Search Results (4,193)

Background: Chronic kidney disease (CKD) is characterized by persistent inflammation, metabolic dysregulation, and mineral and bone disorder (CKD-MBD), all of which may affect ocular tissues. While retinal manifestations of CKD have been increasingly investigated, data regarding clinical anterior segment modifications and their relationship with systemic biochemical parameters remain limited. Methods: We performed a cross-sectional study including 130 participants: 53 non-CKD subjects, 29 patients undergoing maintenance hemodialysis (HD), and 48 kidney transplant recipients (KTRs). All participants underwent comprehensive ophthalmic examination, including best-corrected visual acuity (BCVA), intraocular pressure (IOP) measurement using Goldmann applanation tonometry, Schirmer I test, tear break-up time (TBUT) and assessment of cataract and blepharitis prevalence. Serum creatinine estimated glomerular filtration rate (eGFR), calcium, phosphate, parathyroid hormone (PTH), magnesium, 25-hydroxyvitamin D, and Activin A were recorded. Associations between ocular and systemic parameters were evaluated using correlation and regression analyses. Results: TBUT, Schirmer I and IOP did not differ significantly among groups (all p > 0.05). After adjustment for age, sex, BMI and diabetes mellitus (DM), HD patients showed worse visual acuity than the non-CKD reference group, reflected by higher logMAR BCVA values (adjusted B = +0.128, p = 0.024). In KTRs, higher corrected calcium was independently associated with reduced tear film parameters, correlating with both shorter TBUT (B = −0.903, p = 0.037) and lower Schirmer I values (B = −5.947, p = 0.008). Circulating Activin A increased progressively from controls to KTR to HD patients (median 189.5 vs. 273.0 vs. 314.0 pg/mL, p < 0.001) but showed no independent association with any anterior segment parameter; it was instead associated with cumulative glucocorticoid exposure (B = +1.602, p = 0.024). Conclusions: In CKD, clinical anterior segment and ocular surface differences were largely explained by age, sex, and comorbidity rather than renal replacement modality, with visual acuity deficit persisting in HD after adjusting for these covariates. At the individual level, corrected calcium was the parameter most consistently associated with tear film parameters in KTRs, whereas elevated Activin A was not independently associated with ocular involvement and likely reflects systemic disease activity. Full article

Hypophosphatasia (HPP) is a rare inherited disorder caused by deficient tissue-nonspecific alkaline phosphatase (TNSALP) activity and classically characterized by impaired mineralization processes, although growing evidence suggests broader systemic involvement beyond bone. This cross-sectional study aimed to characterize circulating levels of osteoglycin and sclerostin in patients with HPP and to explore their relationships with TNSALP activity and systemic clinical–biochemical profiles. This cross-sectional study included 25 genetically confirmed HPP patients and 25 age- and sex-matched controls without cardiovascular disease. Circulating osteoglycin and sclerostin were measured by ELISA, and clinical, metabolic, renal, inflammatory, cardiovascular, and bone-related variables were assessed. HPP patients showed lower osteoglycin and higher sclerostin levels compared with controls. Osteoglycin was mainly associated with ALP activity and mineral-related variables, while sclerostin showed broader associations involving glycemic, inflammatory, renal, and cardiovascular domains. In multivariable analyses, osteoglycin was linked to ALP, renal and inflammatory markers, whereas sclerostin was associated with glycemic, mineral, inflammation, and circulatory markers. Overall, osteoglycin variability appeared mainly driven by mineral-related factors, while sclerostin was more influenced by metabolic and inflammatory domains. In conclusion, HPP is associated with an imbalance in circulating bone-derived proteins, characterized by reduced osteoglycin and increased sclerostin, suggesting systemic alterations in bone-related signaling beyond impaired mineralization. Full article

