Frontiers in systems biology最新文献

{"title":"Explainable artificial intelligence (XAI) in schizophrenia: enhancing transparency in clinical decision-making.","authors":"Kshitij Srivastava, Ruby Srivastava","doi":"10.3389/fsysb.2026.1898853","DOIUrl":"10.3389/fsysb.2026.1898853","url":null,"abstract":"<p><p>Schizophrenia is a chronic and severe psychiatric disorder affecting nearly 1% of the global population, characterized by positive symptoms such as hallucinations and delusions, negative symptoms including avolition and affective flattening, and cognitive impairments that compromise social and occupational functioning. Despite advances in psychiatry, diagnosis remains largely symptom-based, relying on criteria from the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and the International Classification of Diseases (ICD-11), highlighting the need for objective biomarkers and improved clinical decision support. Neuroimaging modalities, including structural and functional magnetic resonance imaging (MRI/fMRI), diffusion tensor imaging (DTI), positron emission tomography (PET), as well as electrophysiological techniques such as electroencephalography (EEG) and magnetoencephalography (MEG), have revealed abnormalities in brain connectivity, dopaminergic signaling, sensory processing, and network dysfunction associated with schizophrenia. Recent advances in artificial intelligence (AI), particularly machine learning (ML), have enabled prediction of diagnosis, treatment response, and relapse risk using multimodal clinical, neuroimaging, and genetic data. However, the \"black-box\" nature of many AI models limits transparency, interpretability, and clinician trust, restricting translation into practice. Explainable artificial intelligence (XAI) addresses these challenges by providing interpretable, transparent, and clinically accountable models that support decision-making while preserving ethical and regulatory standards. By integrating explainable models with multimodal data, clinicians can use them as an adjunct for precision psychiatry, facilitating biomarker discovery, personalized treatment strategies, and trustworthy, actionable decisions, ultimately enhancing transparency and improving outcomes in schizophrenia care.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1898853"},"PeriodicalIF":2.6,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149168681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Generative models of living development: an interaction-centered proposal and its implications for artificial life research.","authors":"Bin Yin, Xiao-Rui Wu","doi":"10.3389/fsysb.2026.1904510","DOIUrl":"https://doi.org/10.3389/fsysb.2026.1904510","url":null,"abstract":"<p><p>Artificial life and integrative systems neuroscience increasingly seek to explain how agency is organized through development, not merely how an already-formed controller optimizes a predefined task. This article advances an interaction-centered theory that links computational generative models, which infer hidden causes and candidate action policies, with experimental ecologies, which generate the developmental histories to be explained. The framework distinguishes reward and prior preference from concern, normativity, habit, and action policy. Concerns denote system-relative dimensions of regulatory significance grounded in an agent's organization; habits are historically acquired dispositions; and action policies remain formally defined candidates within a computational model. The code-mediated concern hypothesis proposes that events acquire functional significance when adaptor-implemented mappings make cues informative about viability-linked concerns, thereby changing inference, precision, habit, and action selection. Teleonomic and organizational accounts locate the normative force of these concerns in present self-maintaining organization rather than conscious design or backward causation. The Layered Model of Agency differentiates operative, reflective, joint, material-mediated, sign-mediated, and symbolic agency, preventing evidence for low-level control from being generalized to collective, artifact-mediated, symbolic, or phenomenal agency. The Human-Rat Interaction Paradigm (HRIP) supplies an extensible experimental architecture for studying how structured human-rat interaction histories shape multidomain developmental trajectories. The inaugural male-rat study permits only sex-specific inference; the broader HRIP paradigm accommodates female, male, and mixed-sex samples in comparative and mechanistic research designs. Six propositions and eight predictions define tests of model comparison, cue remapping and adaptor perturbation, habit-policy dissociation, reciprocal coupling, material and sign mediation, multimodal trajectories, developmental and sex moderation, and layer-specific evidence. Together, these elements define a testable program for developmental artificial life while preserving the distinction between functional agency-like organization and phenomenal agency.