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Depression is increasingly linked to microbiota-gut-brain axis dysfunction, yet current monoaminergic antidepressants show limited efficacy. This study investigated the therapeutic potential and underlying mechanisms of GV-971, a marine-derived oligosaccharide, in a chronic restraint stress (CRS) mouse model. We first established that 8 h of daily restraint for 4-8 weeks induces a stable depression-like phenotype characterized by behavioral despair and significant reduction in peripheral monoamine neurotransmitters (5-HT and norepinephrine). GV-971 treatment robustly attenuated CRS-induced depression- and anxiety-like behaviors, restored hippocampal serotonin levels, reduced elevated plasma corticosterone concentrations, and ameliorated CRS-induced adrenal cortical hyperplasia. Mechanistically, GV-971 significantly suppressed neuroinflammation by inhibiting microglial hyperactivation in the prefrontal cortex and hippocampus. Concurrently, it repaired intestinal barrier dysfunction, evidenced by reduced permeability, restored mucosal integrity, and recovered goblet cell numbers. Crucially, integrated shot-gun metagenomics and plasma metabolomics revealed that GV-971 not only reshaped microbial taxonomy but also functionally recalibrated the gut ecosystem. It enriched beneficial taxa (e.g., Bifidobacterium pseudolongum, Bacteroides uniformis) and specific metabolic pathways, leading to increased short-chain fatty acids (valeric and caproic acids) and a significant reduction in plasma levels of tryptophan-kynurenine pathway metabolites, specifically the neurotoxic compounds kynurenine and quinolinic acid. Fecal microbiota transplantation (FMT) from GV-971-treated donors partially recapitulated the antidepressant and gut-protective effects in CRS recipients, confirming a causal role for the remodeled microbiota. Collectively, GV-971 exerts antidepressant effects by coordinately remodeling the gut microbiota, normalizing tryptophan and SCFA metabolism, restoring gut barrier integrity, and dampening central neuroinflammation, supporting its potential as a novel gut-brain axis-targeted therapy for depression.

Cadmium is a widespread environmental xenobiotic that poses serious risks to hepatic, renal, and male reproductive functions. Natural compounds such as silymarin, a bioactive extract from Silybum marianum, have gained attention for their protective potential against xenobiotic-induced toxicity. This study investigated whether subchronic oral administration of silymarin (30 mg/kg) mitigates cadmium-induced toxicity (5 mg/kg) in adult rats over six weeks. Twenty-four rats were assigned to four groups: control, cadmium-exposed, silymarin-treated, and co-treated. Biochemical, hematological, oxidative stress, and reproductive parameters were assessed. Sperm quality was evaluated using CASA, and testicular tissues were examined histologically. Cadmium exposure significantly reduced body weight (-30.8%), elevated transaminases (AST, ALT; p < 0.01), increased serum creatinine and total cholesterol, and induced multi-organ oxidative stress, as reflected by elevated malondialdehyde and markedly reduced SOD, CAT, and thiol group levels in testicular, hepatic, and renal tissues (p < 0.01). Sperm concentration dropped from 75.2 to 21.8 &#xd7; 106/mL, with total motility falling to 35% and progressive motility to 18%, accompanied by severe seminiferous tubule degeneration (Score III in 5 rats). Co-administration of silymarin partially restored these parameters, sperm concentration recovered to 38.5 &#xd7; 106/mL, total motility improved to 50.2%, and antioxidant enzyme activities and liver/kidney biomarkers showed significant but incomplete recovery (p < 0.05). Molecular docking revealed favorable binding affinities of silybin toward GPx (-8.4 kcal/mol), CAT (-8.3 kcal/mol), and SOD (-6.4 kcal/mol), offering a preliminary computational hypothesis suggesting possible interactions between silybin and antioxidant enzymes, pending experimental validation. Silymarin alone exerted no adverse effects. These findings establish silymarin as a partial but promising multi-organ cytoprotectant against cadmium toxicity, and highlight the need for future studies optimizing dosing strategies, exploring longer treatment durations, and investigating combination approaches with metal chelators or Nrf2-activating agents to achieve complete tissue recovery.

