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Copper oxide high-temperature superconductors, such as Bi 2 Sr 2 CaCu 2 O 8+ δ (Bi2212), have garnered extensive research interest due to their high critical temperatures (T c ) surpassing the Bardeen-Cooper-Schrieffer (BCS) limit. The two-dimensional CuO₂ plane is widely regarded as the most crucial element of high-T c cuprate superconductors. The anisotropy of this CuO₂ layer remains a topic of ongoing interest. Although a few experimental results have reported strong optical anisotropy in both ab and ac-planes of Bi2212 through optical "reflectivity" measurements, there is a lack of studies focusing on the optical anisotropy of these materials using optical "transmittance" measurements by utilizing ultraviolet and visible light. Using a generalized high-accuracy universal polarimeter, we observed significant linear birefringence and linear dichroism peaks in the UV region at room temperature. To investigate the origin of the significant optical anisotropy, single crystals of Bi 2- x Pb x Sr 2 CaCu 2 O 8+ δ with different lead contents (x = 0, 0.4, and 0.6) were grown using the floating zone method, and the wavelength dependencies of linear birefringence and linear dichroism along the c axis were measured. The insights gained into the optical anisotropy of Bi 2- x Pb x Sr 2 CaCu 2 O 8+ δ from this study are significant for discussing its origin of the mechanism of high-T c superconductivity., (© 2024. The Author(s).)

When two ecosystems with separate evolutionary histories come into contact (eco-fusion), reciprocal invasions occur during their fusion. Asymmetries in the migration direction or extinction rate then occur (e.g., during the Great American Biotic Interchange, GABI). Hypotheses have been proposed to describe this process, but the ecosystem properties have not been adequately discussed. To identify the ecosystem properties that create vulnerability to species loss during eco-fusion, we conducted computer simulations of the fusion of ecosystems with independent evolutionary histories. With asymmetrical species extinction rates, the ecosystem with a higher extinction rate had a shorter food chain, a higher ratio of animal species to plant species, and a lower ratio of carnivores to herbivores. Most ecosystems that have undergone isolated evolution are vulnerable. These results may explain the vulnerability of South America's ecosystem during the GABI and that of modern Australia.

EZH2 overexpression occurs in various malignancies and is associated with a poor outcome. We have so far demonstrated that EZH2 downregulates the important genes such as E-cadherin and RUNX3 by increasing histone H3K27 trimethylation. However, the mechanism of EZH2 overexpression in various cancer cells remains unclear. In this study we carried out a promoter analysis of the EZH2 gene and investigated whether a survival signal that is upregulated in cancer cells is related to overexpression at the transcription level. We also explored the clinical relevance of the signaling pathway that leads to EZH2 overexpression in breast cancer and demonstrated that MEK-ERK1/2-Elk-1 pathway leads to EZH2 overexpression. The triple-negative and ERBB2-overexpressing subtypes of breast cancer are known to contain more rapidly proliferating breast cancer cells. The signaling pathway connected to EZH2 overexpression was associated with both aggressive subtypes of breast cancer. We show the significance that overexpression of histone modifier protein EZH2 in cancer cells and our study could pave the way for EZH2 inhibition to become an efficient treatment for more aggressive breast cancers.

Cytokine oncostatin M (OM) exerts growth-inhibitory and differentiative effects on breast cancer cells. Previously we showed that the transcription from the p53 gene in breast cancer cells was down regulated by OM. To elucidate the molecular mechanisms underlying the OM effect on p53 transcription, in this study, we dissected the p53 promoter region and analysed the p53 promoter activity in breast tumor cells. We showed that treatment of MCF-7 cells with OM induced a dose- and time-dependent suppression of p53 promoter activity. The p53 promoter activity was decreased to 35% of control at 24 h and further decreased to 20% at 48 h by OM at concentrations of 5 ng/ml and higher. Deletion of the 5'-flanking region of the p53 promoter from -426 to -97 did not affect the OM effect. However, further deletion to -40 completely abolished the repressive effect of OM. The p53 promoter region -96 to -41 contains NF-kappaB and c-myc binding sites, and a newly identified UV-inducible element PE21. Mutations to disrupt NF-kappaB binding or c-myc binding to the p53 promoter decreased the basal promoter activity without affecting the OM-mediated suppression, whereas mutation at the PE21 motif totally abolished the OM effect. We further demonstrated that insertion of PE21 element upstream of the thymidine kinase minimal promoter generated an OM response analogous to that of the p53 promoter. Finally, we detected the specific binding of a nuclear protein with a molecular mass of 87 kDa to the PE21 motif. Taken together, we demonstrate that OM inhibits the transcription of the p53 gene through the PE21 element. Thus, the PE21 element is functionally involved in p53 transcription regulated by UV-induction and OM suppression.