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In recent years, tea leaf spot, caused by the fungus Epicoccum sorghinum, adversely affects both the yield and quality of tea in China. Transient overexpression and antisense oligonucleotide (AsODN) assays revealed that upregulating CsMYB1, a transcription factor located in the nucleus, enhances resistance to E. sorghinum infection in tea leaves. Overexpression of CsMYB1 in transgenic Nicotiana benthamiana conferred resistance to Botrytis cinerea. Multi-omics assays of transiently overexpressed CsMYB1 in tea leaves indicated that CsMYB1 induces the expression of numerous disease resistance genes. DNA affinity purification sequencing assay indicated that CsMYB1 can activate the expression of the disease resistance gene pectinesterase/pectinesterase inhibitor 41 (CsPME41). β-glucuronidase and dual-luciferase assays showed that csi-miR858-3p_L-1 targets and cleaves CsMYB1. Moreover, transient overexpression and AsODN assays in tea leaves and transgenic csi-miR858-3p_L-1 N. benthamiana plants indicated that increasing csi-miR858-3p_L-1 levels heightens susceptibility to E. sorghinum in tea leaves. The relative expression levels of CsMYB1, CsPME41, and csi-miR858-3p_L-1 in tea leaves exhibited distinct spatial and temporal patterns in response to E. sorghinum invasion. This study reveals that the csi-miR858-3p_L-1-CsMYB1-CsPME41 module plays a role in the disease resistance response of tea plants to E. sorghinum infection, providing crucial data for resistance breeding.

Seven new endemic genera and ten new species of Tortricidae are described from the Hawaiian Islands; all are assigned to Archipini (Tortricinae). A further eleven new combinations and one restored status are proposed. Iliahia, gen. nov. (type species: Capuaflavopicta Walsingham), is described for six species which feed on the foliage of 'iliahi (Santalum spp.; Santalaceae): Iliahia flavocincta (Walsingham), comb. nov., Iliahia flavopicta (Walsingham), comb. nov., Iliahia lilinoe, sp. nov., Iliahia pahulu, sp. nov., Iliahia santalata (Swezey), comb. nov., reinst. stat., and Iliahia xanthogona (Walsingham), comb. nov.; Nomewaimea, gen. nov. (type species: Epagoge infaustana Walsingham), is described for four species which feed on the leaves, shoots, and stems of ōpuhe (Touchardia sandwicensis; Urticaceae) and māmaki (Pipturus spp.; Urticaceae): Nomewaimea alaea, sp. nov., Nomewaimea kupenuia, sp. nov., Nomewaimea infaustana (Walsingham), comb. nov., and Nomewaimea urerana (Swezey), comb. nov.; Kumakena, gen. nov. (type species: Capua cassia Swezey), is described for Kumakenacassia (Swezey), comb. nov., which feeds on the leaves of kolomona (Senna gaudichaudii; Fabaceae); Limua, gen. nov. (type species: Archips lichenoides Walsingham), is described for four species which feed on the leaves of olopua (Notelaea sandwicensis; Oleaceae) and kōpiko (Psychotria spp.; Rubiaceae): Limua fuscoviridis (Walsingham), comb. nov., Limua lichenoides (Walsingham), comb. nov., Limua pahole, sp. nov., and Limua trochilidanus (Walsingham), comb. nov.; Paalua, gen. nov. (type species: Panaphelix asteliana Swezey), is described for three species which feed on the leaves of pa'iniu (Astelia spp.; Asteliaceae): Paalua asteliana (Swezey), comb. nov., Paalua maunaloa, sp. nov., and Paalua leleole, sp. nov.; Aipoola kaumualii, gen. nov., sp. nov., is described for a new species which feeds on the leaves of po'olā (Claoxylon sandwicense; Euphorbiaceae); and Maneapakele, gen. nov. (type species: Maneapakelehapalua Austin & Rubinoff), is described for two species which feed in the fruits of pāpala kēpau (Ceodes spp.; Nyctaginaceae): Maneapakele hapalua, sp. nov., and Maneapakele kahaha, sp. nov. Lectotypes are designated for four species. With the exception of K. cassia and possibly I. pahulu and I.santalata, all species are believed to be single-island endemics. We assess the conservation status for all species treated. All previously described species transferred to these new genera are provided with a new diagnosis in the context of the new species. A generic key to Tortricidae in Hawai'i and a species checklist is provided.

