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Background Ambient air pollutants have been suggested to affect pubertal development. Nevertheless, current studies indicate inconsistent effects of these pollutants, causing precocious or delayed puberty onset. This study aimed to explore the associations between long-term exposure to particulate matter with aerodynamic diameters ≤ 2.5 μm (PM 2.5 ) along with its components and menarche timing among Chinese girls. Method Self-reported age at menarche was collected among 855 girls from China Health and Nutrition Survey 2004 to 2015. The pre-menarche annual average concentrations of PM 2.5 and its components were calculated on the basis of a long-term (2000–2014) high-resolution PM 2.5 components dataset. Generalized linear models (GLM) and logistic regression models were used to analyze the associations of exposure to a single pollutant (PM 2.5 , sulfate, nitrate, ammonium, black carbon and organic matter) with age at menarche and early menarche (< 12 years), respectively. Weighted quantile sum methods were applied to examine the impacts of joint exposure on menarche timing. Results In the adjusted GLM, per 1 µg/m 3 increase of annual average concentrations of nitrate and ammonium decreased age at menarche by 0.098 years and 0.127 years, respectively (all P  < 0.05). Every 1 µg/m 3 increase of annual average concentrations of PM 2.5 (OR: 1.04, 95% CI: 1.00-1.08), sulfate (OR: 1.23, 95% CI: 1.01–1.50), nitrate (OR: 1.23, 95% CI: 1.06–1.43) and ammonium (OR: 1.32, 95% CI: 1.06–1.66) were significantly positively associated with early menarche. Higher level of joint exposure to PM 2.5 and its components was associated with 11% higher odds of early menarche ( P  = 0.04). Additionally, the estimated weight of sulfate was the largest among the mixed pollutants. Conclusions Long-term exposure to PM 2.5 and its components could increase the risk of early menarche among Chinese girls. Moreover, sulfate might be the most critical components responsible for this relationship. Our study provides foundation for targeted prevention of PM 2.5 components.

The brown planthopper (BPH), Nilaparvata lugens (Stål), is one of the most important rice pests in Asia rice regions. BPH has monophagy, migration, rapid reproduction and strong environmental adaptability, and its control is a major problem in pest management. Adult BPH exhibit wing dimorphism, and the symbiotic microbiota enriched in the gut can provide energy for wing flight muscles as a source of nutrition. In order to study the diversity of symbiotic microbiota in different winged BPHs, this paper takes female BPH as the research object. It was found that the number of symbiotic microbiota of different winged BPHs would change at different development stages. Then, based on the 16S rRNA and ITS sequences, a metagenomic library was constructed, combined with fluorescent quantitative PCR and high-throughput sequencing, the dominant symbiotic microbiota flora in the gut of different winged BPHs was found, and the community structure and composition of symbiotic microbiota in different winged BPHs were further determined. Together, our results preliminarily revealed that symbiotic microbiota in the gut of BPHs have certain effects on wing morphology, and understanding the mechanisms underlying wing morph differentiation will clarify how nutritional factors or environmental cues alter or regulate physiological and metabolic pathways. These findings also establish a theoretical basis for subsequent explorations into BPH-symbiont interplay.

Cyclic di-GMP (c-di-GMP) is a second messenger that promotes biofilm formation in several bacterial species, but the mechanisms are often unclear. Here, we report that c-di-GMP promotes biofilm formation in mycobacteria in a manner dependent on the nucleoid-associated protein Lsr2. We show that c-di-GMP specifically binds to Lsr2 at a ratio of 1:1. Lsr2 upregulates the expression of HadD, a (3R)-hydroxyacyl-ACP dehydratase, thus promoting the synthesis of keto-mycolic acid and biofilm formation. Thus, Lsr2 acts as a c-di-GMP receptor that links the second messenger’s function to lipid synthesis and biofilm formation in mycobacteria. Cyclic di-GMP (c-di-GMP) is a second messenger that promotes biofilm formation through unclear mechanisms in several bacterial species. Here, Ling et al. report that c-di-GMP promotes biofilm formation in mycobacteria by binding to protein Lsr2, which upregulates the synthesis of keto-mycolic acid and thus biofilm formation.

