The developmental basis of fingerprint pattern formation and variation.

Fingerprints are complex and individually unique patterns in the skin. Established prenatally, the molecular and cellular mechanisms that guide fingerprint ridge formation and their intricate arrangements are unknown. Here we show that fingerprint ridges are epithelial structures that undergo a truncated hair follicle developmental program and fail to recruit a mesenchymal condensate. Their spatial pattern is established by a Turing reaction-diffusion system, based on signaling between EDAR, WNT, and antagonistic BMP pathways. These signals resolve epithelial growth into bands of focalized proliferation under a precociously differentiated suprabasal layer. Ridge formation occurs as a set of waves spreading from variable initiation sites defined by the local signaling environments and anatomical intricacies of the digit, with the propagation and meeting of these waves determining the type of pattern that forms. Relying on a dynamic patterning system triggered at spatially distinct sites generates the characteristic types and unending variation of human fingerprint patterns.

The challenges in finding your home as a multidisciplinary scientist.

Technological advances in a variety of scientific disciplines are being applied in the life sciences leading to an increase in the number scientists who see themselves or are classed as being multidisciplinary. Although their diverse skills are celebrated and needed to understand the immense complexity of life, being a multidisciplinary researcher can pose unique challenges. We asked multidisciplinary researchers and the director of an institute that fosters multidisciplinary research for their thoughts on what they see as the challenges or obstacles that multidisciplinary scientists can often face.

Limb development genes underlie variation in human fingerprint patterns.

Fingerprints are of long-standing practical and cultural interest, but little is known about the mechanisms that underlie their variation. Using genome-wide scans in Han Chinese cohorts, we identified 18 loci associated with fingerprint type across the digits, including a genetic basis for the long-recognized "pattern-block" correlations among the middle three digits. In particular, we identified a variant near EVI1 that alters regulatory activity and established a role for EVI1 in dermatoglyph patterning in mice. Dynamic EVI1 expression during human development supports its role in shaping the limbs and digits, rather than influencing skin patterning directly. Trans-ethnic meta-analysis identified 43 fingerprint-associated loci, with nearby genes being strongly enriched for general limb development pathways. We also found that fingerprint patterns were genetically correlated with hand proportions. Taken together, these findings support the key role of limb development genes in influencing the outcome of fingerprint patterning.

Modeling recent human evolution in mice by expression of a selected EDAR variant.

An adaptive variant of the human Ectodysplasin receptor, EDARV370A, is one of the strongest candidates of recent positive selection from genome-wide scans. We have modeled EDAR370A in mice and characterized its phenotype and evolutionary origins in humans. Our computational analysis suggests the allele arose in central China approximately 30,000 years ago. Although EDAR370A has been associated with increased scalp hair thickness and changed tooth morphology in humans, its direct biological significance and potential adaptive role remain unclear. We generated a knockin mouse model and find that, as in humans, hair thickness is increased in EDAR370A mice. We identify new biological targets affected by the mutation, including mammary and eccrine glands. Building on these results, we find that EDAR370A is associated with an increased number of active eccrine glands in the Han Chinese. This interdisciplinary approach yields unique insight into the generation of adaptive variation among modern humans.

PARP1 UFMylation ensures the stability of stalled replication forks.

The S-phase checkpoint involving CHK1 is essential for fork stability in response to fork stalling. PARP1 acts as a sensor of replication stress and is required for CHK1 activation. However, it is unclear how the activity of PARP1 is regulated. Here, we found that UFMylation is required for the efficient activation of CHK1 by UFMylating PARP1 at K548 during replication stress. Inactivation of UFL1, the E3 enzyme essential for UFMylation, delayed CHK1 activation and inhibits nascent DNA degradation during replication blockage as seen in PARP1-deficient cells. An in vitro study indicated that PARP1 is UFMylated at K548, which enhances its catalytic activity. Correspondingly, a PARP1 UFMylation-deficient mutant (K548R) and pathogenic mutant (F553L) compromised CHK1 activation, the restart of stalled replication forks following replication blockage, and chromosome stability. Defective PARP1 UFMylation also resulted in excessive nascent DNA degradation at stalled replication forks. Finally, we observed that PARP1 UFMylation-deficient knock-in mice exhibited increased sensitivity to replication stress caused by anticancer treatments. Thus, we demonstrate that PARP1 UFMylation promotes CHK1 activation and replication fork stability during replication stress, thus safeguarding genome integrity.

