Search Results (2,392)

Lectins are glycan-binding proteins involved in diverse biological processes and have gained attention for their potential applications in biotechnology and immunomodulation. BOL (Brassica oleracea lectin) is a unique ~34 kDa lectin isolated from Brassica oleracea var. botrytis, composed exclusively of TRAF-like domains, where TRAF stands for tumor necrosis factor receptor–associated factor. To overcome the limitations of plant-based extraction, we aimed to produce recombinant BOL in Escherichia coli. Various strains and expression vectors were tested under distinct induction conditions to optimize solubility and yield. While expression using pET28a was unsuccessful, GST-tagged BOL was efficiently expressed in E. coli BL21-R3-pRARE2(DE3) and purified using affinity chromatography. Functional assays demonstrated that the recombinant protein retained lectin activity, as evidenced by hemagglutination of goat erythrocytes. Protein identity was confirmed by MALDI-TOF/TOF mass spectrometry, with tryptic peptides matching the BOL lectin sequence in the National Center for Biotechnology Information (NCBI) database. Our findings highlight the importance of codon optimization, temperature modulation, and fusion tag selection for the successful expression of eukaryotic lectins in E. coli. This work provides a platform for future functional studies of BOL and supports its potential application in plant immunity and biomedical research. Full article

Background and Objectives: Systemic inflammatory markers from an ordinary complete blood count (CBC) may foreshadow where non-small-cell lung cancer (NSCLC) will first spread, but organ-specific signatures remain poorly defined. Materials and Methods: We retrospectively reviewed 302 adults (mean age 60.7 ± 13.4 years; 80.8% men) with stage IV NSCLC managed at OncoHelp Medical Center, Timișoara, between January 2022 and December 2024. Eligibility demanded a single radiologically confirmed distant site at diagnosis and pre-treatment CBC. Neutrophil-to-lymphocyte (NLR), platelet-to-lymphocyte (PLR), and lymphocyte-to-monocyte (LMR) ratios were compared across pleural (n = 52), bone (n = 86), liver (n = 66), and brain (n = 98) metastases using Kruskal–Wallis tests with Bonferroni adjustment; z-standardized logistic models identified independent predictors. Results: Metastases clustered most often in brain (32.5%), followed by bone (28.5%), liver (21.9%), and pleura (17.2%). Median PLR rose selectively in pleural disease (274 vs. 217–253 in other sites; p = 0.006). LMR fell to 2.0 in bone but climbed to 2.8 in brain lesions (p = 0.032 and 0.008, respectively). NLR was globally elevated (6.7–7.6), yet differed significantly only for bone and liver deposits. Logistic modeling showed that each standard-deviation rise in absolute neutrophil count quadrupled the odds of hepatic involvement (Odd Ratio (OR) 4.26; 99% Confidence inerval (CI) 2.20–6.25), monocytosis nearly doubled bone risk (OR 1.83; 1.01–3.33), while higher erythrocytes, eosinophils, and lymphocytes independently protected against pleural seeding (all p < 0.01). Age-stratified analysis revealed that osseous and cerebral metastases predominated in patients ≤ 50 years, whereas inflammatory indices were age-invariant. Conclusions: Routine CBC ratios encode distinct “inflammatory fingerprints” that mirror the first metastatic destination in NSCLC: platelets herald pleural spread, neutrophils favor liver and bone, and divergent lymphocyte–monocyte balances separate bone from brain. Although no substitute for cross-sectional imaging, these low-cost markers could refine clinical suspicion, guide targeted work-up, and illuminate the biology of organ-selective dissemination, particularly in resource-limited settings. Full article

