Search Results (2,679)

Lithium recovery from salt lake brines with high Mg/Li ratios remains highly challenging due to the comparable physicochemical properties of Mg²⁺ and Li⁺, while lithium–aluminum-layered double hydroxides (Li/Al-LDHs) have emerged as promising lithium-selective adsorbents. However, their practical application is hindered by particle aggregation, limited structural stability, and insufficient processability under continuous-flow conditions. Herein, a mineral-directed synthesis strategy was developed to construct natural mineral-supported Li/Al-LDHs composite adsorbents using three abundant clay minerals, chlorite, montmorillonite, and illite, as structural substrates. The mineral crystal structures were demonstrated to regulate the nucleation, growth behavior, and dispersion of Li/Al-LDH nanosheets, resulting in distinct hierarchical architectures and lithium adsorption performances. Comprehensive structural characterization revealed the successful integration of Li/Al-LDH phases with different mineral matrices while preserving the intrinsic layered structures of both components. The results demonstrated that different mineral substrates significantly influenced the crystal growth, dispersion, and interfacial structure of Li/Al-LDHs. Among the prepared composites, montmorillonite @Li/Al-LDHs exhibited the optimal lithium adsorption performance, achieving a lithium adsorption capacity of 6.0 mg·g⁻¹ and a remarkable Li⁺/Mg²⁺ separation factor of 73.5 in a brine with a high Mg/Li ratio of 61.25. Furthermore, the optimized adsorbent maintained 81.7% of its initial adsorption capacity after 100 adsorption–desorption cycles and demonstrated stable lithium recovery performance under continuous-flow conditions. This work establishes the relationship between natural mineral crystal structures and Li/Al-LDH adsorption behaviors, providing new insights into the rational design of economical, scalable, and environmentally friendly lithium adsorbents for sustainable recovery of lithium resources from Mg-rich brines. Full article

The marine ecosystem remains an unparalleled reservoir of structurally unique macromolecular biomolecules with diverse pharmaceutical applications. Among red macroalgae (Rhodophyta), the genus Gelidium Lamouroux is economically renowned as a primary industrial source of agar. Beyond its traditional hydrocolloid utility, recent molecular evidence reveals that Gelidium biomass possesses a dense matrix of non-digestible sulfated galactans, low-molecular-weight agaro-oligosaccharides, marine bromophenols, polyphenols, and mycosporine-like amino acids that have shown promising biological activities and therapeutic potential in preclinical models. Utilizing advanced green depolymerization and extraction technologies—including enzyme-assisted, ultrasound-assisted, and subcritical water extraction—these structural polysaccharides and specialized secondary metabolites can be efficiently isolated while optimizing yields and preserving bioactive functional integrity. This review comprehensively synthesizes the dual-target therapeutic modalities of Gelidium bioactives, focusing on their prebiotic modulation of the gastrointestinal microbiota and their protective effects on cutaneous tissues. In the gastrointestinal tract, Gelidium polysaccharides resist upper digestive enzymatic hydrolysis, serving as selective fermentable substrates that significantly enrich beneficial saccharolytic taxa while suppressing opportunistic pathobionts. This microbial fermentation accelerates the synthesis of short-chain fatty acids; based on established epithelial models, these organic acids provide a mechanistic rationale for upregulating epithelial tight junction proteins (zonula occludens-1, occludin, and claudin-1), theoretically supporting intestinal barrier integrity and mitigating systemic endotoxemia. Concurrently, in cutaneous tissues, selected Gelidium-derived fractions have been reported to modulate matrix metalloproteinases, including matrix metalloproteinase-1, matrix metalloproteinase-2, and matrix metalloproteinase-9, scavenge reactive oxygen species via nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 pathway activation, and modulate oxidative and melanogenic pathways to support cutaneous homeostasis. Finally, we establish the theoretical framework of the gut–skin axis as an experimentally supported systemic conduit through which Gelidium-mediated intestinal homeostasis attenuates cutaneous inflammation, photoaging, and barrier disruption. We further address current bioavailability limitations, standardization hurdles, and future clinical trajectories required to translate Gelidium biomass into functional nutricosmetics and marine therapeutics. Full article