Metabolic reprogramming within the tumor microenvironment (TME) limits the efficacy of chemo-immunotherapy in triple-negative breast cancer (TNBC). Despite advances in high-resolution profiling, the specific intercellular metabolic crosstalk driving immune evasion remains incompletely understood. Here, we present a comprehensive single-cell metabolic atlas of the TNBC ecosystem to decode spatial and cell-type-specific metabolic vulnerabilities. Our multidimensional analysis reveals a distinct paracrine metabolic communication axis: CXCL9+ macrophages upregulate rate-limiting enzymes (IDO1/2) to become a potential source of local kynurenine, which is subsequently imported by cytotoxic T cells. Through in vitro co-culture and in vivo models, we demonstrate that this kynurenine uptake triggers impaired effector function and phenotypic exhaustion. Crucially, pharmacological blockade of SLC7A5 with the specific inhibitor JPH203 abrogates this metabolic toxicity, restores T cell effector function, and enhances the anti-tumor efficacy of combined cisplatin and anti-PD-1 therapy. Collectively, our findings delineate the Kynurenine-SLC7A5 metabolic axis as a critical driver of immunosuppression, providing a compelling rationale for integrating amino acid transport blockade to overcome resistance to chemo-immunotherapy.

Food-grade titanium dioxide (E171) is widely used as a food additive and has raised concerns about its potential systemic toxicity. However, its impact on cardiac cellular metabolism and mitochondrial function remains incompletely understood. In the present study, we investigated the effects of E171 on intracellular labile iron, oxidative stress, mitochondrial ultrastructure, and mitochondrial bioenergetics in H9c2 cardiomyoblasts. Exposure to E171 leads to a significant increase in intracellular labile iron (Fe2+) levels. This alteration was accompanied by elevated reactive oxygen species (ROS) production and reduced intracellular glutathione levels, consistent with enhanced oxidative stress following E171 exposure. Ultrastructural analysis by transmission electron microscopy (TEM) revealed marked mitochondrial alterations, including reduced cristae density and structural damage. Functional assessment of mitochondrial bioenergetics demonstrated impaired oxidative phosphorylation and reduced maximal respiratory capacity in E171-treated cells. The potential protective role of quercetin (a powerful antioxidant and iron chelator) was explored in mitochondrial respiration assays; however, at the concentration and exposure conditions tested, quercetin treatment did not fully restore the bioenergetic parameters induced by E171. Collectively, these findings indicate that E171 increases intracellular labile iron levels and promotes oxidative stress, associated with alterations in mitochondrial ultrastructure and impaired bioenergetic function in H9c2 cardiomyoblasts, suggesting a potential mechanism by which food additives may affect cardiac cellular metabolism.

Uveitis is a heterogeneous group of intraocular inflammatory diseases and an important cause of visual impairment worldwide. Although current treatments mainly target inflammation, many patients develop chronic or recurrent disease, suggesting that inflammation control alone may not fully restore intraocular homeostasis. Increasing evidence highlights the blood-ocular barrier (BOB), including the blood-retinal barrier and blood-aqueous barrier, as a key regulator of the intraocular microenvironment. This review aims to summarize the bidirectional interaction between intraocular inflammation and blood-ocular barrier dysfunction in uveitis, and to highlight the clinical significance of barrier dysfunction in disease monitoring and management. In addition, this review discusses the potential value of incorporating barrier assessment into dynamic disease evaluation and relapse-aware management strategies. Recent studies suggest that inflammation and BOB dysfunction are bidirectionally linked. Inflammatory mediators disrupt barrier integrity, while barrier breakdown facilitates immune cell infiltration and further amplifies inflammation, forming a self-reinforcing cycle that may drive disease persistence. Importantly, BOB dysfunction also has clinical implications. Findings such as aqueous flare, macular edema on optical coherence tomography, and vascular leakage on fluorescein angiography reflect barrier status and can serve as dynamic indicators for disease monitoring. Persistent abnormalities despite reduced inflammatory cell activity may indicate incomplete barrier recovery or subclinical inflammation, helping to explain discordant clinical findings and the relapse-prone nature of uveitis. Rather than viewing BOB dysfunction solely as a pathological consequence of inflammation, this review highlights the potential clinical value in disease assessment and management. Barrier-related findings may provide additional information beyond conventional inflammatory evaluation, particularly in cases where inflammatory cell activity appears controlled, but underlying barrier alteration persists. Incorporating barrier assessment into monitoring may help interpret discordant clinical findings, improve evaluation of disease control, and support a more relapse-aware management strategy in uveitis. In addition, therapeutic approaches aimed at restoring barrier integrity may provide a more comprehensive strategy for achieving sustained remission and reducing recurrence risk.