Comparative analysis of models in predicting the effects of SNPs on TF-DNA binding using large-scale in vitro and in vivo data.

Non-coding variants associated with complex traits can alter the motifs of transcription factor (TF)-deoxyribonucleic acid binding. Although many computational models have been developed to predict the effects of non-coding variants on TF binding, their predictive power lacks systematic evaluation. Here we have evaluated 14 different models built on position weight matrices (PWMs), support vector machines, ordinary least squares and deep neural networks (DNNs), using large-scale in vitro (i.e. SNP-SELEX) and in vivo (i.e. allele-specific binding, ASB) TF binding data. Our results show that the accuracy of each model in predicting SNP effects in vitro significantly exceeds that achieved in vivo. For in vitro variant impact prediction, kmer/gkm-based machine learning methods (deltaSVM_HT-SELEX, QBiC-Pred) trained on in vitro datasets exhibit the best performance. For in vivo ASB variant prediction, DNN-based multitask models (DeepSEA, Sei, Enformer) trained on the ChIP-seq dataset exhibit relatively superior performance. Among the PWM-based methods, tRap demonstrates better performance in both in vitro and in vivo evaluations. In addition, we find that TF classes such as basic leucine zipper factors could be predicted more accurately, whereas those such as C2H2 zinc finger factors are predicted less accurately, aligning with the evolutionary conservation of these TF classes. We also underscore the significance of non-sequence factors such as cis-regulatory element type, TF expression, interactions and post-translational modifications in influencing the in vivo predictive performance of TFs. Our research provides valuable insights into selecting prioritization methods for non-coding variants and further optimizing such models.

Combined genome-wide association study of 136 quantitative ear morphology traits in multiple populations reveal 8 novel loci.

Human ear morphology, a complex anatomical structure represented by a multidimensional set of correlated and heritable phenotypes, has a poorly understood genetic architecture. In this study, we quantitatively assessed 136 ear morphology traits using deep learning analysis of digital face images in 14,921 individuals from five different cohorts in Europe, Asia, and Latin America. Through GWAS meta-analysis and C-GWASs, a recently introduced method to effectively combine GWASs of many traits, we identified 16 genetic loci involved in various ear phenotypes, eight of which have not been previously associated with human ear features. Our findings suggest that ear morphology shares genetic determinants with other surface ectoderm-derived traits such as facial variation, mono eyebrow, and male pattern baldness. Our results enhance the genetic understanding of human ear morphology and shed light on the shared genetic contributors of different surface ectoderm-derived phenotypes. Additionally, gene editing experiments in mice have demonstrated that knocking out the newly ear-associated gene (Intu) and a previously ear-associated gene (Tbx15) causes deviating mouse ear morphology.

From musk to body odor: Decoding olfaction through genetic variation.