Conjugated linoleic acid (CLA) comprises positional and geometric isomers of linoleic acid (LA) that have attracted interest due to their reported biological activities. In particular, trans-10,cis-12-CLA (t10,c12-CLA) has been associated with distinct metabolic effects, but its selective production remains challenging because conventional chemical synthesis generates mixtures of CLA isomers. In this study, the linoleic acid isomerase from Propionibacterium acnes (PAI) was displayed on Bacillus subtilis spores by fusion to spore crust proteins to develop a biocatalyst for t10,c12-CLA production. Twenty-four recombinant B. subtilis strains were constructed by fusing PAI to six spore crust proteins with different linker architectures. All constructs produced detectable t10,c12-CLA from 5 mg/mL LA, demonstrating that spore-displayed PAI remained catalytically active and accessible to extracellular substrate. The CgeA-L2 construct showed the highest mean CLA production, approximately 1.33 mg/mL CLA under the tested conditions. Time-course experiments revealed that product formation increased during the initial phase of the reaction before reaching a plateau, while recovered spores retained catalytic activity after one reuse cycle. Finally, spore-displayed PAI converted LA released from safflower oil by soluble lipase. Together, these results establish B. subtilis spores as a functional display format for PAI and provide a basis for further development of a recoverable catalyst for CLA production. Full article

Dietary nucleotides and nucleic-acid-derived compounds are considered bioactive nutrients, but their metabolic relevance remains uncertain. This narrative review, supported by a structured literature search, evaluates intestinal handling and evidence on glucose and lipid metabolism, redox homeostasis, immune function, gut barrier regulation, and microbiota. Direct supplementation studies are distinguished from nucleoside/nucleobase evidence, dietary nucleic acids or purine-rich foods, and endogenous extracellular purinergic signaling. Preclinical studies suggest defined nucleotide preparations may modulate AMP-activated protein kinase (AMPK), insulin receptor substrate 1 (IRS-1)/protein kinase B (AKT)/forkhead box protein O1 (FOXO1) signaling, lipid accumulation, and mitochondrial/redox-related endpoints. In contrast, extracellular adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine 5′-monophosphate (AMP) studies provide mechanistic context but do not show that oral supplementation modifies purinergic signaling in humans. Human intervention evidence is sparse and derived from older adults not selected for insulin resistance, type 2 diabetes, or metabolic-dysfunction-associated steatotic liver disease (MASLD). Reductions in homeostatic model assessment of insulin resistance (HOMA-IR) should be interpreted as changes in a surrogate estimate, not proof of therapeutic efficacy. The supplemental doses evaluated in available human intervention studies appear generally well-tolerated, whereas short-term high nucleotide intake can raise circulating uric acid. Dietary nucleotides therefore remain candidate, not established, metabolic or immune therapies. Full article

Antibacterial coatings are essential for preventing infections and maintaining adequate hygiene standards in high-density and high-risk environments, such as public spaces, public transportation systems, schools, and healthcare facilities. In this context, it is essential that such coatings are easy to apply and compatible with large-scale production processes. Among the various strategies for developing antimicrobial surfaces, the incorporation of antibacterial agents into paints represents a particularly practical and versatile approach. In this work, antimicrobial coatings were developed by incorporating curcumin, a naturally derived antibacterial compound, into a commercially available water-based paint. For comparison, coatings were also developed by incorporating a commercially available silver-ion-based additive, a well-established antibacterial agent, into the same paint. Antimicrobial dispersions were deposited onto polycarbonate (PC) and polymethyl methacrylate (PMMA) substrates using a spray coating technique. The produced coatings were evaluated in terms of adhesion and hardness according to the ASTM D3359 and ASTM D3363 standards, respectively, achieving ratings of 4B for adhesion and 4B/5B for hardness. Moreover, after five days of continuous water immersion, no visible signs of cracking, delamination, or discoloration were observed. The resulting curcumin- and silver-based coatings, under the tested surface-contact assay conditions, markedly reduced viable bacterial recovery against both S. aureus and E. coli, with no colonies recovered at the dilution range used for comparison with the Paint-Blank control. These results support the potential of curcumin as a naturally derived antibacterial additive for the development of water-based antibacterial coatings and provide a basis for further investigation of their long-term stability, durability, and practical applicability. Full article