The associations between sialylated anti-cyclic citrullinated peptide (anti-CCP) antibodies bearing α-2,6-sialic acid (SIA), ST6Gal1 and Neu1 enzymes, and clinical disease activity measures such as disease activity score 28 (DAS28), the Simplified Disease Activity Index (SDAI), and Clinical Disease Activity Index (CDAI) are unknown in rheumatoid arthritis (RA). To address this gap, this study included 97 patients with RA evaluated at baseline (month 0) and at 6 and 12 months. At each visit, blood cells were analyzed for B-cell ST6Gal1 and Neu1 expressions, and plasma samples were assessed for ST6Gal1 and Neu1 levels. The erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), monocyte chemotactic protein-1 (MCP-1), and IgG anti-CCP with its α-2,6-SIA modification were measured. Disease activity measures, namely DAS28-ESR, DAS28-CRP, DAS28-MCP-1, SDAI, and CDAI, were calculated. Correlations and Receiver Operating Characteristics among ST6Gal, Neu1, SIA/anti-CCP ratios, and disease activity measures were assessed. Multivariate regression analyses were performed to reveal confounding factors in such correlations. The total SIA content of anti-CCP antibodies was inversely correlated with B-cell Neu1 levels (ρ = −0.317 with p = 0.013. Plasma (free-form) Neu1 levels were inversely correlated with SIA/IgG anti-CCP ratios (ρ = −0.361, p = 0.001) in the DAS28-MCP-1 < 2.2 (remission) subgroup. No such correlation was observed for the DAS28-ESR, DAS28-CRP, SDAI, or CDAI subgroups. B-cell ST6Gal1 levels correlated inversely with SDAI ≤ 11 and DAS28-MCP-1 ≤ 3.6 combined remission and low-disease-activity subgroups (ρ = −0.315 with p = 0.001 and ρ = −0.237 with p = 0.008, respectively). The same was observed for B-cell ST6Gal1/Neu1 ratios correlating with the SDAI ≤ 11 subgroup (ρ = −0.261, p = 0.009). Nevertheless, B-cell ST6Gal1/Neu1 ratios against SDAI ≤ 11 and DAS28-MCP-1 ≤ 3.6 subgroups produced significant area-under-curve (AUC) values of 0.616 and 0.600, respectively (asymptotic p-Values 0.004 and 0.018, respectively). Through multivariate regression analyses, we found that biologics (a confounding factor) interfered with p-Values related to the B-cell ST6Gal1 enzyme but did not interfere with p-Values related to the pure B-cell Neu1 enzyme. In addition, disease duration interfered with p-Values related to the pure Neu1 enzyme on B-cells or in plasma. Moreover, plasma ST6Gal1/Neu1 ratios against the DAS28-MCP-1 < 2.2 remission subgroup produced an AUC of 0.628 and asymptotic p = 0.003. Therefore, it is suggested that B-cell ST6Gal1/Neu1 ratios can be used as clinical indicators for the combined remission and low-disease-activity subgroup of SDAI and DAS28-MCP-1 formulae. Plasma ST6Gal1/Neu1 ratios are also good indicators of DAS28-MCP-1 remission. Full article

Alcohol Use Disorder (AUD) poses global health challenges, and causes hematological alterations such as macrocytosis and oxidative stress. Disruption of protein structures by alcohol and/or its metabolites may exacerbate AUDs; proteomics can elucidate the underlying biological mechanisms. This study examined the proteins differentially expressed in the cytosol and membrane fractions of erythrocytes obtained from 30 male patients with AUD, comparing them to samples from 15 age- and BMI-matched social drinkers (SDs) and 15 non-drinkers (control). The analysis aimed to identify the molecular differences related to alcohol consumption. The AUD patient subgrouping was based on mean corpuscular volume (MCV), with 16 individuals classified as having a normal MCV and 14 having a high MCV. Proteins were separated via two-dimensional(2D)-gel electrophoresis, digested with trypsin, and identified via Matrix-Assisted Laser Desorption/Ionization Time-of-Flight (TOF) mass spectrometry (MALDI-TOF/TOF). Additionally, levels of malondialdehyde and 4-hydroxyalkenals (MDA + HAE), reduced glutathione (GSH), oxidized glutathione (GSSG), serum carbohydrate-deficient transferrin (%CDT), disialotransferrin (%DST), and sialic acid (SA) were analyzed. The results showed increased MDA + HAE and decreased total thiols in AUD patients, with GSSG elevated and the GSH/GSSG ratio reduced in the AUD MCV-high subgroup. Serum %CDT, %DST, and SA were significantly higher in AUD. Compared to the control profiles, the AUD group exhibited differential protein expression. Few proteins, such as bisphosphoglycerate mutase, were downregulated in AUD versus control and SD, as well as in the MCV-high AUD subgroup. Conversely, endoplasmin and gelsolin were upregulated in AUD relative to control. Cytoskeletal proteins, including spectrin-alpha chain, actin cytoplasmic 2, were overexpressed in the AUD group and MCV-high AUD subgroup. Several proteins, such as 14-3-3 isoforms, alpha-synuclein, translation initiation factors, heat shock proteins, and others, were upregulated in the MCV-high AUD subgroup. Under-expressed proteins in this subgroup include band 3 anion transport protein, bisphosphoglycerate mutase, tropomyosin alpha-3 chain, uroporphyrinogen decarboxylase, and WD repeat-containing protein 1. Our findings highlight the specific changes in protein expression associated with oxidative stress, cytoskeletal alterations, and metabolic dysregulation, specifically in AUD patients with an elevated MCV. Understanding these mechanisms is crucial for developing targeted interventions and identifying biomarkers of alcohol-induced cellular damage. The complex interplay between oxidative stress, membrane composition, and cellular function illustrates how chronic alcohol exposure affects cellular physiology. Full article