The olfactory system combines input from multiple receptor types to represent odor information, but there are few explicit examples relating olfactory receptor (OR) activity patterns to odor perception. To uncover these relationships, we performed genome-wide scans on odor-perception phenotypes for ten odors in 1000 Han Chinese and validated results for six of these odors in an ethnically diverse population (n = 364). In both populations, consistent with previous studies, we replicated three previously reported associations (ß-ionone/OR5A1, androstenone/OR7D4, cis-3-hexen-1-ol/OR2J3 LD-band), but not for odors containing aldehydes, suggesting that olfactory phenotype/genotype studies are robust across populations. Two novel associations between an OR and odor perception contribute to our understanding of olfactory coding. First, we found a SNP in OR51B2 that associated with trans-3-methyl-2-hexenoic acid, a key component of human underarm odor. Second, we found two linked SNPs associated with the musk Galaxolide in a novel musk receptor, OR4D6, which is also the first human OR shown to drive specific anosmia to a musk compound. We noticed that SNPs detected for odor intensity were enriched with amino acid substitutions, implying functional changes of odor receptors. Furthermore, we also found that the derived alleles of the SNPs tend to be associated with reduced odor intensity, supporting the hypothesis that the primate olfactory gene repertoire has degenerated over time. This study provides information about coding for human body odor, and gives us insight into broader mechanisms of olfactory coding, such as how differential OR activation can converge on a similar percept.

The receptor kinase RiSho1 in Rhizophagus irregularis regulates arbuscule development and drought tolerance during arbuscular mycorrhizal symbiosis.

In terrestrial ecosystems, most plant species can form beneficial associations with arbuscular mycorrhizal (AM) fungi. Arbuscular mycorrhizal fungi benefit plant nutrient acquisition and enhance plant tolerance to drought. The high osmolarity glycerol 1 mitogen-activated protein kinase (HOG1-MAPK) cascade genes have been characterized in Rhizophagus irregularis. However, the upstream receptor of the HOG1-MAPK cascade remains to be investigated. We identify the receptor kinase RiSho1 from R. irregularis, containing four transmembrane domains and one Src homology 3 (SH3) domain, corresponding to the homologue of Saccharomyces cerevisiae. Higher expression levels of RiSho1 were detected during the in planta phase in response to drought. RiSho1 protein was localized in the plasma membrane of yeast, and interacted with the HOG1-MAPK module RiPbs2 directly by protein-protein interaction. RiSho1 complemented the growth defect of the yeast mutant ∆sho1 under sorbitol conditions. Knock-down of RiSho1 led to the decreased expression of downstream HOG1-MAPK cascade (RiSte11, RiPbs2, RiHog1) and drought-resistant genes (RiAQPs, RiTPSs, RiNTH1 and Ri14-3-3), hampered arbuscule development and decreased plants antioxidation ability under drought stress. Our study reveals the role of RiSho1 in regulating arbuscule development and drought-resistant genes via the HOG1-MAPK cascade. These findings provide new perspectives on the mechanisms by which AM fungi respond to drought.

Smartphone-enabled colorimetric immunoassay for deoxynivalenol based on Mn2+-mediated aggregation of AuNPs.

Deoxynivalenol (DON) is a common mycotoxin in food that mainly pollutes grain crops and feeds, such as barley, wheat and corn. DON has caused widespread concern in the field of food and feed safety. In this study, a colorimetric immunoassay was proposed based on the aggregation of gold nanoparticles (AuNPs) due to the decomposition of Mn2+ from gold-coated manganese dioxide (AuNP@MnO2) nanosheets. In this study, 2-(dihydrogen phosphate)-l-ascorbic acid (AAP) was hydrolyzed by alkaline phosphatase (ALP) and converted to ascorbic acid (AA). Then, AuNP@MnO2 was reduced to Mn2+ and AuNPs aggregation occurred. Using the unique optical characteristics of AuNPs and AuNP@MnO2, visible color changes realized simple detection of DON with high sensitivity and portability. With increasing DON content, the color changed more obviously. To quantitatively detect DON, pictures can be taken and the blue value can be read by a smartphone. The detection limit (Ic10) of this method was 0.098 ng mL-1, which was 326 times higher than that of traditional competitive ELISA, and the detection range was 0.177-6.073 ng mL-1. This method exhibited high specificity with no cross-reaction in other structural analogs. The average recovery rate of DON in corn flour samples was 89.1 %-110.2 %, demonstrating the high accuracy and stability of this assay in actual sample detection. Therefore, the colorimetric immunoassay can be used for DON-related food safety monitoring.

