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The ligand exchange procedure of CsPbI3 perovskite quantum dots (PQDs) enables the fabrication of thick and conductive PQD solids that act as a photovoltaic absorber for solution‐processed thin‐film solar cells. However, the ligand‐exchanged CsPbI3 PQD solids suffer from deterioration in photovoltaic performance and ambient stability due to the surface traps, such as uncoordinated Pb2+ sites on the PQD surface, which are generated after the conventional ligand exchange process using ionic short‐chain ligands dissolved in polar solvents. Herein, a facile surface stabilization is demonstrated that can simultaneously improve the photovoltaic performance and ambient stability of CsPbI3 PQD photovoltaic absorber using covalent short‐chain triphenylphosphine oxide (TPPO) ligands dissolved in a nonpolar solvent. It is found that the TPPO ligand can be covalently bound to uncoordinated Pb2+ sites and the nonpolar solvent octane can completely preserve the PQD surface components. Owing to their synergetic effects, the CsPbI3 PQD photovoltaic absorber stabilized using the TPPO ligand solution dissolved in octane exhibit higher optoelectrical properties and ambient stability than the control absorber. Consequently, CsPbI3 PQD solar cells composed of PQD photovoltaic absorbers fabricated via surface stabilization strategy provide an improved power conversion efficiency of 15.4% and an enhanced device stability. Triphenylphosphine oxide (TPPO) ligand solution dissolved in octane is treated on ligand‐exchanged CsPbI3 perovskite quantum dot (PQD) solids for surface stabilization of PQDs. Through Lewis‐base interactions, the TPPO ligand exhibits strong coordination with PQD surface traps. Moreover, the nonpolar octane enables nondestructive PQD surface. Consequently, the PQD solar cells with TPPO ligand solution show improved performance and durability.

Heavy metals are both integral parts of cells and environmental toxicants, and their deregulation is associated with severe cellular dysfunction and various diseases. Here we show that the Hippo pathway plays a critical role in regulating heavy metal homeostasis. Hippo signalling deficiency promotes the transcription of heavy metal response genes and protects cells from heavy metal-induced toxicity, a process independent of its classic downstream effectors YAP and TAZ. Mechanistically, the Hippo pathway kinase LATS phosphorylates and inhibits MTF1, an essential transcription factor in the heavy metal response, resulting in the loss of heavy metal response gene transcription and cellular protection. Moreover, LATS activity is inhibited following heavy metal treatment, where accumulated zinc directly binds and inhibits LATS. Together, our study reveals an interplay between the Hippo pathway and heavy metals, providing insights into this growth-related pathway in tissue homeostasis and stress response. Han et al. report that the Hippo pathway kinases LATS1 and LATS2 phosphorylate the heavy metal response transcription factor MTF1, leading to attenuation of heavy metal response gene transcription and cellular detoxification.

The MAP4K family, consisting of seven kinases (MAP4K1–7), plays crucial roles in regulating diverse cellular processes, including proliferation, differentiation, migration and apoptosis. Recent studies have highlighted their involvement in multiple signaling pathways such as mitogen-activated protein kinase, Jun N-terminal kinase and Hippo, implicating them in conditions such as cancer, autoimmune and metabolic disorders and neurodegenerative diseases. Notably, MAP4K proteins have demonstrated significant roles in cancer development and progression, including tumor growth, metastasis and immune modulation. Here we summarize current insights into the roles of individual MAP4K members in cancer and other diseases, emphasizing their distinct and overlapping functions within key signaling networks. Furthermore, we discuss the therapeutic potential of targeting MAP4K family members for cancer treatment. These kinases represent promising targets for developing novel therapies for cancer and related diseases. Future research is essential to clarify the specific molecular mechanisms of MAP4K proteins in cancer and to explore their broader relevance in health and disease. MAP4K kinases drive cancer progression and therapeutic potential The MAP4K family of proteins plays a crucial role in various cellular processes, including cell growth and survival. The Review explores how different MAP4K proteins contribute to cancer progression and other diseases. Researchers used various methods, including genetic analysis and experiments on cell lines, to investigate the roles of MAP4K proteins. They found that these proteins are involved in key signaling pathways that regulate cell behavior. For example, MAP4K1 affects immune cell activation, whereas MAP4K4 is linked to cancer cell movement and growth. The Review highlights that MAP4K proteins can act as both promoters and suppressors of cancer, depending on the context. This dual role makes them potential targets for new cancer therapies. The researchers suggest that developing specific inhibitors for these proteins could lead to more effective treatments for cancer and other diseases. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.

