BACKGROUND:Antimicrobial resistance (AMR) poses a serious threat to global public health and requires truthful measurement to assess bacterial susceptibility to antibiotics. Mathematical modeling is a useful tool for quantifying and predicting antimicrobial susceptibility and its relationship to other features. METHOD:This study aimed to identify the most appropriate mathematical model for the relationship between Minimum Inhibitory Concentration (MIC) and bacterial susceptibility. The models assessed were the Michaelis-Menten model, the logistic growth model and the logarithmic regression model. To ensure objective and comprehensive comparisons, various statistical indicators were used, including coefficient of determination (R²), Mean Squared Error (MSE), Root Mean Squared Error (RMSE), and the Akaike Information Criterion (AIC). RESULT:The logarithmic regression model provided the best fit to the data. It yielded the highest R² value and the lowest MSE, RMSE and AIC values compared to Michaelis-Menten and logistic growth models. On the other hand, the logistic growth model provided the poorest fit, with the lowest R² and the largest prediction errors. Although the Michaelis-Menten model outperformed the logistic growth model, the logarithmic regression model consistently achieved lower error metrics and provided a more accurate and informative representation of the relationship between MIC and bacterial susceptibility. DISCUSSION:The logarithmic regression model performed best; thus, this model is appropriate for modeling antimicrobial susceptibility data. The findings indicate that mathematical modeling is important in AST and has the potential to become a powerful predictive tool in the fight against antibiotic resistance. CONCLUSION:The logarithmic regression is the strongest and most valid model for describing the relationship between MIC and bacterial susceptibility, and it can be useful for interpreting and predicting antimicrobial susceptibility data.
Background: Abnormal lipid metabolism plays a crucial role in diabetic foot ulcers (DFU). This study aims to systematically uncover the cell-specific mechanisms of lipid metabolism disorders in DFUs and screen for potential diagnostic biomarkers. Methods: Bulk and single-cell transcriptomic data related to DFUs were integrated from the GEO database. Key cell types were identified through single-cell analysis, and candidate genes were screened by combining differential expression analysis with a lipid metabolism gene set. Random forest analysis, Elastic Net regression, and expression validation were subsequently performed to identify core genes, followed by the construction and validation of a nomogram model. The biological functions of the identified core genes were further investigated using immune infiltration analysis, cell subset analysis, pseudotemporal trajectory inference, and molecular docking. Results: Single-cell analysis identified macrophages as key cells in DFU, yielding 19 lipid metabolism-related candidate genes, with CCL3 and ADAP2 ultimately confirmed as core genes. The nomogram model based on these two genes exhibited good predictive performance (AUC=0.909). Macrophages were classified into three functionally heterogeneous subsets (Macro_ADAP2⁷, Macro_CCL3⁷, and Macro_IGKC⁷), and pseudotemporal analysis revealed their dynamic evolution from inflammation to metabolic regulation. Molecular docking suggested that Wortmannin and BX-471 could stably bind to ADAP2 and CCL3, respectively. Discussion: This single-cell study uncovers a central role for disordered macrophage lipid metabolism in DFU. Heterogeneous expression of CCL3 and ADAP2 defines functional macrophage subsets, linking lipid abnormalities to immune dysfunction and yielding a high-value diagnostic model with drug-target potential for precision interventions Conclusion: This study provides new insights into elucidating the immunometabolic regulatory mechanisms of DFU and developing targeted therapies.