Background/Objectives: Patients with erythropoietic protoporphyria (EPP) have a decreased activity of the ferrochelatase enzyme which converts protoporphyrin IX (PpIX) into heme, causing PpIX to accumulate in erythrocytes. The ensuing release of PpIX to the skin when exposed to visible light causes a phototoxic reaction with severe pain, erythema, and edema. Erythrocyte PpIX levels in adult EPP patients are rather stable and largely unaffected by pharmaceutical treatments. It is important to be aware of drugs causing an increase in PpIX as this may increase the risk of liver toxicity. Method: The patient had blood samples taken regularly for analyses of PpIX, znPpIX, ALT, ALP, iron, leucocytes, C-reactive protein, and hemoglobin before, during, and after treatment with teriflunomide. Additionally, we tested if teriflunomide increased PpIX in vitro. Results: A female EPP patient was treated for 7 years with teriflunomide for multiple sclerosis attacks. During treatment, her natural PpIX level increased from about 30 µmol/L to about 200 µmol/L, without significant simultaneous changes in hemoglobin, iron levels, alanine transaminase (ALT), or alkaline phosphatase (ALP). The patient experienced no increase in photosensitivity. In vitro addition of teriflunomide did not affect PpIX levels. Discussion: In patients with lead intoxication, the release of PpIX from erythrocytes is very slow. The increase in PpIX during treatment with teriflunomide compared to periods with no medication could be caused by a similar slow PpIX release from the erythrocytes. This theory is supported by the patient’s unchanged light sensitivity and stable levels of hemoglobin, iron, and liver enzymes. Full article

Significant progress has been made in developing cell-based drug delivery systems that utilize the intrinsic biological properties of various cell types—erythrocytes, leukocytes, platelets, stem cells, and even spermatozoa—to improve drug targeting, bioavailability, and biocompatibility. This review presents an integrative analysis of the latest advances in cell-based drug delivery systems, focusing on their design, pharmacokinetics, cellular interactions, and therapeutic potential. We specifically focus on hybrid microrobots and membrane-coated nanocarriers as emerging biohybrid platforms. Despite these advances, translation to the clinical phase remains constrained by persistent limitations, such as immune clearance, loss of membrane integrity during cargo loading, limited tissue penetration of carrier cells, and manufacturing challenges. Finally, we highlight future directions, including CAR-cell combinations and artificial cell engineering, that promise to expand the clinical utility of cell-based drug delivery systems in oncology, infectious diseases, and regenerative medicine. Full article

In the pursuit of novel anticancer therapies, assessing their selectivity and safety profile towards healthy cells is crucial. This study investigated chlorochalcones, derivatives of 2′-hydroxychalcone containing a chlorine atom, for their impact on human breast cancer cells (MCF-7 and MDA-MB-231), healthy blood cells (erythrocytes, peripheral blood mononuclear cells (PBMCs), platelets), and microvascular endothelial cells (HMEC-1). Our findings demonstrated that chlorochalcones did not detrimentally affect erythrocytes, showing no hemolysis or preserving osmotic resistance and transmembrane potential. They also exhibited minimal impact on normal PBMC viability and varying effects on platelet metabolic activity at therapeutic concentrations. Importantly, these derivatives displayed lower toxicity towards HMEC-1 endothelial cells than towards breast cancer cells, indicating a degree of selectivity. Chlorochalcones have high antiproliferative activity against cancer cells, primarily by inducing apoptosis with virtually no significant impact on cell cycle progression. Their mechanism of action involves the modulation of reactive oxygen species (ROS) levels and induction of mitochondrial dysfunction, including membrane depolarization and reduced mitochondrial mass. Biological activity, including toxicity and ROS modulation, is dependent on the position and number of chlorine atoms. In conclusion, this study highlights the ability of chlorochalcones to effectively target malignant cells while sparing normal circulatory and endothelial cells, thus positioning them as a promising class of candidates for further anticancer drug development. Full article