Background/Objectives: Lung metastasis (LM) is the most common type of extrahepatic metastasis after hepatectomy for hepatocellular carcinoma. However, the predictive factors for LM after hepatectomy for hepatocellular carcinoma remain incompletely characterized. This study aimed to examine the predictive factors for LM after hepatectomy for hepatocellular carcinoma and clarify the association between preoperative biomarkers and LM. Methods: We analyzed data of 644 consecutive patients with hepatocellular carcinoma who underwent primary hepatectomy between July 2003 and December 2023. Patients were divided into two groups: LM (+) and LM (−). Additionally, the association between perioperative factors and LM was investigated. Subsequently, a risk model was developed to predict LM. Results: Of the 644 patients, 43 (6.7%) experienced LM. Regarding biochemical scores, only the proportion of high Controlling Nutritional Status (CONUT) score (≥3) was significantly different (43.9% in the LM (−) group vs. 60.5% in the LM (+) group, p = 0.04). In multivariable analysis, a high CONUT score, tumor size, and microvascular invasion were identified as independent predictive factors for LM. The risk model exhibited accuracy with an area under the curve of 0.93, 0.85, and 0.83 in the 1-, 3-, and 5-year LM, respectively. Conclusions: The present study demonstrated an association between CONUT score and LM after primary hepatectomy for hepatocellular carcinoma and found that a high CONUT score is a complementary predictive factor for LM. Full article

Background: Acute liver failure (ALF) is a rare, yet potentially fatal clinical syndrome characterized by the rapid deterioration of hepatic function in individuals without pre-existing liver disease, typically occurring over a period of days to weeks. It is associated with substantial morbidity and mortality, particularly in low-income settings, and is clinically defined by the presence of jaundice, coagulopathy, and hepatic encephalopathy. Among its various etiologies, acetaminophen (APAP) overdose is the leading cause of drug-induced liver injury and ALF, especially in industrialized countries such as the United States and the United Kingdom. In the present study, we compared two experimental approaches for inducing APAP-mediated ALF in mice: oral and intraperitoneal (IP) administration. Methods: While most studies reported in the literature rely on a single route of administration, this comparative analysis provides a more comprehensive evaluation of the advantages and limitations associated with each method, thereby enhancing the reproducibility and translational relevance of experimental ALF models. Results: Our results demonstrate that both administration routes effectively recapitulate key clinical and biochemical features of human ALF, including hepatic encephalopathy, marked elevations in serum transaminases, and high mortality rates. However, the effective APAP dose required to achieve these outcomes differed between the two routes, with 400 mg/kg for IP administration and 500 mg/kg for oral administration, as would be expected based on pharmacokinetic considerations. From a clinical assessment perspective, the use of adapted scoring systems, such as the O’Grady criteria, is essential for evaluating encephalopathy in animal models. Notably, oral administration via gastric gavage requires greater technical expertise, which may influence experimental consistency. Conclusions: Taken together, these findings underscore the importance of route selection in experimental design and highlight the value of comparative approaches for optimizing preclinical models of ALF. Full article

Ocular ischemic syndrome (OIS) is a vision-threatening disorder characterized by retinal ischemia, oxidative stress, and inflammation. In this study, the protective effects of anakinra, an interleukin-1 receptor antagonist, were investigated and compared with those of tocilizumab, an interleukin-6 receptor antagonist. Twenty-four male Wistar rats were randomly assigned to four groups (n = 6 per group): sham-operated (SG), carotid artery clamping/unclamping (CUG), anakinra-treated carotid artery clamping/unclamping (ACUG), and tocilizumab-treated carotid artery clamping/unclamping (TCUG). An experimental ocular ischemic injury model induced by transient bilateral common carotid artery occlusion was established by transient bilateral common carotid artery clamping followed by reperfusion. Retinal tissues were analyzed for malondialdehyde (MDA), total glutathione (tGSH), superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) levels, and histopathological examinations were performed. OIS markedly increased MDA, TNF-α, IL-1β, and IL-6 levels while significantly decreasing tGSH, SOD, and CAT activities. Both anakinra and tocilizumab attenuated oxidative stress and inflammatory responses; however, anakinra produced notably greater improvements in MDA, tGSH, SOD, and CAT levels. Histopathological evaluation demonstrated that both treatments reduced retinal injury, edema, vascular congestion, and inflammatory cell infiltration. Although retinal architecture appeared slightly better preserved in the anakinra-treated group, histopathological scores were comparable between the treatment groups. These findings suggest that anakinra may attenuate oxidative and inflammatory retinal damage in this experimental ocular ischemic injury model and may provide greater biochemical protection than tocilizumab, whereas histopathological protection was comparable between treatments. Nevertheless, further experimental and clinical studies are required to confirm these findings. Full article