Introduction: Many therapeutic agents exhibit limited clinical effectiveness due to their poor bioavailability, rapid systemic clearance, and short plasma half-life, which eventually reduce patient compliance. To address these challenges, long-circulating drug delivery systems have been introduced to prolong drug presence in the bloodstream, enhance pharmacokinetic stability, and improve therapeutic outcomes. Methods: This narrative review was conducted through a structured literature search of the Scopus database using the keywords “long-circulating AND drug formulation” and “long-circulating AND nanoparticles,” focusing on articles published between 2000 and 2024. Results: This review offers a comprehensive overview of current strategies to extend drug circulation time, including PEGylation, lipidation, nucleic acid modification, and fusion technologies involving Fc and Human Serum Albumin (HSA). Additionally, the emerging cell-mediated biomimetic approaches that utilize natural biological mechanisms for targeted and sustained drug release are discussed. Furthermore, advanced formulation systems such as microencapsulation, nanocrystal suspensions, multivesicular liposomes, and biomineralization-based nanocarriers are assessed in terms of their design principles, preparation techniques, and mechanisms of controlled drug release. Discussion: These findings highlight the growing importance of rational design in longcirculating drug delivery systems, where modifications at the molecular and formulation levels can significantly influence pharmacokinetic behaviour. The shift from conventional modification strategies toward biomimetic and hybrid systems reflects an evolving focus on achieving more precise and biologically responsive drug delivery. Conclusion: Long-circulating drug delivery systems play a vital role in overcoming pharmacokinetic limitations, enhancing drug stability, and improving therapeutic efficacy. Continued advancements in formulation strategies and emerging technologies are expected to further support the development of safer, more effective, and patient-friendly precision therapeutics.
Objective: This study aimed to investigate the antidepressant mechanism of isorhamnetin based on the common targets and signaling pathways shared by depression and type 2 diabetes mellitus. Method: The targets and mechanisms of isorhamnetin's action on depression were investigated by network pharmacology and molecular docking experiments, combined with 100 ns molecular dynamics simulation to verify the binding stability, and the effects of the related mechanisms were verified at the animal level, including Western blot analysis of p-GSK-3β phosphorylation. Result: The results showed that isorhamnetin could act on 80 potential targets and participate in the regulation of 198 related signaling pathways in the treatment of depression. It exerted potential antidepressant effects by improving glucose metabolism disorders in mice and regulating the signaling pathways comorbid with depression and diabetes. Discussion: An in-depth topological analysis demonstrated that isorhamnetin exhibited the highest degree of interaction. Direct inhibition of depression proteins by isorhamnetin and GSK-3β was validated using reverse docking validation. The effect of isorhamnetin on diabetic mice showed that isorhamnetin inhibits the activity of dipeptidyl peptidase-4 in a dose-dependent manner, promoting the secretion of glucagon-like peptide-1, and then inhibiting the activity of GSK- 3β, which contributes to the lowering of blood glucose while activating the PI3K/AKT signaling pathway, triggering a cascade reaction that subsequently regulates the expression profiles of depression- associated targets in the downstream signaling pathway. Data obtained via molecular docking experiments demonstrated that isorhamnetin binds to GSK-3β in the vicinity of its catalytic region, thereby blocking the binding of GSK-3β to its target substrate. Conclusion: This study elucidated the mechanism by which isorhamnetin exerts potential antidepressant effects by regulating the common targets and signaling pathways of depression and diabetes, and provided a theoretical basis for its clinical application.
INTRODUCTION:Silver Nanoparticles (AgNPs) can be used as antimicrobial agents. Most chemical methods used to prepare AgNPs involve toxic and hazardous materials. Fortunately, "green nanotechnology" is considered safe, environmentally friendly, rapid, viable, scalable, and cost-effective. This method uses microorganisms or plant extracts to fabricate AgNPs. Androcymbium palaestinum is reported to be a rich source of phenethyisoquinoline alkaloids that can be used to prepare AgNPs. The major aim of this work is to prepare AgNPs using the methanolic extract of the corms of A. palaestinum. The prepared nanoparticles were expected to be influenced by different experimental variables and to exhibit antibacterial activity against resistant bacterial strains. METHODS:The methanolic extract of the corms of A. palaestinum was used for the green synthesis of Silver Nanoparticles (AgNPs-AP). The effects of pH and the concentration of the inorganic precursor, AgNO3, on the synthesis of nanoparticles were investigated. The particle size, dispersity, and surface charge of AgNPs-AP were determined. The formation of nanoparticles was confirmed using UV-Vis, XRD, FTIR, and SEM. RESULTS:The results showed that AgNPs-AP were formed only in alkaline media. Increasing the concentration of AgNO3 decreased the sizes of the NPs, lowered their charge, and enhanced their uniformity. SEM images showed spherical and well-dispersed nanoparticles. The antibacterial activity of the AgNPs-AP was assessed by determining the Minimum Bactericidal Concentration (MBC) for resistant strains of Escherichia coli and Staphylococcus aureus. Both strains were sensitive to AgNPs-AP. DISCUSSION:These observations highlight how green synthesis conditions strongly influence nanoparticle quality and biological performance. The behavior of AgNPs-AP suggests that A. palaestinum extract provides effective reducing and stabilizing agents, enabling environmentally friendly production of functional antimicrobial nanoparticles. CONCLUSION:Using A. palaestinum extract to prepare AgNPs-AP as described in this work is eco-friendly and can be used in the future to prepare an antimicrobial agent that affects resistant bacteria.