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1904510"},"PeriodicalIF":2.6,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13650560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149171939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding endurance performance: integrative genomic and epigenetic insights into the molecular basis of athletic adaptation.","authors":"Arij El Haddouchi, Amina Marrouh, Souad Kartti, Elmostafa El Fahime, Saber Boutayeb, Younes Chagar, Christophe Baudot, Lahcen Belyamani, Rachid Eljaoudi, Taoufiq Dakka","doi":"10.3389/fsysb.2026.1858520","DOIUrl":"https://doi.org/10.3389/fsysb.2026.1858520","url":null,"abstract":"<p><p>Applied genomics in sports performance has rapidly evolved into a multidisciplinary field aimed at elucidating the biological determinants of complex athletic traits, particularly endurance. Endurance performance represents a highly polygenic and multifactorial phenotype, shaped by the dynamic interplay between genetic predisposition and training-induced adaptations. This review provides a comprehensive synthesis of evidence from candidate gene studies, genome-wide association studies (GWAS), and meta-analyses to identify genetic variants consistently associated with endurance-related phenotypes. GWAS and candidate gene approaches have identified over 44 polymorphisms relevant to endurance-oriented sports, with <i>HFE</i> rs1799945 emerging as a strong predictor of endurance ability. Key variants, including <i>ACE</i> rs1799752, <i>CDKN1A</i> rs236448, <i>PPARGC1A</i> rs8192678, and <i>PPARA</i> rs4253778, are highlighted for their roles in modulating critical physiological pathways such as oxygen transport, mitochondrial biogenesis, energy metabolism, and muscle fiber composition. Beyond static genetic variation, this review emphasizes the pivotal contribution of epigenetic mechanisms, including DNA methylation, histone modifications, and non-coding RNAs. In particular, exercise-responsive microRNAs (miR-1, miR-206, miR-21, miR-146, miR-208, and miR-222) are discussed as key regulators of gene expression and molecular adaptation to endurance training. Although more than 200 genetic polymorphisms have been associated with athlete status, only a limited subset demonstrates consistent and replicated associations with endurance athlete status. This underscores the limitations of single-marker approaches and highlights the need for integrative frameworks that incorporate genomics, epigenomics, and transcriptomics. Advancing toward such multi-omics strategies is essential for a more comprehensive understanding of the biological architecture of endurance, and for the development of personalized training interventions aimed at optimizing performance and adaptation.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1858520"},"PeriodicalIF":2.6,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13650432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149171241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting gut dysbiosis: a new frontier in MASLD management.","authors":"Shweta Sharma, Arun Pachauri, Harshal Nagar, Vishwa Thakkar, Kajal Patel","doi":"10.3389/fsysb.2026.1937809","DOIUrl":"https://doi.org/10.3389/fsysb.2026.1937809","url":null,"abstract":"<p><p>Globally, Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prominent leading cause of CLD, which is intricately linked with obesity, T2D, and metabolic syndrome. Recent insights in pathophysiologically of MASLD have shifted from the traditional \"two-hit\" model to a \"multiple-hit\" paradigm, demonstrating the importance of understanding the gut-liver axis and gut dysbiosis as central drivers of disease progression. Hence, this narrative review explores the mechanistic pathways through which an altered gut microbiome contributes to MASLD, by specifically emphasizing intestinal barrier disruption, endotoxemia, altered bile acid metabolism, and SCFA imbalance. These dysregulations trigger oxidative stress, leading to systemic inflammation and insulin resistance, propelling simple steatosis toward steatohepatitis and fibrosis at last. Furthermore, we also highlighted the diagnostic utility of microbial signatures and multi-omics approaches in identifying disease-specific microbial shifts, such as the depletion of beneficial SCFA-producing bacteria like <i>Faecalibacterium</i> and <i>Akkermansia</i>. Eventually, to address the growing hepatic-associated health burden, microbiome-targeted therapeutics can emerge as one of the promising contributors. In this review, we synthesise and demonstrate the current and prospective interventions, including dietary modifications, biotics (probiotics, prebiotics, synbiotics), and FMT. Additionally, we also show the transition of care toward precision microbiome therapies utilizing engineered bacteria, bacteriophages, and AI-guided patient stratification. While current microbiome-centric treatments demonstrate promise in modulating hepatic inflammation and restoring mucosal integrity, their clinical translation remains hindered by patient heterogeneity and a lack of standardized protocols. Ultimately, managing MASLD effectively will require moving beyond broad ecosystem resets toward highly tailored, multi-omics-driven precision medicine to accurately target individualized microbial deficits.