Rice blast, caused by the fungus Magnaporthe oryzae, is a devastating disease that threatens global food security, causing annual yield losses of 10–30%. Consequently, novel control strategies beyond conventional fungicides are urgently needed. Tetramycin, a polyene macrolide antibiotic, is known for its broad-spectrum antifungal activity. However, the specific mechanisms underlying its efficacy against rice blast remain to be fully elucidated. In this study, we demonstrate that tetramycin confers resistance through a dual mode of action. First, in vitro assays revealed that tetramycin directly inhibits M. oryzae mycelial growth. Second, and more critically, it functions as a potent immune elicitor in Oryza sativa. Transcriptome analysis coupled with physiological assays showed that tetramycin treatment triggers a rapid oxidative burst, characterized by significantly elevated activities of key defense enzymes, including superoxide dismutase, peroxidase, phenylalanine ammonia lyase, and polyphenol oxidase (PPO). This oxidative response is further orchestrated through the simultaneous activation of the jasmonic acid (JA) and salicylic acid (SA) signaling pathways, as evidenced by the distinct upregulation of their respective biosynthetic genes and hormone levels. Collectively, these findings indicate that tetramycin not only acts as a direct fungicide but also primes the rice innate immune system via a synergistic reactive oxygen species-JA-SA signaling network, offering a sustainable strategy for rice blast management.

In recent years, nonalcoholic fatty liver disease (NAFLD) has become the most important chronic liver disease worldwide. The prevalence of NAFLD in China has also increased year by year. This study aimed to detect NAFLD early by developing a nomogram model in Chinese individuals. A total of 8861 subjects who underwent physical examination in Karamay and were 18 to 62 years old were enrolled. Clinical information, laboratory results and ultrasound findings were retrieved. The participants were randomly assigned to the development set (n = 6203) and the validation set (n = 2658). Significant variables independently associated with NAFLD were identified by least absolute shrinkage and selection operator (LASSO) regression and the multiple logistic regression model. Six variables were selected to construct the nomogram: age, sex, waist circumference (WC), body mass index (BMI), alanine aminotransferase (ALT), triglycerides and glucose index (TyG). The area under the receiver operating characteristic curve (AUROC) of the development set and validation set was 0.886 and 0.894, respectively. The calibration curves showed excellent accuracy of the nomogram model. This physical examination and laboratory test-based nomogram can predict the risk of NAFLD intuitively and individually.

Transition metal‐based nanotherapeutics, such as chemodynamic therapy and ferroptosis‐ or cuproptosis‐induced strategies, hold great potential for cancer treatment. Copper‐ and iron‐based nanozymes enhance reactive oxygen species (ROS) generation and regulate metal ion homeostasis, driving ferroptosis and cuproptosis. However, simultaneous delivery of copper and iron ions and the role of mitochondria‐targeted copper in inducing cuproptosis remain underexplored. Here, a dual‐functional nano‐heterojunction platform, MIL‐Cu1.8S‐TPP/FA, is reproted, integrating iron‐ and copper‐based components for synergistic ferroptosis and cuproptosis induction. Mitochondria‐targeted Cu1.8S nanodots demonstrated high biocompatibility and efficiently induced cuproptosis by disrupting mitochondrial iron‐sulfur proteins. Combined with MIL‐88B, the iron‐based metal‐organic framework, the MIL‐Cu1.8S heterojunction exhibited enhanced ROS catalytic activity, confirmed by density functional theory (DFT) analysis, with improved H2O2 adsorption and lower energy barriers for peroxidase (POD)‐like reactions. The dual‐targeting MIL‐Cu1.8S‐TPP/FA nanoplatform effectively delivered copper ions to mitochondria and iron ions to tumor cells, modulating key ferroptosis‐ and cuproptosis‐related markers, such as GPX4, GSH, FDX‐1, and HSP70. The platform synergistically combined photothermal effects with multi‐pathway cell death mechanisms, achieving significant anti‐tumor efficacy in vitro and in vivo. This study underscores the therapeutic potential of synchronously delivering copper and iron ions and highlights mitochondria‐targeted strategies in advancing multi‐modal cancer therapies. This work reports a mitochondria‐targeted nanozyme platform, MIL‐Cu1.8S‐TPP/FA, which induces potent cuproptosis via localized delivery of Cu1.8S nanodots to mitochondria. Surface‐anchoring these nanodots onto MIL‐88B metal‐organic frameworks enhances both passive and active tumor targeting. The resulting heterojunction structure exhibits synergistic POD‐like and GPx‐like catalytic activity, enabling coordinated disruption of iron and mitochondrial copper homeostasis to trigger ferroptosis and cuproptosis in tumor cells.

