Driscollhanson7171

As the technology development, the future advanced combustion engines must be designed to perform at a low temperature. Thus, it is a great challenge to synthesize high active and stable catalysts to resolve exhaust below 100 °C. Here, we report that bismuth as a dopant is added to form platinum-bismuth cluster on silica for CO oxidation. The highly reducible oxygen species provided by surface metal-oxide (M-O) interface could be activated by CO at low temperature (~50 °C) with a high CO2 production rate of 487 μmolCO2·gPt-1·s-1 at 110 °C. Experiment data combined with density functional calculation (DFT) results demonstrate that Pt cluster with surface Pt-O-Bi structure is the active site for CO oxidation via providing moderate CO adsorption and activating CO molecules with electron transformation between platinum atom and carbon monoxide. These findings provide a unique and general approach towards design of potential excellent performance catalysts for redox reaction.Formamidinium lead iodide perovskites are promising light-harvesting materials, yet stabilizing them under operating conditions without compromising optimal optoelectronic properties remains challenging. We report a multimodal host-guest complexation strategy to overcome this challenge using a crown ether, dibenzo-21-crown-7, which acts as a vehicle that assembles at the interface and delivers Cs+ ions into the interior while modulating the material. This provides a local gradient of doping at the nanoscale that assists in photoinduced charge separation while passivating surface and bulk defects, stabilizing the perovskite phase through a synergistic effect of the host, guest, and host-guest complex. The resulting solar cells show power conversion efficiencies exceeding 24% and enhanced operational stability, maintaining over 95% of their performance without encapsulation for 500 h under continuous operation. Moreover, the host contributes to binding lead ions, reducing their environmental impact. This supramolecular strategy illustrates the broad implications of host-guest chemistry in photovoltaics.Cells infected with pathogens can contribute to clearing infections by releasing signals that instruct neighbouring cells to mount a pro-inflammatory cytokine response, or by other mechanisms that reduce bystander cells' susceptibility to infection. Here, we show the opposite effect epithelial cells infected with Salmonella Typhimurium secrete host factors that facilitate the infection of bystander cells. We find that the endoplasmic reticulum stress response is activated in both infected and bystander cells, and this leads to activation of JNK pathway, downregulation of transcription factor E2F1, and consequent reprogramming of microRNA expression in a time-dependent manner. These changes are not elicited by infection with other bacterial pathogens, such as Shigella flexneri or Listeria monocytogenes. Remarkably, the protein HMGB1 present in the secretome of Salmonella-infected cells is responsible for the activation of the IRE1 branch of the endoplasmic reticulum stress response in non-infected, neighbouring cells. Furthermore, E2F1 downregulation and the associated microRNA alterations promote Salmonella replication within infected cells and prime bystander cells for more efficient infection.It is known that an RNA's structure determines its biological function, yet current RNA structure probing methods only capture partial structure information. The ability to measure intact (i.e., full length) RNA structures will facilitate investigations of the functions and regulation mechanisms of small RNAs and identify short fragments of functional sites. Here, we present icSHAPE-MaP, an approach combining in vivo selective 2'-hydroxyl acylation and mutational profiling to probe intact RNA structures. We further showcase the RNA structural landscape of substrates bound by human Dicer based on the combination of RNA immunoprecipitation pull-down and icSHAPE-MaP small RNA structural profiling. We discover distinct structural categories of Dicer substrates in correlation to both their binding affinity and cleavage efficiency. And by tertiary structural modeling constrained by icSHAPE-MaP RNA structural data, we find the spatial distance measuring as an influential parameter for Dicer cleavage-site selection.Human pluripotent stem cell (hPSC)-derived pancreatic β cells are an attractive cell source for treating diabetes. However, current derivation methods remain inefficient, heterogeneous, and cell line dependent. To address these issues, we first devised a strategy to efficiently cluster hPSC-derived pancreatic progenitors into 3D structures. Through a systematic study, we discovered 10 chemicals that not only retain the pancreatic progenitors in 3D clusters but also enhance their potentiality towards NKX6.1+/INS+ β cells. We further systematically screened signaling pathway modulators in the three steps from pancreatic progenitors toward β cells. The implementation of all these strategies and chemical combinations resulted in generating β cells from different sources of hPSCs with high efficiency. The derived β cells are functional and can reverse hyperglycemia in mice within two weeks. Our protocol provides a robust platform for studying human β cells and developing hPSC-derived β cells for cell replacement therapy.Since their discovery as drivers of proliferation, cyclin-dependent kinases (CDKs) have been considered therapeutic targets. Small molecule inhibitors of CDK4/6 are used and tested in clinical trials to treat multiple cancer types. Despite their clinical importance, little is known about how CDK4/6 inhibitors affect the stability of CDK4/6 complexes, which bind cyclins and inhibitory proteins such as p21. We develop an assay to monitor CDK complex stability inside the nucleus. Unexpectedly, treatment with CDK4/6 inhibitors-palbociclib, ribociclib, or