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1937809"},"PeriodicalIF":2.6,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13650556/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149171355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Latent multimorbidity classes and antithrombotic medication distributions among patients hospitalized for bleeding after dental surgery: a retrospective study.","authors":"Juliane Wagner, Johannes Heinrich Spille, Jill Flor, Zeyue Ouyang, Jonas Conrad, Christof Dörfer, Jörg Wiltfang, Hendrik Naujokat","doi":"10.3389/fsysb.2026.1917159","DOIUrl":"10.3389/fsysb.2026.1917159","url":null,"abstract":"<p><strong>Objectives: </strong>To characterize patients hospitalized for postoperative intraoral bleeding after dental surgery and to describe latent multimorbidity classes and their observed antithrombotic medication distributions.</p><p><strong>Materials and methods: </strong>This single-center retrospective study included 700 patients hospitalized between 2011 and 2021. Demographic characteristics, clinical measurements, comorbidities, and antithrombotic medication categories were extracted from medical records. Latent class analysis was performed in 458 patients with at least two documented comorbidities using 11 binary indicators. Models containing one to six classes were compared using information criteria, entropy, the bootstrap likelihood ratio test, class size, and clinical interpretability. Stability of the selected solution was assessed using 100 bootstrap resamples.</p><p><strong>Results: </strong>The median age was 74 years, 460 patients (65.7%) were male, and 581 (83.0%) were receiving at least one antithrombotic medication. A five-class solution was selected. Class 1 (n = 26, 5.7%) was characterized by deep venous thrombosis, hypertension, and cardiac disease; Class 2 (n = 97, 21.2%) by heart valve replacement and cardiac disease; Class 3 (n = 55, 12.0%) by stroke, cardiac disease, and hypertension; Class 4 (n = 151, 33.0%) by hypertension and cardiac disease; and Class 5 (n = 129, 28.2%) by a broader multisystem profile involving cardiac disease, hypertension, diabetes, renal disease, and gastrointestinal disease. Vitamin K antagonist (VKA) use was most frequent in Classes 1 and 2, whereas direct oral anticoagulant (DOAC) use was most frequent in Class 4. Bootstrap analysis indicated moderate overall stability.</p><p><strong>Conclusion: </strong>The study describes clinically relevant heterogeneity among hospitalized bleeding cases.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1917159"},"PeriodicalIF":2.6,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13646137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149139565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic determinants of tendon and ligament injuries in athletes: a narrative review from single variants to gene-gene interactions.","authors":"Amina Marrouh, Arij El Haddouchi, Souad Kartti, Elmostafa El Fahime, Saber Boutayeb, Younes Chagar, Christophe Baudot, Lahcen Belyamani, Taoufiq Dakka, Rachid Eljaoudi","doi":"10.3389/fsysb.2026.1858521","DOIUrl":"10.3389/fsysb.2026.1858521","url":null,"abstract":"<p><p>Tendon and ligament injuries are common in athletes and can result in significant functional impairment. Genetic factors are increasingly recognized as key contributors to individual susceptibility. A structured narrative literature search was conducted in PubMed, Scopus, Web of Science, and Google Scholar to identify studies investigating genetic polymorphisms associated with tendon and ligament injuries in athletic populations. Eligible studies published in English and involving elite, professional, recreational, or physically active individuals were narratively synthesized. This review synthesizes current evidence on polymorphisms associated with these injuries, identifying 70 genes and 107 variants across candidate-gene studies, haplotype analyses, and genome-wide association studies (GWAS). Specifically, the evidence included 33 candidate genes with 43 polymorphisms, 25 polymorphisms evaluated in haplotype analyses involving these candidate genes as well as three additional genes, and 34 genes identified through GWAS encompassing 39 variants. These genes are involved in extracellular matrix (ECM) organization, inflammation, tissue remodeling, angiogenesis, and muscle function. Structural genes, particularly collagens (<i>COL1A1, COL3A1, COL5A1</i>), proteoglycans (<i>ACAN, DCN, BGN</i>), matrix remodeling (<i>MMPs, TIMP2</i>), and glycoproteins (<i>FMOD, TNC</i>), as well as genes related to inflammatory (<i>IL1B, IL6, TNF-</i>α), and vascular pathways (<i>VEGFA, VEGFR2)</i>, were frequently implicated. Importantly, gene-gene interactions and haplotypes appear to be more informative than single polymorphisms for explaining injury risk. Although GWAS studies remain limited, they have identified novel loci, reinforcing the polygenic nature of these conditions. Overall, these findings highlight the complexity of genetic influences and support integrating genetic, biomechanical, and environmental factors to improve personalized prevention and rehabilitation strategies in sports medicine.