Grain number per panicle critically determines rice yield. Although many underlying genes have been reported, yet the molecular mechanisms linking ethylene to panicle development remain unclear. Here, we identify GRAIN NUMBER PER PANICLE 3 (GNP3) as a regulator of GNP through genome-wide association study (GWAS) combined with map-based cloning. GNP3 encodes a MITOGEN-ACTIVATED PROTEIN KINASE KINASE KINASE 22 (OsMKKK22) that phosphorylates S -adenosyl-L-methionine synthetase 1 (SAMS1), triggering its degradation to suppress ethylene biosynthesis. Ethylene overaccumulation in gnp3 −1 mutants reduces grain number, while GNP3 overexpression enhances panicle branching and grain yield by lowering ethylene levels. We demonstrate that a natural haplotype GNP3 Hap-T prevalent in indica subspecies strengthens GNP3-SAMS1 interaction, accelerating SAMS1 degradation and improving grain number. Furthermore, overexpressing GNP3 increases grain yield by approximately 20% in field plot conditions. Our findings unveil a MAPK-ethylene regulatory module and highlight GNP3 Hap-T as a valuable genetic resource for breeding high-yield rice. Grain number per panicle (GNP) is a critical yield component trait of rice. Here, the authors clone a MAPKKK encoding gene GNP3 positively regulating grain yield and show its role in rice panicle development by interacting and destabilizing ethylene biosynthesis related enzyme SADENOSYLMETHIONINE SYNTHETASE 1.

The evidence linking meat intake to early menarche has been contradictory. We aimed to estimate meat intake and time trends among Chinese girls, and to assess the associations between long-term meat intake and menarche. This study used seven rounds of data from the China Health and Nutrition Survey, and 5175 girls aged 6–17 years were analyzed. Cox proportional hazard and restricted cubic spline models were used to analyze the associations and dose-response relationships between meat intake and menarche. Over the 15-year period, total meat intake almost doubled, and meat subtype consumption increased among Chinese girls. Increased total meat, red meat, white meat and poultry intake was significantly associated with the risk of earlier menarche. When extreme tertiles were compared, the multivariable-adjusted hazard ratios (95% confidence intervals) for total meat, red meat, white meat and poultry were 1.28 (1.06–1.54), 1.19 (1.01–1.42), 1.23 (1.02–1.47) and 1.23 (1.06–1.44), respectively. An approximately U-shaped association was observed: compared to the reference (75 g/day), early menarche risk decreased at lower intakes (25–75 g/day), showed no association at moderate intakes (75–175 g/day), and increased significantly at higher intakes (> 175 g/day). Increased long-term meat consumption was associated with an increased risk of early menarche in Chinese girls.

Culm diameter directly affects lodging and yield traits in cereal crops. However, the underlying molecular mechanisms of these interrelated, complex agronomic traits remain unclear. Here, we identify a quantitative trait locus for culm diameter in rice ( Oryza sativa ) and cloned the candidate gene, STRONG1 . This gene encodes MICROTUBULE-ASSOCIATED PROTEIN 70 (MAP70), which localizes to cortical microtubules and alters the arrangement of the microtubule skeleton. Knockout or knockdown of STRONG1 enhances grain yield by synchronously improving lodging resistance, panicle architecture, and plant architecture. One single-nucleotide polymorphism, SNP − 1304 (C to A), in a MYB61-binding site within the STRONG1 promoter affects its expression, resulting in changes in cellulose content and sclerenchyma cell wall development. Rice accessions harboring the Hap- STRONG1 C haplotype derived from wild rice, with reduced STRONG1 expression, show enhanced lodging resistance and yield, compared to accessions carrying Hap- STRONG1 A . Knockout of STRONG1 results in a 9.3–15.4% increase in yield, compared to the wild type in a field plot trial. Knockout of STRONG1 also improves panicle and plant architecture, facilitating high-density planting. This study provides a candidate gene for the development of improved rice varieties with stable, high yields. Lodging resistance is critical for rice yield. Here, the authors demonstrate that STRONG1 alters the arrangement of the microtubule skeleton, resulting in changes in secondary cell wall development, thereby negatively regulating lodging resistance and grain yield.

Natural variations provide valuable genetic resources for improving rice grain number per panicle (GNP). Here, our genome-wide association study (GWAS) identifies GNP2 and GNP5 as key regulators of GNP that enhance rice yield. GNP5 encodes a bZIP transcription factor binding to the S5779181 locus in the GNP2 promoter, where natural variation significantly influences GNP. GNP2 encodes a conserved GSK3-like kinase that phosphorylates and stabilizes Gnp4/LAX2. The phosphorylated Gnp4/LAX2 T175,262D promotes yield by modulating transcription factors involved in panicle development. Haplotype analysis reveals an elite allele combination (Type I) of GNP5 and GNP2 that significantly increases GNP. Field trials demonstrate that enhanced GNP2 expression raises yield by approximately 10%. Our findings thus uncover a genetic resource with application potential for enhancing rice yield. Grain number per panicle (GNP) is a yield-determining trait of rice. Here, the authors identify a GSK3-like kinase-encoding gene GNP2 and a bZIP transcription factor-encoding gene GNP5 , demonstrating their synergistic regulation of GNP and showing that specific allele combinations of these genes enhance rice yield in field conditions.