An 11-year-old male neutered domestic shorthair cat underwent investigations for right mandibular and prescapular lymph node enlargement and weight loss. Cytology of the mandibular and prescapular lymph nodes revealed marked pyogranulomatous inflammation and mild neutrophilic, non-septic inflammation, respectively. Excisional biopsy of both lymph nodes was performed. Histopathology of the mandibular lymph node revealed severe pyogranulomatous inflammation, with prominent Splendore-Hoeppli phenomenon. Histopathology of the prescapular lymph node was consistent with reactive lymphoid hyperplasia. A Neisseria species was cultured from tissue samples obtained from both lymph nodes, with sensitivity testing confirming susceptibility to amoxicillin-clavulanate. After a 4-week course of amoxicillin-clavulanate (20 mg kg-1 PO q12h), clinical signs resolved. The cat was clinically well with no evidence of recurrence of infection 2.5 years after presentation.

Bone and joint infections (BJI), particularly periprosthetic joint infections (PJI), remain major postoperative complications. Although international guidelines have clarified diagnostic criteria, recommendations on clinical strain preservation remain scarce. Microbiology laboratories routinely store isolates from severe infections, but protocols and storage duration vary widely. This narrative review synthesizes international and national guidelines (ICM, EBJIS, IDSA, SPILF), French regulatory texts, and published data on bacterial preservation techniques. Methods of conservation (serial subculture, preservation media, freezing at various temperatures, desiccation, and lyophilization) and their impact on strain viability and genetic stability were examined. Most guidelines recommend preserving strains involved in BJI or infective endocarditis for molecular comparison, follow-up, or medico-legal purposes, yet few specify concrete duration or storage conditions. French SPILF guidelines require at least one year at - 80 °C. Preservation methods differ in cost, practicality, and long-term genetic integrity, with - 80 °C-- 130 °C offering optimal stability. Inadequate storage conditions-temperature fluctuations, humidity, oxygen exposure-may lead to contamination, DNA degradation, or genetic drift. Given the clinical, epidemiological, and medico-legal value of archived isolates, long-term standardized storage in dedicated biobanks is essential. A minimum five-year preservation period appears both feasible and beneficial to strengthen diagnostic reliability, outbreak investigations, and future research.

Aging is marked by progressive physiological decline driven by chronic inflammation, mitochondrial dysfunction, and impaired metabolic and musculoskeletal resilience. As the global population ages, dietary supplements have gained attention as potential tools to support healthy longevity. This review summarizes current evidence on nutritional compounds that target aging-related pathways, focusing on interventions that influence mitochondrial health, cognitive performance, immune function, metabolic regulation, and maintenance of muscle mass in older adults. Thirty-two human studies were identified through PubMed, Scopus, and Web of Science.

Aging is recognized as the most significant risk factor for neurodegenerative diseases. Emerging evidence indicates that inflammation contributes to the progression of aging-related neurodegeneration. As a transmembrane immune receptor, triggering receptor expressed on myeloid cells 1 (TREM1) plays a crucial role in the regulation of inflammatory responses. Previously, our research group and others showed that the levels of a soluble form of TREM1 (sTREM1) were increased in the plasma or cerebrospinal fluid (CSF) of patients with Alzheimer's disease, the most common type of neurodegenerative disease among the elderly. Moreover, the elevated levels of CSF sTREM1 were closely associated with a more rapid rate of hippocampal degeneration in cognitively impaired older adults. However, the precise mechanisms by which sTREM1 contributes to aging-related neurodegeneration remain largely unclear. In this study, by utilizing senescence accelerated mouse prone 8 mice, an animal model of accelerated aging, we confirmed that serum sTREM1 levels were significantly increased during the aging process. Importantly, we demonstrated that roundabout guidance receptor 2 (ROBO2) functioned as a receptor for sTREM1 in hippocampal neurons, and its expression was also upregulated with aging. Additionally, we revealed for the first time that knockdown of neuronal ROBO2 mitigated aging-related hippocampal synaptic degeneration and cognitive impairments. Furthermore, we provided the first evidence that sTREM1 reduced the expression of synaptic proteins via the ROBO2/extracellular signal-regulated kinase pathway. These findings elucidated the mechanisms through which sTREM1 contributed to aging-related neurodegeneration and suggested that the inhibition of sTREM1-mediated signaling might represent a novel therapeutic strategy for the treatment of neurodegeneration and cognitive decline induced by aging.