Developing new therapies and discovering bioactive compounds to treat cutaneous leishmaniasis are critical to improving patients' quality of life. More effective, less toxic, and affordable compounds are needed. Thus, discovering such compounds could significantly enhance the management and control of cutaneous leishmaniasis. Brazil has a biodiversity of flora and microorganisms that remains unexplored, mainly for evaluating extracts and compounds with anti-Leishmania activity. This study aimed to screen the leishmanicidal activity of extracts and fractions from leaves of Eugenia pyriformis Cambess. collected during different seasons (winter and summer) in Rio de Janeiro, Brazil. Extracts from summer-collected leaves showed higher effectiveness against Leishmania (Leishmania) amazonensis promastigotes and amastigotes. The IC50 values for the extract from leaves collected in summer (Ep1) were significantly lower than those for winter extracts. Extracts showed low toxicity to human macrophages and a high selectivity index (SI > 12). In addition, the Ep1 extract induced G0/G1 phase arrest and necrosis in promastigotes. UHPLC-HR-ESI-MS/MS analysis combined with molecular networking revealed that flavonoids and terpenoids were predominant in active fractions. The study highlights the potential of E. pyriformis Cambess. as a source of leishmanicidal compounds from leaves collected during the summer season.

Chronic obstructive pulmonary disease (COPD) is a major public health concern due to its high prevalence, morbidity, and mortality. Although COPD is recognized as a systemic inflammatory disease, the specific circulating inflammatory proteins associated with its development and progression remain poorly understood. We performed a Mendelian randomization (MR) study to investigate the association between circulating inflammatory proteins and COPD risk. Genetic data were obtained from a genome-wide association study of 20,066 COPD cases and 338,303 controls from the FinnGen consortium and circulating inflammatory protein data were derived from a genome-wide association study of 14,824 participants. The inverse-variance weighted method was used as the primary analysis. Depending on the number of available instrumental variables, complementary methods including the Wald ratio, Weighted Median, MR-Egger, Weighted Mode, and Simple Mode were applied to assess robustness. Sensitivity analyses were conducted to evaluate heterogeneity and pleiotropy using Cochran's Q test, the MR-Egger intercept, MR-PRESSO, and leave-one-out analysis. In addition, cis-acting protein quantitative trait locus -restricted analyses were performed to further reduce potential pleiotropy. Our findings showed that higher genetically predicted levels of CCL28 (odds ratio [OR] = 0.83, 95% confidence interval [CI]: 0.69-0.99, P = .0394), CD40 (OR = 0.94, 95% CI: 0.89-0.99, P = .0170), and urokinase-type plasminogen activator (OR = 0.91, 95% CI: 0.85-0.99, P = .0212) were associated with a lower risk of COPD, whereas higher levels of Flt3L (OR = 1.09, 95% CI: 1.01-1.18, P = .0344) and CD6 (OR = 1.06, 95% CI: 1.02-1.12, P = .0099) were associated with a higher risk. Sensitivity analyses showed no evidence of heterogeneity or directional pleiotropy, and leave-one-out analyses indicated that the results were not driven by any single nucleotide polymorphism. These findings suggest that circulating inflammatory proteins, including CCL28, CD40, urokinase-type plasminogen activator, Flt3L, and CD6, may be involved in COPD pathogenesis. Further studies are needed to validate these findings and clarify their potential biological relevance.

BBX transcription factors can respond to UV-B signals, promote plant photomorphogenesis, and regulate plant anthocyanin biosynthesis. Based on transcriptome sequencing analysis, this study analyzed the transcription factors of StBBXs under UV-B treatment and identified two differentially expressed genes, StBBX19 and StBBX24. We explored the protein structures, promoters, and phylogenetics of StBBX19 and StBBX24, speculating that they respond to UV-B treatment and regulate anthocyanin biosynthesis. We constructed overexpression vectors, YFP, and bimolecular fluorescence complementation vectors for the transient transformation of tobacco. The results suggest that StBBX19 and StBBX24 may not function as direct regulators of anthocyanin biosynthesis, but rather enhance anthocyanin accumulation through interaction with StMYB308. Still, after interacting with StMYB308, purple spots appeared on tobacco leaves, suggesting that the interaction between StBBX19, StBBX24, and StMYB308 increases anthocyanin content in tobacco leaves. This study provides significant evidence for the adaptation mechanism of plants under UV-B treatment and offers new insights for molecular plant breeding of pigmented potatoes.