Introduction: Chemotherapy-induced alopecia (CIA) is a common and distressing side effect of cancer therapy. Phenylephrine hydrochloride can reduce follicular exposure to chemotherapeutic drugs through localized vasoconstriction, but its topical effectiveness is limited by poor skin penetration. Invasomal nanocarriers provide an efficient platform for enhancing dermal delivery and sustaining local drug action Methods: A rotatable three-level two-factor Central Composite Design (CCD) was employed to optimize invasomal formulations. The optimized invasomal dispersion was formulated using lipoid 80, and D-limonene was incorporated into a Carbopol-based hydrogel for sustained drug release. Formulations were characterized for vesicular morphology, zeta potential, drug entrapment, in vitro drug release, and ex vivo permeation studies using goat skin. Statistical models were validated using ANOVA. Results: The optimized formulation exhibited a vesicle size of 162 ± 1.8 (nm), EE% of 63.09 ± 3.2 %, and a steady-state flux of 0.6251 µg/cm²/h—over fivefold higher than the conventional gel. Optimization was performed using a Central Composite Design based on phospholipid and terpene concentrations. The invasomal gel exhibited significantly higher cumulative drug permeation (59.34 ± 2.34%) compared to the conventional gel (19.97 ± 0.86%) (p < 0.005), confirming enhanced dermal delivery. Drug release followed a Higuchi diffusion model, indicating controlled and sustained release for deeper dermal penetration. Discussion: The results compellingly demonstrate that the phenylephrine-loaded invasomal gel markedly outperforms conventional formulations by achieving superior dermal penetration and sustained drug release. This optimized nanocarrier system presents a transformative, non-invasive strategy for combating chemotherapy-induced alopecia. Conclusion: The developed phenylephrine-loaded invasomal gel demonstrated superior drug penetration and sustained release, suggesting its potential as a novel, non-invasive strategy for chemotherapy-induced alopecia management. Future studies should focus on in vivo validation and long-term stability assessments for clinical translation.
Introduction: To establish a universal method based on LC-MS for the structural characterization of mAbs. This method includes determining the intact molecular weight, deglycosylated intact molecular weight, reduced molecular weight, and deglycosylated-reduced molecular weight of mAbs, along with peptide mapping (amino acid sequence coverage) and glycan profiling. Methods: LC-MS analysis was performed using mAb injections as test samples. A MAbPac™ RP column was coupled to intact mass spectrometry for molecular weight measurement. For peptide mapping, trypsin-digested samples were analyzed using an ACQUITY UPLC Peptide CSH C18 column with tandem mass spectrometry (MS/MS) to assess amino acid sequence coverage. Glycan profiling was performed using an ACQUITY UPLC Glycan BEH Amide column, with 2-ABlabeled glycans analyzed via secondary mass spectrometry. Results: For bevacizumab (three manufacturers), sintilimab, and camrelizumab, the intact molecular weight, deglycosylated molecular weight, reduced molecular weight, and deglycosylatedreduced molecular weight of mAbs showed errors of less than 10 ppm when compared with theoretical sequences, confirming consistency with theoretical values. Peptide mapping demonstrated that the amino acid sequence coverage of bevacizumab and sintilimab matched the theoretical sequences. Glycan profiling identified distinct glycan profiles for the tested mAbs. Discussion: A universal LC-MS-based method was developed for comprehensive structural characterization of monoclonal antibodies, including molecular weight, peptide mapping (sequence coverage), and glycan profiling. The method is efficient, straightforward, and validated across three mAb therapeutics, providing reliable support for the development and analysis of mAbbased therapeutics. Conclusion: This method allows companies to directly apply it to quality control. It has been validated with several target biologics, demonstrating its versatility and general applicability.