Only a limited number of neuroimaging studies have explored the effects of ambient air pollution in adults. The prior studies have investigated only cortical volume, and they have reported mixed findings, particularly for gray matter. Furthermore, the association between nitrogen dioxide ( ) and neuroimaging markers has been little studied in adults. We investigated the association between long-term exposure to air pollutants ( , particulate matter (PM) with aerodynamic diameters of (PM10) and (PM2.5), and neuroimaging markers. The study included 427 men and 530 women dwelling in four cities in the Republic of Korea. Long-term concentrations of PM10, , and PM2.5 at residential addresses were estimated. Neuroimaging markers (cortical thickness and subcortical volume) were obtained from brain magnetic resonance images. A generalized linear model was used, adjusting for potential confounders. A increase in PM10 was associated with reduced thicknesses in the frontal [ (95% CI: , )] and temporal lobes [ (95% CI: , )]. A increase in PM2.5 was associated with a thinner temporal cortex [ (95% CI: , )]. A 10-ppb increase in was associated with reduced thicknesses in the global [ (95% CI: , 0.00)], frontal [ (95% CI: , )], parietal [ (95% CI: , )], temporal [ (95% CI: , )], and insular lobes [ (95% CI: , 0.00)]. The air pollutants were also associated with increased thicknesses in the occipital and cingulate lobes. Subcortical structures associated with the air pollutants included the thalamus, caudate, pallidum, hippocampus, amygdala, and nucleus accumbens. The findings suggest that long-term exposure to high ambient air pollution may lead to cortical thinning and reduced subcortical volume in adults. https://doi.org/10.1289/EHP7133.

The Hippo pathway is a central regulator of organ size and a key tumor suppressor via coordinating cell proliferation and death. Initially discovered in Drosophila , the Hippo pathway has been implicated as an evolutionarily conserved pathway in mammals; however, how this pathway was evolved to be functional from its origin is still largely unknown. In this study, we traced the Hippo pathway in premetazoan species, characterized the intrinsic functions of its ancestor components, and unveiled the evolutionary history of this key signaling pathway from its unicellular origin. In addition, we elucidated the paralogous gene history for the mammalian Hippo pathway components and characterized their cancer-derived somatic mutations from an evolutionary perspective. Taken together, our findings not only traced the conserved function of the Hippo pathway to its unicellular ancestor components, but also provided novel evolutionary insights into the Hippo pathway organization and oncogenic alteration.

The Hippo pathway is commonly altered in cancer initiation and progression; however, exactly how this pathway becomes dysregulated to promote human cancer development remains unclear. Here we analyze the Hippo somatic mutations in the human cancer genome and functionally annotate their roles in targeting the Hippo pathway. We identify a total of 85 loss-of-function (LOF) missense mutations for Hippo pathway genes and elucidate their underlying mechanisms. Interestingly, we reveal zinc-finger domain as an integral structure for MOB1 function, whose LOF mutations in head and neck cancer promote tumor growth. Moreover, the schwannoma/meningioma-derived NF2 LOF mutations not only inhibit its tumor suppressive function in the Hippo pathway, but also gain an oncogenic role for NF2 by activating the VANGL-JNK pathway. Collectively, our study not only offers a rich somatic mutation resource for investigating the Hippo pathway in human cancers, but also provides a molecular basis for Hippo-based cancer therapy. The Hippo signalling pathway is commonly mutated across cancer types. Here, the authors identify 85 loss-of-function missense mutations within Hippo signalling genes and highlight the mechanisms underpinning mutations in MOB1 and NF2.

