Search Results (29,612)

Objective: This study aimed to evaluate the long-term degradation behavior, biostimulatory effects, and biocompatibility of a novel poly-L-lactic acid-block-polyethylene glycol/hyaluronic acid (PLLA–b–PEG/HA) composite filler for soft tissue augmentation. Methods: PLLA–b–PEG/HA microsphere properties were characterized via scanning electron microscopy (SEM), X-ray diffraction (XRD), Fourier-transform infrared spectroscopy (FTIR), nuclear magnetic resonance hydrogen spectroscopy (¹H NMR), thermogravimetry (TG) and differential scanning calorimetry (DSC). A 104-week in vivo rabbit model was established to systematically observe filler degradation and tissue responses. Ultrasound monitoring, histological staining, ELISA and RT-PCR were performed to assess volumetric changes, inflammatory reactions and collagen synthesis-related signaling. Results: Physicochemical property tests demonstrated that PLLA–b–PEG retains the fundamental physicochemical properties of pristine PLLA while exhibiting enhanced hydrophilicity. B-ultrasound demonstrated a presented uniform in vivo distribution without displacement or diffusion over time, confirming steady and predictable degradation. SEM verified progressive morphological degradation and porous evolution of the microspheres. The filler induced a mild, balanced inflammatory microenvironment with early expression of both pro-inflammatory (IL-12, TNF-α) and anti-inflammatory (IL-4) cytokines, which resolved gradually over time. Sustained TGF-β upregulation persisted throughout the 104-week observation period, driving continuous neocollagenesis and prominent neoelastogenesis, thereby achieving favorable and long-term tissue remodeling with excellent biocompatibility. Conclusions: The PLLA–b–PEG/HA composite filler exhibits controllable degradation properties and homeostatic regulatory effects, along with outstanding long-term biosafety and tissue integration capacity. As an ideal biostimulatory filler for soft tissue augmentation, it can effectively facilitate the regeneration of high-quality functional extracellular matrix rich in collagen fibers and elastic fibers, and holds promising clinical prospects for natural and long-lasting soft tissue filling applications. Full article

Ovarian cancer remains a major cause of gynecological cancer-related mortality, highlighting the need for novel therapeutic strategies capable of enhancing antitumor activity while targeting multiple mechanisms involved in tumor progression. Everolimus, an inhibitor of the mammalian target of rapamycin pathway, and carboplatin are established antineoplastic agents with distinct mechanisms of action, whereas astaxanthin is a bioactive carotenoid with antioxidant, anti-inflammatory, and potential anticancer properties. This study compared the individual and pairwise combination effects of carboplatin, everolimus, and astaxanthin on cell viability, migratory capacity, and inflammatory and tumor-associated biomarkers in SKOV3 ovarian cancer cells. Human SKOV3 ovarian cancer cells were cultured under standard conditions and exposed to different concentrations of carboplatin, everolimus, and astaxanthin, either individually or as pairwise two-drug combinations, for 24–72 h. Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay. Cell migration was evaluated using a scratch wound-healing assay. Based on the experimental treatment protocol, 100 nM everolimus, 100 μM carboplatin, and 100 μM astaxanthin, alone and in combination, were further evaluated for their effects on β-defensin 1, β-defensin 2, α-defensin 1, tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β) levels. Biomarker concentrations were determined by ELISA. Experiments were independently performed in triplicate. Everolimus, carboplatin, and astaxanthin produced concentration- and time-dependent alterations in SKOV3 cell viability, with more pronounced cytotoxic effects generally observed following prolonged exposure. The pairwise combination treatments also substantially affected cell viability, particularly at later experimental time points. Assessment of migratory capacity demonstrated significant differences in wound closure among treatment groups at 24, 48, and 72 h (p = 0.0224, p = 0.0155, and p = 0.0028, respectively), indicating a time-dependent inhibitory effect on SKOV3 cell migration. Treatment with carboplatin, everolimus, and astaxanthin, individually or in pairwise combinations, also significantly modulated β-defensin 1, β-defensin 2, α-defensin 1, TNF-α, and IL-1β levels compared with control cells, with the magnitude and direction of these changes varying according to treatment regimen and exposure duration. Everolimus, carboplatin, and astaxanthin exerted significant time- and treatment-dependent effects on the viability and migratory behavior of SKOV3 ovarian cancer cells and markedly modulated defensin and pro-inflammatory cytokine responses. The findings demonstrate distinct treatment- and time-dependent responses to the individual agents and their pairwise combinations in SKOV3 ovarian cancer cells. These observations represent preliminary comparative in vitro effects rather than evidence of pharmacological synergy or therapeutic benefit. Further mechanistic studies using additional ovarian cancer cell lines, formal drug interaction analyses, and in vivo models are required to establish the biological and potential therapeutic relevance of these treatment combinations. Full article