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1858521"},"PeriodicalIF":2.6,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642649/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149139616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GPCR signaling systems facilitate precision interventions for multi-oncology therapy.","authors":"Ashley Del Pozo, Mia Pardo, Tabitha Boeringer, Carter J Craig, Ramzia Sorathia, Madeline Millican, Stuart Maudsley","doi":"10.3389/fsysb.2026.1940022","DOIUrl":"10.3389/fsysb.2026.1940022","url":null,"abstract":"<p><p>Precision oncology has undergone a transformative evolution from static genomic profiling toward dynamic, multi-omics frameworks capable of capturing tumor heterogeneity and adaptive resistance in real time. Central to this paradigm shift is the emerging recognition that G protein-coupled receptors (GPCRs) constitute a vastly underexploited axis of oncogenic signaling, tumor microenvironment (TME) modulation, and non-genetic adaptive resistance. Here we delineate the effective transition to GPCR-focused precision oncology, emphasizing the integrated deployment of next-generation sequencing (NGS), single-cell transcriptomics, expression-based liquid biopsies (ctRNA, exosomal miRNA, circulating tumor cells), and AI-driven quantitative systems network modeling to interrogate GPCR signaling dynamics across solid and hematologic malignancies. GPCRs, comprising approximately 800 human receptors with extensive pharmacological plasticity, encompassing biased agonism, allosteric modulation, receptor heterodimerization, and ligand-independent signaling, serve as critical integrators of extracellular cues and intracellular transcriptional programs. Their overexpression, mutation, and epigenetic dysregulation in multiple cancer types positions them as both prognostic biomarkers and actionable therapeutic targets. We discuss recent advances in integrative genomic platforms, liquid biopsy evolution, case studies of GPCR-driven tumor evolution, and cutting-edge therapeutic modalities, including PROTACs (Proteolysis Targeting Chimeras), biased ligands, RNA therapeutics, and digital twin modeling, to articulate a forward-looking vision for GPCR-centric precision oncology. By harnessing real-time tumor monitoring and AI-optimized adaptive therapies, this framework promises to overcome the limitations of static genomic approaches, enabling mid-treatment recalibration to combat resistance and improve durable survival in heterogeneous solid tumors.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1940022"},"PeriodicalIF":2.6,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13639398/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149119497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The causal integration ladder: a multilevel evidence framework for therapeutic target evaluation in cervical cancer.","authors":"Shishir Singh, Manyata Srivastava, Pragathi Uppada, Diksha Ameta, Aesha Singh, Monisha Banerjee, Atar Singh Kushwah","doi":"10.3389/fsysb.2026.1874355","DOIUrl":"https://doi.org/10.3389/fsysb.2026.1874355","url":null,"abstract":"<p><p>Cervical-cancer genomic studies nominate many altered genes, but the evidence needed to distinguish disease association from a causal, therapeutically tractable mechanism is rarely stated explicitly. We present the Causal Integration Ladder (CIL), an evidence-accounting framework that distinguishes Level I association, inherited Level II-G evidence, acquired Level II-S evidence, Level III computational and direct functional evidence, and Level IV translational validation, while treating viral etiology as an explicit context modifier. An exploratory TCGA-CESC screen (306 tumours, 3 normal samples) supplied 25 Level I candidates. HPV annotations were available for 291 primary tumours (280 positive, 9 negative, 2 indeterminate). Restriction to HPV-positive tumours preserved the direction of all 25 Level I effects; HPV-positive versus HPV-negative comparisons were exploratory because the negative group was small and histologically heterogeneous. Somatic analysis used 194 mutation-evaluable and 295 copy-number-evaluable tumours. Ten candidates showed false-discovery-rate-significant copy-number-expression associations, including CDKN2A, whereas recurrent protein-altering mutation was uncommon. Eight genes were additionally audited using public cis-eQTL, GWAS, dependency, pharmacogenomic, and cell-compartment resources. The revised CIL reports inherited, somatic, etiological, and functional evidence independently; absence of germline support is not interpreted as evidence against somatic, viral, or functional relevance. No observational result is presented as experimental validation, and Level III direct perturbation and Level IV translational claims remain prospective.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1874355"},"PeriodicalIF":2.6,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13630610/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149119601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional saturation of Earth's habitable domains: constraints on land systems and potential in marine environments.","authors":"I Valentin Petrescu-Mag, Ioan G Oroian, Benone Păsărin, O Călin Safirescu, Petru Burduhos, Ioan Braşovean, Daniela Bordea, Bianca Moldovan, Tudor N Pojar, Ioan Bănățean-Dunea, F Camelia Oroian, Praveen Pandey","doi":"10.3389/fsysb.2026.1941138","DOIUrl":"https://doi.org/10.3389/fsysb.2026.1941138","url":null,"abstract":"<p><p>In this context, functional saturation is defined as the state in which a system's capacity to sustain additional productive or regulatory functions becomes constrained due to cumulative anthropogenic pressures, even if some physical space remains available. This review examines whether the progressive contraction of terrestrial plant communities under intensifying anthropogenic pressure can be functionally compensated by the expansion of marine macroalgal