Laminated Perovskite Photovoltaics: Enabling Novel Layer Combinations and Device Architectures

High‐efficiency perovskite‐based solar cells can be fabricated via either solution‐processing or vacuum‐based thin‐film deposition. However, both approaches limit the choice of materials and the accessible device architectures, due to solvent incompatibilities or possible layer damage by vacuum techniques. To overcome these limitations, the lamination of two independently processed half‐stacks of the perovskite solar cell is presented in this work. By laminating the two half‐stacks at an elevated temperature (≈90 °C) and pressure (≈50 MPa), the polycrystalline perovskite thin‐film recrystallizes and the perovskite/charge transport layer (CTL) interface forms an intimate electrical contact. The laminated perovskite solar cells with tin oxide and nickel oxide as CTLs exhibit power conversion efficiencies of up to 14.6%. Moreover, they demonstrate long‐term and high‐temperature stability at temperatures of up to 80 °C. This freedom of design is expected to access both novel device architectures and pairs of CTLs that remain usually inaccessible

Tracing molybdenum attenuation in mining environments using molybdenum stable isotopes

Molybdenum contamination is a concern in mining regions worldwide. Better understanding of processes controlling Mo mobility in mine wastes is critical for assessing potential impacts and developing water-quality management strategies associated to this element. Here, we used Mo stable isotope (δ98/95Mo) analyses to investigate geochemical controls on Mo mobility within a tailings management facility (TMF) featuring oxic and anoxic environments. These isotopic analyses were integrated with X-ray absorption spectroscopy, X-ray diffraction, Raman spectroscopy, transmission electron microscopy, and aqueous chemical data. Dissolved Mo concentrations were inversely correlated with δ98/95Mo values such that enrichment of heavy Mo isotopes in solution reflected attenuation processes. Inner-sphere complexation of Mo(VI) with ferrihydrite was the primary driver of Mo removal and was accompanied by a circa 1 ‰ isotope fractionation. Limited Mo attenuation and isotope fractionation was observed in Fe(II)- and Mo-rich anoxic TMF seepage, while attenuation and isotope fractionation were greatest during discharge and oxidation of this seepage after discharge into a pond where Fe-(oxyhydr)oxide precipitation promoted Mo sorption. Overall, this study highlights the role of sorption onto Fe-(oxyhydr)oxides in attenuating Mo in oxic environments, a process which can be traced by Mo isotope analyses

Akt kinase C-terminal modifications control activation loop dephosphorylation and enhance insulin response.

The Akt protein kinase, also known as protein kinase B, plays key roles in insulin receptor signalling and regulates cell growth, survival and metabolism. Recently, we described a mechanism to enhance Akt phosphorylation that restricts access of cellular phosphatases to the Akt activation loop (Thr(308) in Akt1 or protein kinase B isoform alpha) in an ATP-dependent manner. In the present paper, we describe a distinct mechanism to control Thr(308) dephosphorylation and thus Akt deactivation that depends on intramolecular interactions of Akt C-terminal sequences with its kinase domain. Modifications of amino acids surrounding the Akt1 C-terminal mTORC2 (mammalian target of rapamycin complex 2) phosphorylation site (Ser(473)) increased phosphatase resistance of the phosphorylated activation loop (pThr(308)) and amplified Akt phosphorylation. Furthermore, the phosphatase-resistant Akt was refractory to ceramide-dependent dephosphorylation and amplified insulin-dependent Thr(308) phosphorylation in a regulated fashion. Collectively, these results suggest that the Akt C-terminal hydrophobic groove is a target for the development of agents that enhance Akt phosphorylation by insulin

Halogen Oxidation Reactions of (C5Ph5)Cr(CO)3 and Lewis Base Addition To [(C5Ph5)Cr(μ-X)X]2: Electrochemical, Magnetic, and Raman Spectroscopic Characterization of [(C5Ph5)CrX2]2 and (C5Ph5)CrX2(THF) (X = Cl, Br, I). X-ray Crystal Structure of [(C5Ph5)Cr(μ-Cl)Cl]2

The 17-electron complex (C5Ph5)Cr(CO)3 reacts with halogens (C6H5I•Cl2, Br2, and I2) in C6H6 to yield the dimeric oxidation products [(C5Ph5)Cr(m-X)X]2 as thermally stable solids. Reactions with other chlorinating agents similarly yield [(C5Ph5)CrCl2]2. An X-ray crystal structure of [(C5Ph5)Cr(m-Cl)Cl]2 was obtained. The magnetic properties of the Cl2 bridged dimer have been determined and modeled using the usual isotropic hamiltonian which yields J/k = –30 K. Low-temperature (77 K) Raman spectra of solid [(C5Ph5)CrX2]2 (X = Cl, I) allow assignments to be made for the metal-ring and metal halogen stretching modes in the low frequency region (\u3c 600 cm-1). Tetrahydrofuran (THF) cleaves these dimers to yield complexes of the form (C5Ph5)CrX2(THF)

PPARα siRNA–Treated Expression Profiles Uncover the Causal Sufficiency Network for Compound-Induced Liver Hypertrophy