Tumorous IRE1α facilitates CD8+T cells-dependent anti-tumor immunity and improves immunotherapy efficacy in melanoma.

BACKGROUND: Tumor cells frequently suffer from endoplasmic reticulum (ER) stress. Previous studies have extensively elucidated the role of tumorous unfolded protein response in melanoma cells, whereas the effect on tumor immunology and the underlying mechanism remain elusive. METHODS: Bioinformatics, biochemical assays and pre-clinical mice model were employed to demonstrate the role of tumorous inositol-requiring transmembrane kinase/endoribonuclease 1α (IRE1α) in anti-tumor immunity and the underlying mechanism. RESULTS: We firstly found that IRE1α signaling activation was positively associated with the feature of tumor-infiltrating lymphocytes. Then, pharmacological ER stress induction by HA15 exerted prominent anti-tumor effect in immunocompetent mice and was highly dependent on CD8+T cells, paralleled with the reshape of immune cells in tumor microenvironment via tumorous IRE1α-XBP1 signal. Subsequently, tumorous IRE1α facilitated the expression and secretion of multiple chemokines and cytokines via XBP1-NF-κB axis, leading to increased infiltration and anti-tumor capacity of CD8+T cells. Ultimately, pharmacological induction of tumorous ER stress by HA15 brought potentiated therapeutic effect along with anti-PD-1 antibody on melanoma in vivo. CONCLUSIONS: Tumorous IRE1α facilitates CD8+T cells-dependent anti-tumor immunity and improves immunotherapy efficacy by regulating chemokines and cytokines via XBP1-NF-κB axis. The combination of ER stress inducer and anti-PD-1 antibody could be promising for increasing the efficacy of melanoma immunotherapy.

De novo engineering riboflavin production Bacillus subtilis by overexpressing the downstream genes in the purine biosynthesis pathway.

BACKGROUND: Bacillus subtilis is widely used in industrial-scale riboflavin production. Previous studies have shown that targeted mutagenesis of the ribulose 5-phosphate 3-epimerase in B. subtilis can significantly enhance riboflavin production. This modification also leads to an increase in purine intermediate concentrations in the medium. Interestingly, B. subtilis exhibits remarkable efficiency in purine nucleoside synthesis, often exceeding riboflavin yields. These observations highlight the importance of the conversion steps from inosine-5'-monophosphate (IMP) to 2,5-diamino-6-ribosylamino-4(3 H)-pyrimidinone-5'-phosphate (DARPP) in riboflavin production by B. subtilis. However, research elucidating the specific impact of these reactions on riboflavin production remains limited. RESULT: We expressed the genes encoding enzymes involved in these reactions (guaB, guaA, gmk, ndk, ribA) using a synthetic operon. Introduction of the plasmid carrying this synthetic operon led to a 3.09-fold increase in riboflavin production compared to the control strain. Exclusion of gmk from the synthetic operon resulted in a 36% decrease in riboflavin production, which was further reduced when guaB and guaA were not co-expressed. By integrating the synthetic operon into the genome and employing additional engineering strategies, we achieved riboflavin production levels of 2702 mg/L. Medium optimization further increased production to 3477 mg/L, with a yield of 0.0869 g riboflavin per g of sucrose. CONCLUSION: The conversion steps from IMP to DARPP play a critical role in riboflavin production by B. subtilis. Our overexpression strategies have demonstrated their effectiveness in overcoming these limiting factors and enhancing riboflavin production.

Tandem mass tag-based quantitative proteomics analyses of the spermatogenesis-ameliorating effect of Youjing granule on rats.

