The past 5 years have witnessed the rise of highly efficient organometal halide perovskite-based solar cells. In conventional perovskite solar cells, compact n-type metal oxide film is always required as a blocking layer on the transparent conducting oxide (TCO) substrate for efficient electron-selective contact. In this work, an interface engineering approach is demonstrated to avoid the deposition of compact n-type metal oxide blocking film. Alkali salt solution was used to modify the TCO surface to achieve the optimized interface energy level alignment, resulting in efficient electron-selective contact. A remarkable power conversion efficiency of 15.1% was achieved under AM 1.5 G 100 mW · cm(-2) irradiation without the use of compact n-type metal oxide blocking layers.
The prognostic, especially predictive, values of inflammation indexes in advanced colorectal cancer were not established. Therefore, the both values of neutrophil lymphocyte ratio (NLR) and platelet lymphocyte ratio (PLR) in patients with initially metastatic colorectal cancer (mCRC) were investigated and compared. Samples were collected from 243 patients who were initially diagnosed with mCRC between 2005 and 2010 in the Sun Yat-sen University Cancer Center. Elevated NLR (p < 0.001), PLR (p = 0.008), and CEA (p < 0.001) were identified as statistically significant poor prognostic factors for overall survival (OS), while only NLR (p = 0.029) and CEA (p < 0.001) were validated as independent predictors. Univariate analysis identified elevated NLR (p < 0.001), PLR (p = 0.023), and CEA (p < 0.001) as statistically significant poor predict factors for the progression-free survival (PFS) of first-line chemotherapy, while NLR (p = 0.013) and CEA (p = 0.001) were independent. In addition, we observed significantly different OS (p < 0.001) and PFS (p < 0.001) among patients who had elevations in both NLR and CEA levels and those having one elevation or neither elevation. NLR, PLR, and CEA were significant predictors of OS and PFS in mCRC. However, only NLR and CEA play as independent. When coupled with CEA, NLR may lead to improved prognostic predictors.
Epstein-Barr virus (EBV) causes endemic Burkitt lymphoma (BL) and immunosuppression-related lymphomas. These B cell malignancies arise by distinct transformation pathways and have divergent viral and host expression programs. To identify host dependency factors resulting from these EBV+, B cell-transformed cell states, we performed parallel genome-wide CRISPR/Cas9 loss-of-function screens in BL and lymphoblastoid cell lines (LCLs). These highlighted 57 BL and 87 LCL genes uniquely important for their growth and survival. LCL hits were enriched for EBV-induced genes, including viral super-enhancer targets. Our systematic approach uncovered key mechanisms by which EBV oncoproteins activate the PI3K/AKT pathway and evade tumor suppressor responses. LMP1-induced cFLIP was found to be critical for LCL defense against TNFα-mediated programmed cell death, whereas EBV-induced BATF/IRF4 were critical for BIM suppression and MYC induction in LCLs. Finally, EBV super-enhancer-targeted IRF2 protected LCLs against Blimp1-mediated tumor suppression. Our results identify viral transformation-driven synthetic lethal targets for therapeutic intervention.
We study the electronic contribution to the main thermoelectric properties of a molecular junction consisting of a single quantum dot coupled to graphene external leads. The system electrical conductivity (G), Seebeck coefficient (S), and the thermal conductivity (κ), are numerically calculated based on a Green's function formalism that includes contributions up to the Hartree-Fock level. We consider the system leads to be made either of pure or gapped-graphene. To describe the free electrons in the gapped-graphene electrodes we used two possible scenarios, the massive gap scenario, and the massless gap scenario, respectively. In all cases, the Fano effect is responsible for a strong violation of the Wiedemann-Franz law and we found a substantial increase of the system figure of merit ZT due to a drastic reduction of the system thermal coefficient. In the case of gapped-graphene electrodes, the system figure of merit presents a maximum at an optimal value of the energy gap of the order of ∆/D ∼ 0.002 (massive gap scenario) and ∆/D ∼ 0.0026 (massless gap scenario). Additionally, for all cases, the system figure of merit is temperature dependent.
Circadian clocks coordinate behaviour, physiology and metabolism with Earth's diurnal cycle. These clocks entrain to both light and temperature cycles, and daily environmental temperature oscillations probably contribute to human sleep patterns. However, the neural mechanisms through which circadian clocks monitor environmental temperature and modulate behaviour remain poorly understood. Here we elucidate how the circadian clock neuron network of Drosophila melanogaster processes changes in environmental temperature. In vivo calcium-imaging techniques demonstrate that the posterior dorsal neurons 1 (DN1s), which are a discrete subset of sleep-promoting clock neurons, constantly monitor modest changes in environmental temperature. We find that these neurons are acutely inhibited by heating and excited by cooling; this is an unexpected result when considering the strong correlation between temperature and light, and the fact that light excites clock neurons. We demonstrate that the DN1s rely on peripheral thermoreceptors located in the chordotonal organs and the aristae. We also show that the DN1s and their thermosensory inputs are required for the normal timing of sleep in the presence of naturalistic temperature cycles. These results identify the DN1s as a major gateway for temperature sensation into the circadian neural network, which continuously integrates temperature changes to coordinate the timing of sleep and activity.
Highlights d CRISPR/Cas9 screen highlights host epigenetic suppressors of the EBV lytic cycle d EBV senses MYC abundance to maintain B cell latency d MYC depletion alters three-dimensional EBV genomic architecture d FACT is a druggable target for Burkitt B cell EBV latency reversal
Highlights d Cystine starvation induces g-glutamyl-peptide accumulation in NSCLC cells d GCLC catalyzes g-glutamyl-peptide synthesis via a GSHindependent mechanism d NRF2 protects against ferroptosis via g-glutamyl-peptide synthesis d g-glutamyl-peptide synthesis prevents ferroptosis by reducing glutamate stress
SummaryEpstein-Barr virus (EBV) replication contributes to multiple human diseases, including infectious mononucleosis, nasopharyngeal carcinoma, B cell lymphomas, and oral hairy leukoplakia. We performed systematic quantitative analyses of temporal changes in host and EBV proteins during lytic replication to gain insights into virus-host interactions, using conditional Burkitt lymphoma models of type I and II EBV infection. We quantified profiles of >8,000 cellular and 69 EBV proteins, including >500 plasma membrane proteins, providing temporal views of the lytic B cell proteome and EBV virome. Our approach revealed EBV-induced remodeling of cell cycle, innate and adaptive immune pathways, including upregulation of the complement cascade and proteasomal degradation of the B cell receptor complex, conserved between EBV types I and II. Cross-comparison with proteomic analyses of human cytomegalovirus infection and of a Kaposi-sarcoma-associated herpesvirus immunoevasin identified host factors targeted by multiple herpesviruses. Our results provide an important resource for studies of EBV replication.
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