Despite its critical role in disease diagnosis as a radiopharmaceutical, Fluorine-18 generates medical wastewater that necessitates efficient treatment, for which membrane adsorption stands out as a potent method, albeit one that demands high-performance membranes with exceptional permeability and adsorption capacity. This study presents a novel cerium-loaded amyloid fibril hybrid membrane designed for efficient removal of fluorine-18 from such wastewater. The membrane is fabricated through a facile process involving oxidation-precipitation of cerium species onto amyloid fibrils, followed by vacuum filtration, with further compositional tuning via incorporation of porous silica or activated carbon dopants. The resulting membrane retains the characteristic amyloid fibril structure and exhibits high water permeability with a flux of up to 803.3 L/(m2&#xb7;h&#xb7;bar), superior to most of the other membrane materials. It effectively removes fluoride ions (F-) from both low and high-concentration solutions, achieving a removal efficiency of up to 99% and a maximum adsorption capacity of 580 mg/g, outperforming many existing membrane materials. The hybrid membrane also demonstrates notable resistance to ionic interference, enabling selective F- adsorption from solutions containing high concentrations of Cl-, NO3- and SO42-, with a distribution coefficient (Kd) as high as 4.1 &#xd7; 104 mL/g; furthermore, it maintains a fluoride removal rate above 51% after ten consecutive adsorption cycles. The membrane retains 51% of its initial fluoride removal efficiency after 10 cycles, indicating potential for repeated use, although further optimization or regeneration strategies would be required to fully restore performance. Mechanistic investigations reveal that F- adsorption occurs mainly through ion exchange with hydroxyl groups on CeO2. This work introduces a promising novel material with significant potential for the efficient treatment of medical radioactive wastewater containing fluorine-18.

Brain dysfunction is a primary symptom of Gulf War illness (GWI). The present study investigated the effects of an amorphous formula of curcumin (CUR) and &#x3b1;-glycosyl isoquercitrin (AGIQ) on neurobehaviors and adult neurogenesis and following synaptic plasticity of produced neurons in the hippocampal dentate gyrus (DG) in a rat GWI model. Ten-week-old rats received GWI-related chemicals and restraint stress for 28 days; thereafter, animals were fed either a diet without supplement or mixed with 0.1% CUR or 0.5% AGIQ for 126 days. GWI treatment adversely affected behavioral endpoints, including novel object recognition, sucrose preference, novelty-suppressed feeding, and contextual fear conditioning. CUR ameliorated all these effects, while AGIQ caused anxiety-like behavior and improved fear extinction learning. GWI treatment downregulated NRF2-KEAP1 pathway-related genes in the DG; both phytochemicals reversed most of these changes. GWI treatment increased CD68+ and CD163+ microglia populations in the DG hilus; both phytochemicals reversed the increase of CD68+ microglia. In the neurogenic niche, GWI treatment decreased GFAP+ neural stem cells but increased DCX+ and PCNA+ cells, decreased hilar SST+ and GAD67+ GABAergic interneurons, and downregulated Pvalb. CUR reversed decreases in GFAP+ cell and SST+ interneuron numbers. Both phytochemicals increased VGLUT1 immunoreactivity, restored the VGLUT1/VGAT ratio, and upregulated Bdnf, Gria1, Gria2, Gria3, Slc17a7, Ptgs2, and Mapk1. AGIQ further increased COX2+ cell numbers and upregulated Grin2a, Grin2b, and Mapk3. In summary, both phytochemicals may have exerted antioxidant effects and modulated excitatory/inhibitory balance via glutamatergic signaling in GWI animals; CUR was superior to AGIQ at normalizing aberrant neurobehaviors and neurogenesis.

Renal aging shortens healthspan and propagates organ dysfunction beyond the kidney, yet its molecular drivers remain incompletely defined. Here we identify microsomal prostaglandin E synthase-2 (mPGES-2) as a critical regulator of renal aging and its skeletal consequence. Genetic ablation of Ptges2 improved health indices in aged mice, prolonged median survival, and markedly alleviated glomerulosclerosis, podocyte injury, and renal senescence. Single-cell transcriptomic analysis, together with podocyte- and tubule-specific knockout models, showed that podocyte mPGES-2, rather than tubular mPGES-2, is the dominant intrarenal driver of aging-related kidney injury. Mechanistically, mPGES-2 promoted podocyte senescence through a PGE2/EP1 signaling axis. Podocyte-specific Ptges2 deletion also mitigated age-related osteoporosis and restored renal calcitriol and &#x3b1;-klotho, supporting a kidney-bone mechanism secondary to impaired renal endocrine function. Consistent with the genetic models, pharmacological inhibition of mPGES-2 with SZ0232 attenuated renal aging and improved bone microarchitecture in aged mice. Both genetic deficiency and pharmacological inhibition of mPGES-2 were well tolerated, with no overt adverse effects on major organs. These findings identify podocyte mPGES-2 as a druggable determinant of renal aging and a potential therapeutic target for aging-associated osteoporosis.

