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Throughout the 1950s, the Daily Mirror led a campaign by the popular press against petty, tyrannical discipline, commonly known as 'bull(shit)', within the British Army. Acting as moral entrepreneurs, tabloid newspapers positioned what they regarded to be the deviant behaviour exhibited by over-zealous non-commissioned officers towards national servicemen as a threat to the normative contours of British society. By doing so, the campaign against 'bull' sought to exploit latent fears about large standing armies in peacetime to pressure the Army to reform and modernize its methods of discipline. The article argues that the campaign against 'bull' was effective in that it elevated military discipline as an issue of public concern during a period in which the British Army was actively seeking to enhance its public image to improve soldier recruitment and retention as it prepared to revert back to being an all-volunteer force after the decision was made in 1957 to terminate National Service. By framing 'bull' as an archaic form of social control that was damaging to both morale and efficiency, the moral crusade compelled the Army to explain and justify its methods of discipline amidst increasing public and parliamentary concern.

Chlamydia psittaci is an obligate intracellular zoonotic pathogen that causes atypical pneumonia. Pyroptosis is a type of regulated cell death mediated by gasdermin-family proteins and plays an important role in the response to intracellular infection. This study investigates whether C. psittaci infection triggers GSDME-mediated pyroptosis through the ROS-JNK signaling pathway. Our study revealed that infection with C. psittaci induces pyroptosis through caspase-3 activation and subsequent GSDME cleavage in human cervical epithelial (HeLa) cells. Mechanistically, the infection increased intracellular levels of reactive oxygen species (ROS) and phosphorylated c-Jun N-terminal kinase (JNK). Treatment with either the ROS scavenger NAC or the JNK inhibitor SP600125 significantly suppressed pyroptosis. Furthermore, inhibition of either the caspase-3-GSDME axis or the ROS-JNK pathway significantly increased the number of C. psittaci inclusion bodies. Taken together, our findings suggest that the ROS/JNK signaling pathway modulates GSDME-mediated pyroptosis and concurrently restricts C. psittaci replication in host cells, identifying the ROS-JNK-GSDME axis as a key mechanism in C. psittaci-induced pyroptosis. These findings reveal novel therapeutic targets for the treatment of psittacosis.

Cranioectodermal dysplasia (CED) (OMIM #218330) is an autosomal recessive multisystemic disorder. While many studies have diagnosed this condition postnatally, few cases have been identified during the prenatal period. This study aimed to investigate genetic mutations in a Han Chinese fetus and conduct a literature review, integrating ultrasonographic findings with molecular analysis to expand the genotype-phenotype spectrum of this ciliopathy. A 22-year-old Han Chinese woman conceived naturally. Prenatal ultrasound revealed multiple fetal congenital anomalies, including limb shortening, generalized fetal edema, cystic hygroma, and bilateral echogenic kidneys. Whole-exome sequencing revealed two bi-parental inherited compound heterozygous variants in WDR35: [c.1600C > T (p.Arg534Cys)] and [c.2375_2383del (p.Asn792_ Ala794del)]. The couple ultimately opted to terminate the pregnancy. The WDR35 mutations are associated with CED and exhibit a complex prenatal phenotype. Comprehensive prenatal ultrasound, whole-exome sequencing, and multidisciplinary genetic counseling are essential for accurate diagnosis and informed reproductive counseling.