INTRODUCTION/OBJECTIVE:CDS1 is a phospholipid-metabolism enzyme with potential value as a biomarker for immune checkpoint blockade response across cancers. We evaluated the pan-cancer prognostic, immune, and functional significance of CDS1 in tumor progression and immunotherapy stratification. METHODS:We integrated multi-omics data from TCGA, GTEx, and cBioPortal across more than 10,000 samples to assess CDS1 expression, survival outcomes, immune correlations, genomic alterations, and immune checkpoint blockade responses. Functional validation was performed in cervical squamous cell carcinoma (CESC) using HeLa and SiHa cells after CDS1 overexpression. RESULTS:High CDS1 expression was associated with favorable outcomes in PD-L1-targeted therapy, including atezolizumab (HR 0.62), and showed similar benefit across nivolumab (HR 0.65) and pembrolizumab (HR 0.71) in seven clinical cohorts totaling 2,847 patients. CDS1 explained 42% of response variance, outperforming tumor mutation burden (28%). In contrast, high CDS1 was associated with resistance to CTLA-4 therapy, including ipilimumab (HR 1.28, p = 0.03). CDS1 correlated with CD8+ T-cell infiltration (r = 0.64), CXCL9/CXCL10 expression (r = 0.52- 0.67), and TNFRSF9 (r = 0.42). In CESC, CDS1 was top-ranked by stage/grade correlation (r = 0.71), and its overexpression induced a 4.8-fold increase in invasion (p < 0.0001). DISCUSSION:These findings suggest that CDS1 links phospholipid metabolism to immune regulation, membrane remodeling, and tumor aggressiveness. Its associations with immune infiltration and differential checkpoint response indicate that CDS1 may help explain immunotherapy outcomes across cancer types. CONCLUSION:CDS1 emerges as a phospholipid-based biomarker for identifying patients likely to benefit from PD-L1 therapy while predicting CTLA-4 resistance.
The increasing occurrence of pharmaceuticals and other bioactive contaminants in aquatic environments has raised significant concern due to their potential toxicological effects, continuous human exposure, and implications for public health. These compounds, including drug residues, metabolites, and biologically active pollutants, often persist at trace concentrations that challenge conventional analytical methodologies commonly used in medicinal and pharmaceutical chemistry. Biosensor-based analytical strategies have emerged as powerful tools for the detection and quantification of pharmaceuticals and bioactive compounds in complex aqueous matrices, offering high sensitivity, molecular selectivity, reduced analysis time, and the potential for decentralized monitoring. By integrating biological recognition elements with physicochemical transducers, biosensors enable the detection of compounds of medicinal relevance while providing insights into bioavailability, toxicity, and exposure pathways. From a pharmaceutical biotechnology perspective, biosensor platforms based on enzymes, whole cells, nucleic acids, and nanostructured transducers represent scalable analytical tools that complement conventional methods used in pharmaceutical analysis and exposure assessment. This review critically examines recent advances in biosensor technologies applied to the detection of pharmaceuticals and bioactive contaminants in water, with particular emphasis on electrochemical, surface plasmon resonance, whole-cell, bacterial, DNA-based, and microarray biosensing platforms. Attention is given to analytical performance parameters, target analytes of pharmacological relevance, and the suitability of different biosensing approaches for complex aqueous matrices. Selected examples from Mexican research are discussed as a case study illustrating contributions to current analytical challenges. Finally, current limitations and future perspectives are addressed, highlighting the role of biosensor-based strategies as complementary analytical tools in pharmaceutical biotechnology, medicinal chemistry, and toxicological assessment.