Background/Objectives: Meningiomas frequently involve the adjacent skull bone. The bone tumor microenvironment (TME) represents a unique niche in bone-invasive tumors and bone metastases, and can promote tumor progression through tumor–stromal interactions. We hypothesized that the bone TME may contribute to tumor cell transcriptional changes and tumor growth in meningioma. Methods: Human malignant meningioma cell lines, IOMM-Lee and HKBMM, were implanted over the calvarial bone (bone TME) and into the dorsal skin (non-bone TME) of BALB/c-nu/nu mice. Tumors from the IOMM-Lee model underwent bulk RNA sequencing with computational separation of human- and mouse-derived reads, enabling ligand–target interaction analysis of stromal cell-to-tumor cell signaling. Differential gene expression analysis, enrichment analysis, ligand–target interaction analysis, multiplex immunofluorescence, and immunohistochemistry were performed. Results: Tumor volume was significantly greater in the bone TME than in the non-bone TME in both models, whereas the Ki-67 labeling index was significantly reduced. Transcriptomic analysis revealed distinct tumor cell transcriptional states in the bone TME, characterized by upregulation of inflammation-related genes and enrichment of inflammatory signaling pathways, including interferon responses and NF-κB signaling. Ligand–target interaction analysis of stromal cell-to-tumor cell signaling identified stromal IL1B as a candidate regulator of inflammatory transcriptional programs in tumor cells. F4/80-positive macrophages expressed IL-1β, and tumor cells were positive for phospho-IKKα/β and phospho-IκBα in the bone TME. Conclusions: Tumor–stromal interactions potentially involving macrophage-derived IL-1β may be associated with inflammatory transcriptional programs in meningioma cells and with meningioma enlargement in the bone TME. These interactions may be therapeutically relevant in meningioma with bone involvement. Full article

Staphylococcus aureus is an ESKAPE pathogen, defined by its ability to evade antibacterial treatment, and together with S. epidermidis is a leading Gram-positive cause of wound infection. The emergence of methicillin- and vancomycin-resistant strains further limits conventional antibiotic treatment. The staphylococcal endolysin LysSte134_1 was produced recombinantly, its proper folding confirmed by zymography, and its lytic activity demonstrated against planktonic cultures of both S. aureus and S. epidermidis. The combination of LysSte134_1 with 10% 1,3-propanediol and Zn²⁺ increased CFU reduction in both species relative to LysSte134_1 with Zn²⁺ alone. In a murine wound model, topical application of LysSte134_1 significantly reduced the bacterial burden in wound tissue, achieving a 2–3-log reduction in MRSA and below the detection limit for S. epidermidis. Treatment was accompanied by normalization of peripheral leukocyte counts and a shift in the serum cytokine profile from a sustained pro-inflammatory state with elevated IL-6, IL-17 and IL-10 toward levels comparable to non-infected controls. These results suggest the potential utility of LysSte134_1 as a component of topical antibacterial formulations and support further investigation in models of staphylococcal wound infection. Full article