Stimuli-responsive, cell-mediated drug delivery systems represent a dynamic interface between biological functionality and engineered control. Leveraging the inherent targeting properties of erythrocytes, immune cells, stem cells, and exosomes, these systems offer a promising strategy for precise therapeutic delivery. In this review, we provide a comprehensive analysis of the design principles and biological underpinnings of stimuli-responsive carriers that release payloads in response to endogenous triggers (e.g., pH, redox, enzymatic activity) or external stimuli (e.g., light, ultrasound, magnetic fields). We further examine current strategies for loading and functionalizing cellular carriers, highlight key therapeutic applications across oncology and regenerative medicine, and assess translational progress and regulatory challenges. This review underscores the emerging clinical potential of intelligent cell-based delivery vehicles and outlines future directions for their optimization and implementation. Full article

Background: The phenomenon of pink teeth represents a notable observation in forensic science, although its interpretation remains complex and not directly attributable to a specific cause of death. Methods: This systematic review provides an updated and comprehensive overview of the morphological and histological mechanisms associated with this finding, with a focus on hemoglobin diffusion and pigment accumulation during putrefaction rather than on detailed biochemical pathways. Results: Environmental conditions, especially high humidity and moderate temperatures, are identified as key facilitators. The synthesis of the available evidence, including case reports, observational series, and experimental studies, confirms that pink discoloration is primarily linked to postmortem hemoglobin diffusion following erythrocyte breakdown and release of heme groups into dentinal structures. This process occurs more frequently under conditions that preserve hemoglobin and facilitate its migration into dental tissues. Importantly, pink teeth have been documented across a wide spectrum of postmortem scenarios, such as hanging, drowning, carbon monoxide poisoning, and prolonged exposure to humid environments, indicating that their presence is neither pathognomonic nor exclusively associated with a specific cause of death. Assessment methods include semi-quantitative visual scoring systems (e.g., SPTC and SPTR), spectrophotometric assays, and histochemical analyses for hemoglobin derivatives. Recent advances in digital forensics, particularly micro-computed tomography and artificial intelligence–based segmentation, may further support the objective evaluation of chromatic dental changes. Conclusions: This review underscores the need for standardized approaches to the identification, classification, and analysis, both qualitative and quantitative, of pink teeth in medico-legal practice. Although not diagnostic in isolation, their systematic study enhances our understanding of decomposition processes and contributes supplementary interpretive data in forensic investigations. Full article

Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease characterized by inflammation of the synovial tissue, leading to joint destruction, pain, stiffness, and progressive impairment of motor functions. Despite significant advances in diagnosis and treatment, RA remains a major clinical and social challenge, negatively impacting patients’ quality of life. The aim of this study was to assess the relationship between the expression of selected microRNAs (miRNAs) and the activity of the disease. A total of 46 RA patients and 20 healthy controls (HCs) were enrolled in the study. A quantitative real-time polymerase chain reaction was used to evaluate the expression of miRNAs in whole blood. MiRNA-186 exhibited decreased concentrations in RA patients compared to HCs (p = 0.03). Patients with an active form of the disease (DAS28 > 3.2) exhibited lower expression of miRNA-186 than HCs (p = 0.04). Additionally, ACPA-negative patients also demonstrated reduced miRNA-186 expression compared to controls. AUC analysis confirmed that the combination of miRNA-186, the erythrocyte sedimentation rate (ESR), and Visual Analog Scale—Patient Global Assessment (VAS PGA) may be effective in identifying RA exacerbation. The combination of classical laboratory markers, clinical data, and molecular markers enhances the ability to assess RA exacerbation. MiRNA-186 may be considered a potential marker of disease activity in RA. Full article

