10 research outputs found

    Possible signatures of mixed-parity superconductivity in doped polar SrTiO3 films

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    Superconductors that possess both broken spatial inversion symmetry and spin-orbit interactions exhibit a mix of spin singlet and triplet pairing. Here, we report on measurements of the superconducting properties of electron-doped, strained SrTiO3 films. These films have an enhanced superconducting transition temperature and were previously shown to undergo a transition to a polar phase prior to becoming superconducting. We show that some films show signatures of an unusual superconducting state, such as an in-plane critical field that is higher than both the paramagnetic and orbital pair breaking limits. Moreover, nonreciprocal transport, which reflects the ratio of odd versus even pairing interactions, is observed. Together, these characteristics indicate that these films provide a tunable platform for investigations of unconventional superconductivity

    Anomalous superconducting diode effect in a polar superconductor

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    A superconductor with broken time reversal and inversion symmetry may exhibit nonreciprocal charge transport, including a nonreciprocal critical current, also known as superconducting diode effect. We report an intrinsic superconducting diode effect in a polar strontium titanate film. Differential resistance measurements reveal a superconducting state whose depairing current is polarity dependent. There is, however, no measurable deviation from Ohmic behavior, implying that this state does not arise from a bulk magnetochiral anisotropy. In the entire measurement range, the only deviation from linearity in the differential resistance is on the edge of the superconducting transition at high magnetic fields, likely due to the motion of flux vortices. Furthermore, the magnitude of the effect is preserved even when the in-plane magnetic field is oriented parallel to the current, indicating that this effect truly does not originate from a bulk magnetochiral anisotropy

    Targeted Protein Degradation to Overcome Resistance in Cancer Therapies: PROTAC and N-Degron Pathway

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    Extensive progress in understanding the molecular mechanisms of cancer growth and proliferation has led to the remarkable development of drugs that target cancer-driving molecules. Most target molecules are proteins such as kinases and kinase-associated receptors, which have enzymatic activities needed for the signaling cascades of cells. The small molecule inhibitors for these target molecules greatly improved therapeutic efficacy and lowered the systemic toxicity in cancer therapies. However, long-term and high-dosage treatment of small inhibitors for cancer has produced other obstacles, such as resistance to inhibitors. Among recent approaches to overcoming drug resistance to cancers, targeted protein degradation (TPD) such as proteolysis-targeting chimera (PROTAC) technology adopts a distinct mechanism of action by which a target protein is destroyed through the cellular proteolytic system, such as the ubiquitin–proteasome system or autophagy. Here, we review the currently developed PROTACs as the representative TPD molecules for cancer therapy and the N-degrons of the N-degron pathways as the potential TPD ligands

    Regulation of Inflammation-Mediated Endothelial to Mesenchymal Transition with Echinochrome a for Improving Myocardial Dysfunction

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    Endothelial–mesenchymal transition (EndMT) is a process by which endothelial cells (ECs) transition into mesenchymal cells (e.g., myofibroblasts and smooth muscle cells) and induce fibrosis of cells/tissues, due to ischemic conditions in the heart. Previously, we reported that echinochrome A (EchA) derived from sea urchin shells can modulate cardiovascular disease by promoting anti-inflammatory and antioxidant activity; however, the mechanism underlying these effects was unclear. We investigated the role of EchA in the EndMT process by treating human umbilical vein ECs (HUVECs) with TGF-β2 and IL-1β, and confirmed the regulation of cell migration, inflammatory, oxidative responses and mitochondrial dysfunction. Moreover, we developed an EndMT-induced myocardial infarction (MI) model to investigate the effect of EchA in vivo. After EchA was administered once a day for a total of 3 days, the histological and functional improvement of the myocardium was investigated to confirm the control of the EndMT. We concluded that EchA negatively regulates early or inflammation-related EndMT and reduces the myofibroblast proportion and fibrosis area, meaning that it may be a potential therapy for cardiac regeneration or cardioprotection from scar formation and cardiac fibrosis due to tissue granulation. Our findings encourage the study of marine bioactive compounds for the discovery of new therapeutics for recovering ischemic cardiac injuries
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