Myocardial ischemia-reperfusion (I/R) injury is a frequent complication of acute myocardial infarction (AMI), yet clinical biomarkers and targets remain limited. Although tRNA-derived small RNAs (tsRNAs) are emerging cardiovascular regulators, their roles in I/R injury are not fully elucidated. We identified tsRNA-3025a via sequencing in mouse I/R models and validated its clinical significance. Circulating tsRNA-3025a was significantly upregulated in AMI and unstable angina patients, independently predicting adverse events within 30 days. Functionally, tsRNA-3025a exacerbated apoptosis and mitochondrial dysfunction in vitro, while its in vivo silencing reduced infarct size, improved cardiac function and increased the proportion of Ki67- and pH3-positive cardiomyocytes. Mechanistically, tsRNA-3025a aggravated injury by targeting PIK3C2A, thereby suppressing autophagosome formation and impairing protective autophagic flux during reperfusion. In conclusion, circulating tsRNA-3025a serves as a prognostic biomarker for post-PCI patients. Targeting tsRNA-3025a attenuates myocardial I/R injury and restores myocardial regeneration and repair by regulating PIK3C2A-mediated protective autophagy flux.

Acute pancreatitis (AP) frequently triggers intestinal barrier dysfunction, yet the underlying molecular mechanisms remain poorly understood. This study investigated whether small extracellular vesicle (sEV)-enriched serum preparations from healthy individuals protect against AP-induced intestinal barrier dysfunction through microRNA-mediated regulation of pyroptosis. sEV-enriched preparations were isolated from 10 AP patients (AP-sEV) and 10 healthy controls (HC-sEV) using ExoQuick precipitation followed by ultracentrifugation. A murine AP model was established using cerulein and lipopolysaccharide, and human intestinal epithelial cells were stimulated with lipopolysaccharide for in vitro studies. HC-sEV preparations significantly ameliorated AP-induced tissue damage, restored tight junction proteins (claudin-1, occludin, ZO-1), reduced intestinal permeability, and suppressed inflammatory cytokines (TNF-&#x3b1;, IL-6, IL-1&#x3b2;) and pyroptosis-related proteins including NLRP3, gasdermin D, and cleaved caspase-1. Conversely, AP-sEV preparations exacerbated barrier dysfunction. Bioinformatics analysis identified miR-579-3p as significantly downregulated in AP-sEV. Inhibition of miR-579-3p reversed HC-sEV protective effects. ANXA3 was validated as a direct miR-579-3p target, and ANXA3 overexpression counteracted miR-579-3p-mediated protection. These findings demonstrate that HC-sEV preparations protect against AP-induced intestinal barrier dysfunction through miR-579-3p delivery targeting ANXA3 to suppress NLRP3 inflammasome-mediated pyroptosis. The miR-579-3p/ANXA3/NLRP3 axis represents a novel therapeutic target for preserving intestinal barrier integrity during acute pancreatitis.

Quadriceps muscle and tendon injuries are a significant cause of impairment of the knee extensor mechanism, ranging from minor muscle strains to complete tendon ruptures and extensive defects following oncologic resections. This narrative review provides a comprehensive analysis of contemporary concepts in anatomy, biomechanics, diagnosis, surgical management, and rehabilitation, with a particular focus on reconstructive techniques and functional outcomes. While most muscle injuries respond well to conservative management, complete quadriceps tendon ruptures typically require surgical repair to restore extensor continuity. Both transosseous suture techniques and suture anchor fixation demonstrate reliable outcomes, with no clear superiority in clinical results. Chronic ruptures present additional challenges due to tendon retraction and poor tissue quality, often necessitating advanced reconstruction methods such as V-Y tendon lengthening and augmentation with autografts, allografts, or synthetic materials. In cases of large defects, especially following soft-tissue sarcoma resection, free functional muscle transfer (FFMT) has emerged as a key reconstructive strategy. Common donor muscles include the latissimus dorsi, gracilis, rectus abdominis, and vastus lateralis, each offering specific biomechanical advantages. Functional recovery is strongly influenced by the extent of quadriceps preservation, with better outcomes observed when at least two muscle heads remain functional. Rehabilitation protocols vary depending on the surgical approach. Early controlled mobilisation is generally recommended after tendon repair, whereas FFMT requires a more cautious and prolonged rehabilitation process to allow for flap integration and reinnervation. Overall, optimal outcomes depend on a multidisciplinary approach combining appropriate surgical technique, individualized rehabilitation, and careful patient selection.