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) deposition and cognitive decline. Clinical evidence indicates that Hericium erinaceus whole fruiting body powder offers limited therapeutic efficacy, which is suggested to be constrained by whole-food matrix interference and uncertainties in central nervous system (CNS) exposure. Therefore, we hypothesized that erinacine C (EC)—a purified active component from Hericium erinaceus mycelia—could resolve these limitations and potentially exhibit favorable neuroprotective effects owing to its low molecular weight and lipophilicity. In this study, we investigated the neuroprotective potential and associated signaling alterations of EC using APP/PS1 transgenic mice and Aβ_25-35-induced PC12 cells. In vivo, oral administration of EC alleviated deficits in activities of daily living, as evidenced by improvements in nesting and burrowing behaviors, along with enhanced short-term spatial memory in the Y-maze test. EC treatment was associated with a reduction in hippocampal Aβ plaque accumulation, suppression of glial activation (GFAP and IBA1), and decreased IL-6 levels in both serum and hippocampal tissues. In vitro, EC intervention counteracted Aβ_25-35-induced cytotoxicity in PC12 cells. Analysis of signaling markers revealed that EC treatment was accompanied by a restoration of p-Akt/Akt levels and a suppression of p-GSK3β (Tyr216) activation. Consequently, EC treatment was correlated with reduced tau hyperphosphorylation, the up-regulation of the anti-apoptotic protein Bcl-2, and the down-regulation of pro-apoptotic markers including Bax and cleaved-caspase-3, thereby lowering the total apoptotic rate. Taken together, these findings suggest that EC may mitigate cognitive impairment and neurodegeneration in parallel with alterations in the Akt/GSK3β/tau/caspase-3 signaling response, thereby representing a potentially promising therapeutic candidate for the intervention of AD. Full article

Psoriasis is a chronic, relapsing skin disease driven by failed immune tolerance toward self-antigens and sustained IL-23/IL-17 signaling. Systemic drugs and biologics control disease in many patients, yet they do not restore lasting tolerance, and most patients relapse after treatment withdrawal. Tolerogenic vaccines aim to re-educate the cutaneous immune system: when administered under non-inflammatory conditions, they push antigen-presenting cells toward tolerogenic dendritic cells (tDCs) and regulatory T cells (Tregs) instead of pathogenic effectors. Because the hyperkeratotic stratum corneum of psoriatic plaques blocks macromolecular vaccines, microneedle (MN) arrays can deposit nanocarriers directly into the dermal-epidermal junction. The narrative review asks whether MN-delivered tolerogenic nanovaccines can advance psoriasis therapy beyond broad immunosuppression. We first define tolerogenic vaccination and explicitly distinguish antigen-specific tolerogenic vaccines, antigen-independent immune-reprogramming nanocarriers, and conventional local drug delivery, then survey MN engineering and nanocarrier architectures, the immunomodulatory pathways involved, and translational barriers spanning manufacturing, safety, and regulation. Because most evidence is preclinical, the level of evidence is reported for each platform, and the unresolved autoantigen problem, the limitations of imiquimod-based models, and the need for human-relevant validation are emphasized. Full article

Background/Objectives: This study evaluated the metabolic effects of empagliflozin, an SGLT2 inhibitor (SGLT2i), in type 2 diabetes patients. Methods: In an observational cohort study, 42 patients received empagliflozin for 1 month, with serum and urine analyzed for IL-6, NT-proBNP, iron metabolism markers, and electrolytes. Another group was treated for 3 months, assessing lipoprotein and glycoprotein profiles, IL-6, and NT-proBNP. Results: Empagliflozin increased serum magnesium (mean difference = 0.26 ± 0.38 mg/dL, p < 0.0001), hemoglobin (mean difference = 0.45 ± 0.78 g/dL, p = 0.0005), and hematocrit (mean difference = 1.74 ± 2.08%, p < 0.0001), while decreasing ferritin (mean difference = −29.23 ± 51.97 ng/mL) and transferrin saturation (mean difference = −3.65 ± 7.22%). NT-proBNP and IL-6 levels trended lower (non-significant). Lipoprotein profiling showed a neutral effect. Conclusions: Empagliflozin positively affected serum magnesium, iron metabolism, and inflammatory markers without altering lipoprotein profiles. Further research is needed to elucidate SGLT2i’s molecular mechanisms underlying their pleiotropic–cardioprotective effects. Full article

