Optical Response of Aged Doped and Undoped GaAs Samples.

We studied epitaxial GaAs samples doped with Ge and Sn up to 1×1019 cm -3, which were stored in a dry and dark environment for 26 years. The optical response of the GaAs samples was determined through the photoluminescence and photoreflectance techniques, taken at different times: just after their fabrication in 1995, 2001 and 2021. The evolution of defects formed by the action of O 2 in the samples and their correlation with doping with Ge and Sn impurities were studied. We obtained the result that aging formed defects of type vacancies, mainly As, which produced energy levels of deep traps linked to the L band. The concentration of vacancies over the 26 years could be as large as 1017 cm -3, and these vacancies form complexes with doping impurities.

Formation of Point Defects Due to Aging under Natural Conditions of Doped GaAs.

The aging dynamics of materials used to build the active part of optoelectronic devices is a topic of current interest. We studied epitaxial samples of GaAs doped with Ge and Sn up to 1×1019 cm-3, which were stored in a dry and dark environment for 26 years. Photoluminescence spectra were taken in three periods: 1995, 2001 and 2021. In the last year, time-resolved photoluminescence, Raman, and X-ray measurements were also performed to study the evolution of defects formed by the action of O2 in the samples and its correlation with the doping with Ge and Sn impurities. We found that oxygen formed oxides that gave off Ga and As atoms, leaving vacancies mainly of As. These vacancies formed complexes with the dopant impurities. The concentration of vacancies over the 26 years could be as large as 1×1018 cm-3.

Wnt2 Contributes to the Development of Atherosclerosis.

Atherosclerosis, is a chronic inflammatory disease, characterized by the narrowing of the arteries resulting from the formation of intimal plaques in the wall of arteries. Yet the molecular mechanisms responsible for maintaining the development and progression of atherosclerotic lesions have not been fully defined. In this study, we show that TGF-ß activates the endothelial-to-mesenchymal transition (EndMT) in cultured human aortic endothelial cells (HAECs) and this transition is dependent on the key executor of the Wnt signaling pathway in vitro. This study presents the first evidence describing the mechanistic details of the TGF-ß-induced EndMT signaling pathway in HAECs by documenting the cellular transition to the mesenchymal phenotype including the expression of mesenchymal markers α-SMA and PDGFRα, and the loss of endothelial markers including VE-cadherin and CD31. Furthermore, a short hairpin RNA (shRNA) screening revealed that Wnt2 signaling is required for TGF-ß-mediated EndMT of HAECs. Also, we found that LDLR-/- mice fed on a high-fat western-type diet (21% fat, 0.2% cholesterol) expressed high levels of Wnt2 protein in atherosclerotic lesions, confirming that this signaling pathway is involved in atherosclerosis in vivo. These findings suggest that Wnt2 may contribute to atherosclerotic plaque development and this study will render Wnt2 as a potential target for therapeutic intervention aiming at controlling atherosclerosis.

DSTYK Enhances Chemoresistance in Triple-Negative Breast Cancer Cells.

Breast cancer, as the most prevalent cancer in women, is responsible for more than 15% of new cancer cases and about 6.9% of all cancer-related death in the US. A major cause of therapeutic failure in breast cancer is the development of resistance to chemotherapy, especially for triple-negative breast cancer (TNBC). Therefore, how to overcome chemoresistance is the major challenge to improve the life expectancy of breast cancer patients. Our studies demonstrate that TNBC cells surviving the chronic treatment of chemotherapeutic drugs show significantly higher expression of the dual serine/threonine and tyrosine protein kinase (DSTYK) than non-treated parental cells. In our in vitro cellular models, DSTYK knockout via the CRISPR/Cas9-mediated technique results in apoptotic cell death of chemoresistant cells upon drug treatment. Moreover, DSTYK knockout promotes chemotherapeutic drug-induced tumor cell death in an orthotopic mouse model. These findings suggest that DSTYK exerts an important and previously unknown role in promoting chemoresistance. Our studies provide fundamental insight into the role of DSTYK in chemoresistance in TNBC cells and lay the foundation for the development of new strategies targeting DSTYK for improving TNBC therapy.