Accumulating evidence underscores the therapeutic benefits of exercise in the prevention and treatment of various diseases. However, many patients are unable to engage in sufficient physical training because of frailty, disability, or disease burden. This challenge has stimulated considerable interest in exercise mimetics, which are pharmacological or biological interventions designed to activate exercise-responsive pathways and recapitulate the key adaptive responses elicited by physical activity. In this Review, we outline the conceptual foundations, classification, historical evolution, and biological rationale of exercise mimetics, and organize the field according to its major mechanisms, including neurotrophic signaling, redox regulation, immune modulation, mechanotransduction, vascular coupling, mitochondrial metabolism, epigenetic remodeling, and inter-organ crosstalk. We further examine how these pathways shape normal physiology and development, with an emphasis on metabolic homeostasis, neurodevelopment, cognition, aging, angiogenesis, and inflammation. Building on this framework, we evaluate emerging applications in major human diseases, including cancer, traumatic injury, cardiovascular disorders, neurodegenerative disorders, and inflammatory or immune-mediated conditions, with particular attention to neuroregeneration and systems-level repair. Finally, we assess clinical and translational advances in biomarker-guided diagnosis, personalized treatment, circulating mediators, drug delivery, combination therapy, and clinical trials. Although exercise mimetics offer a scalable and mechanism-informed therapeutic strategy, most evidence to date remains preclinical, and substantial challenges related to pharmacokinetics, safety, target engagement, and patient heterogeneity must be overcome before clinical implementation.

Exercise physiology is evolving from an organ-based framework toward a systems-level understanding, where molecular interactions between muscle, brain, and the gut microbiome critically influence performance and health. This review systematically examines the genetic, molecular, and cellular bases of this triad, with a focus on translational insights for disease prevention and human optimization. A systematic search of PubMed, Embase, and Web of Science was conducted up to October 2023 to identify studies exploring molecular pathways linking skeletal muscle, cognitive/affective function, and gut microbiota in exercise contexts. Inclusion criteria were original research articles investigating at least two components of the muscle-brain-gut axis. Exclusion criteria included non-English articles, conference abstracts, and studies without molecular data. The PRISMA 2020 guidelines were followed. The search strategy is detailed in Supplementary Material. Evidence was categorized into Grades 1 through 4 based on methodological rigor, omics integration, reproducibility, and translational relevance to human physiology and disease models. Analysis included 154 studies encompassing 987 molecular associations. Among these, 59 associations (Grades 1-2) provided robust evidence for genetically and functionally validated pathways, including myokine-mediated (e.g., irisin, BDNF) and microbially derived metabolites (e.g., SCFAs, tryptophan derivatives) that modulate neuroplasticity, mitochondrial function, inflammation, and HPA axis activity. Psychobiological factors influenced microbial composition, illustrating bidirectional gut-brain-muscle signaling. Most associations (n = 952) were limited by methodological variability or insufficient mechanistic depth. The integration of multi-omics platforms (metagenomics, metabolomics, proteomics) emerges as a key tool for personalized exercise interventions and biomarker discovery. This review synthesizes molecular evidence for the muscle-gut-brain axis as an integrative determinant of exercise responsiveness and disease resilience. We highlight genetic and metabolic pathways with diagnostic and therapeutic potential, aligning with the development of molecular tools for precision medicine. Future interdisciplinary research should leverage artificial intelligence and longitudinal omics to translate these mechanisms into targeted strategies for performance enhancement and disease prevention.