Beta-glucans, which existed in the cell walls of cereals, bacteria, and fungi, comprise a group of β- d -glucose polysaccharides. We investigated the effects of four kinds of beta-glucan, that are derived from barley, yeast, mushroom, and euglena on wound healing. The migration and viability of keratinocyte or fibroblast were analyzed using the in vitro scratch wound healing assay, invasion assay, MTT assay, and in vivo assay. All the beta-glucans had a significant effect on keratinocyte migration at 20 μM and showed no toxicity on dermal fibroblast. Moreover, treatment of keratinocytes with the beta-glucan derived from the mushroom ( Schizophyllum commune ) promoted in vivo wound closure. The Integrin/FAK/Src pathway is known to affect cell migration by forming lamellipodia. Beta-glucan from S. commune activates the Integrin/FAK/Src signaling pathway in a time-dependent. Reactive oxygen species are associated with fibroblast differentiation to contract dermal layer and synthesize collagens. We found that fibroblast was activated by increasing NOX4 expression. We propose that beta-glucan derived from mushroom is capable of promoting keratinocyte migration via the induction of FAK/Src phosphorylation there by accelerating wound closure and activating dermal fibroblast differentiation through NADPH oxidase for matrix remodeling.

A dual‐functional electron transport layer (ETL) is reported for PbS colloidal quantum dot (CQD) photovoltaics by incorporating 9‐anthracenecarboxylic acid (ACA) into a zinc oxide (ZnO) matrix. Despite its favorable electron transport characteristics and appropriate band alignment, intrinsic defects in ZnO, such as oxygen vacancies, remain a limiting factor in device performance. The carboxylate functional group of ACA effectively passivates these defects, thereby reducing trap‐assisted recombination. Moreover, ACA, an acene‐based π‐conjugated molecule, efficiently generates triplet excitons. These triplets undergo triplet energy transfer to the PbS CQD layer, enhancing photocurrent generation. Owing to these synergistic effects, CQD photovoltaics (PVs) incorporating ACA‐treated ZnO ETLs exhibit enhanced open‐circuit voltage and short‐circuit current density, resulting in a higher power conversion efficiency of 11.55% compared to 10.48% for control devices. This strategy highlights the combined advantages of electronic defect passivation and triplet exciton harvesting in PbS CQD PVs. An acene‐based donor incorporated into the electron transport layer enables triplet energy transfer to PbS colloidal quantum dots and improves defect passivation, resulting in enhanced photovoltaic device performance.

The Hippo pathway is a key regulator of tissue homeostasis, organ size and cancer. Identification of microcolin B and its analog molecules as Hippo pathway activators connects PtdIns4P-dependent lipid signaling with the Hippo pathway, suggesting potential targets for cancer therapy.

Low-field benchtop nuclear magnetic resonance (NMR) spectroscopy has emerged as an accessible analytical platform for rapid, routine, and application-oriented analysis. However, its broader analytical adoption remains constrained by intrinsic limitations, including reduced spectral resolution, severe signal overlap, and lower sensitivity compared with conventional high-field instruments. To address these limitations, artificial intelligence (AI), including machine learning and deep learning approaches, has increasingly been explored alongside conventional chemometric strategies to enhance information extraction from low-field spectral data. This review examines recent developments in AI-assisted benchtop NMR across three major application domains: classification and authentication, quantitative analysis, and spectral processing or automated interpretation. Current evidence suggests that classification and authentication currently represent the most mature application area, whereas quantitative analysis shows promising but often condition-dependent performance. In contrast, spectral reconstruction and automated interpretation remain comparatively early-stage and exploratory, despite their potential long-term relevance for addressing intrinsic information limitations. Key challenges, including limited dataset diversity, poor model transferability, validation pitfalls, limited interpretability, and the lack of benchmarking and standardized workflows, are critically discussed. Future progress will likely depend not only on advances in AI algorithms, but also on the development of robust, reproducible, and analytically meaningful workflows. Overall, AI-assisted benchtop NMR is evolving from proof-of-concept applications toward a more structured analytical framework for extracting chemically meaningful information from spectrally constrained low-field data.