To address the challenge of quantitatively identifying thermal-resistance contributions from multi-layer packaging structures within liquid-cooled insulated-gate bipolar transistor (IGBT) modules, this study establishes a three-dimensional conjugate heat-transfer model incorporating the chip, solder layer, direct-bonded copper (DBC) ceramic layer, substrate, elliptical pin-fin heat sink, and fluid domain. The IGBT and fast-recovery diode (FRD) power losses under typical motor controller operating conditions are modeled as volumetric heat sources applied to the chip region. Based on model validation, an internal thermal bottleneck evaluation method is proposed using inter-layer temperature-drop decomposition, introducing the thermal bottleneck number (BN) to quantify the temperature-drop contribution of each packaging layer along the target chip’s heat-dissipation path. Results show that in the baseline structure, the DBC ceramic layer is the critical internal thermal bottleneck, with a BN value of 11.05%. When the DBC thermal conductivity increases from 20 W/(m·K) to 80 W/(m·K), the maximum junction temperature of the IGBT decreases from 413.32 K to 396.79 K, and the BN drops from 11.05% to 3.69%. Conversely, when the DBC thickness increases from 0.20 mm to 0.50 mm, the maximum junction temperature rises from 405.45 K to 424.42 K. Further analysis reveals that after weakening the DBC thermal bottleneck, the relative temperature-drop contribution of the solder interface becomes increasingly apparent; notably, a central 20% low-conductivity defect in the solder layer raises the maximum junction temperature to 517.16 K, 103.84 K higher than under normal solder conditions. These findings provide valuable insights for identifying internal thermal bottlenecks and optimizing packaging structures in liquid-cooled IGBT modules. Full article

Rumen viruses may influence methane-related fermentation indirectly by altering microbial populations that produce or consume hydrogen, formate, and methylated substrates, but evidence in sheep remains limited. The objective of this exploratory study was to determine whether the viral component recovered from bulk rumen metagenomes was associated with diet-induced differences in in vitro methane production through variation in viral community structure, predicted host associations, or metabolic functions. Forty-eight Hu rams were assigned to two dietary treatments with four pen replicates per treatment; one animal per pen was sampled, yielding eight rumen-fluid samples for 12 h in vitro methane determination and metagenomic sequencing. We characterized the viral component recovered bioinformatically from bulk rumen metagenomes. Phage-derived sequences predominated in both the low-methane (LMEG; 80.72%) and high-methane (HMEG; 79.95%) groups, with Uroviricota and Caudoviricetes as the dominant lineages. Global diversity, predicted-host composition, and KEGG and UniProtKB/ViralZone profiles did not show statistically supported group separation; however, two putative genus-level labels, Pakpunavirus and Fromanvirus, were enriched in LMEG after the reported false-discovery-rate correction. More than 99% of CHERRY host assignments were bacterial, and the conservative PHP–CHERRY consensus set was dominated by Bacillota and Bacteroidota. No methanogen-associated viral contig received concordant genus-level support. HMEG showed numerical increases in mtd, cofF, and fdhA, but none remained significant after correction, and canonical methyl-coenzyme M reductase genes were not detected. These findings identify candidate diet-associated viral signals consistent with a possible indirect virus–bacteria–fermentation relationship, but they do not establish a causal role of rumen viruses in methane production or identify phages for direct methane mitigation. Further studies with larger sample sizes, direct virus–host validation, and measurements of rumen fermentation and animal performance are required before potential methane-mitigation applications can be considered. Full article