The transition period in dairy cows, spanning late pregnancy and early lactation, is associated with substantial metabolic and immunological challenges, leading to increased oxidative stress and inflammation. Selenium (Se), particularly in organic forms, supports antioxidant defenses, immune function, and metabolic regulation. This study investigated the effects of supplementing periparturient Holstein–Friesian cows with orally administered selenitetriglycerides (0.5 mg Se/kg body weight/day starting 12 days before the expected calving date and continuing until parturition) on antioxidant enzyme activity and on the hepatic expression of key inflammatory and metabolic genes. Serum selenium concentrations and erythrocyte glutathione peroxidase (GSH-Px) activity were assessed before and after parturition, and hepatic gene expression levels of tumor necrosis factor alpha (TNF-α), peroxisome proliferator-activated receptor alpha (PPAR-α) and delta (PPAR-δ) were assessed 24 h and 7 days postpartum. Supplemented cows showed significantly elevated serum Se levels and increased GSH-Px activity, reflecting improved antioxidant capacity. Moreover, hepatic expression of TNF-α and PPAR-δ was significantly reduced postpartum in the supplemented group, whereas PPAR-α expression remained stable. These findings indicate that selenitetriglycerides effectively enhance antioxidant defenses, moderate inflammation, and stabilize metabolic pathways during the periparturient phase, potentially reducing postpartum metabolic disorders and improving dairy-cow health. Full article

Background: Experimental studies suggest that some insecticides, fungicides, and herbicides can result in liver cell death, but population-based evidence is lacking. We investigated associations between urinary pesticide metabolites and liver biomarkers among adolescents and adults in an Ecuadorian agricultural area. Methods: We examined participants in 2016 (N = 528, 11–17 years) and 2022 (N = 505, 17–24 years). Plasma alanine aminotransferase (ALT), aspartate aminotransferase, soluble cytokeratin-18, and erythrocytic acetylcholinesterase were measured. Urinary biomarkers included four organophosphates, six neonicotinoids, three pyrethroids, two herbicides, and two fungicides. Generalized estimating equation (GEE) models examined associations and introduced sex and age interaction terms and quadratic terms. Quantile g-computation evaluated the effects of pesticide mixtures. Results: No significant associations were observed between pesticide biomarkers and liver biomarkers in longitudinal or cross-sectional analyses. A curvilinear association was found between 3-phenoxybenzoic acid (3-PBA; pyrethroid) and ALT (β_quadratic = −0.35, 95% CI: [−0.67, −0.04]) in 2016, but not in 2022. Sex modified the associations of 3-PBA with AST, ALT, and CK18-M65 in adolescents (2016), with non-significant positive associations observed in males and non-significant negative associations observed in females. No pesticide mixture effects were observed. Conclusions: Urinary biomarkers of various insecticides, herbicides, fungicides, and their mixtures were not associated with liver biomarkers among adolescents and young adults in agricultural settings. These largely null findings, consistent across time points, suggest background-level exposures in these settings possibly do not harm liver health in this population, though effects at higher exposures cannot be ruled out. Full article

Background/Objectives: Human leukocyte antigen B27 (HLA-B27) is a genetic marker strongly associated with various inflammatory rheumatic diseases, particularly those within the spondyloarthritis spectrum. Its presence influences disease onset, clinical severity, and therapeutic strategies. However, comparative data between HLA-B*27-positive and -negative patients, especially in Eastern European populations, remain limited. The study aimed to investigate the clinical, paraclinical, and psychosocial differences between HLA-B*27-positive and -negative individuals diagnosed with rheumatic diseases, in order to better understand the implications of HLA-B27 status on disease expression and patient quality of life. Methods: A cross-sectional, observational study was conducted between June 2023 and December 2024 at the Emergency Clinical Hospital for Children “Sf Ioan” in Galati, Romania, in collaboration with “Dunarea de Jos” University. Fifty adult patients with various rheumatic conditions were enrolled and stratified into HLA-B*27-positive (n = 22) and -negative (n = 28) groups. Data collection included clinical evaluations, laboratory biomarkers (CRP = C-reactive protein; ESR = erythrocyte sedimentation rate), and a structured quality-of-life questionnaire. Statistical analysis was performed using SPSS v27. Results: HLA-B*27-positive patients were significantly younger (mean age 46.00 vs. 55.07 years, p = 0.018) and had higher CRP levels (>1 mg/dL in 53.33% vs. 0%, p = 0.001). Ankylosing spondylitis was more prevalent in this group (22.73% vs. 3.57%, p = 0.039). Magnetic resonance imaging (MRI) was more frequently used (68.18% vs. 39.29%, p = 0.042), indicating greater suspicion of axial involvement. HLA-B27-positive patients also reported higher perceived stress (mean score 2.41 vs. 1.21, p < 0.001). Conclusions: HLA-B*27 positivity is associated with earlier disease onset, increased systemic inflammation, greater axial involvement, and higher psychological stress. These findings emphasise the need for personalised, multidisciplinary care that integrates both medical and psychological support for HLA-B*27-positive patients. Full article

