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The perovskite solar cell has emerged rapidly in the field of photovoltaics as it combines the merits of low cost, high efficiency, and excellent mechanical flexibility for versatile applications. However, there are significant concerns regarding its operational stability and mechanical robustness. Most of the previously reported approaches to address these concerns entail separate engineering of perovskite and charge-transporting layers. Herein we present a holistic design of perovskite and charge-transporting layers by synthesizing an interpenetrating perovskite/electron-transporting-layer interface. This interface is reaction-formed between a tin dioxide layer containing excess organic halide and a perovskite layer containing excess lead halide. Perovskite solar cells with such interfaces deliver efficiencies up to 22.2% and 20.1% for rigid and flexible versions, respectively. Long-term (1000 h) operational stability is demonstrated and the flexible devices show high endurance against mechanical-bending (2500 cycles) fatigue. Mechanistic insights into the relationship between the interpenetrating interface structure and performance enhancement are provided based on comprehensive, advanced, microscopic characterizations. This study highlights interface integrity as an important factor for designing efficient, operationally-stable, and mechanically-robust solar cells., Operational stability and mechanical robustness remain as engineering bottlenecks in perovskite solar cells technology. Here, Dong et al. introduce an interpenetrating perovskite at the electron-transporting-layer interface that enables a 1000-hour stable operation and high endurance against bending fatigue over 2500 cycles.

Several studies show that the immunosuppressive drugs targeting the interleukin-6 (IL-6) receptor, including tocilizumab, ameliorate lethal inflammatory responses in COVID-19 patients infected with SARS-CoV-2. Here, by employing single-cell analysis of the immune cell composition of two severe-stage COVID-19 patients prior to and following tocilizumab-induced remission, we identify a monocyte subpopulation that contributes to the inflammatory cytokine storms. Furthermore, although tocilizumab treatment attenuates the inflammation, immune cells, including plasma B cells and CD8+ T cells, still exhibit robust humoral and cellular antiviral immune responses. Thus, in addition to providing a high-dimensional dataset on the immune cell distribution at multiple stages of the COVID-19, our work also provides insights into the therapeutic effects of tocilizumab, and identifies potential target cell populations for treating COVID-19-related cytokine storms., Tocilizumab has been used to treat the excessive inflammatory responses in COVID-19 patients. Here, the authors use single-cell RNA sequencing results from two severe COIVD-19 patients to provide high-dimensional immune profiling data, and to implicate potential cellular and molecular insights for the therapeutic effects of tocilizumab.

Growing evidences suggest that cancer stem cells exhibit many molecular characteristics and phenotypes similar to their ancestral progenitor cells. In the present study, human embryonic stem cells are induced to differentiate into hepatocytes along hepatic lineages to mimic liver development in vitro. A liver progenitor specific gene, RALY RNA binding protein like (RALYL), is identified. RALYL expression is associated with poor prognosis, poor differentiation, and metastasis in clinical HCC patients. Functional studies reveal that RALYL could promote HCC tumorigenicity, self-renewal, chemoresistance, and metastasis. Moreover, molecular mechanism studies show that RALYL could upregulate TGF-β2 mRNA stability by decreasing N6-methyladenosine (m6A) modification. TGF-β signaling and the subsequent PI3K/AKT and STAT3 pathways, upregulated by RALYL, contribute to the enhancement of HCC stemness. Collectively, RALYL is a liver progenitor specific gene and regulates HCC stemness by sustaining TGF-β2 mRNA stability. These findings may inspire precise therapeutic strategies for HCC., RALYL is a liver progenitor cell-specific gene but its role in hepatocellular carcinoma (HCC) remains unknown. Here, the authors demonstrate that RALYL regulates HCC stemness through upregulation of TGF-β2 mRNA stability by decreasing N6-methyladenosine modification.

The search for quantum spin liquids in frustrated quantum magnets recently has enjoyed a surge of interest, with various candidate materials under intense scrutiny. However, an experimental confirmation of a gapped topological spin liquid remains an open question. Here, we show that circularly-polarized light can provide a novel knob to drive frustrated Mott insulators into a chiral spin liquid (CSL), realizing an elusive quantum spin liquid with topological order. We find that the dynamics of a driven Kagome Mott insulator is well-captured by an effective Floquet spin model, with heating strongly suppressed, inducing a scalar spin chirality $S_i \cdot (S_j \times S_k)$ term which dynamically breaks time-reversal while preserving SU(2) spin symmetry. We fingerprint the transient phase diagram and find a stable photo-induced CSL near the equilibrium state. The results presented suggest employing dynamical symmetry breaking to engineer quantum spin liquids and access elusive phase transitions that are not readily accessible in equilibrium., Comment: Accepted version, with supplementary info. 36 pages, 8 figures

Beta-transducin repeat containing E3 ubiquitin protein ligase (BTRC) is crucial for the degradation of IκBα. Our previous transcriptome sequencing analysis revealed that tetraspanin 15 (TSPAN15) was significantly upregulated in clinical oesophageal squamous cell carcinoma (OSCC) tissues. Here, we show that high TSPAN15 expression in OSCC tissues is significantly associated with lymph node and distant metastasis, advanced clinical stage, and poor prognosis. Elevated TSPAN15 expression is, in part, caused by the reduction of miR-339-5p. Functional studies demonstrate that TSPAN15 promotes metastatic capabilities of OSCC cells. We further show that TSPAN15 specifically interacts with BTRC to promote the ubiquitination and proteasomal degradation of p-IκBα, and thereby triggers NF-κB nuclear translocation and subsequent activation of transcription of several metastasis-related genes, including ICAM1, VCAM1, uPA, MMP9, TNFα, and CCL2. Collectively, our findings indicate that TSPAN15 may serve as a new biomarker and/or provide a novel therapeutic target to OSCC patients., BTRC can activate NF-κB signaling through the ubiquitination and degradation of IκB-α. Here the authors show that TSPAN15 promotes metastasis of oesophageal squamous cell cancer by enhancing BTRC induced degradation of IκB-α and subsequent activation of NF-κB.

Inositol polyphosphate 5-phosphatases can terminate downstream signalling of phosphatidylinositol-3 kinase; however, their biological role in the pathogenesis of cancer is controversial. Here we report that the inositol polyphosphate 5-phosphatase, phosphatidylinositol 4,5-bisphosphate 5-phosphatase, has a tumour suppressive role in melanoma. Although it is commonly downregulated in melanoma, overexpression of phosphatidylinositol 4,5-bisphosphate 5-phosphatase blocks Akt activation, inhibits proliferation and undermines survival of melanoma cells in vitro, and retards melanoma growth in a xenograft model. In contrast, knockdown of phosphatidylinositol 4,5-bisphosphate 5-phosphatase results in increased proliferation and anchorage-independent growth of melanocytes. Although DNA copy number loss is responsible for downregulation of phosphatidylinositol 4,5-bisphosphate 5-phosphatase in a proportion of melanomas, histone hypoacetylation mediated by histone deacetylases HDAC2 and HDAC3 through binding to the transcription factor Sp1 at the PIB5PA gene promoter appears to be another commonly involved mechanism. Collectively, these results establish the tumour suppressive role of phosphatidylinositol 4,5-bisphosphate 5-phosphatase and reveal mechanisms involved in its downregulation in melanoma., Inositol polyphosphate 5-phosphatases, such as PIB5PA, terminate signalling downstream of phosophoinositide-3 kinase; however, their biological roles remain unclear. Here the authors report that PIB5PA has a tumour suppressive role in melanoma.