FatB acyl-ACP thioesterases play an important role in plant fatty acid metabolism, determining the chain length and saturation of acyl groups that feed both storage oil and membrane lipid biosynthesis. In sunflower (Helianthus annuus L.), only one isoform, HaFatB1, has been characterized to date. Here, we report the identification and functional characterization of a novel sunflower plastidial thioesterase, HaFatB2, which exhibits low expression in developing seeds but is relatively abundant in leaves, suggesting a metabolic role beyond oil biosynthesis. Structural modelling and molecular docking predicted efficient accommodation of palmitoyl- and oleoyl-ACPs, a preference confirmed by in vitro assays and kinetic studies. When expressed in Escherichia coli, HaFatB2 markedly modified the fatty acid profile, leading to the unexpected accumulation of 4-hydroxymyristic acid (23% of total FAs), a rare fatty acid with potential industrial relevance. In contrast, expression in the photosynthetic cyanobacterium Anabaena sp. PCC 7120 and in Nicotiana benthamiana leaves did not significantly alter fatty acid composition, likely due to differences in substrate availability and endogenous regulatory mechanisms. Altogether, these findings identify HaFatB2 as a thioesterase with high preference for the export of palmitic and oleic fatty acids and highlight its biotechnological potential for producing uncommon hydroxylated fatty acids in heterologous systems.

Atmospherically deposited cadmium (Cd) can accumulate in crops through uptake by above-ground parts; however, the key organs, pathways, and mechanisms involved in Cd uptake and accumulation in plants under this mode remain unclear. To clarify these issues, this study carefully designed a pot experiment with wheat, exposing various above-ground organs for different durations (daytime and nighttime) using CdS nanoparticles to simulate atmospherically deposited Cd. Results showed that exposure of above-ground parts to CdS significantly increased Cd content in all tissues of wheat, indicating that Cd in wheat plants from above-ground uptake could be transferred upward to grains and downward to roots. Furthermore, spike and foliar uptake contributed 11-34% and 66-89%, respectively, to the increased Cd levels in wheat grains, while these two uptake modes contributed 1-49% and 51-99%, respectively, to the increased Cd levels in other tissues (including roots, stems, leaves, and husks). These findings suggest that, in addition to leaves, spikes were also important organs responsible for the uptake of simulated atmospherically deposited Cd. Regarding absorption pathways, the contributions of stomatal and cuticular penetration to Cd accumulation in grains were quantified as 42-66% and 34-58%, indicating that both pathways played key roles in the internalization of atmospheric Cd in plants. Subcellular distribution of Cd in above-ground tissues showed that the cell wall, particularly its pectin component, served as the primary barrier to simulated deposited Cd influx into the cytoplasm. This study highlights that controlling foliar and spiked Cd uptake-particularly by regulating stomatal opening and enhancing the cell wall's Cd-binding capacity-could be a promising strategy to prevent Cd accumulation in crops resulting from atmospheric deposition.

While antibiotic use is recognized to contribute to antimicrobial resistance (AMR), the magnitude of its impact on AMR-related harms is not well understood. This study quantifies the association between antibiotic consumption and AMR-related mortality and costs. Antibiotic consumption expressed in defined daily dose per 1,000 inhabitants per day (DID) was sourced from pharmaceutical sales data from 30 European countries. Linear regression models were fitted to assess the association between antibiotic consumption and (a) AMR-related mortality in 2023 and (b) AMR-related healthcare costs in 2021. Estimates were adjusted for key confounders, including median age, gross domestic product (GDP) and hospital bed density. Leave-one-out and time-lag sensitivity analysis were performed to test robustness. Each unit increase in DID of average antibiotic consumption was associated with 0.3 (95% Confidence Interval [CI]:0.2-0.5) additional AMR-related deaths per 100,000, and an increase in AMR-related costs of 5.6% (95% CI: 1.8%-9.3%), holding all other variables constant. Mortality estimates were robust across sensitivity analyses, while cost-estimates were sensitive to excluding outliers. Using antibiotic consumption from earlier years did not significantly affect the results. This ecological study demonstrated that antibiotic consumption is positively associated with AMR-related mortality and costs across European countries. Despite the ecological nature of this study, the presented quantitative estimates can be used to inform health policy analyses of antibiotic interventions. Although missing data and context-specific factors may have limited the robustness of the cost association, these findings suggest that reducing unnecessary antibiotic consumption could help lower AMR-related mortality and healthcare costs.