Background and Objectives: Visual evoked potentials (VEPs) are established tools for detecting optic pathway involvement in multiple sclerosis (MS); however, the distinct clinical significance of longitudinal changes in latency and amplitude remains unclear. This exploratory study aimed to evaluate the clinical utility of serial VEP assessments in patients with relapsing–remitting MS (RRMS) by examining the associations between temporal changes in latency and amplitude and concurrent markers of disease activity and disability. Materials and Methods: We retrospectively analyzed 83 patients with RRMS from three centers who underwent at least two pattern-reversal VEP assessments ≥ 1 year apart. Patients with recent optic neuritis were excluded. Longitudinal changes in VEP latency and amplitude were evaluated in relation to relapse activity during the same inter-assessment interval, baseline MRI and CSF findings, and disability assessed by the Expanded Disability Status Scale (EDSS). Sensitivity analyses were stratified and adjusted for disease-modifying therapy (DMT) efficacy tier, and progression independent of relapse activity (PIRA) was examined using a formal definition. Results: Over a median follow-up of 2 years, 43.4% of patients developed P100 latency prolongation, which was independently associated with a higher annualized relapse rate during the same interval (odds ratio [OR] 2.91, p = 0.005; area under the curve (AUC) 0.72 for concurrent on-study relapse activity), an association that persisted after adjustment for DMT efficacy tier, but not with disability worsening. In contrast, 56.6% of patients exhibited amplitude reduction, which was associated with greater disability accumulation at the group level, with higher EDSS scores at follow-up despite similar baseline values (p < 0.05); the corresponding inverse correlation between amplitude decline and EDSS change was only nominally significant (ρ = −0.231, p = 0.036), did not survive correction for multiple comparisons, and was attenuated after adjustment for baseline EDSS. Formally defined PIRA events were rare (n = 3), precluding inference. Baseline magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) findings differed in the latency group, with fewer MRI lesions and a lower immunoglobulin G (IgG) index, whereas no corresponding differences were observed in the amplitude group. Conclusions: In this exploratory cohort, longitudinal prolongation of VEP latency was associated with concurrent relapse activity, whereas amplitude decline showed a weaker, group-level association with disability. These findings are consistent with, but do not demonstrate, distinct inflammatory and neurodegenerative substrates, and warrant prospective validation before serial VEP monitoring can inform individualized management in MS. Full article

When does a complex adaptive system (CAS) (like a thermostat, a market, a flock, or a large language model) become a complex adaptive autopoietic system (CAAS), one that actively produces and sustains itself rather than merely adapting to its environment? We argue that this transition requires two simultaneous conditions. The first, established in a companion work, is architectural sufficiency. The system’s decision structure must achieve recursive closure at the third cybernetic order, the so-called fractal-seed point. The second, derived here, is corporeal viability. The system must pay a structural cost (the enactment tension E) large enough to hold its organization in place against perturbation. Working within Fisher-Generative Informational Realism (FGIR), an informational-realist framework in which information, not matter or energy, is the primary generative substrate of reality, we derive a scalar invariant E = I_pc², where I_p is the integrated informational potential of the operative field and c is the global coherence conductance at which informational structure locks into place. This invariant marks the threshold at which a proto-autopoietic system crosses into full autopoiesis. Because FGIR treats physical mass-energy as the result of a freezing projection acting on an incorporeal informational manifold rather than as the foundation of reality, the same invariant that governs autopoietic closure in social and organizational systems also projects, under appropriate bridge conditions, for instance, onto the classical physical law $\widehat{E}=\widehat{m}\hspace{0.17em}{\widehat{c}}^2$, or in a quantum context, the Schrödinger equation. The physical projection is stated as a conditional equivalence (T-BRIDGE), but it is not the focus of this paper. Rather, the central contribution is the cybernetic threshold itself and its operationalization. We show how a systems theorist can assess a system’s distance from critical admissibility, even when the absolute magnitudes of I_p and c are unavailable in domains that lack R(6) closure; we connect the coercivity threshold explicitly to Ashby’s Law of Requisite Variety, supplying the energetic constraint that Ashby’s purely combinatorial criterion leaves implicit. The contemporary case of large language models illustrates the framework. LLMs display transient, externally-scaffolded R(3)-like decision structure but fail the coercivity threshold, and so remain proto-autopoietic. The paper thus offers systems science a derived criterion, additional to architectural closure, for distinguishing full from proto-autopoiesis, with a specified but as yet unexecuted test program across physical, biological, cognitive, and social domains. Full article