Huntington's disease [HD] is a progressive, autosomal dominant neurodegenerative disorder caused by a pathogenic CAG repeat expansion in the HTT gene, resulting in mutant huntingtin [mHTT] protein accumulation, neuronal dysfunction, and selective neurodegeneration. Current pharmacological management remains largely symptomatic, with no approved therapies capable of modifying disease progression. In recent years, however, significant advances in molecular neuroscience and translational medicine have accelerated the development of disease-modifying strategies targeting the underlying pathogenic mechanisms of HD. This review synthesizes emerging pharmacological therapies with a particular focus on insights derived from recent and ongoing clinical trials. Key therapeutic approaches discussed include gene-silencing technologies such as antisense oligonucleotides, RNA interference, and CRISPRCas9- based strategies, as well as small-molecule modulators targeting mutant huntingtin aggregation, proteostasis, autophagy, mitochondrial dysfunction, and neuroinflammation. In addition, advances in symptomatic treatments addressing motor, cognitive, and psychiatric manifestations are reviewed. The article critically examines translational challenges encountered in clinical development, including blood-brain barrier penetration, allele selectivity, dosing paradigms, patient heterogeneity, biomarker integration, and ethical considerations associated with irreversible genetic interventions. Lessons learned from both successful and failed trials highlight the importance of precision medicine approaches, biomarker-guided trial designs, and combination therapies targeting multiple pathogenic pathways. Collectively, this review provides an updated and clinically relevant overview of the evolving HD therapeutic landscape and outlines key considerations for translating molecular advances into effective and safe pharmacological interventions.
Delta hepatitis, caused by the Hepatitis Delta Virus (HDV), is considered a satellite virus as it uses proteins from the hepatitis B virus for its assembly and release. Currently, serological and molecular tests are available for the diagnosis of HDV, with limitations such as standardization, for molecular tests, a short detection window in the acute phase, and the formation of antigen-antibody complexes during the chronic phase, for serological tests, which can cause variability in sensitivity and specificity values. Furthermore, molecular tests are more expensive and require specialized infrastructure as compared to serological tests. Due to these limitations, studies focused on the development of diagnostic tests are crucial, and the commercialization of these tests would help fill existing gaps in the detection and management of the disease. However, despite the severity of the disease and the limitations of diagnostic tests, publications, such as articles and patents using serological diagnosis, are scarce. Literature reviews are fundamental for disseminating information, describing advances related to the topic and its difficulties, and fostering academic and commercial interest among researchers. Therefore, the objective of this review is to explore patent databases for serological diagnostic technologies for HDV infection. The results identified only nine patents related to serological diagnosis. Most of these patents showed promising results, achieving a sensitivity and specificity above 90%. However, the small number of registered patents highlights the need for greater investment and partnerships to boost research, validate technologies, and facilitate the commercialization of tests.
INTRODUCTION:Fulvic acid (FA) is a mineral-based traditional Chinese medicine, which is commonly used to treat gastrointestinal diseases. The aim of this study is to investigate the protective effects of FA against 5-FU-induced intestinal injury in vivo and elucidate its potential mechanisms. METHODS:Mice are randomly divided into 8 groups, including a control group, a model group, PPI treated group (omeprazolea, positive drug), LPDA treated group (loperamidean, positive drug), and four doses (25 mg/kg, 50 mg/kg, 100 mg/kg, 150 mg/kg) of FA treated groups (FA-25, FA- 50, FA-100, FA-150). Histopathological examinations were carried out to assess the protective impact of FA. Transcriptome sequencing, qPCR (quantitative PCR), and western blot analyses were conducted to explore the mechanism of FA. RESULTS:Intragastric administration of 5 g/kg FA did not cause acute toxicity in mice. Histopathological examination of the mouse small intestine showed that FA-treated groups had improved morphology. Transcriptome sequencing revealed 69 DEGs that were significantly different between the FA-treated group and the model group. KEGG pathway analysis revealed that these genes were predominantly associated with the cytokine-cytokine receptor interaction pathway. qPCR validation confirmed the expression profiles of crucial differentially expressed genes, specifically Csf3r, Csf2rb, and Csf2rb2. Western blot analysis confirmed the Csf3r and Csf2rb protein expression results. DISCUSSION:This study suggests that FA protects against 5-FU-induced intestinal injury and is associated with upregulation of granulocyte-related gene expression. CONCLUSION:These observations suggest that FA has a protective effect against 5-FU-induced intestinal injury. However, these findings are still preclinical, and their therapeutic potential remains to be further validated in large-animal models and human cell-based systems.