Broodiness is a natural behavior whereby female birds stop laying eggs to sit on and hatch them. This behavior is regulated through genetic, hormonal, and environmental factors. The Taihe Black-Boned Silky Fowl (TBSF), a Chinese traditional domestic breed, exhibits a strong brooding tendency; however, the molecular mechanisms underlying this trait remain unclear. In this study, we performed an integrated multi-omics analysis to characterize differences between two groups of TBSF hens: 8 individuals undergoing 30 days of active brooding (BR30) and 8 individuals in the normal laying egg stage (NB), selected from a total group of 230 hens. We combined 16S rRNA sequencing, untargeted metabolomics, and hepatic transcriptome sequencing, with statistical analyses including QIIME 1.9.1, OPLS-DA (VIP > 1), Student’s t-test (p ≤ 0.05), and DESeq2 (|log₂FC| ≥ 1, FDR < 0.05) for differentially expressed genes (DEGs), respectively, and Pearson’s correlation analysis for multi-omics integration. Phenotypically, brooder hens showed significantly reduced feed intake, body weight, and main digestive tissue indices, alongside altered liver and blood biochemical parameters. Hepatic transcriptome analysis identified 1582 DEGs between groups, enriched in pathways related to fatty acid oxidation and the amino acid degradation pathway. In addition, 16S rRNA sequencing revealed distinct gut microbial community structures: the NB group was enriched in Bacilliota and Pseudomonadota, while the BR30 group was enriched in Spirochaetota and Synergistota. Metabolomic profiling identified a total of 143 differential metabolites, which were enriched in lipid and amino acid metabolites, including alpha-linolenic acid and pyruvate metabolites. Multi-omics correlation analysis revealed tight associations between gut microbial taxa, circulating metabolites, and hepatic gene expression. Specifically, beneficial lipid metabolites, including phospholipids, lysophosphatidylcholines, and sphingomyelins, were positively correlated with Synergistes and the Christensenellaceae R-7, as well as with key hepatic lipid metabolism genes FABP1, LPL, and FADS2. In summary, this study reveals that the gut–liver axis plays a critical part in the modulation of energy metabolism during broodiness, and further highlights new insights into metabolic targets that could optimize reproductive behavior and enhance poultry production. Full article

Ovarian ischemia/reperfusion (I/R) injury is a major cause of tissue damage following the surgical detorsion of ovarian torsion and is characterized by excessive oxidative stress, inflammation, and progressive cellular injury. Although ranolazine has been reported to exert antioxidant and anti-inflammatory effects in various experimental models, its potential protective effects against ovarian I/R injury have not yet been investigated. This study aimed to evaluate whether pretreatment with ranolazine protects ovarian tissue against experimental I/R injury in rats. Twenty-four female Wistar albino rats were randomly assigned to four groups: a healthy group (HG), sham-operated group (SOG), ovarian ischemia/reperfusion (OIR) group, and ranolazine-treated ovarian ischemia/reperfusion (ROIR) group. Ovarian ischemia was induced by 1 h of torsion followed by 6 h of reperfusion. Ranolazine (50 mg/kg) was administered 1 h before the induction of ischemia as a preventive pretreatment. Oxidative stress markers (MDA, tGSH, SOD, and CAT), pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6), histopathological alterations, and the expression of COX-1, COX-2, IL-1β, and IL-6 were evaluated by double immunofluorescence staining. Ovarian I/R significantly increased MDA and pro-inflammatory cytokine levels while markedly decreasing tGSH levels and SOD and CAT activities (p < 0.001). These biochemical alterations were accompanied by severe follicular degeneration, mononuclear cell infiltration, interstitial edema, decreased COX-1 immunoreactivity, and increased expression of COX-2, IL-1β, and IL-6. Ranolazine treatment significantly attenuated oxidative stress and inflammatory responses, preserved the antioxidant defense system, ameliorated histopathological damage, restored COX-1 immunoreactivity, and inhibited the expression of COX-2, IL-1β, and IL-6. This is the first experimental study evaluating ranolazine in ovarian I/R injury. These findings suggest that preventive pretreatment with ranolazine attenuates experimental ovarian I/R injury through antioxidant and anti-inflammatory mechanisms. Future studies are needed to determine whether similar protective effects can be achieved when ranolazine is administered after ovarian torsion or following surgical detorsion. Full article