Petroleum hydrocarbon (PHC) degradation in oxygen-limited soils is constrained by scarce terminal electron acceptors and poor redox connectivity. Coupling Fe and S transformations with conductive electron snorkels is expected to stimulate anaerobic PHC turnover by promoting Fe/S redox cycling and syntrophic electron exchange, yet the underlying mechanism remains unclear. Here, a dual electron-transfer framework was developed by integrating in situ biogenic FeSx-associated assemblages with electron snorkels. In systems amended with exogenous γ-FeOOH + snorkel + S0 or Fe-rich natural soil + snorkel + S0 (HFe-SN+S), PHC removal increased by ∼2.4-4.1-fold relative to corresponding controls, and comparable enhancements were reproduced in an independent agricultural soil. These gains were accompanied by higher bulk ionic conductivity, transient Fe2+ accumulation, and FeSx-enriched aggregate coatings, indicating enhanced ion release and Fe/S redox turnover. HFe-SN + S reshaped Fe/S cycling and enriched Fe-S-transforming and PHC-degrading consortia carrying genes for PHC catabolism and extracellular electron transfer. Redox-coupled N transformation provided an auxiliary electron sink, mitigating electron accumulation and coinciding with faster TOC depletion and IC production. Overall, these findings support a mechanistic framework in which FeSx-associated interfacial structures may facilitate local electron exchange, while snorkels provide a potential electron-disposal route, establishing a theoretical basis for Fe-S-snorkel-assisted remediation strategies.

The plant endoplasmic reticulum (ER) forms a highly dynamic tubular network whose architecture depends on ER-shaping proteins and its interaction with the cytoskeleton. While actin is well known to drive ER movement in plants, how the ER associates with microtubules and how this affects ER network architecture remain poorly understood. Here, we identify Arabidopsis thaliana reticulon 17 (RTN17) as an atypical reticulon that links the ER to the microtubule cytoskeleton. RTN17 features extended, intrinsically disordered N- and C-terminal domains enriched in low-complexity regions, consistent with a scaffolding or hub function. Topology analysis using redox-sensitive roGFP2 constructs shows that both termini face the cytosol, yet RTN17 lacks the amphipathic helix typical of ER-shaping reticulons and does not induce membrane constriction. Instead, RTN17 localises to punctate foci on curved ER membranes, recruits the ER fusogen ROOT HAIR DEFECTIVE3 (RHD3), and co-expression alters ER architecture and dynamics. RTN17 puncta preferentially co-localise with microtubules, and its over-expression promotes ER alignment with the microtubule network. We propose that RTN17 acts as a multifunctional scaffold linking curved ER domains with the microtubule cytoskeleton and localising RHD3 to these sites to regulate ER fusion events. By integrating curvature sensing, cytoskeletal attachment and fusion regulation, RTN17 represents a new class of plant reticulons with scaffolding rather than shaping functions. This work highlights an unrecognised mechanism coordinating ER organisation with the cytoskeleton, providing insights into how plants achieve spatial control of endomembrane architecture and potentially adapt membrane dynamics to developmental or stress cues.

Population genomic workflows frequently rely on fragmented command-line utilities, custom conversion scripts, and programming language-specific environments, complicating computational reproducibility and obscuring data provenance. As analytical workflows become increasingly automated and computationally intensive, dependence on disparate preprocessing tools can introduce friction between raw genotype files, quality-control decisions, statistical analyses, and downstream workflows. We developed SNPio, a Python-native framework that consolidates single nucleotide polymorphism data parsing, filtering, visualization, numerical genotype encoding, and population genomic summary-statistic calculation within a unified software architecture. VCF file parsing and filtering benchmarks were compared against vcfR and SNPfiltR. SNPio demonstrated faster execution times but used more memory than its R-based comparators, reflecting SNPio's retention of genotype arrays, metadata, and provenance-tracking attributes. Pairwise Weir and Cockerham's FST and Nei's genetic distance estimates aligned with HierFstat expectations based on Pearson correlations and aggregate error metrics. D-statistics conformed to theoretical expectations across eleven simulated datasets spanning a range of introgression signal strengths. SNPio provides a reproducible Python-native workflow for processing, filtering, encoding, visualizing, and analyzing SNP datasets. It integrates common early-stage population genomic operations into a transparent, scriptable framework, which ultimately promotes workflow provenance and reduces reliance on disjointed software tools, unsaved terminal commands, and custom scripts. SNPio is particularly suited for population genomic studies of non-model organisms in ecological, evolutionary, and conservation contexts, where reproducible preprocessing and interoperability with downstream analyses are becoming increasingly important.