Allergic asthma is characterized by Th2-driven airway inflammation. Indoleamine 2,3-dioxygenase (IDO) maintains immune tolerance, but its role in modulating the anti-inflammatory actions of Curcumin (CN) is unclear. This study investigated whether CN retains efficacy in a rat model of Ovalbumin (OVA)-induced airway inflammation under pharmacological IDO inhibition. Rats were sensitized and challenged with OVA and treated with methylprednisolone (MP, 15 mg/kg), CN (200 mg/kg), the IDO inhibitor 1-MT (70 mg/kg), or CN+1-MT. Assessments included systemic and pulmonary leukocyte profile, delayed-type hypersensitivity (DTH), OVA-specific IgE, bronchoalveolar lavage fluid (BALF) inflammatory cells and nitric oxide (NO) levels, lung wet/dry weight ratio, gene expression of tumor necrosis factor alpha (TNF-α), interleukin (IL)-4, IL-6, Cxcr2 and transcription factor Nfkb1 and lung histopathology. CN alone or combined with 1-MT normalized leukocyte counts, suppressed eosinophilic and neutrophilic infiltration, restored BALF NO levels, reduced DTH response and OVA-specific IgE, decreased pulmonary edema, and preserved pulmonary vascular integrity. CN significantly attenuated TNF-α, IL-4, IL-6, and Cxcr2 gene expression despite pharmacological IDO inhibition. Histopathology revealed reduced inflammatory infiltration and maintained alveolar structure. CN maintains anti-inflammatory, immunomodulatory and tissue-protective efficacy in allergic airway inflammation despite pharmacological IDO inhibition. These findings call for future research on CN as a potential adjunctive therapy method for inflammatory airway diseases. However, to elucidate the underlying processes, more research on IDO activity and downstream immunometabolic pathways is needed. Full article

Background/Objectives: Thrombotic cardiovascular diseases remain a major cause of morbidity and mortality worldwide. Current antithrombotic therapies are limited by insufficient thrombus targeting. This study aimed to develop a fibrin-binding peptide-functionalized, hydrogen peroxide (H₂O₂)-responsive polymeric micelle and to evaluate its physicochemical properties and biological effects under H₂O₂-induced endothelial oxidative stress and preliminary FeCl₃-induced thrombosis conditions. Methods: A fibrin-binding peptide, P2 (VTFIKC), was screened using computer-aided drug design and evaluated through microscale thermophoresis and in vitro thrombus adhesion assays. An all-trans retinoic acid (atRA)-based boronate ester prodrug, BORA, was synthesized to enable H₂O₂-triggered degradation and drug release. BORA was co-assembled with P2-modified Mal-PEG-b-PAsp to prepare P2-Mal-PEG-b-PAsp/BORA micelles. Their physicochemical properties, H₂O₂ responsiveness, H₂O₂-scavenging activity, cytocompatibility, cytoprotective effects, anti-inflammatory activity, and preliminary in vivo efficacy were evaluated. Results: The resulting micelles exhibited a suitable nanoscale size, acceptable cytocompatibility, H₂O₂-responsive changes in particle size distribution, and concentration-dependent H₂O₂-scavenging activity. In H₂O₂-stimulated human umbilical vein endothelial cells, micelle treatment was associated with improved cell viability, lower intracellular ROS-associated fluorescence, and reduced TNF-α and IL-1β concentrations. In a FeCl₃-induced rat carotid artery thrombosis model, P2-Mal-PEG-b-PAsp/BORA micelles altered platelet- and leukocyte-related hematological indices and exhibited preferential accumulation in the thrombotic carotid artery. Conclusions: P2-Mal-PEG-b-PAsp/BORA micelles combine P2-mediated fibrin-binding potential, H₂O₂-responsive release behavior, and H₂O₂-scavenging activity. The findings provide preliminary support for further investigation of this peptide-functionalized nanoplatform. Full article