RATIONALE: Male infertility is a common reproductive system disease manifested as aberrant spermatogenesis and identified as "kidney deficiency and dampness" in Chinese traditional medicine. Youjing granule (YG) is a Chinese material medica based on tonifying kidneys and removing dampness. It has proven to be able to regulate semen quality in clinical application, but the underlying mechanism has not been clarified. METHODS: Using serum containing YG to treat primarily cultured spermatogonial stem cells (SSCs), the apoptotic rate and mitosis phase ratio of SSCs were measured. The liquid chromatography-tandem mass spectrometry with tandem mass tags method was applied for analyzing the serum of rats treated with YG/distilled water, and proteomic analyses were performed to clarify the mechanisms of YG. RESULTS: Totally, 111 proteins in YG-treated serum samples were differentially expressed compared with control groups, and 43 of them were identified as potential target proteins, which were further annotated based on their enrichment in Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways. Proteomic analyses showed that the mechanisms of YG may involve regulation of glycolysis, gluconeogenesis and nucleotide-binding and oligomerization domain-like receptor signaling pathway. In addition, RhoA and Lamp2 were found to be possible responders of YG through reviewing the literature. CONCLUSIONS: The results demonstrate that our serum proteomics platform is clinically useful in understanding the mechanisms of YG.

Pesticides in Greenhouse Airborne Particulate Matter: Occurrence, Distribution, Transformation Products, and Potential Human Exposure Risks.

Pesticides are frequently sprayed in greenhouses to ensure crop yields, where airborne particulate matter (PM) may serve as a carrier in depositing and transporting pesticides. However, little is known about the occurrence and fate of PM-borne pesticides in greenhouses. Herein, we examined the distribution, dissipation, and transformation of six commonly used pesticides (imidacloprid, acetamiprid, prochloraz, triadimefon, hexaconazole, and tebuconazole) in greenhouse PM (PM1, PM2.5, and PM10) after application as well as the associated human exposure risks via inhalation. During 35 days of experiment, the six pesticides were detected in all PM samples, and exhibited size- and time-dependent distribution characteristics, with the majority of them (>64.6%) accumulated in PM1. About 1.0-16.4% of initially measured pesticides in PM remained after 35 days, and a total of 12 major transformation products were elucidated, with six of them newly identified. The inhalation of PM could be an important route of human exposure to pesticides in the greenhouse, where the estimated average daily human inhalation dose (ADDinh) of the six individual pesticides was 2.1-1.2 × 104 pg/kg day-1 after application (1-35 days). Our findings highlight the occurrence of pesticides/transformation products in greenhouse PM, and their potential inhalation risks should be further concerned.

From Water to Water: Insight into the Translocation of Pesticides from Plant Rhizosphere Solution to Leaf Guttation and the Associated Ecological Risks.

Plant guttation is an important source of water/nutrients for many beneficial insects, while the presence of pesticides in guttation has been considered as a new exposure route for nontarget insects. This study aimed to elucidate how 15 diverse pesticides are translocated from growth media to guttation by maize plants through a hydroponic experiment. All pesticides were effectively translocated from the growth solution to maize guttation and reached a steady state within 5 days. The strong positive correlation (R2 = 0.43-0.84) between the concentrations of pesticides in guttation and in xylem sap demonstrated that xylem sap was a major source of pesticides in guttation. The relationship between the bioaccumulation of pesticides in guttation (BCFguttation) and the chemical Kow was split into two distinct patterns: for pesticides with log Kow > 3, we identified a good negative linear correlation between log BCFguttation and log Kow (R2 = 0.71); however, for pesticides with log Kow < 3, all data fall close to a horizontal line of BCFguttation ≅ 1, indicating that hydrophilic pesticides can easily pass through the plants from rhizosphere solution to leaf guttation and reach saturation status. Besides, after feeding with pesticide-contaminated guttation, the mortality of honeybees was significantly impacted, even at very low levels (e.g., ∑600 µg/L with a mortality of 93%). Our results provide essential information for predicting the contamination of plant guttation with pesticides and associated ecological risks.

Molecular basis and current insights of atypical Rho small GTPase in cancer.