Pancreatic ductal adenocarcinoma (PDAC) growth and metastasis are influenced by the tumor microenvironment (TME), which includes immune cells, endothelial cells, macrophages, and cancer-associated fibroblasts (CAFs). Since the novel integrin-targeted cytotoxin ProAgio can inhibit activated CAFs and endothelial cells, we investigated its combination with standard of care chemotherapies in genetically engineered mouse (GEM) and orthotopic murine models of PDAC. We established metastatic murine KPC-Ganji & Bassel-Luc (mKPC-GB-Luc) cell lines and validated them using bulk RNA sequencing. Two in vivo orthotopic mouse model were used to evaluate ProAgio with chemotherapy. mKPC-GB-Luc was used to evaluate the 5FU, oxaliplatin, and irinotecan (FOI combination), and KPC-ML1-Luc was used to evaluate the gemcitabine, nab-paclitaxel (GPTx combination). Immunohistochemistry was used to measure integrin β3, E-cadherin, and HIF-1α. Hypoxia was evaluated using pimonidazole. Stem cells, CAFs, and immune cell subtypes were quantified by flow cytometry. We evaluated the combination of ProAgio plus gemcitabine in a KPC genetically engineered mouse model (KPC GEM). Two sets of KPC GEM were developed. The first set was used for a survival study. The second set was terminated early and tumors were used for single-cell RNA seq and sequential multiplex immunofluorescence (COMET). Compared with the chemo regimen (GPTx or FOI), ProAgio, or sham, the combination of ProAgio plus chemo significantly modulated the TME, reduced tumor weight, reduced hypoxia, and eliminated metastasis to the lungs and liver. The combination of ProAgio and gemcitabine increased overall survival in KPC GEM mice compared with either treatment alone. Single-cell RNA sequencing, flow cytometry, immunofluorescence, immunohistochemistry, and COMET analyses demonstrated that ProAgio plus chemotherapy reprogrammed the PDAC-TME by changing activated CAFs toward a qCAFs (quiescent CAFs), macrophages from protumor to proinflammatory polarization, and activating natural killer (NK) cells, CD4⁺, and CD8⁺ T cells. Combination therapy inhibited PDAC stemness. ProAgio-treated CAFs in vitro exhibited reduced secretion of glycine and cysteine, vital metabolites that support stemness and tumor progression. These results confirm the novel mechanism of action of ProAgio, which includes reducing hypoxia and modulating TME. The current data provide evidence for potentiation of chemotherapy efficacy by ProAgio.