Extracellular vesicles (EVs) have emerged as fundamental pillars of intercellular communication, acting as primary mediators of the bidirectional biochemical crosstalk within the integrated bone–muscle unit. This review provides a comprehensive synthesis of EV-mediated signaling across the bone–muscle axis, offering a side-by-side mapping of vesicular biogenesis, cargo composition, and functional roles in both tissues. Under physiological conditions, skeletal muscle- and bone-derived EVs orchestrate tissue homeostasis, adaptations to physical exercise, myogenesis, and bone remodeling by transferring unique molecular cargos of proteins and specific microRNAs. However, aging induces a profound remodeling of the EV secretome toward a senescent profile characterized by harmful vesicular factors. This dysfunctional vesicular signaling impairs both muscle regeneration and osteogenesis, directly contributing to the pathogenesis of interconnected age-related disorders like sarcopenia, osteoporosis, and osteosarcopenia. Concurrently, circulating EVs represent valuable, minimally invasive biomarkers for early diagnosis. On the therapeutic front, this review critically evaluates emerging EV-based approaches, utilizing mesenchymal stem cell-derived, bioengineered, or biomaterial-incorporated EVs, offering promising, low-immunogenic alternatives to cell transplantation to enhance musculoskeletal tissue repair and restore bone–muscle homeostasis. Despite persisting technical challenges regarding large-scale production and standardization, targeting or leveraging EV-mediated communication represents one of the most innovative and revolutionary strategies to counteract age-related musculoskeletal decline. By unifying physiological mechanisms, age-related molecular reprogramming, and therapeutic engineering across both muscle and bone into a single narrative, this review provides a comprehensive framework to guide future research and clinical translation in musculoskeletal health. Full article

Congenital hypothyroidism (CH) is a common endocrine disorder characterized by thyroid hormone deficiency and has dramatic consequences if diagnosis and treatment are delayed. Although neonatal screening (NNS) and early levothyroxine (L-T4) treatment have markedly improved neurodevelopmental outcomes, evidence suggests that cardiovascular alterations may persist into later life. Thyroid hormones regulate lipid metabolism, endothelial nitric oxide (NO) availability, myocardial relaxation, vascular tone and arterial wall homeostasis. Early clinical studies in patients with CH reported variable lipid and lipoprotein abnormalities, whereas more recent studies have demonstrated endothelial dysfunction, increased arterial stiffness, and elevated carotid intima–media thickness (IMT), even in the absence of classical cardiovascular risk factors. These alterations appear to be associated with cumulative exposure to thyroid-stimulating hormone (TSH) abnormalities rather than isolated biochemical measurements. These findings suggest that CH may affect cardiovascular biology through multiple pathways, including dyslipidemia, endothelial dysfunction, vascular remodeling, and cumulative exposure to thyroid-stimulating hormone abnormalities. This review summarizes the available evidence linking congenital hypothyroidism to early vascular and atherosclerotic changes and discusses its conceptual relationship to familial hypercholesterolemia as another model of early-life cumulative cardiovascular risk. Full article

The multifractal properties of ion-channel currents recorded from Beta vulgaris L. vacuoles were analyzed using multifractal detrended fluctuation analysis (MFDFA) and the Wavelet Transform Modulus Maxima (WTMM) method. The study covered a range of membrane potentials, different incubation times with indole-3-acetic acid (IAA), and regimes with single and multiple active channels. Clear multifractal behavior was observed, with the spectrum width, $\Delta \alpha$, varying with voltage, biochemical modulation, and channel occupancy. A comparative analysis shows that WTMM provides a more reliable and detailed characterization of the scaling properties. In particular, WTMM yields stronger nonlinearity in the scaling exponents $\tau \left(q\right)$, clearer scaling regimes, and higher sensitivity to variations in $\Delta \alpha$, whereas MFDFA results are affected by deviations from ideal scaling. The presence of multiple channels introduces a structured, non-monotonic dependence of $\Delta \alpha$ on voltage, indicating collective dynamics. These results demonstrate that WTMM is better suited for analyzing nonstationary, dichotomous ion-channel signals. Full article