This study was designed to investigate the impact of Lamotrigine (LTG) on astrocyte activation in epilepsy during pregnancy and to elucidate its potential underlying mechanisms. A rat model of epilepsy during pregnancy was established using pentylenetetrazole (PTZ) injection. CTX-TNA2 cells were treated with IL-1β to activate astrocytes. NLRP3 expression was modulated using NLRP3 inhibitor and pcDNA 3.1-NLRP3 overexpression. Neuronal damage, apoptosis, and astrocyte activation were evaluated by HE staining, TUNEL staining, and immunofluorescence, respectively. Levels of inflammatory cytokines were determined by ELISA. Protein and mRNA expression levels associated with inflammation and astrocyte activation were analyzed by Western blot and RT-qPCR. LTG significantly reduced the expression of NLRP3, TXNIP, and suppressed inflammatory responses. In vivo, LTG attenuated neuronal damage and apoptosis in the cerebral cortex and hippocampal CA1 region, accompanied by decreased levels of TNF-α, IL-1β, and IL-6, as well as reduced expression of GFAP, GLAST, and phosphorylated p65. Co-treatment with the NLRP3 inhibitor MCC950 further enhanced these effects. In vitro, LTG inhibited astrocyte proliferation and activation, whereas NLRP3 overexpression partially reversed these effects. LTG alleviates astrocyte activation and neuroinflammation in pregnancy-associated epilepsy, potentially through modulation of the NLRP3/TXNIP axis. These findings provide novel insights into the pathogenesis of epilepsy during pregnancy and suggest potential therapeutic strategies.

Immune cell-cell interaction plays a critical role in the regulation of inflammatory responses. IL-10-expressing regulatory B cells (B10) alleviate the periodontal inflammation and bone loss by secreting IL-10, which can stimulate pro-resolving macrophage differentiation. However, little is known about the dynamic B10-macrophage interaction and the specific B10-induced pro-resolving functions in vivo in periodontitis. This study aimed to determine the dynamic local infiltration of B10 and macrophages, and the B10-induced macrophage differentiation and functions in experimental periodontitis. B10 were adoptively transferred via tail vein injection in a mouse model of experimental periodontitis. In some experiments, macrophages were depleted by intraperitoneal injection of clodronate liposomes. Dynamic gingival infiltration of B10 and macrophages were evaluated by in vivo imaging system (IVIS). The level of bone loss was evaluated by Micro-CT and TRAP staining. Cytokine productions, macrophage efferocytosis and autophagy were assessed by immunohistochemical / immunofluorescence analysis. Production of specialized pro-resolving mediators (SPMs) was detected by LC-MS/MS. B10 adoptive transfer inhibited alveolar bone resorption and osteoclast differentiation. B10 adoptive transfer promoted the number of pro-resolving macrophages compared with the control groups. A significant increase in IL-10, Arg-1, and YM-1, ATG5⁺, LC3B⁺, CD68⁺LC3B⁺, CD68+ATG5+ and CD68⁺Ly6G⁺ cells were detected in gingival tissues following B10 transfer, accompanied by a marked decrease in IL-17 A, TNF-α, and IL-1β expression. However, the B10-mediated suppression of alveolar bone resorption, osteoclast differentiation, TNF-α and IL-1β expression, as well as the upregulation of IL-10, ATG5, and LC3B, was attenuated upon macrophage depletion, whereas IL-17 A expression remained suppressed regardless of the macrophage presence. Notably, B10 adoptive transfer promoted RvD2 release in a macrophage-dependent manner. This study suggested that B10 adoptive transfer inhibited inflammation and bone loss in experimental periodontitis through the induction of macrophage-mediated pro-resolving functions, including RvD2 production, enhanced neutrophil clearance, and induction of macrophage autophagy.