ConspectusThe innovative exploration of non-fullerene acceptors (NFAs) such as ITIC, Y6, and others, has boosted the power conversion efficiencies (PCEs) of organic solar cells (OSCs) surpassing 21%. However, organic photovoltaics still suffer from significant efficiency gaps compared to inorganic photovoltaics, particularly in open-circuit voltage under similar bandgaps. This notable disparity is largely driven by the stark difference in nonradiative recombination energy losses: OSCs typically incur losses exceeding 0.2 eV, whereas their inorganic counterparts suffer only minimal losses, ranging from a mere 0.03 to 0.04 eV. This insurmountable nonradiative recombination is closely associated with some intrinsic features of organic photovoltaic light-harvesting materials: relatively flexible molecular frameworks, loose and disordered molecular aggregates, large exciton binding energies, etc. Therefore, a multiscale regulation spanning single-molecular properties and aggregation behaviors in further molecular design is required, if a remarkable PCE improvement is expected.In this Account, we first present a brief review of the development of electron acceptor materials, with a focus on analyzing the prominent merits of current high-efficiency acceptor molecular skeletons (especially Y6 analogs) in terms of intermolecular packing modes, photodynamic, etc. Meanwhile, great challenges for further material design also arises from the quite limited structural optimization room for Y-series backbones. In order to break through the dilemma of molecular design, we developed CH-series NFAs with multi-functionalized central units and an "acceptor-donor-acceptor" architecture. Subsequently, a systematic discussion about CH-series NFAs will be made to reveal their advantages in (1) inducing a directional transformation of molecular packing mode toward a more favorable one, through multiple intermolecular weak interactions such as fluorine-hydrogen/sulfur/π bonds, thus rendering multidimensional long-range ordered molecular stacking to minimize energy loss pathways in OSCs; (2) breaking through the limitations of traditional dimeric/trimeric/polymeric acceptor design by pioneering the construction of relatively rigid central-units-linked dimeric/trimeric NFAs with multiple free terminals to enhance intermolecular packings; (3) proposing a novel "functional reconfiguration" strategy for the central units, aiming to explore new photoelectric conversion mechanisms in organic photovoltaic materials.Thus far, CH-series NFAs based binary OSCs have achieved the highest PCE of approaching 21%, ranking among the best NFAs. If further considering their great structural modification possibilities, CH-series NFAs hold exceptional promise as a versatile platform for developing OSCs with record-breaking PCEs. Therefore, we further propose some perspectives for CH-series NFAs, for example, more precise structural and packing optimization to reduce exciton binding energies and improve molecular packing ordering; further in-depth exploration of a "functional reconfiguration" strategy to apply new photoelectric conversion mechanisms, such as triplet excitons, singlet fission, etc.; extending the absorption edge of NFAs to near-infrared II region to harvest more low-energy photons, especially for tandem OSCs. These strategies may have the potential to overcome the critical challenge existing in OSCs and shrink the PCE gap comparing to inorganic platforms.

Dysesthesia-such as tingling and numbness-remains refractory to pharmacological treatment and poses therapeutic challenges within neuropathic pain. Dysesthesia-matched transcutaneous electrical nerve stimulation (DM-TENS) is a perceptually guided neuromodulation approach in which stimulation parameters are iteratively adjusted to synchronize with the perceived temporal patterns and intensity of the patient's abnormal sensory experience. However, immediate responses to DM-TENS across heterogeneous neuropathic pain conditions, as well as the feasibility of both direct and indirect (remote-site) stimulation approaches have not been described. This retrospective observational case series included consecutive patients with refractory neuropathic pain referred from the pain clinic to the rehabilitation department at our university hospital between December 2024 and August 2025. Dysesthesia intensity was assessed before and during stimulation using the Numerical Rating Scale (NRS), and pain quality was evaluated using the Short-Form McGill Pain Questionnaire-2 (SF-MPQ-2) as an exploratory measure. Within-session changes were examined using session-level linear mixed-effects models, with aggregated non-parametric analyses performed as sensitivity analyses. As an exploratory analysis, within-patient consistency of stimulation parameters (frequency, pulse width, and intensity) across repeated sessions was evaluated using intraclass correlation coefficients (ICCs). DM-TENS was well tolerated in all participants, with no stimulation-related adverse events requiring session termination. Fifteen patients underwent 66 DM-TENS sessions, of which 64 provided NRS data. A session-level linear mixed-effects model showed significantly lower NRS scores during stimulation (p&#x2009;<&#x2009;1&#x2009;&#xd7;&#x2009;10&#x207b;8). Aggregated sensitivity analyses showed a median NRS change of&#x2009;-&#x2009;2.0 (interquartile range&#x2009;-&#x2009;2.75 to&#x2009;-&#x2009;1.43). Indirect stimulation was applied only in trigeminal neuropathic presentations; lower within-session symptom scores were observed during palm stimulation, and these findings should be considered exploratory. SF-MPQ-2 total scores were also significantly lower during stimulation (p&#x2009;=&#x2009;0.002). Stimulation parameters showed good to excellent within-patient consistency across repeated sessions (ICC range 0.78-0.85). In this retrospective observational case series, lower within-session symptom scores were observed during DM-TENS across heterogeneous neuropathic pain conditions, including trigeminal, spinal, and peripheral presentations. These findings raise the hypothesis that individualized, perceptually guided adjustment of stimulation parameters warrants prospective evaluation.