Identifying physiological changes during the transition period is essential for improving the health and productivity of dairy goats. This study evaluated hematological, biochemical, hormonal, oxidative stress, and molecular alterations in Shami goats during the pre-pregnancy, late pregnancy, and early lactation periods. Eighty clinically healthy goats were examined, and blood samples were analyzed for hematological indices, metabolic and hormonal profiles, oxidative stress biomarkers, and relative expression of genes associated with energy metabolism, antioxidant defense, inflammation, and autophagy. Late pregnancy was characterized by significant (p < 0.05) increases in red blood cell count (RBCs), hemoglobin concentration (Hb), neutrophils, albumin, globulin, urea, insulin-like growth factor-1 (IGF-I), and malondialdehyde (MDA), accompanied by decreased glucose, cholesterol, total protein (TP), antioxidant markers, total leukocyte count, packed cell volume, and monocytes. Early lactation was associated with higher non-esterified fatty acid, triiodothyronine (T3), and thyroxine (T4) levels. Genes involved in lipid mobilization and oxidation, ketogenesis, inflammation, cellular stress, and autophagy; sirtuin 1 (SIRT1), peroxisome proliferator-activated receptor alpha (PPARA), carnitine palmitoyltransferase 1a (CPT1A), 3-hydroxy-3-methylglutaryl-coenzyme a synthase 2 (HMGCS2), cluster of differentiation 36 (CD36), lipase E (LIPE), protein kinase amp-activated catalytic subunit alpha 1 (PRKAA1), solute carrier family 2 member 1 (SLC2A1), haptoglobin (HP), interleukin 6 (IL6), heat shock protein 70 (HSP70), heme oxygenase 1 (HMOX1), beclin 1 (BECN1), and autophagy-related protein 5 (ATG5) were significantly upregulated, whereas antioxidant- and glucose transport-related genes nuclear factor erythroid 2-related factor 2 (Nrf2), glutathione peroxidase 1 (GPX1), catalase (CAT), thioredoxin (TXN), and solute carrier family 2 member 4 (SLC2A4) were downregulated during the transition period. The results indicate well-orchestrated metabolic and molecular adaptations that can be employed as biological indicators to track the physiological status of Shami goats. These findings fulfilled the study objective and identified potential biomarkers of the transition period in Shami goats. Full article

Non-communicable diseases (NCDs), including type 2 diabetes mellitus (DM), hypertension (HTA), obesity (OB), and cardiovascular disease (CVD), represent a major global health burden and disproportionately affect socially vulnerable populations. Small extracellular vesicles (EVs) are stable carriers of proteins and regulatory RNAs that may reflect endothelial dysfunction and cardiometabolic stress. This study explored plasma-derived EV-associated biomarkers in adults from La Guajira, Colombia, with emphasis on miR-126-3p, miR-21-5p, miR-92a-3p, and SNAIL. Anthropometric, clinical, and biochemical data were obtained from a cross-sectional cohort. Representative plasma samples were selected for EVs isolation by size-exclusion chromatography. Vesicles were characterized by nanoparticle tracking analysis, scanning transmission electron microscopy, protein quantification, Western blotting, and bead-based flow cytometry. Candidate miRNAs were identified by small RNA sequencing and validated by stem-loop RT-qPCR. Bioinformatic enrichment analyses were performed using miRNet 2.0 and KEGG pathway analysis. The epidemiological cohort showed a high cardiometabolic burden, with waist-to-height ratio (WHtR) and triglyceride-glucose (TyG) index emerging as key markers of central adiposity and metabolic dysfunction. Plasma-derived EVs displayed the expected nanoscale morphology and expressed canonical vesicle markers. Protein cargo analyses revealed EMT- and remodeling-associated proteins, including SNAIL and GAL-3. EV-associated miR-126-3p, miR-21-5p, and miR-92a-3p were enriched predominantly in hypertensive and hypertensive-diabetic groups. In an exploratory sub-cohort, CD31-positive EVs showed a trend toward increased expression in individuals with previous myocardial infarction or stroke (p = 0.057). KEGG enrichment analysis linked the identified miRNA signature to pathways involved in endothelial dysfunction, inflammation, vascular remodeling, apoptosis, and extracellular matrix organization. Plasma-derived EVs from individuals with cardiometabolic disorders carry molecular signatures consistent with endothelial stress and vascular remodeling. These findings identify miR-126-3p, miR-21-5p, miR-92a-3p, SNAIL, and CD31-positive EVs as exploratory candidate biomarkers that require validation in larger prospective cohorts. Full article