Introduction/Objective: Bone regeneration plays a critical role in the treatment of maxillofacial and musculoskeletal diseases by restoring lost or damaged bone tissue to support function and structural integrity. In this systematic review, we aimed to investigate the effects and mechanisms of Resveratrol (RSV) Nanoparticles (NPs) on bone regeneration in bone diseases and maxillofacial surgery. Methods: This study followed the PRISMA 2020 guidelines. A comprehensive search on PubMed/MEDLINE, Scopus, Web of Science (WOS), Embase, and the Cochrane Library was conducted for studies published before July 2, 2025. Data extraction was conducted for the included studies, and the results were reviewed. Results: RSV-NPs upregulated key osteogenic markers, including Runt-Related Transcription Factor 2 (Runx2), Alkaline Phosphatase (ALP), Osteocalcin (OCN), Osteopontin (OPN), Type I Collagen (Col-I), Bone Morphogenetic Protein-2 (BMP-2), and Insulin-Like Growth Factor-2 (IGF-2), and increased ALP activity, calcium deposition, and extracellular matrix mineralization. It promoted human bone marrow proliferation and induced osteoblast-like morphology. RSV-NPs reduced pro-inflammatory cytokines and Reactive Oxygen Species (ROS). Additionally, RSVNPs demonstrated anti-senescence and mitochondrial-protective effects. It also enhanced bone defect healing, increased Bone Volume Fraction (BV/TV) and Bone Mineral Density (BMD), promoted neovascularization, and synchronized scaffold degradation with new bone formation. Discussion: RSV-NPs enhance bone regeneration. These results align with previous evidence supporting nanoparticle-mediated drug delivery. However, limitations include a lack of standardized formulation techniques and limited clinical translation to date. Further research should prioritize toxicity profiling, scalability, and clinical trials. Conclusion: RSV-NPs show promise for bone regeneration, offering more effective, targeted treatment with reasonable safety and low cytotoxicity.
In the originally published article [1], a phrase was unclear, which may have affected readability. This has now been revised to improve clarity and ensure that the intended meaning is accurately conveyed. The corrections do not affect the results, interpretations, or conclusions of the article. The original article can be found online at: https://www.eurekaselect.com/article/138842 Details of the error and its correction are provided below: ORIGINAL: Abstract: Treatment of hepatic diseases presents a significant challenge due to their diverse nature. Ginsenosides, bioactive compounds derived from the root of Panax ginseng and widely used in traditional Chinese medicine, offer multifaceted protection to various organs in the body. Their versatile effects, including antioxidant, anti-inflammatory, anti-apoptotic and more, make them a promising approach for addressing hepatic disorders. This review explores the intricate molecular mechanisms and properties of ginsenosides in the prevention and treatment of liver ailments, from mild conditions to severe damage and liver fibrosis. Given the increasing prevalence of hepatic disorders, this article sheds light on the significant pharmaceutical potential of ginsenosides in the realm of hepatic disease management. CORRECTED: Abstract: Treatment of hepatic diseases presents a significant challenge due to their diverse nature. Ginsenosides, bioactive compounds derived from the root of Panax ginseng and widely used in traditional Chinese medicine, offer multifaceted protection to various organs in the body. Their versatile effects, including antioxidant, anti-inflammatory, anti-apoptotic and more, make them a promising approach for addressing hepatic disorders. This review explores the intricate molecular mechanisms and properties of ginsenosides in the prevention and treatment of liver diseases, from mild conditions to severe damage and liver fibrosis. Given the increasing prevalence of hepatic disorders, this article sheds light on the significant pharmaceutical potential of ginsenosides in the realm of hepatic disease management. ORIGINAL: Ginsenosides refer to a collection of bioactive substances discovered in the root of Panax ginseng, a medicinal plant that has been employed in traditional Chinese medicine for many centuries [8]. The medicinal properties of ginseng have been extensively documented in the fields of the central nervous, cardiovascular, endocrine, and immune systems. Furthermore, it exhibits anti-cancer, anti-stress, and antioxidant properties [9, 10]. Even the protective effects of ginseng against coronavirus disease 2019 (COVID-19) have been recently reported [11]. The positive impacts of ginseng can be credited to its diverse array of pharmacologically active constituents; however, the majority of its pharmacological benefits are linked to ginsenosides [12]. Studies have extensively explored the hepatoprotective properties of ginsenosides, ranging from mild to severe liver damage with various etiologies and liver fibrosis. In this review, we provide a summary of the present knowledge and recent advancements regarding the effects of ginsenosides in mitigating various liver ailments. CORRECTED: Ginsenosides refer to a collection of bioactive substances discovered in the root of Panax ginseng, a medicinal plant that has been employed in traditional Chinese medicine for many centuries [8]. The medicinal properties of ginseng have been extensively documented in the fields of the central nervous, cardiovascular, endocrine, and immune systems. Furthermore, it exhibits anti-cancer, anti-stress, and antioxidant properties [9, 10]. Even the protective effects of ginseng against coronavirus disease 2019 (COVID-19) have been recently reported [11]. The positive impacts of ginseng can be credited to its diverse array of pharmacologically active constituents; however, the majority of its pharmacological benefits are linked to ginsenosides [12]. Studies have extensively explored the hepatoprotective properties of ginsenosides, ranging from mild to severe liver damage with various etiologies and liver fibrosis. In this review, we provide a summary of the present knowledge and recent advancements regarding the effects of ginsenosides in mitigating various liver diseases. The publishers apologize for any inconvenience caused.