Atypical Rho GTPases are a subtype of the Rho GTPase family that are involved in diverse cellular processes. The typical Rho GTPases, led by RhoA, Rac1 and Cdc42, have been well studied, while relative studies on atypical Rho GTPases are relatively still limited and have great exploration potential. With the increase in studies, current evidence suggests that atypical Rho GTPases regulate multiple biological processes and play important roles in the occurrence and development of human cancers. Therefore, this review mainly discusses the molecular basis of atypical Rho GTPases and their roles in cancer. We summarize the sequence characteristics, subcellular localization and biological functions of each atypical Rho GTPase. Moreover, we review the recent advances and potential mechanisms of atypical Rho GTPases in the development of multiple cancers. A comprehensive understanding and extensive exploration of the biological functions of atypical Rho GTPases and their molecular mechanisms in tumors will provide important insights into the pathophysiology of tumors and the development of cancer therapeutic strategies.

Epigenome-wide association study on ambient PM2.5 exposure in Han Chinese, the NSPT study.

Ambient PM2.5 exposure has been recognized as a major health risk and related to aging, cardiovascular, respiratory and neurologic diseases, and cancer. However, underlying mechanism of epigenetic alteration and regulated pathways still remained unclear. The study on methylome effect of PM2.5 exposure was quite limited in Chinese population, and cohort-based study was absent. The study included blood-derived DNA methylation for 3365 Chinese participants from the NSPT cohort. We estimated individual PM2.5 exposure level of short-medium-, medium- and long-term, based on a validated prediction model. We preformed epigenome-wide association studies to estimate the links between PM2.5 exposure and DNA methylation change, as well as stratification and sensitive analysis to examined the robustness of the association models. A systematic review was conducted to obtain the previously published CpGs and examined for replication. We also conducted comparison on the DNA methylation variation corresponding to different time windows. We further conducted gene function analysis and pathway enrichment analysis to reveal related biological response. We identified a total of 177 CpGs and 107 DMRs associated with short-medium-term PM2.5 exposure, at a strict genome-wide significance (P < 5 × 10-8). The effect sizes on most CpGs tended to cease with the exposure of extended time scale. Associated markers and aligned genes were related to aging, immunity, inflammation and carcinogenesis. Enriched pathways were mostly involved in cell cycle and cell division, signal transduction, inflammatory pathway. Our study is the first EWAS on PM2.5 exposure conducted in large-scale Han Chinese cohort and identified associated DNA methylation change on CpGs and regions, as well as related gene functions and pathways.

The COP9 signalosome reduces neuroinflammation and attenuates ischemic neuronal stress in organotypic brain slice culture model.

The constitutive photomorphogenesis 9 (COP9) signalosome (CSN) is a deNEDDylase controlling ubiquitination activity of cullin-RING-E3 ligases (CRLs) and thus the levels of key cellular proteins. While the CSN and its catalytic subunit CSN5 have been extensively studied in cancer, its role in inflammatory and neurological diseases is less understood. Following verification that CSN5 is expressed in mouse and human brain, here we studied the role of the CSN in neuroinflammation and ischemic neuronal damage employing models of relevant brain-resident cell types, an ex vivo organotypic brain slice culture model, and the CRL NEDDylation state-modifying drugs MLN4924 and CSN5i-3, which mimic and inhibit, respectively, CSN5 deNEDDylase activity. Untargeted mass spectrometry-based proteomics revealed that MLN4924 and CSN5i-3 substantially alter the microglial proteome, including inflammation-related proteins. Applying these drugs and mimicking microglial and endothelial inflammation as well as ischemic neuronal stress by TNF and oxygen-glucose-deprivation/reoxygenation (OGD/RO) treatment, respectively, we could link CSN5/CSN-mediated cullin deNEDDylation to reduction of microglial inflammation, attenuated cerebral endothelial inflammation, improved barrier integrity, as well as protection from ischemic stress-induced neuronal cell death. Specifically, MLN4924 reduced phagocytic activity, motility, and inflammatory cytokine expression of microglial cells, and this was linked to inhibition of inflammation-induced NF-κB and Akt signaling. Inversely, Csn5 knockdown and CSN5i-3 increased NF-κB signaling. Moreover, MLN4924 abrogated TNF-induced NF-κB signaling in cerebral microvascular endothelial cells (hCMECs) and rescued hCMEC monolayers from OGD/RO-triggered barrier leakage, while CSN5i-3 exacerbated permeability. In an ex vivo organotypic brain slice model of ischemia/reperfusion stress, MLN4924 protected from neuronal death, while CSN5i-3 impaired neuronal survival. Neuronal damage was attributable to microglial activation and inflammatory cytokines, as indicated by microglial shape tracking and TNF-blocking experiments. Our results indicate a protective role of the CSN in neuroinflammation via brain-resident cell types involved in ischemic brain disease and implicate CSN activity-mimicking deNEDDylating drugs as potential therapeutics.