The LW-9 peptide was previously identified through screening of purified molecules from the venom of the spider Phoneutria nigriventer and has been described as an immunomodulatory compound with potential application in cancer therapy. The molecule was biochemically characterized and subjected to in silico analyses to evaluate its toxicity and efficacy profiles. LW-9 exhibits a molecular mass of 1235.522 Da and the amino acid sequence PyrKKDRFLGLM-CONH₂. Secondary and tertiary structures were modeled using computational approaches. The results indicated low permeability across biological membranes, including the blood–brain barrier. In silico predictions further suggested that LW-9 is neither carcinogenic nor mutagenic; however, it may act as a potent inhibitor of the CYP3A4 enzyme, raising concerns regarding potential drug–drug interactions. Overall, LW-9 shows promise as an immunomodulatory agent for cancer applications, while its pharmacokinetic properties and possible interactions with other drugs continue to be investigated. Full article

Background and Clinical Significance: Endoscopic ureterocele incision is the preferred initial treatment for ureteroceles associated with duplex collecting systems due to its capability for rapid decompression via a minimally invasive technique with generally favorable outcomes among pediatric patients. However, the postoperative trajectory in children with solitary functioning renal units remains inadequately characterized. We present a severe, yet reversible, case of postrenal acute kidney injury (AKI) following endoscopic ureterocele incision in an infant with a contralateral multicystic dysplastic kidney (MCDK). This case emphasizes the pathophysiological implications of failed ureterocele decompression and the vital importance of rigorous postoperative monitoring. Case Presentation: A female infant with a right MCDK and a left duplex collecting system featuring an upper pole ureterocele underwent transurethral endoscopic incision due to progressive hydronephrosis. Within 24 h following surgery, the patient exhibited oliguria, oedema, worsening hydronephrosis, hyponatremia (125 mmol/L), metabolic acidosis, and increasing serum creatinine levels, indicative of postrenal AKI. Arterial blood gas analyses indicated severe renal-driven metabolic acidosis with bicarbonate levels of 13.9 mmol/L, accompanied by respiratory compensation and normal lactate levels. Imaging studies revealed deteriorating hydronephrosis of the upper and lower poles of the left kidney. Emergency open nephrostomy placement in the lower pole, after failed jj insertion in the lower pole ureteral orifice, resulted in the immediate restoration of urinary drainage and progressive biochemical recovery. The patient required a brief period of intensive care monitoring, followed by hospitalization in pediatric and urological departments. Longitudinal imaging demonstrated persistent but stable upper pole dilatation with preserved parenchyma. Definitive management was later achieved through right nephrectomy of the non-functioning MCDK. Conclusions: In patients with solitary functioning renal units, the endoscopic ureterocele incision may result in postoperative local oedema, potentially leading to clinically significant obstructive AKI. This case underscores the necessity for intensified surveillance and individualized postoperative management strategies in anatomically complex pediatric patients. Full article

Lys49 phospholipase A2 (Lys49-PLA₂) homologues are catalytically inactive snake venom toxins with diverse biological activities, but their functional characterization requires recombinant production strategies to overcome the limitations inherent to native venom-derived proteins. Here, we produced recombinant BaMtx (rBaMtx), a Lys49-PLA₂ homologue from Bothrops atrox, in the Pichia pastoris KM71 expression system and evaluated whether its biochemical and biological properties were preserved. rBaMtx was secreted into the culture medium, purified by cation-exchange chromatography, and characterized by SDS-PAGE, Western blotting, RP-HPLC (85.9% purity), and MALDI-TOF mass spectrometry, confirming a molecular mass of 13,821 Da. Despite lacking PLA₂ activity, rBaMtx retained pronounced myotoxicity in vivo, inducing dose-dependent plasma creatine kinase release and skeletal muscle damage comparable to or greater than native BaMtx. In vitro, rBaMtx reduced viability of murine 4T1 breast carcinoma cells (IC₅₀ = 60.94 µg/mL), altered cell morphology, modestly increased IL-1β release, and produced context-dependent effects in paired human tumor and non-tumor cell models, differing from native BaMtx and crude venom. These findings establish rBaMtx as a reproducible model for investigating the mechanisms and biomedical potential of catalytically inactive Lys49-PLA₂ homologues. Full article