Periodontitis is a chronic inflammatory disease initiated by dysbiotic subgingival biofilms and characterized by local tissue destruction, epithelial ulceration, immune-cell activation, and extracellular-matrix remodeling. Increasing evidence suggests that periodontal inflammation may extend beyond the oral cavity through recurrent bacteremia, dissemination of microbial products, systemic cytokine activation, endothelial dysfunction, oxidative stress, and thrombo-inflammatory signaling. These mechanisms are also implicated in atrial structural remodeling and atrial fibrillation (AF), but the molecular bridge between periodontal lesions, systemic inflammatory–fibrotic activity, and the atrial substrate remains incompletely defined. This structured narrative review synthesizes mechanistic, translational, biomarker-based, observational, and interventional evidence linking periodontal inflammation with cardiovascular remodeling and AF. Literature was identified through searches of PubMed/MEDLINE, Scopus, and Web of Science, complemented by reference-list screening. Particular attention was given to thrombospondin-1 (TSP-1), transforming growth factor-β (TGF-β)-related signaling, galectin-3 (Gal-3), and SGLT2-related cardiometabolic pathways. Because of heterogeneity in study populations, periodontal definitions, biomarker measurements, interventions, and cardiovascular endpoints, findings were synthesized thematically rather than quantitatively. Periodontitis is associated with systemic inflammatory activation, endothelial dysfunction, oxidative stress, and cardiovascular phenotypes, including atherosclerotic disease, hypertension, heart failure, and AF. Epidemiological studies support an association between periodontitis and incident AF, while human tissue data link periodontal inflammatory burden with atrial fibrosis, non-paroxysmal AF, and left atrial appendage thrombosis in selected AF populations. The strength of evidence differs across the proposed pathways: Gal-3 has the most consistent clinical evidence in AF and cardiac fibrosis; TSP-1/TGF-ß signaling is supported mainly by mechanistic periodontal-tissue and selected cardiovascular studies; and SGLT2-related pathways remain indirect systemic modifiers of the cardiometabolic and inflammatory milieu. Evidence regarding periodontal therapy and AF-related outcomes remains promising but limited and does not establish a direct antiarrhythmic effect. The available evidence supports a biologically plausible inflammatory–fibrotic continuum linking periodontitis, systemic immune activation, endothelial dysfunction, atrial remodeling, and AF susceptibility. However, causality, temporal sequence, tissue-level concordance, and biomarker-based clinical utility remain insufficiently established. Future studies integrating standardized periodontal assessment, circulating biomarkers, tissue-level inflammatory–fibrotic markers, cardiac imaging, and rhythm monitoring are needed to clarify whether local periodontal molecular signatures reflect systemic or cardiac remodeling relevant to AF vulnerability. Full article

For decades, post-mining sites were considered biological deserts requiring intensive technical reclamation. This statement is increasingly challenged by evidence demonstrating that mineral extraction creates heterogeneous, nutrient-poor habitats capable of supporting self-organizing ecosystems with high conservation value. In urban-industrial landscapes, where eutrophication and habitat homogenization dominate, oligotrophic mineral substrates represent increasingly rare environmental conditions that promote functional diversity and ecosystem resilience. Their spatial heterogeneity and broad hydrological gradients generate a mosaic of ecological niches that facilitate spontaneous succession and the establishment of diverse terrestrial and aquatic communities, including numerous rare and protected species. Despite growing recognition of post-mining sites as novel ecosystems, research has primarily focused on species composition, whereas ecosystem functioning, functional traits, and long-term resilience remain insufficiently understood. Moreover, the contribution of mineral habitat heterogeneity to biodiversity maintenance and ecosystem multifunctionality has not been adequately incorporated into management frameworks or environmental policy. This review hypothesizes that mineral post-mining habitats constitute critical reservoirs of ecosystem functions within urban-industrial landscapes and argues that spontaneous succession should be recognized as a legitimate, nature-based management pathway. Integrating functional ecology with the novel ecosystem concept offers a robust scientific framework for developing evidence-based, biodiversity-oriented management strategies for urban-industrial landscapes. Full article