Naturalistic threat viewing provides a useful context for examining how observers align their neural responses to shared, continuously unfolding stimulus structure. This study used electroencephalography inter-subject correlation (EEG-ISC) of band-limited power time courses to characterize condition-related neural alignment during rest, threat-related viewing, and neutral viewing. Seventeen healthy adults viewed an eyes-open resting baseline, a high-arousal parkour clip labeled as the fear condition, and an emotionally neutral parkour clip while 64-channel EEG was recorded. Band-limited power was extracted using sliding-window fast Fourier transform, and ISC was estimated using leave-one-out correlation followed by Fisher z transformation. We examined condition-related ISC differences across delta, theta, alpha, and beta bands, as well as time-dynamics, window-length sensitivity, matched-duration controls, and exploratory associations with trait anxiety. Across the analyzed delta-beta frequency bands, ISC differed reliably across conditions, showing stronger synchrony during video viewing than rest and higher ISC during fear viewing than neutral viewing. This effect was most pronounced for alpha-band power ISC, although frequency-specific interpretation remains tentative because periodic and aperiodic spectral components were not separated. Time-dynamics analyses showed that ISC was largely stable within clips, with a selective attenuation of fear-alpha ISC over time. Window-length and matched-duration control analyses broadly preserved the qualitative condition pattern. Exploratory individual-differences analyses did not provide robust evidence for an association between fear-evoked ISC and trait anxiety in this small sample. These findings support EEG-ISC as a marker of shared, stimulus-locked processing during naturalistic threat viewing. Threat-related events may promote more convergent tracking of unfolding stimulus structure, yielding stronger neural alignment at the group level. The exploratory anxiety-related findings require confirmation in larger samples.

Excessive iron availability (EIA) in marine ecosystems often occurs as a result of anthropogenic activities and represents a stressful and damaging condition for many marine organisms. The gray mangrove Avicennia marina, the dominant vegetation along the Red Sea shoreline, is frequently exposed to such conditions; however, its physiological responses remain unknown. The current results indicate that, under controlled conditions, EIA had contrasting effects on the growth of A. marina seedlings, depending on the salinity of the medium. Under saline conditions (600 mM NaCl), excessive iron reduced total dry weight (by 35%), photosynthetic assimilation rate (by 20.6%), stomatal conductance (by 40%), transpiration rate (by 46%), iron accumulation in leaves (by 42%), stems (by 18.4%), and roots (by 36.1%), as well as iron absorption efficiency (FeAE) (by 39.4%). In contrast, under nonsaline conditions, EIA enhanced total dry weight (by 39.8%), net photosynthetic assimilation rate (by 19%), and photosynthetic pigment content, while having no significant effect on iron accumulation in different plant organs or on iron use efficiency. Salt excretion occurred only under saline conditions, and EIA had no effect on the rate or composition of the excreted salt crystals. In conclusion, A. marina seedlings appear to cope with excessive iron by sequestering excess Fe in the roots and enhancing root growth and photosynthetic activity under nonsaline conditions. Under saline treatment, however, the plants adopt a restrictive Fe uptake strategy, and despite that, the detrimental effects of EIA were noted only under saline conditions.

Aging and its associated diseases are characterized by a complex interplay of cellular dysfunction, chronic inflammation, and tissue degeneration. Dysregulated cell death and the resulting inflammatory responses are pivotal drivers of this pathological synergy. Among various cell demise pathways, programmed cell death (PCD) mechanisms, including apoptosis, necroptosis, and pyroptosis, are critical for maintaining homeostasis but can drive pathology when aberrantly activated. Crucially, they leave specific and reliable biomarkers, allowing for their distinct assessment in complex aging tissues. This review synthesizes recent insights into the intricate regulation and execution of these PCD pathways, their interconnections with inflammatory signaling, and their impact on the pathogenesis of aging and aging-related diseases. We further highlight how the integrated understanding of these cell death pathways opens avenues for targeted therapies in aging-associated disorders.