Background/Objectives: Chronic low-grade inflammation drives cardiometabolic risk; functional SNPs may influence individual cytokine and hematologic phenotypes. We investigated genotype-specific relationships between circulating immuno-inflammatory biomarkers and routine blood indices in apparently healthy adults. Methods: In this cross-sectional study, 155 fasting volunteers (26–72 years) were genotyped for IL1RN rs1149222 and TNF-proximal rs2071645. Serum IL-1β, TNF-α, oxidized LDL (oxLDL) and C-reactive protein (CRP) were quantified by ELISA, and complete blood counts were recorded simultaneously. Genotype effects were tested with ANOVA/Kruskal–Wallis; Spearman correlations and age-, sex-, BMI-adjusted linear models explored genotype-stratified associations. Results: Among 155 adults, IL1RN rs1149222 significantly affected IL-1β (TT > TG ≈ GG; ANOVA p = 0.042) and oxLDL (overall p = 0.036), with the clearest difference between heterozygotes and major-allele homozygotes. The same variant produced a modest fall in erythrocyte count and hemoglobin restricted to heterozygotes (RBC p = 0.036; Hb p = 0.041). TNF-proximal rs2071645 strongly raised TNF-α (GG > GA > AA; p < 0.0001) and led to a moderate oxLDL increase, driven by GA versus AA carriers (pairwise p = 0.013), while leaving red-cell indices and CRP unchanged. Baseline leukocyte counts, differentials and derived ratios showed no genotype dependence, and multivariable models revealed no epistatic interaction between the two loci. Conclusions: IL1RN rs1149222 and TNF-related rs2071645 generate two independent inflammatory signatures—an IL-1β-oxidative axis linked to mild erythropoietic suppression and a TNF-lipid axis without hematologic shift. Integrating targeted genotyping with inexpensive hematologic ratios may refine early risk stratification and guide tailored preventive strategies in ostensibly healthy populations. Full article

Bacterial infection is a cause of life-threatening diseases. The emergence of antimicrobial-resistant bacteria exacerbates this situation, highlighting the need for the discovery of new antimicrobial agents. Our previous study identified a novel antimicrobial peptide, BrSPR20-P1 (P1), which showed potential activity against MRSA. Additionally, silver nanoparticles (AgNPs) exhibit broad-spectrum antibacterial activity, capable of killing multidrug-resistant bacteria. The combination of antimicrobial agents presents a novel strategy for combating these pathogens. This study aimed to evaluate the antibacterial activity of the combination of P1 and AgNPs. It revealed that the combinations showed synergy. The P1 and AgNP mixture at a concentration of 1 and 8 µg/mL (1:8) doubled the activity against S. aureus and MRSA, while that combination of 64 and 64 µg/mL (64:64) exhibited broad-spectrum activity, expanding to E. coli with a 32-fold increase. These combinations exhibited a bactericidal effect, showing the rapid killing of tested bacteria at 10× MIC, with killing rates during the first 3 h ranging from 4.04 ± 0.01 to 4.31 ± 0.03 h⁻¹. The P1 and AgNP mixtures caused a low risk of antibacterial resistance up to 30 passages. It was demonstrated that the synergistic activity of P1 and AgNPs occurred through the disruption of cell walls and membranes, leakage of intracellular materials, and cell lysis. Additionally, the mixtures appeared to interact with bacterial genomic DNA, as indicated by a gel retardation assay. These activities of the combinations were concentration-dependent. The 1:8 µg/mL mixture caused low hemolysis and cytotoxicity and did not impede the wound healing process. In contrast, although the 64:64 µg/mL mixture showed excellent antibacterial efficacy, it was toxic to erythrocytes and mammalian cells. It implies that dose optimization is required to balance its efficacy and toxicity. Therefore, the P1 and AgNP combinations exhibit synergistic antimicrobial activity and have the potential to resolve bacterial infections. Full article