and metastasis.
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| 9. |
- Looy, Cindy V., et al.
(författare)
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Biological and physical evidence for extreme seasonality in central Permian Pangea
- 2016
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Ingår i: Palaeogeography, Palaeoclimatology, Palaeoecology. - : Elsevier BV. - 0031-0182 .- 1872-616X. ; 451, s. 210-226
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Tidskriftsartikel (refereegranskat)abstract
- Climate models indicate increased desertification in the continental interior of Pangea during the Permian, which would have affected the composition of the flora and fauna. We present a multi-proxy paleoenvironmental reconstruction of a terrestrial ecosystem in central Pangea of Lopingian age. The reconstruction is based on biological and physical data from the Moradi Formation, located in the Tim Mersoi sub-Basin, northern Niger. Paleosols and sedimentological evidence indicate that the prevailing climate was semi-arid to very arid with marked intervals of high water availability. Carbon stable isotope data from organic matter and paleosols suggest that both the soil productivity and actual evapotranspiration were very low, corresponding to arid conditions. Histological analysis of pareiasaur bones shows evidence of active metabolism and reveals distinct growth marks. These interruptions of bone formation are indicative of growth rhythms, and are considered as markers for contrasting seasonality orepisodic climate events. The macrofossil floras have low diversity and represent gymnosperm dominated woodlands. Most notable are ovuliferous dwarf shoots of voltzian conifers, and a 25-m long tree trunk with irregularly positioned branch scars. The combined biological and physical evidence suggests that the Moradi Formation was deposited under a generally arid climate with recurring periods of water abundance, allowing for a well-established ground water-dependent ecosystem. With respect to its environment, this system is comparable with modern ecosystems such as the southern African Namib Desert and the Lake Eyre Basin in Australia, which are discussed as modern analogues.
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| 10. |
- Pang, M-F, et al.
(författare)
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TGF-beta 1-induced EMT promotes targeted migration of breast cancer cells through the lymphatic system by the activation of CCR7/CCL21-mediated chemotaxis
- 2016
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Ingår i: Oncogene. - : Nature Publishing Group. - 0950-9232 .- 1476-5594. ; 35:6, s. 748-760
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Tidskriftsartikel (refereegranskat)abstract
- Tumor cells frequently disseminate through the lymphatic system during metastatic spread of breast cancer and many other types of cancer. Yet it is not clear how tumor cells make their way into the lymphatic system and how they choose between lymphatic and blood vessels for migration. Here we report that mammary tumor cells undergoing epithelial-mesenchymal transition (EMT) in response to transforming growth factor-beta (TGF-beta 1) become activated for targeted migration through the lymphatic system, similar to dendritic cells (DCs) during inflammation. EMT cells preferentially migrated toward lymphatic vessels compared with blood vessels, both in vivo and in 3D cultures. A mechanism of this targeted migration was traced to the capacity of TGF-beta 1 to promote CCR7/CCL21-mediated crosstalk between tumor cells and lymphatic endothelial cells. On one hand, TGF-beta 1 promoted CCR7 expression in EMT cells through p38 MAP kinase-mediated activation of the JunB transcription factor. Blockade of CCR7, or treatment with a p38 MAP kinase inhibitor, reduced lymphatic dissemination of EMT cells in syngeneic mice. On the other hand, TGF-beta 1 promoted CCL21 expression in lymphatic endothelial cells. CCL21 acted in a paracrine fashion to mediate chemotactic migration of EMT cells toward lymphatic endothelial cells. The results identify TGF-beta 1-induced EMT as a mechanism, which activates tumor cells for targeted, DC-like migration through the lymphatic system. Furthermore, it suggests that p38 MAP kinase inhibition may be a useful strategy to inhibit EMT and lymphogenic spread of tumor cells.
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