Saccharina Japonica Polysaccharides Suppress High-Fat Diet-Induced Obesity and Modulate Gut Microbiota Composition and Function.

Recent studies have highlighted the potential of Saccharina japonica Polysaccharides (SJPs) in alleviating high-fat diet (HFD)-induced obesity by regulating gut microbiota, which warrants further exploration to elucidate the underlying structure-activity relationship. In this study, five polysaccharide fractions (Sj-T, Sj-T-1, Sj-T-2, Sj-T-3, and Sj-T-4) with different structure characteristics were prepared from S. japonica, and their effects on HFD-induced obesity and gut microbiota composition were investigated using C57BL/6J mice. The results revealed that oral administration of Sj-T considerably suppressed HFD-induced obesity, glucose metabolic dysfunction, and other disordered symptoms. While, Sj-T-2, which has the lowest molecular weight, was the most effective in alleviating HFD-induced obesity and had the second-best effect on improving HFD-induced impaired glucose tolerance among the five SJPs. Supplementation with SJPs significantly modulated HFD-induced gut microbiota dysbiosis both at the phylum and species levels, such as enriching Desulfobacterota and Actinobacteriota, while suppressing the abundance of Bacteroidota. Sj-T also dramatically restored the gut microbiota composition by modulating the abundance of many crucial gut bacterial taxa, including s_Bacteroides_acidifaciens, s_Lachnospiraceae _bacterium, and g_Lachnospiraceae_NK4A136_group. Besides, SJPs also dramatically altered the function of gut microbiota, including many carbohydrate-metabolism enzymes. This study highlights the potential of SJPs in preventing obesity and restoring intestinal homeostasis in obese individuals.

Blue Long Afterglow and Ultra Broadband Vis-NIR Emission from All-Inorganic Copper-Doped Silver Halide Single Crystals.

All-inorganic metal halides with afterglow emission have attracted increasing attention due to their significantly longer afterglow duration and higher stability compared to their organic-inorganic hybrid counterparts. However, their afterglow colors have not yet reached the blue spectral region. Here, we report all-inorganic copper-doped Rb2AgBr3 single crystals with ultralong blue afterglow (>300 s) by modulating defect states through doping engineering. The introduction of copper(I) ions into Rb2AgBr3 facilitates the formation of bromine vacancies, thus increasing the density of trap states available for charge storage and enabling bright, persistent emission after ceasing the excitation. Moreover, cascade energy transfer between distinct emissive centers in the crystals results in ultra-broadband photoluminescence, not only covering the whole white light with near-unity quantum yield but also extending into the near-infrared region. This 'cocktail' of exotic light-emission properties, in conjunction with the excellent stability of copper-doped Rb2AgBr3 crystals, allowed us to demonstrate their implementation to solid-state lighting, night vision, and intelligent anti-counterfeiting.