systems in a high-CO₂ world. Integrating perspectives from Earth system ecology, biogeochemistry, and spatial analysis, the study evaluates three interdependent dimensions: the saturation of habitable terrestrial space, the relative openness yet ecological constraint of marine environments, and the dynamic coupling between atmospheric CO₂ and ocean chemistry. The synthesis reveals a fundamental asymmetry between land and ocean systems. Terrestrial ecosystems are undergoing direct structural transformation through land-use change, resulting in a measurable contraction of ecologically functional space and increasing transgression of planetary boundaries. In contrast, marine systems retain substantial geometric space but are subject to diffuse, cumulative stressors, particularly in productive coastal zones where macroalgal communities are most viable. Elevated CO₂ exerts dual effects on marine primary producers, simultaneously enhancing photosynthetic potential while intensifying ocean acidification, with temporally lagged responses mediated by air-sea exchange dynamics. Although macroalgae may exhibit localized increases in productivity, their capacity to provide long-term carbon sequestration and ecosystem stability remains inherently limited due to rapid biomass turnover, susceptibility to regime shifts, and the interaction of multiple stressors. The available evidence suggests that marine macroalgal expansion is unlikely to fully compensate for terrestrial vegetation loss at global ecological and biogeochemical scales. Instead, the Earth system is undergoing a net reduction in biospheric resilience, characterized by declining terrestrial complexity and increasingly unstable marine productivity. These findings challenge assumptions of compensatory redistribution of primary production and underscore the necessity of preserving terrestrial ecosystems alongside mitigating pressures on marine environments.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1941138"},"PeriodicalIF":2.6,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149119443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined abdominal and transcranial photobiomodulation is associated with fecal microbiome restructuring: a systems microbiology pre-post case report.","authors":"Gabriela N F Guimarães, Douglas W Barrett, F Gonzalez-Lima","doi":"10.3389/fsysb.2026.1920618","DOIUrl":"10.3389/fsysb.2026.1920618","url":null,"abstract":"<p><p>Photobiomodulation (PBM) has been proposed as a non-invasive strategy capable of modulating mitochondrial, inflammatory, vascular, and gut-brain axis-related pathways. However, its potential effects on fecal microbiome ecology in neurobehavioral conditions remain poorly characterized. This case report describes paired fecal microbiome findings before and after a 90-day combined abdominal and transcranial PBM protocol in a 6-year-old female with autism spectrum disorder and chronic constipation. PBM was delivered daily using a 1064-nm near-infrared LED device with 54 mW/cm² irradiance, applied for 10 min over the right prefrontal cortex and for 10 min over the infraumbilical and right lower abdomen. Fecal samples collected before and after the intervention were analyzed by 16 S rRNA amplicon sequencing. The baseline sample showed limited taxonomic resolution, with 93.14% assigned to \"Other/unclassified,\" whereas the post-intervention sample showed a more taxonomically resolved microbial profile, including Firmicutes (53.37%), Bacteroidetes (29.66%), Actinobacteria (7.97%), Verrucomicrobia (4.21%), Euryarchaeota (2.89%), Proteobacteria (1.14%), and a markedly reduced unclassified fraction (0.03%) at the phylum level. At the genus level, the post-intervention profile showed detection or increased representation of taxa commonly discussed in relation to gut microbial ecology, mucosal biology, and short-chain fatty acid metabolism, including Faecalibacterium (7.03%), Bifidobacterium (4.25%), <i>Bacteroides</i> (18.82%), Alistipes (5.38%), preserved Akkermansia (3.92%-4.21%), and low-abundance Roseburia. Taxa with context-dependent or uncertain significance, including Sarcina, Collinsella, Parabacteroides, and residual unclassified genera, were also observed and are reported transparently. Caregiver behavioral observations included improved bowel regularity, reduced abdominal distension, more stable mood, reduced irritability and impulsivity, improved communication, and greater social tolerance. The intervention was well tolerated with no reported adverse effects. As a single-patient pre-post case report without sham control, repeated baseline sampling, or functional metagenomic confirmation, these findings cannot establish causality. Nevertheless, they provide a biologically plausible systems-level observation linking combined abdominal and transcranial PBM with a shift in fecal microbiome structure and gastrointestinal-behavioral regulation, supporting future controlled studies integrating longitudinal microbiome profiling, metabolomics, inflammatory biomarkers, autonomic measures, and validated behavioral outcomes.</p>","PeriodicalId":73109,"journal":{"name":"Frontiers in systems biology","volume":"6 ","pages":"1920618"},"PeriodicalIF":2.6,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13600810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149042379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}