The liver is a vital organ in the human body, responsible for multiple functions, including immunity, digestion, detoxification, and vitamin storage. Liver diseases cause approximately 2 million deaths annually, accounting for 4% of global mortality, making it a worldwide health challenge. The NAD⁷-dependent deacetylase SIRT6 plays a crucial role in key physiological and pathological processes of liver diseases. With an emphasis on its regulatory mechanisms in lipid metabolism, inflammatory responses, oxidative stress, and various liver diseases, this review summarizes the multifaceted role of SIRT6 in hepatic physiology and pathology. SIRT6 maintains hepatic lipid homeostasis and regulates hepatic inflammation and oxidative stress via multiple signaling pathways, thereby alleviating liver diseases such as liver fibrosis, NAFLD, and liver cancer. The study also discusses how natural and chemical activators, such as MDL- 800 and diosgenin, can activate SIRT6 or upregulate its expression, thereby improving liver damage. Consequently, SIRT6 represents a promising therapeutic target for the development of novel strategies against liver disorders.
Introduction: The rise of antibiotic-resistant bacteria poses a significant threat to healthcare systems, warranting the development of novel antibiotics with enhanced efficacy. Methodology: In this study, silver nanorods (AgNR) were synthesized for the first time using a Callistemon viminalis leaf extract and evaluated for their DPPH antioxidant property and antibacterial properties against gentamicin-resistant Escherichia coli. Results: The synthesis success of AgNR was confirmed by UV-Vis spectroscopy, as evidenced by a clear LSPR peak at 466 nm. X-ray diffraction analysis validated the crystalline form of metallic AgNR. Meanwhile, TEM analysis revealed that the silver nanomaterials were rectangular nanorods with an average size of 85 nm. Fourier transform infrared analysis confirmed the presence of carboxylic acids, alkanes, alkenes, aromatic compounds, alkyl and aryl functional groups on the surface of silver nanorods (AgNR) with efficient antioxidant property. The bandgap energy calculated from the Tauc plot was 2.0 eV. Antimicrobial analysis revealed that E. coli demonstrated resistance to gentamicin, even at concentrations 125 and 1250 times those recommended by the Swedish Reference Group on Antibiotics (SRGA) and Clinical Laboratory Standards Institute (CLSI), respectively. Similarly, 0.1% m/V AgNR exhibited zones of inhibition measuring 17 mm and 18 mm, respectively, at 125 and 1250 times higher than the standard concentration, confirming E. coli is susceptible but exhibiting resistance behaviour. Under Ultraviolet-A (UVA) irradiation, the photocatalytic antibacterial activity of AgNR was substantially higher than the standard value of 2, demonstrating ≥99% reduction in bacterial viability. Discussions: Biogenic AgNR is suitable for antibacterial activities and photocatalysis activities, which are important in the future to combat bacterial resistant problems. Conclusion: This indicates that UVA irradiation significantly enhanced the antibacterial properties of AgNR. The external UVA irradiation promotes electron excitation and transfer from the valence to the conduction band, leading to the inactivation of E. coli. Therefore, the antimicrobial activity of biogenic AgNR amplified by UVA irradiation presents a potent and sustainable approach for combating gentamicin-resistant E. coli.