Background: Prostate cancer (PC) is a heterogeneous disease in which the histopathological grade does not always reflect underlying biological behavior. While transcriptomic studies have provided insight into tumor biology, grade-associated molecular changes remain incompletely defined, particularly in underrepresented populations such as those from the Middle East and North Africa (MENA) region. Methods: In this study, we used a pathology-guided transcriptomic approach to examine gene expression patterns across PC grades in a MENA cohort. RNA sequencing was performed on formalin-fixed paraffin-embedded (FFPE) tissues, including benign prostatic hyperplasia (BPH, n = 7), low-grade tumors (Gleason 6–7 [3 + 4]; LG; n = 7), and high-grade tumors (Gleason 7 [4 + 3]–10; HG; n = 7). Differential expressions, pathway-level enrichment analyses and the estimation of immune cell composition were carried out, followed by comparison with publicly available datasets (TCGA-PRAD, n = 496), including LG tumors (n = 292) and HG tumors (n = 204), using the GEPIA2 and UALCAN platforms. Selected genes were further assessed using qRT-PCR in an independent set of samples (n = 21). Representative immunohistochemical images from the Human Protein Atlas were reviewed to provide descriptive protein-level context across tumor grades. Results: Transcriptomic comparisons of tumor samples with benign controls identified a set of shared transcriptional changes present in both low- and high-grade disease. Among these, SLC29A2 and IL2RA showed consistent upregulation across tumor grades and similar expression trends in external datasets. Direct comparison between HG and LG tumors revealed distinct transcriptional profiles with patterns indicative of increased proliferative activity and altered immune-related signaling in higher-grade disease. Pathway-level analyses showed the enrichment of cell-cycle and metabolic gene signatures in HG tumors, whereas inflammatory and NF-κB-associated transcriptional signatures showed a comparatively reduced expression. Additional genes, including AAMDC, ASAH2, TNFRSF1B, NFKBIL1, and NFKBIZ, were associated with these grade-dependent differences. qRT-PCR findings were generally consistent with the RNA-seq results for selected targets. Conclusions: This study describes transcriptional patterns associated with the PC grade in a MENA cohort using a pathology-guided framework. The findings highlight candidate genes associated with tumor presence and grade progression and provide a foundation for further investigation in larger, well-annotated cohorts, particularly in populations that remain underrepresented in transcriptomic studies. Full article

Diosmin, a flavonoid, is widely used to alleviate the symptoms of chronic venous disease (CVD), while compression stockings remain a key component of its conservative management. This study used an ex vivo model of human skin explants to evaluate the vasomotor and anti-inflammatory effects of a class II elastic venous compression model (EVC2), applied alone or in combination with diosmetin-3-O-β-D-glucuronide (DT), the major circulating metabolite of diosmin. The explants were exposed to substance P to induce neurogenic inflammation, after which they were treated with EVC2, DT at a concentration of 2700 pg/mL, or both. Compared with substance P alone, all treatments led to a significant reduction in capillary dilation and IL-8 secretion, as well as a change in endothelial CD34 expression. While the combination improved all parameters, only significant additional effects were observed for reducing low CD34 expression versus DT alone (77% for score 0, no CD34 expression, p = 0.043; 62.1% for score 1, low CD34 expression, p = 0.013), and for decreasing IL-8 versus EVC2 alone (41.2%, p = 0.033). These findings suggest vasomotor and anti-inflammatory effects of DT and mechanical compression, and highlight their combined effects on inflammatory parameters in CVD. Full article