Potyvirus rapae (turnip mosaic virus, TuMV) is widely used as a model system in plant-virus interaction studies. The TuMV RNA genome encodes 11 proteins, some of which remain poorly characterized, while the functions of others are well defined. Studying individual proteins in isolation may not recapitulate native expression levels, subcellular localization, and interaction with host factors during virus replication and movement. An alternative approach is to tag individual viral proteins in the context of an infectious clone. Epitope tags may alter protein functions and affect viral replication, movement, or a combination of essential steps, thus leading to changes in pathogenicity. Because they have central roles in viral infection, here we measured the effect of individually tagging the helper component proteinase (HC-Pro) and nuclear inclusion protein b (NIb) with a 6His-3xFLAG tag. Epitope tags were placed at the N-terminus of HC-Pro and the N- and C-termini of NIb within a TuMV infectious clone carrying coding sequences for the green fluorescent protein (TuMV-GFP). Constructs carrying a tagged HC-Pro displayed pathogenicity similar to that observed for TuMV-GFP in Nicotiana benthamiana and Arabidopsis thaliana plants. In contrast, infectivity of NIb-tagged clones became temperature sensitive and, even at the permissive temperature, showed reduced pathogenicity compared to TuMV-GFP. Providing a silencing suppressor in trans did not restore infection efficiency, suggesting reduced viral fitness due to structural or functional disruption caused by the epitope tags. Structural models generated using AlphaFold2 showed no effect of the tag on HC-Pro. In contrast, structural models illustrated tag interference with the NIb catalytic site. AlphaFold2 was further used to predict the structural impact of several tags on NIb and to predict the effect of a 6HIS-3xFlag tag on all other TuMV proteins. This study provides a broadly applicable framework for selecting suitable epitope tags to mark viral proteins and maintain function in the context of virus infection.

Autism is a multifactorial neurodevelopmental disorder characterized by social deficits, stereotypical behaviour, and neurotransmitter imbalance. This study evaluated the neuroprotective potential of Puerarin (PUN) and Magnesium Acetyl Taurate (MGAT) in a propionic acid (PPNA)-induced rat model of autism. PPNA was administered intracerebroventricularly for 11 consecutive days to induce autism-like features, followed by a 44-day treatment period with PUN (300&#xa0;mg/kg, i.p.) and MGAT (500&#xa0;mg/kg, p.o.). A comprehensive assessment was conducted, including behavioural analysis, biochemical and molecular evaluations, cerebrospinal fluid and plasma profiling, and histopathology. Treatment with PUN and MGAT, particularly in combination, improved behavioural outcomes, restored neurotransmitter balance, reduced neuroinflammation and apoptotic signaling, and attenuated activation of the glutaminase-glutamate/NMDAR and MAPK pathways (C-JNK, ERK1/2, P38 MAPK). Additionally, treatment increased magnesium levels and PSD-95 expression, indicating significant neuroprotection. These findings support the potential of PUN and MGAT as a multitarget therapeutic strategy for autism and warrant further translational investigation.