Introduction: Antibiotic resistance that has been found among pathogenic bacteria has propelled the development of alternative antimicrobial agents. This study explores the antimicrobial properties of Terminalia catappa L. (Indian almond) leaf extracts as a natural antimicrobial agent in aquaculture, focusing on their effects on pathogenic bacteria and their ability to support beneficial nitrifying bacteria in recirculating aquaculture systems (RAS). Methods: Different extracts (Methanol, Ethanol and Aqueous) of T. catappa leaves were prepared and subjected to phytochemical analysis, revealing the presence of alkaloids, flavonoids, phenols, tannins, and terpenoids. The agar well diffusion test, Minimum inhibitory concentration (MIC), and Minimum bactericidal concentration test were used to determine antibacterial efficacy against pathogenic bacteria (Aeromonas caviae, A. veronii) and nitrifying bacteria (Rhodococcus rhodochrous, Bacillus oceanisediminis). Results: The in vitro antibacterial assay results indicate that methanolic extracts at 25-250 mg/ml may inhibit pathogenic bacteria, but were less effective than other extracts against nitrifying bacteria. Electron microscopy (Field-Emission Scanning Electron Microscopy (FE-SEM) and Transmission Electron Microscopy (TEM)) was used to visualise structural damage in bacterial cells, including membrane rupture and cytoplasmic leakage, particularly in pathogenic strains. Discussion: The methanol extract of Terminalia catappa leaves was found to have strong antibacterial activity, which could be attributed to the fact that it contained higher levels of phenolics, flavonoids, and other bioactive phytochemicals than aqueous extracts. The extract was more active in inhibiting pathogenic bacteria, with a relatively weaker effect on nitrifying bacteria, suggesting a selective antibacterial action in vitro. Future research should focus on in vivo validation and dose optimisation. Conclusion: The present study has shown that, in vitro, the extracts of Terminalia catappa leaves exhibit different antibacterial activity, with high levels of inhibition against pathogenic bacterial strains, compared with the action of selected heterotrophic nitrifying bacteria. Such findings provide preliminary data on selective antibacterial activity. However, the results are limited to in vitro confirmation and require in vivo validation before proceeding to further applications in aquaculture.
The advancement of targeted cancer therapy has driven the exploration of cancer-associated miRNA modulation to achieve specific therapeutic outcomes. Despite similarities to other oligonucleotide therapeutics, miRNA-based approaches present unique challenges due to the biological complexity, including rapid degradation, poor tumour tissue penetration, and potential immunotoxicity. To address this limitation, numerous chemical modifications and advanced nanodelivery strategies have been developed and evaluated across preclinical and clinical settings. Overall, while significant progress has been made, optimising stability, delivery efficiency, and safety remain critical to fully realise the clinical potential of miRNA-based cancer therapeutics.
The introduction of individualized biochemical profiles is allowing to revolutionize modern medicinal chemistry by providing more comprehensive data for the development of drugs, their refinement and clinical application. Conventional methods frequently underestimate inter-individual variability, resulting in inferior efficacy or adverse reactions. This new approach highlights the importance of personalized biochemical signatures in moulding pharmacokinetics and pharmacodynamics of drug candidates in accordance with the genomic variations, epigenetic alterations, and interaction of the host with its microbiome. The said parameters influence the absorption, distribution, metabolism, and excretion (ADME), forcing a re-evaluating the classical drug designing model. Individualized biochemical profiling will be fuelled by the combined impact of pharmacogenomics, high-throughput screening, and quantitative structure-activity relationship (QSAR) models, enabling the improvement of drug candidates better suited to an individual's metabolic and enzymatic ranges. This approach will notably help in predicting druginduced liver injury (DILI) and other organ-specific toxicities, allowing improved safety with novel treatments before clinical trials. In addition, individualized biochemical data can also enhance the accuracy of nanocarrier-based drug delivery systems by combining enzyme and receptor expression patterns, resulting in better tissue targeting and fewer off-target effects. This narrative review was conducted through a structured search of peer-reviewed literature from leading scientific databases, with emphasis on recent and translationally relevant studies. The article aims to explore how the amalgamation of these three fields (metabolomics, targeted nanotechnology, and machine learning) has the potential to reshape clinical interventions and allow researchers to refine drug reactions at the individual level.