Controlling local chemical environments within porous crystalline materials is essential for selective adsorption and catalysis, yet remains difficult in stable frameworks with precisely oriented functional sites. Here we use reticular chemistry to programme tunable confinement in triazolate metal-organic frameworks constructed from Kuratowski-type Zn5Cl4 nodes. Linker geometry directs the formation of the ith-d topology, in which terminal Zn-bound groups point inwards to generate confined and chemically addressable pores. This strategy yields two isoreticular frameworks, NU-6000 and NU-6001, with distinct cage dimensions and apertures, while preserving the same topology. Post-synthetic chloride-to-hydroxide exchange installs dense arrays of inward-facing Zn-OH groups without loss of crystallinity, enabling reversible CO2 chemisorption through bicarbonate formation. Single-crystal analysis of a CO2 adduct reveals that confinement imposes a geometric accessibility limit on reactive hydroxyl sites within the smallest cage of NU-6000. Under this confinement regime, NU-6000 exhibits strong low-pressure CO2 capture, including at 30&#x2009;ppm, and achieves 61.4% site utilization at 420&#x2009;ppm, among the highest reported for metal-organic frameworks under comparable conditions.

R-loops and D-loops are three-stranded nucleic acid structures that have emerged as central regulators of genome stability, gene expression, and DNA metabolism. R-loops form co-transcriptionally or post-transcriptionally when nascent RNA re-anneals with the template DNA strand, generating an RNA: DNA hybrid that displaces the non-template strand into a single-stranded state. These structures are enriched at CpG island promoters, transcription termination sites, and immunoglobulin class-switch regions, where they coordinate transcription regulation, chromatin remodeling, and DNA damage signaling. D-loops are formed when a single-stranded DNA segment pairs with one strand of a duplex and displaces the other, arising through context-dependent mechanisms that include RAD51- or DMC1-mediated strand invasion in homologous recombination, shelterin-assisted invasion at telomeres, and replication-coupled strand displacement at the mitochondrial DNA origin. They serve as indispensable intermediates in double-strand break repair, telomere maintenance, and mitochondrial DNA replication. Recent cryo-electron microscopy studies have resolved the stepwise RAD51-mediated strand exchange mechanism at near-atomic resolution, substantially advancing structural understanding of D-loop biogenesis. Despite their differences in molecular composition, both structures remodel Watson-Crick base pairing and, when dysregulated, are associated with replication fork stalling, transcription-replication conflicts, and aberrant recombination. This review systematically compares the structural features, formation mechanisms, regulatory networks, and biological functions of R-loops and D-loops, with emphasis on their convergent roles in safeguarding genome integrity. We further discuss rapidly evolving detection technologies and emerging therapeutic strategies targeting these structures in cancer and neurodegeneration, identifying key unresolved questions for future investigation.