Oxidative stress is a central and well-established driver of cardiovascular disease, contributing to mitochondrial dysfunction, endothelial injury, inflammatory activation, and progressive myocardial and vascular remodeling. Although the major endogenous sources of cardiovascular reactive oxygen species (ROS), including NADPH oxidases, mitochondrial electron transport chain leakage, and uncoupled nitric oxide synthase, are well characterized, an additional and underappreciated contributor has recently emerged: cytochrome P450 2D6 (CYP2D6), an enzyme classically regarded as a hepatic drug-metabolizing protein. Accumulating evidence indicates that CYP2D6 is expressed extrahepatically in cardiac, vascular, and neural tissue, where uncoupled catalytic cycling is proposed to generate ROS independently of its canonical xenobiotic-metabolizing role, although direct experimental evidence for this pathway in human cardiac and vascular tissue remains limited. CYP2D6-derived oxidative processes may interact with mitochondrial respiratory function, endothelial nitric oxide bioavailability, and redox-sensitive inflammatory pathways, potentially contributing to cardiovascular vulnerability under specific genetic or pathological conditions. Critically, the magnitude of this oxidative contribution is not fixed: it is dynamically shaped by inherited CYP2D6 genetic variation, with poor and ultra-rapid metabolizer phenotypes exhibiting divergent oxidative burden and pharmacokinetic vulnerability, and is further amplified by polypharmacy, multimorbidity, and inflammation-driven phenoconversion, whereby clinically expressed CYP2D6 activity diverges from inherited genotype in ways that intensify redox imbalance. These dynamics are particularly relevant in East Asian populations, where the decreased-function CYP2D6*10 allele is highly prevalent. In this narrative, hypothesis-generating review, we integrate evidence from pharmacogenomics, redox biology, and cardiovascular pharmacology to propose a conceptual framework that reframes CYP2D6 as a genetically and pharmacologically tunable node within cardiovascular redox biology. We further examine emerging redox biomarkers, multi-omics platforms, and AI-assisted modeling as translational strategies for capturing this dynamic oxidative risk in real time. This framework supports a shift from static genotype-guided prescribing toward oxidative-risk-informed, adaptive cardiovascular precision medicine. Importantly, our focus on CYP2D6 should not be interpreted as evidence that it is a major cardiovascular CYP isozyme or an established driver of cardiovascular pathology. Rather, CYP2D6 is examined here as a deliberately hypothesis-generating candidate whose unusually strong pharmacogenetic variability, clinically important cardiovascular drug substrates, dynamic susceptibility to phenoconversion, extrahepatic expression, and mechanistically plausible links to endogenous substrate metabolism and CYP-associated ROS generation provide a convergent rationale for focused investigation. The mechanistic framework proposed in this review has not yet been experimentally and prospectively validated and should not be applied directly to clinical decision-making without supporting clinical data. Full article

Type 2 diabetes (T2D) is increasingly understood as a chronic, low-grade inflammatory disease in which immune and metabolic signalling are bidirectionally coupled. Nutrient excess drives glucolipotoxic stress in adipose tissue, liver, skeletal muscle and pancreatic islets, engaging innate immune sensors. Responding immune cells then reconfigure their own intermediary metabolism, and the resulting metabolites—succinate, which stabilises hypoxia-inducible factor-1α, and the itaconate that opposes it—themselves specify inflammatory output. These signals converge on NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome assembly, gasdermin D-mediated pyroptosis and interleukin-1β (IL-1β) release, which interrupt insulin signalling through inhibitory serine phosphorylation of insulin receptor substrate-1. Mitochondrial dysfunction, impaired mitophagy and cytosolic mitochondrial DNA sensing sustain the loop, while gut barrier failure supplies a parallel systemic input that converges on beta-cell dysfunction. This narrative review synthesises these mechanisms and examines how metformin, glucagon-like peptide-1 receptor agonists, sodium–glucose cotransporter 2 inhibitors and inflammasome-directed agents intersect with them. The chain described is that of obesity-associated T2D, and the heterogeneity that limits its generalisation across the recognised subgroups of the disease is addressed explicitly rather than assumed away. We give particular weight to a dissociation that constrains the field: sustained IL-1β neutralisation reduced cardiovascular events without preventing incident diabetes. Establishing why is, in our view, the central question for immunometabolic therapeutics in T2D. Full article