Central airway obstruction can be caused by lung cancer and may severely diminish respiratory function to necessitate airway stenting. However, the mechanical properties of airway tissues remain poorly characterized, leading to a mismatch between stent mechanical behavior and airway compliance, which can reduce stent biocompatibility and clinical effectiveness. Such mismatches can result in abnormal stress transfer at the stent-airway interface and cause stent migration, local tissue irritation or inflammation, and impaired long-term performance. Predictive models are often used in treatment planning, however, without a comprehensive understanding of airway properties, advancements in modeling remain highly limited. In this study, we develop an experimental to numerical pipeline for identifying the mechanical properties of the human airway branching network, specifically the trachea, right bronchus, and left bronchus tissues. Biaxial planar tensile tests are used to capture the tissues' unique, anisotropic mechanical response in order to inform the computational routine-where inverse finite element analysis is employed to calibrate a Holzapfel-Gasser-Ogden constitutive model. To overcome the computational burden of traditional IFEA, a neural network (NN) surrogate model is trained to enable rapid material identification. We identify parameter values for the various tissues, such as C10 = 0.53 ± 0.25 kPa, k1 = 0.17 ± 0.30 kPa, k2 = 6.1 ± 2.0, and κ = 0.08 ± 0.01 for the trachea. Notably, this NN-approach reduced computational time from weeks to mere minutes, enabling fast material characterization. Thus, we also provide an efficient modeling framework and user-friendly MATLAB application for future studies. Ultimately, the findings here critically contribute to our current understanding of airway biomechanics and provide essential data for accurate modeling and optimization of airway stenting strategies.

Traumatic brain injury (TBI) and the resulting brain damage and dysfunction are one of the leading causes of death for individuals under 40 worldwide. TBI can occur due to any external force causing deformation in the brain, and it involves a complicated timeline of the initial mechanical damage followed by a subsequent inflammatory response. The details and extent of the effects of TBI on the brain are understudied; however, researchers have developed a vast array of experimental and computational models in order to investigate the complex physiological dynamics and interactions in TBI. This review summarizes the hallmarks of TBI, focusing on the inflammatory response mechanisms within the secondary injury and how they have been modeled computationally. Finally, we highlight potential areas of improvement for computational models of TBI to enhance their relevance for translational and clinical research.

Ammonia (Amm) is the largest nitrogenous waste product of fish, causing damage to vital organs, leading to respiratory difficulties and inhibited growth and reproductive performance of fish. This study explored the protective mechanism of rutin (RUT), a natural antioxidant of plant origin, against oxido-inflammatory stress of ammonia in Nile tilapia. A total of 60 monosex Nile tilapia were randomly distributed into four experimental groups: control, RUT (1 g/kg in feed), Amm (50 mg/L), and Amm + RUT. Daily exposure to Amm for 4 weeks significantly disrupted the hematological profile (↓ RBCs count and Hb by 50%, ↑ WBCs by 46%), increased MDA (+ 42%) and NO (+ 18%) levels, and suppressed the total antioxidant capacity by 42% compared to the control group. It also led to elevating the liver enzyme activity (ALT ↑ 50%, AST ↑ 35% compared to the control group), accompanied by marked histopathological changes in gills, liver, and brain. There was strong HSP70, Cox-2, and GFAP immunostaining alongside upregulation of the transcript levels of NF-κB, TNF-α, and IL-1β genes. The co-treatment of RUT with Amm alleviated all the aforementioned toxicological parameters, restoring RBCs (3.3 ± 0.07 × 106/mm3), Hb (3.2 ± 0.12 g/dL), WBCs (27 ± 0.89 × 103/mm3), and total antioxidant capacity (1.5 ± 0.05 mmol/L) close to control values and normalizing the microscopic histology of gills, liver, and brain. We conclude that the dietary supplementation with RUT attenuates Amm-induced toxicity via its antioxidant and anti-inflammatory potentials.