Gram-negative bacteria pose a threat to global healthcare mainly because their outer membrane (OM) provides an intrinsic barrier to many antimicrobials. Key to this barrier function is the asymmetric structure of the OM, with phospholipids constituting the inner leaflet and lipopolysaccharides, the outer leaflet. Although the mechanism of phospholipid transport between the inner membrane (IM) and OM remains poorly understood, recent studies implicate TamB, YhdP, and YdbH as functionally redundant proteins mediating this process in Escherichia coli. Accordingly, the collective loss of these three paralogs is lethal, and any one of them is sufficient for growth. YdbH is anchored to the IM, and its periplasmic repeating &#x3b2;-sheet groove domain interacts with the OM lipoprotein YnbE via &#x3b2;-strand augmentation to form an intermembrane bridge. Additionally, YnbE multimerizes, and the periplasmic protein YdbL is proposed to modulate YnbE multimerization to facilitate its stacking on the C-terminus of YdbH. Here, we demonstrate that excess YdbL specifically inhibits the function of the YdbH-YnbE complex since overexpression of ydbL causes lethality in the &#x394;yhdP &#x394;tamB double mutant, but the presence of both ydbH and ynbE in trans abrogates this lethality. We resolve high-resolution structural data for YdbL and ascertain its interaction site with the YnbE C-terminal &#x3b1;-helix, with residues mediating this interface highly conserved and critical for YdbL function. Finally, we show that YdbL is protected from degradation by the protease DegP when complexed with YnbE. Overall, our data support a model in which YdbL ensures proper YdbH-YnbE intermembrane bridge formation by directly interacting with YnbE. The mechanism underlying phospholipid transport between the inner and outer membranes of gram-negative bacteria remains enigmatic. Bacterial bridge-like protein systems such as the YdbH-YnbE complex resemble proteins found at membrane contact sites between eukaryotic organelles. These proteins are proposed to mediate intermembrane phospholipid transport, which is essential for growth of the outer membrane (OM). Here, we define the role of YdbL, a periplasmic protein that specifically modulates the YdbH-YnbE system. YdbL directly interacts with YnbE and controls the formation of the YdbH-YnbE complex. Additionally, we reveal that YdbL is selectively degraded by the periplasmic protease DegP. We propose a regulatory model that connects the YdbH-YnbE complex assembly and controls the levels of YdbL, providing new insight into OM homeostasis in gram-negative bacteria.

Pseudorabies virus (PRV) reprograms host inflammatory responses and epitranscriptomics, yet how these processes are connected remains unclear. Here, we report a JNK-WTAP-m&#x2076;A-DUSP5 regulatory circuit that coordinates viral replication and inflammatory responses. PRV infection activated c-Jun N-terminal kinase (JNK), which phosphorylated wilms tumor-associated protein (WTAP) to drive its nuclear export and disrupt the activity of the m&#x2076;A methyltransferase complex. Methylated RNA immunoprecipitation sequencing (MeRIP-seq) and biochemical analyses revealed a global reduction of N6-methyladenosine (m&#x2076;A) on host transcripts, particularly on proinflammatory cytokines, alongside widespread m&#x2076;A modification sites on viral transcripts. Consequently, reduced m&#x2076;A prolonged the half-lives of tumor necrosis factor-&#x3b1; (TNF-&#x3b1;), interleukin-1&#x3b2; (IL-1&#x3b2;), and interleukin-18 (IL-18) mRNAs, as well as viral transcripts, thereby synergistically promoting PRV replication. Inhibition of JNK activity or restoration of m&#x2076;A modification suppressed PRV replication in vitro and in vivo. Moreover, the m&#x2076;A hypomethylation stabilized dual-specificity phosphatase 5 (DUSP5) transcripts at early infection, transiently restraining JNK activation and forming a negative feedback loop. These findings demonstrate that PRV reprograms the m&#x2076;A machinery via JNK-mediated WTAP phosphorylation and highlights RNA methylation restoration as a promising antiviral strategy.

Nonsense-mediated mRNA decay (NMD) is a translation-coupled mRNA decay pathway triggered by a premature termination codon (PTC). While in-frame stop codons are typically defined by cytoplasmic ribosomes, unexpected changes in transcription have been reported in genes containing PTCs. This observation suggests the possibility of PTC detection at the transcription site (TS), which has not been thoroughly investigated with high temporal and spatial resolution. Here, we use a real-time imaging approach to simultaneously detecting transcription sites (TSs) expressing wild-type or NMD-targeted &#x3b2;-globin reporter genes in the same cell. Our data indicate a dynamic change in the transcription of PTC-containing &#x3b2;-globin mRNA that depends on translation, NMD, and nuclear protein import, supporting the existence of rapid transcriptional feedback following NMD in the cytoplasm. This study establishes a robust temporal link between cytoplasmic mRNA decay and nuclear transcription.