Vanishing twin syndrome (VTS) denotes the spontaneous loss of one conceptus from an initially recognized multiple pregnancy, most often during the first trimester. Its clinical relevance has increased with in vitro fertilization and embryo transfer (IVF-ET), as multiple embryo transfer creates the substrate for dizygotic VTS, while blastocyst transfer may be followed by monozygotic splitting and serial early ultrasonography increases detection. However, the literature remains heterogeneous, with empty gestational sacs, losses after fetal cardiac activity, and later single fetal demise often grouped together despite different biological and prognostic implications. New evidence published in recent years on frozen embryo transfer outcomes, cell-free DNA screening, and early childhood development warrants an updated synthesis of vanishing twin syndrome to inform individualized risk assessment, counselling, and standardized research reporting. Overall, the surviving singleton appears to have a lower risk than an ongoing twin pregnancy but a higher risk than a primary singleton, particularly for preterm birth, low birthweight, and small-for-gestational-age birth, with risk increasing when loss occurs after fetal cardiac activity or later in gestation. Nevertheless, evidence is not unanimous, as several well-characterized cohorts and earlier meta-analyses reported no measurable perinatal disadvantage. Two reports from a single tertiary center, based on substantially overlapping recruitment periods, further suggest that VTS may be proportionally less frequent among established twin pregnancies after IVF/ICSI than after spontaneous conception, while IVF-associated VTS has been linked to placental abnormalities, diabetes, and fetal growth restriction; this observation requires independent confirmation. Contemporary frozen embryo transfer cohorts indicate that VTS remains relevant in modern practice, whereas limited long-term data have not demonstrated impaired early childhood growth or development. Management should document the initial number of gestational sacs, embryonic structures, cardiac activity, chorionicity, and timing of loss, while adapting aneuploidy screening to residual trophoblastic DNA and individualizing fetal-growth surveillance. Elective single-embryo transfer remains the most effective preventive strategy, although it cannot eliminate monozygotic twinning. Standardized definitions and long-term offspring follow-up are needed. Full article

Coprinellus comprises mushroom-forming saprotrophic fungi that colonize decomposing plant-derived substrates, yet chromosome-complete genomic resources for this genus remain limited. To resolve chromosome architecture and lineage-specific evolution in this fungal group, we generated chromosome-complete assemblies of Coprinellus xanthothrix and C. saccharinus by integrating Oxford Nanopore Technologies (ONT) long reads, DNA nanoball sequencing (DNBSEQ) short reads, Hi-C, and RNA-seq data. Each genome comprised 13 gapless chromosomes with all 26 telomeres recovered; assembly sizes were 46.92 and 54.81 Mb, with BUSCO completeness of 99.20% and 99.10%, respectively. The larger C. saccharinus genome was primarily associated with greater retroelement content, whereas functional annotation profiles and CAZyme repertoires were broadly comparable between species. Phylogenomic analyses grouped C. xanthothrix with C. radians and C. saccharinus with C. micaceus, with estimated divergence times of 54.4 and 32.8 Ma, respectively. Both divergence events occurred within the Paleogene. Gene family analyses identified lineage-specific expansions enriched in nucleotide metabolism, DNA replication and repair, glutathione metabolism, redox regulation, endocytosis, cytoskeletal organization, and cell-cycle processes. Synteny and Ks analyses further revealed chromosome-level rearrangements and lineage-specific small-scale duplication but no strong evidence of recent whole-genome duplication. Together, the temporal placement of these divergences and the associated genomic patterns raise a testable hypothesis that long-term climatic and vegetation reorganization, together with changes in plant-derived substrates and microhabitats, may have contributed to lineage establishment and ecological differentiation. However, because direct paleoecological evidence and functional validation are currently lacking, this proposed relationship should not be interpreted as causal. These chromosome-complete assemblies provide important resources for comparative genomics in Coprinellus and future experimental studies of saprotrophic adaptation. Full article