The aryl hydrocarbon receptor (AHR) and the vitamin D receptor (VDR) were long regarded as independent transcription factors governing distinct physiology—xenobiotic sensing and calcium–vitamin D homeostasis, respectively. AHR, a basic helix–loop–helix/PAS protein, heterodimerizes with ARNT and binds xenobiotic response elements (XREs) to drive cytochrome P450 genes such as CYP1A1; VDR, a nuclear receptor activated by 1,25-dihydroxyvitamin D₃, heterodimerizes with RXR and binds vitamin D response elements (VDREs). Although their genes reside on separate chromosomes (AHR, Chr 7; VDR, Chr 12), an integrated view recognizes the two pathways as extensively cross-regulatory. This review synthesizes the molecular, immunological, and tissue-level evidence for VDR–AHR interplay. At the molecular level, the receptors cooperate at composite promoter architectures—most notably an everted-repeat VDRE positioned adjacent to an XRE in the CYP1A1 promoter—while AHR ligands reciprocally enhance CYP24A1-mediated catabolism of active vitamin D. Tryptophan metabolism provides a bidirectional hub: kynurenine and the UVB photoproduct FICZ serve as endogenous AHR ligands whose balance, modulated by VDR, shapes signaling output. The tumor suppressor p53 functions as a shared upstream regulator coupling genotoxic stress to both receptors, with convergence on the CDKN1A (p21) checkpoint. Functionally, AHR and VDR converge on the regulatory T cell (Treg)/Th17 axis to influence immune tolerance: sustained AHR activation by TCDD favors Foxp3⁺ Treg differentiation, transient FICZ-driven activation promotes Th17 responses, and VDR reinforces the tolerogenic arm while independently repressing IL-17. The receptors further cooperate in maintaining intestinal epithelial barrier integrity and NF-κB restraint, with parallel impairment in inflammatory bowel disease, and are co-activated in skin by solar UVB, which simultaneously generates vitamin D₃ and the AHR ligand FICZ within keratinocytes. In cancer, VDR acts as a tumor suppressor, AHR exhibits context-dependent pro- and anti-tumor roles, and a three-way AHR–VDR–p53 interaction—inverted by mutant p53—forms a critical regulatory node. Throughout, the direction and magnitude of cross-talk prove highly dependent on cell type, ligand identity and kinetics, and species—distinctions often underappreciated in the literature. Clarifying these context-specific determinants is essential for translating AHR–VDR cross-regulation into rational therapies in autoimmunity, mucosal inflammation, dermatology, and oncology. Full article

Background and Objectives: Traditional open anterior cruciate ligament transection (ACLT) surgical models performed through arthrotomy may introduce capsular trauma and postoperative inflammatory responses that can interfere with the interpretation of post-traumatic osteoarthritis (OA). This study aimed to evaluate the feasibility of a minimally invasive, arthroscopic ACLT rabbit model performed entirely under arthroscopic visualization, without arthrotomy, using a 2.4-mm arthroscope and 2.5-mm shaver, and to provide preliminary structural, histological, synovial, and systemic biochemical characterization of the model for future therapeutic testing. Materials and Methods: Bilateral arthroscopic ACLT was performed in three skeletally mature New Zealand rabbits, followed by a supervised 12-week exercise protocol. Joint degeneration was evaluated macroscopically and histopathologically using the standardized Pritzker-Osteoarthritis Research Society International (OARSI) grading system. Collagen matrix remodeling was assessed via Picrosirius Red staining. Local intra-articular catabolism was quantified via Enzyme-Linked Immunosorbent Assay (ELISA) for matrix metallopeptidase 13 (MMP-13) and interleukin-1β (IL-1β) from synovial fluid. Systemic oxidative stress, including lipid peroxidation biomarkers, malondialdehyde (MDA), and nitric oxide (NO), was evaluated in serum. Results: The arthroscopic approach induced osteoarthritic changes, with severity varying across the cohort. Histopathology revealed vertical matrix fissures and disruption of the normal columnar chondrocyte organization, yielding a median comprehensive Pritzker-OARSI score of 6 (range 6–10), with horizontal degradation restricted to stage 2. Synovial fluid analysis demonstrated measurable concentrations of MMP-13 (188.77 ± 93.87 ng/mL) and IL-1β (174.93 ± 95.51 pg/mL). Furthermore, serum oxidative stress parameters at the 12-week endpoint included lipid peroxidation (MDA: 1.01 ± 0.03 nmol/mL) and NO levels (82.72 ± 0.32 µmol/L), presented descriptively in the absence of a comparator group. Conclusions: This study establishes the first multifaceted pathological baseline of a minimally invasive arthroscopic ACLT rabbit model before therapeutic intervention. The arthroscopic ACLT model produced structural cartilage degeneration alongside measurable intra-articular catabolic and systemic oxidative stress changes, establishing a baseline phenotype and a starting point for future therapeutic studies. Full article