Uncovering pathways underlying drug-induced toxicity is a fundamental objective in the field of toxicogenomics. Developing mechanism-based toxicity biomarkers requires the identification of such novel pathways and the order of their sufficiency in causing a phenotypic response. Genome-wide RNA interference (RNAi) phenotypic screening has emerged as an effective tool in unveiling the genes essential for specific cellular functions and biological activities. However, eliciting the relative contribution of and sufficiency relationships among the genes identified remains challenging. In the rodent, the most widely used animal model in preclinical studies, it is unrealistic to exhaustively examine all potential interactions by RNAi screening. Application of existing computational approaches to infer regulatory networks with biological outcomes in the rodent is limited by the requirements for a large number of targeted permutations. Therefore, we developed a two-step relay method that requires only one targeted perturbation for genome-wide de novo pathway discovery. Using expression profiles in response to small interfering RNAs (siRNAs) against the gene for peroxisome proliferator-activated receptor α (Ppara), our method unveiled the potential causal sufficiency order network for liver hypertrophy in the rodent. The validity of the inferred 16 causal transcripts or 15 known genes for PPARα-induced liver hypertrophy is supported by their ability to predict non-PPARα–induced liver hypertrophy with 84% sensitivity and 76% specificity. Simulation shows that the probability of achieving such predictive accuracy without the inferred causal relationship is exceedingly small (p < 0.005). Five of the most sufficient causal genes have been previously disrupted in mouse models; the resulting phenotypic changes in the liver support the inferred causal roles in liver hypertrophy. Our results demonstrate the feasibility of defining pathways mediating drug-induced toxicity from siRNA-treated expression profiles. When combined with phenotypic evaluation, our approach should help to unleash the full potential of siRNAs in systematically unveiling the molecular mechanism of biological events

Brief Definitive Report The CCR7 Ligand ELC (CCL19) Is Transcytosed in High Endothelial Venules and Mediates T Cell Recruitment

Abstract Lymphocyte homing to secondary lymphoid tissue is defined by a multistep sequence of interactions between lymphocytes and endothelial cells in high endothelial venules (HEVs). After initial selectin-mediated tethering and rolling, firm adhesion of lymphocytes requires rapid upregulation of lymphocyte integrin adhesiveness. This step is mediated in part by the HEVderived chemokine SLC (secondary lymphoid-tissue chemokine, or CCL21) that binds to the CC chemokine receptor (CCR)7 on lymphocytes. However, the CC chemokine ELC (EpsteinBarr virus-induced molecule 1 ligand chemokine, or CCL19) shares the same receptor, and ELC transcripts have been observed in the T cell areas of lymphoid organs. Here, we show that perivascular ELC is transcytosed to the luminal surfaces of HEVs and enables efficient T cell homing to lymph nodes. In situ hybridization on sections of human tonsil showed no ELC mRNA in HEVs, but immunostaining revealed ELC protein in cytoplasmic vesicles of HEV cells. Furthermore, ELC injected into the footpads of mice entered the draining lymph nodes and was presented by HEVs. Finally, intracutaneous injections of ELC in mice lacking functionally relevant ELC and SLC ( plt/plt mice) restored T cell trafficking to draining lymph nodes as efficiently as SLC. We conclude that perivascular ELC is transcytosed to the luminal surfaces of HEVs and participates in CCR7-mediated triggering of lymphocyte arrest

Transcriptional and phenotypic comparisons of Ppara knockout and siRNA knockdown mice

RNA interference (RNAi) has great potential as a tool for studying gene function in mammals. However, the specificity and magnitude of the in vivo response to RNAi remains to be fully characterized. A molecular and phenotypic comparison of a genetic knockout mouse and the corresponding knockdown version would help clarify the utility of the RNAi approach. Here, we used hydrodynamic delivery of small interfering RNA (siRNA) to knockdown peroxisome proliferator activated receptor alpha (Ppara), a gene that is central to the regulation of fatty acid metabolism. We found that Ppara knockdown in the liver results in a transcript profile and metabolic phenotype that is comparable to those of Ppara(−/−) mice. Combining the profiles from mice treated with the PPARα agonist fenofibrate, we confirmed the specificity of the RNAi response and identified candidate genes proximal to PPARα regulation. Ppara knockdown animals developed hypoglycemia and hypertriglyceridemia, phenotypes observed in Ppara(−/−) mice. In contrast to Ppara(−/−) mice, fasting was not required to uncover these phenotypes. Together, these data validate the utility of the RNAi approach and suggest that siRNA can be used as a complement to classical knockout technology in gene function studies

Targeted Use of Sustainable Aviation Fuel to Maximize Climate Benefits

Sustainable aviation fuel (SAF) can reduce aviation’s CO2 and non-CO2 impacts. We quantify the change in contrail properties and climate forcing in the North Atlantic resulting from different blending ratios of SAF and demonstrate that intelligently allocating the limited SAF supply could multiply its overall climate benefit by factors of 9-15. A fleetwide adoption of 100% SAF increases contrail occurrence (+5%), but lower nonvolatile particle emissions (-52%) reduce the annual mean contrail net radiative forcing (-44%), adding to climate gains from reduced life cycle CO2 emissions. However, in the short term, SAF supply will be constrained. SAF blended at a 1% ratio and uniformly distributed to all transatlantic flights would reduce both the annual contrail energy forcing (EFcontrail) and the total energy forcing (EFtotal, contrails + change in CO2 life cycle emissions) by ~0.6%. Instead, targeting the same quantity of SAF at a 50% blend ratio to ~2% of flights responsible for the most highly warming contrails reduces EFcontrail and EFtotal by ~10 and ~6%, respectively. Acknowledging forecasting uncertainties, SAF blended at lower ratios (10%) and distributed to more flights (~9%) still reduces EFcontrail (~5%) and EFtotal (~3%). Both strategies deploy SAF on flights with engine particle emissions exceeding 1012 m-1, at nighttime, and in winter