The impact of glucagon-like peptide-1 receptor agonists (GLP-1RAs) on peripheral artery disease (PAD) remains uncertain. We assessed the association between GLP-1RA use and major limb events in individuals with type 2 diabetes (T2D) and PAD. We performed a literature search from inception to 31 March 2026 for randomized controlled trials and cohort studies comparing GLP-1RA use versus placebo, active comparators or non-use on lower limb outcomes in individuals with T2D and PAD. The primary outcome was a composite of major limb events, as defined by the investigators of the original studies included in the meta-analysis. Secondary outcomes included lower extremity amputation (LEA), revascularization, gangrene, major adverse cardiovascular events (MACE) and all-cause mortality. Subgroup analyses, leave-one-out sensitivity analyses, and meta-regression analysis were also performed. Twelve studies (2 RCTs and 10 matched cohort studies) with thirteen arms involving 418,282 participants were included. Treatment with GLP-1RAs was associated with a significantly lower risk of major limb events by 27% (thirteen arms, RR 0.73, 95% CI 0.65-0.82). Reduced risks were also observed for LEA (RR 0.76, 95% CI 0.66-0.87), revascularization (RR 0.81, 95% CI 0.77-0.86), gangrene (RR 0.80, 95% CI 0.77-0.85), MACE (RR 0.76, 95% CI 0.63-0.90) and all-cause mortality (RR 0.67, 95% CI 0.61-0.73). Subgroup and sensitivity analyses did not substantially change point estimates. Among adults with T2D and PAD, treatment with GLP-1RAs was associated with a lower risk of major limb events. There is a need of dedicated studies with standardized limb-specific endpoints to confirm the protective role of GLP-1RAs on limb events in people with T2D and PAD.

To clarify whether specific immune cell phenotypes exert a causal influence on diabetic nephropathy (DN), we conducted a Mendelian randomization (MR) investigation using large-scale genetic datasets. Summary-level data for immune cell traits and DN were obtained from recent genome-wide association studies and the FinnGen consortium. Genetic instruments were selected under the core MR assumptions, ensuring strong relevance and minimal confounding. The inverse-variance weighted approach served as the primary analytical framework. Complementary analyses, including MR-Egger regression, Cochran Q test, and leave-one-out procedures, were performed to detect horizontal pleiotropy, assess heterogeneity, and evaluate the stability of the findings. Genetically predicted increases in several immune cell phenotypes were associated with higher genetic susceptibility to DN, including CD25 on IgD- CD38dim (odds ratio [OR]: 1.153, P&#x2005;=&#x2005;.026), CD8dim AC (OR: 1.144, P&#x2005;=&#x2005;.045), HLA DR on CD33br HLA DR+ CD14- (OR: 1.142, P&#x2005;<&#x2005;.001), CD39+ CD8br %CD8br (OR: 1.094, P&#x2005;=&#x2005;.047), and CD25hi CD45RA+ CD4 not Treg %T cell (OR: 1.051, P&#x2005;=&#x2005;.041). Conversely, higher SSC-A on CD4+ cells was associated with lower genetic susceptibility to DN (OR: 0.385, P&#x2005;<&#x2005;.001). No evidence of horizontal pleiotropy was detected (P&#x2005;&#x2265;&#x2005;.05). Cochran Q indicated no significant heterogeneity. Sensitivity analyses confirmed the robustness of all associations. This MR analysis suggests that HLA DR on CD33br HLA DR+ CD14- is associated with increased genetic susceptibility to DN, whereas SSC-A on CD4+ is associated with decreased susceptibility. These findings offer genetic evidence of immune involvement in DN susceptibility and warrant further validation and investigation to clarify mechanisms and relevance.