Immune dysregulation is a key driver of metabolic dysfunction-associated steatotic liver disease (MASLD). Double-negative regulatory T (DNT) cells, which are essential for hepatic immune homeostasis, are functionally impaired in MASLD. CD39, an ectoenzyme that converts ATP to adenosine, sustains DNT cell viability and immunoregulatory function. However, the mechanisms of MASLD-induced CD39 dysregulation remain unknown. In this study, a transcriptomic analysis of hepatic DNT cells from MASLD mice revealed reduced ATP hydrolysis, as confirmed by flow cytometry, and lower CD39 level compared to normal control diet-fed mice. Similarly, single-cell transcriptomic data showed that CD39 was downregulated in hepatic DNT cells from MASLD patients, and higher CD39 expression was associated with enhanced cytotoxicity and viability. Furthermore, in vitro experiments confirmed that CD39 maintained the immunosuppressive function of DNT cells by hydrolyzing ATP and suppressing monocyte activation. Mechanistically, arachidonic acid (AA), which is enriched in the livers of MASLD, suppressed CD39 via hypoxia-inducible factor-1&#x3b1; (HIF-1&#x3b1;). This AA-HIF-1&#x3b1;-CD39 axis impaired DNT cell-mediated monocyte immunosuppression, accelerating immune imbalance and MASLD progression. These findings establish the AA-HIF-1&#x3b1;-CD39 axis as a key pathway driving DNT cell dysfunction in MASLD, highlighting potential therapeutic strategies targeting metabolic-immune crosstalk to restore hepatic immune balance.

Objectives: Circadian rhythms regulate key physiological processes, including metabolism and energy balance. Emerging evidence suggests that the timing of physical activity may influence metabolic outcomes. However, how the timing of endurance exercise impacts long-term metabolic health and the role of the circadian clock in this process remain unclear. This study aimed to investigate whether time-dependent endurance exercise improves metabolic health via circadian rhythm regulation. Methods: A 12-week endurance exercise protocol was established using wild-type (WT) and circadian-disrupted Clock&#x394;19 mice. Mice were assigned to exercise at Zeitgeber time 0 (ZT0) or Zeitgeber time 0 (ZT12), or to sedentary controls. Assessments included rotarod fatigue test, body weight, epididymal fat ratio, fasting blood glucose, serum triglycerides, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), non-esterified fatty acids (NEFA), intraperitoneal glucose tolerance test (IPGTT), and insulin tolerance test (ITT). Results: Clock&#x394;19 mice exhibited circadian phase-dependent fatigue susceptibility on the rotarod, particularly at ZT0. Both exercised Clock&#x394;19 groups (ZT0 and ZT12) showed significant weight reduction compared to sedentary controls, indicating that endurance exercise may counteracts circadian disruption-induced weight gain independent of timing. In WT mice, evening exercise (ZT12) led to enhanced lipid regulation and better glucose tolerance. These time-dependent benefits were absent in Clock&#x394;19 mutants, demonstrating that the full metabolic advantages of exercise require a functional circadian clock. Notably, endurance training also partially restored serum HDL-C levels in Clock&#x394;19 mice, suggesting compensatory metabolic responses. Conclusions: Aligning endurance exercise with the body's internal clock provides greater metabolic benefits than untimed exercise. The circadian clock is essential for time-dependent improvements in glucose and lipid metabolism, although some beneficial effects occur independently of a functional clock.

Iron deficiency remains a critical global nutritional challenge, and food iron fortification is the primary intervention strategy for alleviating iron deficiency anemia (IDA). In this study, iron complexes based on fibrous aggregates (FA-Fe) and amorphous aggregates (AA-Fe) of Antarctic Krill protein were fabricated to investigate their structure-activity relationships and iron supplementation efficacy. Both complexes coordinated Fe2+ via carboxyl and amino groups, with FA-Fe exhibiting higher iron chelation capacity and structure-dependent functional divergence. In vitro digestion revealed sustained gastric release of FA-Fe, resulting in higher intestinal soluble iron content (19.05%) and bioaccessibility than AA-Fe and FeSO4. In the IDA model, FA-Fe restored hemoglobin, tissue iron stores, and iron homeostasis-related gene expression while mitigating gastric inflammation and oxidative stress, demonstrating superior biocompatibility. Thus, FA-Fe combines high efficacy with low gastrointestinal irritation, positioning structurally diverse Antarctic Krill protein aggregates as promising iron supplement carriers.