The cell-based mucin array is a versatile platform for expressing and interrogating recombinant mucin reporter proteins with representative patterning and customizable O-glycan structures. The platform is based on glycoengineered mammalian cell lines (HEK293/CHO), in which the glycosylation machinery is genetically rewritten to enable controlled display of specific O-glycan core structures and terminal epitopes with defined sialylation, fucosylation, and sulfation. Uniquely, the platform presents glycans in their native protein context, enabling investigation of how O-glycan density, clustering, and multivalency influence interactions with mucins. A conceptual framework for recognition of such glycan-context cues is provided by the patterned arrangement of O-glycans within mucin O-glycodomains, often composed of tandem repeat (TR) sequences with distinct O-glycosites resembling molecular barcodes. Mucin reporters mimic the serine-, threonine-, and proline-rich domains of natural mucins and mucin-like proteins or they can be designed as artificial Glycocarriers with model O-glycan cluster motifs. Reporters expressed as membrane-bound forms for cell display or as secreted fusion proteins for production can be applied in diverse bioassays. They have been used to probe glycan/mucin binding by viral and microbial adhesins, as well as human Siglec immune receptors. Moreover, the platform provides defined substrates for functional analyses of mucin and O-glycodomain degradation by microbial O-glycopeptidases or mucinases, revealing information of substrate specificities, cleavage points, and catalytic mechanisms. This chapter describes how the cell-based mucin array can be used to dissect interactions with mucins by glycan- and mucin-binding receptors as well as mucinases. The platform overcomes limitations of contemporary technologies by enabling studies with mimics of natural mucins and O-glycodomains that preserve clustered and patterned O-glycan contexts.

Spontaneous solid-state fermentation (SSF) efficiency and product quality depend on microbial consortia regulation under dynamic temperature regimes, yet how spatially heterogeneous temperature trajectories are linked to community assembly, volatile profiles, and abundance modeling remains unclear. Using high-temperature daqu SSF as a model, this study integrates spatial multi-omics, machine learning, and physiological characterizations to characterize microbial responses across a 35-65&#x202f;&#xb0;C gradient. Results revealed pronounced phylogenetic clustering and niche partitioning along the observed thermal gradient, consistent with temperature-associated structuring of microbial communities into temperature-sensitive and temperature-resistant groups. Microbial succession showed a marked temperature-associated transition around 45&#x202f;&#xb0;C within the sampled batch. Lower thermal exposure was associated with the enrichment of temperature-sensitive Lactobacillaceae, whereas higher thermal exposure was associated with temperature-resistant taxa and pyrazine-related volatile profiles. In internal five-fold cross-validation within the single-batch terminal dataset, the Extra Trees regression model showed moderate-to-high fitting performance for selected core bacterial genera (R2&#x202f;=&#x202f;0.75-0.97). By linking intra-batch thermal trajectories with microbial abundance and volatile profiles, this study provides an exploratory framework for understanding spatial thermal heterogeneity in solid-state fermentation systems.

Many invertebrates lack erythrocytes and instead rely on extracellular hemoglobin assemblies, termed erythrocruorins, for oxygen transport. Here we report a 2.84 &#xc5; cryo-electron microscopy (cryo-EM) structure of Perinereis linea erythrocruorin (PlEc). PlEc is a &#x223c;3.3 MDa megacomplex composed of 180 polypeptide chains organized into 12 protomers, forming a hexagonal bilayer with D6 symmetry. Each protomer consists of 12 globin subunits and three linker subunits, adopting a mushroom-like architecture. The cap of the mushroom is formed by a globin dodecamer associated with a heterotrimeric linker head, and the stem consists of a triple-stranded coiled coil derived from the N-terminal helices of three linker subunits. Biochemical assays show that PlEc has thermal stability and auto-oxidation rate comparable to those of other erythrocruorins, but displays relatively lower oxygen-binding affinity. These findings provide mechanistic insights into the quaternary assembly of invertebrate erythrocruorins and lay the groundwork for the potential biomedical applications.