Soil salinization severely restricts the growth and productivity of ginger (Zingiber officinale Rosc.). The PYL gene family encodes core components of the abscisic acid (ABA) signaling pathway, which plays a pivotal role in plant responses to abiotic stresses. However, the PYL gene family in ginger has not been systematically characterized to date. In this study, 11 ZoPYL genes were identified from the ginger genome and phylogenetically clustered into four subfamilies. Promoter sequence analysis revealed the presence of multiple stress-responsive cis-elements, and transcriptional regulatory network prediction suggested that ZoPYL proteins are potentially regulated by MYB, bZIP, and other transcription factor families. Expression profiling indicated that most ZoPYL genes were upregulated in response to ABA treatment, while salt stress induced tissue-specific expression patterns of ZoPYLs, with ZoPYL11 being significantly upregulated in both leaves and roots. Silencing of ZoPYL11 enhanced ginger sensitivity to salt stress, accompanied by reduced activities of antioxidant enzymes and increased accumulation of reactive oxygen species (ROS). Concomitantly, the expression levels of ZoPP2C and ZoSnRK2 genes were dysregulated in ZoPYL11-silenced plants, indicating disrupted ABA signaling. This study provides a comprehensive characterization of the PYL gene family in ginger and demonstrates that ZoPYL11 plays a crucial role in enhancing salt tolerance by mediating ABA signaling and antioxidant defense.

Per-base quality scores are widely treated as technical metadata in next-generation sequencing. Here, we show that in rigorously controlled whole-genome sequencing of cell-free DNA, quality profiles may carry fragmentomic-associated signal that enables classification of cancer samples against matched controls. Analyzing four independent batches (23 cancer samples: pancreatic and breast; 22 matched controls) sequenced in a within-lane regime and further normalized per flow-cell tile to reduce technical confounders, we demonstrate through unsupervised analysis that boundary-enriched dynamics captured in these quality scores consistently separate cancer from control samples. A leave-one-batch-out classifier trained on quality-derived scores achieved a pooled area under the curve of 0.81. Furthermore, we show that the quality-derived metric correlates with short-fragment enrichment and tumor-associated 5'-end motifs, performing comparably to established, motif-based orthogonal methods. These results provide initial evidence that quality scores could serve as a low-cost, alignment-free surrogate signal for cfDNA-based cancer detection.

The observational association between obesity and atrial fibrillation has been well-established. However, its causal mediators underlying this association remain unclear. This study aimed to investigate the causal relationship between body mass index (BMI), as well as potential mediating factors underlying this association, using Mendelian randomization (MR). Genetically predicted BMI was significantly associated with an increased risk of atrial fibrillation (inverse-variance weighted odds ratio [OR]&#x2005;=&#x2005;1.350, 95% confidence interval [CI]&#x2005;=&#x2005;1.268-1.436, P&#x2005;<&#x2005;.001). Sensitivity analyses using multiple methods yielded consistent results, and no evidence of directional pleiotropy was detected after outlier correction. A total of 91 inflammatory cytokines and 4907 plasma proteins were included as potential mediators. Among the screened mediators, SLIT2 exhibited a significant inverse mediating effect on the association between BMI and atrial fibrillation (OR&#x2005;=&#x2005;1.019, 95% CI&#x2005;=&#x2005;1.005-1.034), accounting for 7% of the total effect. These results suggest that higher BMI is associated with reduced SLIT2 expression, which in turn increases the risk of atrial fibrillation. In contrast, ANGPTL3 showed a significant positive mediating effect (OR&#x2005;=&#x2005;1.010, 95% CI&#x2005;=&#x2005;1.003-1.017), accounting for 3.64% of the total effect, indicating that elevated BMI increases ANGPTL3 levels, thereby further increasing the risk of atrial fibrillation. This MR study provides genetic evidence supporting a causal association between obesity and atrial fibrillation and suggests that SLIT2 and ANGPTL3 may be involved as mediators linking obesity-related inflammation and lipid dysregulation to atrial fibrillation susceptibility. First, a 2-sample MR analysis was conducted using genome-wide association studies meta-analysis of European ancestry to estimate the causal effect of genetically proxied BMI on atrial fibrillation. Subsequently, inflammatory cytokines and plasma proteins were considered as candidate mediators, with their cis-protein quantitative trait locus used as instrumental variables. The inverse-variance weighted method was applied as the primary MR approach, while MR-Egger, weighted median, weighted mode, MR-Pleiotropy Residual Sum and Outlier, and leave-one-out methods were used for sensitivity analyses. Shared causal variants were further evaluated using false discovery rate correction and colocalization analysis within a&#x2005;&#xb1;&#x2005;500&#x2009;kb window (PPH4&#x2005;>&#x2005;0.75).