The human facial skin microbiome is a complex and dynamic ecosystem that plays a central role in maintaining skin health, immune regulation, and preventing dermatological skin conditions. Cutibacterium acnes (C. acnes) and Staphylococcus epidermidis (S. epidermidis) are the most prominent bacterial species, with shifts in their relative abundance correlating with skin site, age, skin site, and health status. Exploring the facial microbiome offers exciting opportunities, though it requires careful methodological consideration. Sampling techniques vary in invasiveness and depth, which can influence the accuracy and reproducibility of microbiome profiles. While traditional cultivation methods provide valuable insights, they often miss nonculturable microbes, limiting the view of microbial diversity. Molecular approaches such as amplicon sequencing and metagenomics enable a more comprehensive understanding of microbial communities, even though they currently cannot distinguish between viable and nonviable microbes. Addressing these challenges will help unlock the full potential of facial microbiome research. A balanced facial skin microbiome is associated with healthy skin, whereas a dysbiosis of C.&#xa0;acnes and S. epidermidis is commonly observed in acne-prone skin and more pronounced clinically manifest acne. A comprehensive understanding of the diversity and distribution of C. acnes phylotypes, as well as distinct lineages of S. epidermidis associated with skin disorders, is crucial for developing targeted, microbiome-based cosmetic and medical treatments. Emerging strategies aim to restore microbial balance by leveraging the skin's native microbiota, including probiotic approaches. These strategies represent a promising yet still emerging approach, as current clinical evidence remains limited and further well-controlled studies are required, although they may offer benefits by enhancing microbial diversity and supporting skin barrier function.

Oxidative stress plays a central role in the pathophysiology of type 2 diabetes and contributes to multiorgan dysfunction. Non-pharmacological strategies targeting redox imbalance may provide complementary benefits beyond glycemic control. This study investigated the effects of combined respiratory muscle training (RMT) and photobiomodulation (PBM) on systemic and tissue-specific redox homeostasis in an experimental model of type 2 diabetes. Male rats were allocated into four groups: sedentary Sham (non-diabetic), Sham submitted to RMT combined with PBM, sedentary type 2 diabetes, and type 2 diabetes submitted to the RMT/PBM protocol. Type 2 diabetes was induced by a high-fat diet associated with low-dose streptozotocin. Interventions were performed five days per week for six weeks. Hematological and biochemical parameters were evaluated. Oxidative stress was assessed by lipid peroxidation (thiobarbituric acid reactive substances) and reactive oxygen species production (dichlorofluorescein), while antioxidant defenses were determined by superoxide dismutase activity and non-protein thiol levels in plasma and multiple tissues. In diabetic rats, the combined RMT/PBM protocol increased mean corpuscular hemoglobin concentration, reduced leukocyte and monocyte counts, and restored plasma protein levels. Oxidative damage was attenuated in plasma, diaphragm, lungs, and kidneys, while antioxidant defenses were enhanced, particularly in the diaphragm, heart, and kidneys. In normoglycemic rats, RMT/PBM also enhanced tissue antioxidant capacity, indicating preserved redox responsiveness. Combined RMT and PBM promote systemic and tissue-specific redox adaptations and improve hematological and biochemical parameters in diabetic rats. These findings support the potential of this combined intervention as a non-pharmacological strategy to mitigate oxidative dysfunction associated with type 2 diabetes.

The present study was conducted to evaluate the hepatoprotective potential of Strobilanthes callosa using a well-established rat model of experimentally induced liver injury. The investigation assessed biochemical, hematological, oxidative stress, and histopathological parameters to determine the protective efficacy of the plant extract. Body weight was recorded at the beginning and end of the treatment period, while liver weight was measured after sacrifice to evaluate physiological changes associated with hepatic injury. Serum biochemical markers, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), bilirubin, albumin, and triglycerides, were analyzed using standardized enzymatic assay kits. Treatment with S. callosa significantly reduced serum ALT, AST, and ALP levels respectively, compared with the toxic control group (p&#x2009;<&#x2009;0.05), indicating improved liver function. Bilirubin levels were significantly decreased, whereas albumin levels were restored toward normal values following treatment. Oxidative stress biomarkers revealed a significant reduction in malondialdehyde (MDA) levels by along with increased antioxidant defense through restoration of catalase and glutathione levels respectively (p&#x2009;<&#x2009;0.05). Hematological parameters, including hemoglobin (Hb), red blood cell (RBC), white blood cell (WBC) counts, packed cell volume (PCV), and differential leukocyte count, were evaluated to assess systemic toxicity, inflammatory response, and general physiological status. Histopathological examination of liver tissues using hematoxylin and eosin staining demonstrated marked improvement in hepatic architecture, with reduced necrosis, fatty degeneration, inflammatory infiltration, and tissue disorganization in treated groups compared with toxin-treated animals. Statistical analysis was performed using GraphPad Prism 8.0, with results expressed as mean&#x2009;&#xb1;&#x2009;SD. Data were analyzed using one-way and two-way ANOVA followed by appropriate post hoc tests, and differences were considered statistically significant at p&#x2009;<&#x2009;0.05.