abemaciclib-immediately dissociates p21 selectively from CDK4 but not CDK6 complexes. This effect mediates indirect inhibition of CDK2 activity by p21 but not p27 redistribution. Our work shows that CDK4/6 inhibitors have two roles non-catalytic inhibition of CDK2 via p21 displacement from CDK4 complexes, and catalytic inhibition of CDK4/6 independent of p21. By broadening the non-catalytic displacement to p27 and CDK6 containing complexes, next-generation CDK4/6 inhibitors may have improved efficacy and overcome resistance mechanisms.Metal halide perovskites are an important class of emerging semiconductors. Their charge carrier dynamics is poorly understood due to limited knowledge of defect physics and charge carrier recombination mechanisms. Nevertheless, classical ABC and Shockley-Read-Hall (SRH) models are ubiquitously applied to perovskites without considering their validity. Herein, an advanced technique mapping photoluminescence quantum yield (PLQY) as a function of both the excitation pulse energy and repetition frequency is developed and employed to examine the validity of these models. While ABC and SRH fail to explain the charge dynamics in a broad range of conditions, the addition of Auger recombination and trapping to the SRH model enables a quantitative fitting of PLQY maps and low-power PL decay kinetics, and extracting trap concentrations and efficacies. However, PL kinetics at high power are too fast and cannot be explained. The proposed PLQY mapping technique is ideal for a comprehensive testing of theories and applicable to any semiconductor.Plants utilise intracellular nucleotide-binding, leucine-rich repeat (NLR) immune receptors to detect pathogen effectors and activate local and systemic defence. NRG1 and ADR1 "helper" NLRs (RNLs) cooperate with enhanced disease susceptibility 1 (EDS1), senescence-associated gene 101 (SAG101) and phytoalexin-deficient 4 (PAD4) lipase-like proteins to mediate signalling from TIR domain NLR receptors (TNLs). The mechanism of RNL/EDS1 family protein cooperation is not understood. Here, we present genetic and molecular evidence for exclusive EDS1/SAG101/NRG1 and EDS1/PAD4/ADR1 co-functions in TNL immunity. Using immunoprecipitation and mass spectrometry, we show effector recognition-dependent interaction of NRG1 with EDS1 and SAG101, but not PAD4. An EDS1-SAG101 complex interacts with NRG1, and EDS1-PAD4 with ADR1, in an immune-activated state. NRG1 requires an intact nucleotide-binding P-loop motif, and EDS1 a functional EP domain and its partner SAG101, for induced association and immunity. Thus, two distinct modules (NRG1/EDS1/SAG101 and ADR1/EDS1/PAD4) mediate TNL receptor defence signalling.Phenotypic plasticity is the variation in phenotype that a single genotype can produce in different environments and, as such, is an important component of individual fitness. However, whether the effect of new mutations, and hence evolution, depends on the direction of plasticity remains controversial. Here, we identify the cis-acting modifications that have reshaped gene expression in response to dehydration stress in three Arabidopsis species. Our study shows that the direction of effects of most cis-regulatory variants differentiating the response between A. thaliana and the sister species A. lyrata and A. halleri depends on the direction of pre-existing plasticity in gene expression. A comparison of the rate of cis-acting variant accumulation in each lineage indicates that the selective forces driving adaptive evolution in gene expression favors regulatory changes that magnify the stress response in A. lyrata. The evolutionary constraints measured on the amino-acid sequence of these genes support this interpretation. In contrast, regulatory changes that mitigate the plastic response to stress evolved more frequently in A. halleri. Our results demonstrate that pre-existing plasticity may be a stepping stone for adaptation, but its selective remodeling differs between lineages.Activation of systemic immune responses using PD-1 checkpoint inhibitors is an essential approach to cancer therapy. Yet, the extent of benefit relative to risk of immune related adverse events (irAE) varies widely among patients. Here, we study endocrine irAE from 7 clinical trials across 6 cancers where atezolizumab (anti-PD-L1) was combined with chemotherapies and compared to standard of care. We show that atezolizumab-induced thyroid dysfunction is associated with longer survival. We construct a polygenic risk score (PRS) for lifetime risk of hypothyroidism using a GWAS from the UK Biobank and apply this PRS to genetic data collected from 2,616 patients of European ancestry from these trials. Patients with high PRS are at increased risk of atezolizumab-induced thyroid dysfunction and lower risk of death in triple negative breast cancer. Our results indicate that genetic variation associated with thyroid autoimmunity interacts with biological pathways driving the systemic immune response to PD-1 blockade.Mid-infrared free-space optical communication has a large potential for high speed communication due to its immunity to electromagnetic interference. However, data security against eavesdroppers is among the obstacles for private free-space communication. Here, we show that two uni-directionally coupled quantum cascade lasers operating in the chaotic regime and the synchronization between them allow for the extraction of the information that has been camouflaged in the chaotic emission. This building block represents a key tool to implement a high degree of privacy directly on the physical layer. We realize a proof-of-concept communication at a wavelength of 5.7 μm with a message encryption at a bit rate of 0.5 Mbit/s. Our demonstration of private free-space communication between a transmitter and receiver opens strategies for physical encryption and decryption of a digital message.