Rice husk (RH) is a renewable siliceous lignocellulosic waste providing a unique, greener and less toxic alternative to conventional synthetic polymeric precursors in the production of carbon-based materials for biomedical applications. In this work we studied the porous structure of RH-lignin-based activated carbon produced in the form of honeycomb carbon monoliths and assessed their potential as hemoadsorbents for blood purification in the treatment of patients with serious medical conditions, such as kidney failure and sepsis. To determine their clinical suitability for such an application, the hemocompatibility and cytotoxicity of the monoliths were investigated using the standard ISO guidelines. The monoliths did not cause any changes in the cell viability or cell lysis. High micro/mesoporosity and surface chemistry of the initial monolith-C, N- and P-doped nanostructured carbon honeycomb monoliths were established by low-temperature nitrogen adsorption (LTNA) studies, mercury porosimetry data (MIP), SEM/EDS analysis and FT-IR spectroscopy. The micro-mesoporous, activated carbon-based filtration/adsorbent prototype devices, in the form of three-dimensional (3D) carbon matrix, functionalized with ion-exchange amino- and phosphate groups and encased in polyolefin heat shrink cable sleeve, have been developed with the capacity to remove protein-bound uremic toxins (PBUTs), such us PCS and IS, as well as inflammatory cytokines (IL-6 and IL-8) from human plasma in a flowing model system. The ammoxidized monolith-N, derived from the monolith-C, had the highest removal efficiency (40.05% for PCS, and 28.4% for IL-6). By contrast, phosphorylated monolith-P demonstrated the highest removal efficiency (54.62% for IS, and 54.4% for IL-8), whilst the monolith-C has the lowest removal efficiency for these adsorbates. These results do not correlate with the LTNA and MIP study results, suggesting that the interaction of surface chemical functional groups with the solutes play key roles in the adsorption mechanism. The ion-exchange mechanism of PBUTs and inflammatory cytokine chemisorption by the monoliths, modified with surface N- and P-containing functional groups, has been proposed. Full article

Background/Objectives: Obesity is frequently associated with chronic low-grade inflammation, which contributes to metabolic dysfunction. However, the comparative effects of nutritional supplements on inflammatory biomarkers in adults with overweight or obesity remain unclear. To address this gap, this paper presents a systematic review and network meta-analysis comparing 14 supplementation strategies for their effects on inflammatory biomarkers in this population. Methods: PubMed, Embase, EBSCO, Web of Science, and the Cochrane Library were searched for randomized controlled trials published between January 2000 and January 2026. A frequentist random-effects network meta-analysis was conducted. Effects were reported as mean differences (MDs) with 95% confidence intervals (CIs), and interventions were ranked using the surface under the cumulative ranking curve (SUCRA). The confidence in network estimates was assessed using the Confidence in Network Meta-Analysis (CINeMA) framework. Results: A total of 60 randomized controlled trials were included. Green tea extract (MD = −2.57, 95% CI [−3.99, −1.15]) and curcumin (MD = −1.75, 95% CI [−2.74, −0.76]) both significantly reduced IL-6 levels. Synbiotics (MD = −12.25, 95% CI [−16.7, −7.8]), curcumin (MD = −2.59, 95% CI [−3.83, −1.35]) and probiotics combined with omega-3 (MD = −6.19, 95% CI [−9.12, −3.26]) had a favorable effect on TNF-α. Probiotics combined with omega-3 (MD = −1.74, 95% CI [−3.03, −0.46]), synbiotics (MD = −1.19, 95% CI [−1.85, −0.53]), zinc (MD = −1.18, 95% CI [−2.24, −0.11]), and curcumin (MD = −1.11, 95% CI [−2.14, −0.07]) all reduced CRP levels. Synbiotics (MD = 15.37, 95% CI [12.13, 18.61]) increased adiponectin levels. In contrast, no nutritional supplement significantly reduced leptin levels. Exploratory meta-regression suggested that age, exercise co-interventions, and the proportion of male participants may partly explain heterogeneity in selected outcomes. Conclusions: Nutritional supplements showed biomarker-specific effects. Probiotics combined with omega-3 fatty acids, synbiotics, green tea extract, and curcumin may improve selected inflammatory biomarkers. However, differences in supplement dose, intervention duration, and participant characteristics warrant cautious interpretation and call for further high-quality trials. Full article