Although over 15,000 unique phage genomes have been sequenced, many isolates remain uncharacterised and accessible only within individual laboratories. The BASEL (BActeriophage SElection for your Laboratory) collection comprises 106 newly isolated and characterised virulent bacteriophages that infect the laboratory strain Escherichia coli K-12 and provide an open resource for phage biology. Here, we used cryo-electron microscopy (cryo-EM) to determine the structure of Bas18, a Dhillonvirus siphophage from the BASEL collection. Bas18 assembles an icosahedral capsid with T=7(d) triangulation. The asymmetric unit contains seven copies of the major capsid protein (MCP; gp09) and one dimeric decoration protein (gp64) bound at the centre of each hexamer. The MCP adopts the canonical HK97 fold but features a distinct insertion between the A and P domains, which we designate as G2 and E2 loop. The neck assembly consists of the portal, adaptor, stopper and terminator. The helical tail is built from hexameric rings of the tail tube protein, and the tail tip consists of the distal tail protein, hub and central fibre. Despite low sequence similarity, the overall architecture of the neck, tail, and tail tip closely resembles that of bacteriophage T1. In contrast, structural protein sequences are highly conserved (85-99% sequence similarity) across Dhillonviruses indicating a conserved virion architecture within this genus. These results expand the structural knowledge of the BASEL collection and provide a detailed architectural framework for Dhillonvirus phages, contributing to a broader understanding of siphophage structural diversity.

Timely and accurate diagnosis of mild traumatic brain injury (mTBI) remains challenging in acute care. In the Asia-Pacific (APAC) region, marked heterogeneity in healthcare infrastructure, computed tomography (CT) utilization, and diagnostic pathways underscores the need for practical, standardized approaches to assessment. Blood-based biomarkers, particularly glial fibrillary acidic protein (GFAP) and ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), have shown promising diagnostic performance and have been incorporated into clinical pathways in other regions. However, their role in APAC emergency care workflows has not been systematically addressed. This study aimed to develop expert consensus on the definition, diagnosis, and clinical integration of these biomarkers into mTBI assessment across APAC. A structured modified Delphi process was employed, involving ten expert panelists representing emergency medicine, neurosurgery, and neurology from APAC countries including Australia, India, Indonesia, the Philippines, Singapore, Taiwan, and Thailand. A targeted literature review informed the development of 34 preliminary statements, consolidated into 11 statements covering mTBI definition, diagnostic approach, and biomarker integration. Panelists rated each statement using a 4-point Likert scale across two anonymous online voting rounds, with consensus defined as &#x2265;&#x2009;70% agreement. Voting results were reviewed at a face-to-face meeting in Bangkok in May 2025, where statements were refined before Round 2 voting. All 11 final consensus statements achieved agreement ratings of 90% to 100% following Round 2 voting. Seven statements reached 100% agreement and four achieved 90% agreement. Statements addressed definitions of TBI and mTBI, the adjunctive diagnostic role of GFAP and UCH-L1 within a 12-hour post-injury window, their utility in diagnostically challenging subgroups such as anticoagulated and intoxicated patients, and the continued primacy of clinical assessment and local imaging pathways in guiding triage, imaging, discharge, and follow-up decisions. This modified Delphi study produced 11 high-consensus statements that provide a regional framework for the diagnosis of mTBI and for integration of GFAP and UCH-L1 into biomarker-supported assessment pathways across APAC. These biomarkers may help reduce avoidable CT imaging and support triage in selected patients when used as adjuncts to clinical assessment and established imaging decision-making. The statements are intended to support locally adapted protocols and future APAC-specific implementation and validation studies.