Low temperature dipolar echo in amorphous dielectrics: Significance of relaxation and decoherence free two level systems

The nature of dielectric echoes in amorphous solids at low temperatures is investigated. It is shown that at long delay times the echo amplitude is determined by a small subset of two level systems (TLS) having negligible relaxation and decoherence because of their weak coupling to phonons. The echo decay can then be described approximately by power law time dependencies with different powers at times longer and shorter than the typical TLS relaxation time. The theory is applied to recent measurements of two and three pulse dipolar echo in borosilicate glass BK7 and provides a perfect data fit in the broad time and temperature ranges under the assumption that there exist two TLS relaxation mechanisms due to TLS-phonons and TLS-TLS interaction. This interpretation is consistent with the previous experimental and theoretical investigations. Further experiments verifying the theory predictions are suggested.Comment: 10 pages, 8 figure

2D/3D Heterostructure for Semitransparent Perovskite Solar Cells with Engineered Bandgap Enables Efficiencies Exceeding 25% in Four‐Terminal Tandems with Silicon and CIGS

Wide-bandgap perovskite solar cells (PSCs) with optimal bandgap (E$_{g}$) and high power conversion efficiency (PCE) are key to high-performance perovskite-based tandem photovoltaics. A 2D/3D perovskite heterostructure passivation is employed for double-cation wide-bandgap PSCs with engineered bandgap (1.65 eV ≤ E$_{g}$ ≤ 1.85 eV), which results in improved stabilized PCEs and a strong enhancement in open-circuit voltages of around 45 mV compared to reference devices for all investigated bandgaps. Making use of this strategy, semitransparent PSCs with engineered bandgap are developed, which show stabilized PCEs of up to 25.7% and 25.0% in fourterminal perovskite/c-Si and perovskite/CIGS tandem solar cells, respectively. Moreover, comparable tandem PCEs are observed for a broad range of perovskite bandgaps. For the first time, the robustness of the four-terminal tandem configuration with respect to variations in the perovskite bandgap for two state-of-the-art bottom solar cells is experimentally validated

Optimization of SnO2_{2} electron transport layer for efficient planar perovskite solar cells with very low hysteresis†

Nanostructured tin oxide (SnO$_{2}$) is a very promising electron transport layer (ETL) for perovskite solar cells (PSCs) that allows low-temperature processing in the planar n–i–p architecture. However, minimizing current–voltage (J–V) hysteresis and optimizing charge extraction for PSCs in this architecture remains a challenge. In response to this, we study and optimize different types of single- and bilayer SnO$_{2}$ ETLs. Detailed characterization of the optoelectronic properties reveals that a bilayer ETL composed of lithium (Li)-doped compact SnO$_{2}$ (c(Li)-SnO$_{2}$) at the bottom and potassium-capped SnO$_{2}$ nanoparticle layers (NP-SnO$_{2}$) at the top enhances the electron extraction and charge transport properties of PSCs and reduces the degree of ion migration. This results in an improved PCE and a strongly reduced J–V hysteresis for PSCs with a bilayer c(Li)-NP-SnO$_{2}$ ETL as compared to reference PSCs with a single-layer or undoped bilayer ETL. The champion PSC with c(Li)-NP-SnO$_{2}$ ETL shows a high stabilized PCE of up to 18.5% compared to 15.7%, 12.5% and 16.3% for PSCs with c-SnO$_{2}$, c(Li)-SnO$_{2}$ and c-NP-SnO$_{2}$ as ETL, respectively

Alarmins MRP8 and MRP14 Induce Stress Tolerance in Phagocytes under Sterile Inflammatory Conditions

Hyporesponsiveness by phagocytes is a well-known phenomenon in sepsis that is frequently induced by low-dose endotoxin stimulation of Toll-like receptor 4 (TLR4) but can also be found under sterile inflammatory conditions. We now demonstrate that the endogenous alarmins MRP8 and MRP14 induce phagocyte hyporesponsiveness via chromatin modifications in a TLR4-dependent manner that results in enhanced survival to septic shock in mice. During sterile inflammation, polytrauma and burn trauma patients initially present with high serum concentrations of myeloid-related proteins (MRPs). Human neonatal phagocytes are primed for hyporesponsiveness by increased peripartal MRP concentrations, which was confirmed in murine neonatal endotoxinemia in wild-type and MRP14(-/-) mice. Our data therefore indicate that alarmin-triggered phagocyte tolerance represents a regulatory mechanism for the susceptibility of neonates during systemic infections and sterile inflammation

JAK-STAT signaling in inflammatory breast cancer enables chemotherapy-resistant cell states

Inflammatory breast cancer (IBC) is a difficult-to-treat disease with poor clinical outcomes due to high risk of metastasis and resistance to treatment. In breast cancer, CD44+CD24- cells possess stem cell-like features and contribute to disease progression, and we previously described a CD44+CD24-pSTAT3+ breast cancer cell subpopulation that is dependent on JAK2/STAT3 signaling. Here we report that CD44+CD24- cells are the most frequent cell-type in IBC and are commonly pSTAT3+. Combination of JAK2/STAT3 inhibition with paclitaxel decreased IBC xenograft growth more than either agent alone. IBC cell lines resistant to paclitaxel and doxorubicin were developed and characterized to mimic therapeutic resistance in patients. Multi-omic profiling of parental and resistant cells revealed enrichment of genes associated with lineage identity and inflammation in chemotherapy resistant derivatives. Integrated pSTAT3 ChIP-seq and RNA-seq analyses showed pSTAT3 regulates genes related to inflammation and epithelial to mesenchymal transition (EMT) in resistant cells, as well as PDE4A, a cAMP-specific phosphodiesterase. Metabolomic characterization identified elevated cAMP signaling and CREB as a candidate therapeutic target in IBC. Investigation of cellular dynamics and heterogeneity at the single cell level during chemotherapy and acquired resistance by CyTOF and single cell RNA-seq identified mechanisms of resistance including a shift from luminal to basal/mesenchymal cell states through selection for rare pre-existing subpopulations or an acquired change. Lastly, combination treatment with paclitaxel and JAK2/STAT3 inhibition prevented the emergence of the mesenchymal chemo-resistant subpopulation. These results provide mechanistic rational for combination of chemotherapy with inhibition of JAK2/STAT3 signaling as a more effective therapeutic strategy in IBC