Archives of Advances in Biosciences

Background and Aim: Automated hematology analyzers generate platelet indices and histograms that can provide insight into platelet dynamics. This study evaluates a novel parameter—the pre-peak to post-peak ratio from platelet histograms—and its associations with the percentage of giant platelet, standard platelet indices, and clinical recovery in patients with thrombocytopenia.

Methods: In an observational cohort study, 250 thrombocytopenic patients (platelet count <150,000/μL) were monitored over six days at a tertiary care center. Platelet histograms were analyzed using a 5-part automated hematology analyzer. The pre-peak/post-peak ratio was manually calculated, and its correlations with mean platelet volume (MPV), platelet distribution width (PDW), giant platelet percentage (from peripheral smears), and platelet recovery were assessed.

Results: Hyper-destructive thrombocytopenia predominated (82.4%, n=206), with dengue identified as the leading cause (53.9%). In these cases, giant platelet percentages surged by day 3 (p<0.001), positively correlating with post-peak length and inversely with the ratio. The ratio declined on day 3 and rose on day 6 in 82.4% of recovering patients. In contrast, hypo-productive cases (17.6%, n=44) showed no significant changes or correlations.

Conclusion: The pre-peak to post-peak ratio appears to be a simple and economical prognostic indicator for recovery in hyper-destructive thrombocytopenia, potentially guiding transfusion decisions and monitoring.

Background and Aim: Brain cancer is a leading cause of mortality, posing significant treatment challenges. CircRNAs are emerging as innovative biomarkers and therapeutic targets for various diseases, including cancer. This study evaluates the half-maximal inhibitory concentration (IC50) of Vitamin C, Ag, and TiO2 nanoparticles (NPs) against the GL-261 tumor cell line and their impact on expression of hsa_circ_0001518 in cancerous and healthy mice.

This investigation aims to determine the impact of Vitamin C antioxidants and Ag and TiO2 NPs, individually and in combination, on the gene expression patterns of CircRNAs in brain cancer.

Methods: The GL-261 cell line was cultured and treated with Vitamin C (25, 50, 75, and 100 µg/ml), Ag (11, 24, 42.24, and 65 µg/ml), and TiO2 NPs (5, 7, 10.5, and 17.5 µg/ml). The MTT test was performed to determine cell viability. The expression of investigated circular RNA after treatment with the IC50 of Vitamin C in healthy and brain tumor-bearing mice was assessed by qRT-PCR.

Results: The IC50 values after 48h were 81.25 µg/ml for Vitamin C, 45.47 µg/ml for Ag NPs, and 8.73 µg/ml for TiO2 NPs. qRT-PCR results indicated that the combination of the antioxidant and NP significantly decreased circ0001518 expression in brain tumor-bearing animals more than any single treatment.

Conclusion: The combination of TiO2 and Vitamin C, as well as Ag and Vitamin C, significantly alters the expression of the investigated circ and shows potential as a novel therapeutic approach for brain cancer.

Background and Aim: Breast cancer remains a major cause of cancer mortality in women, and tumor-driven cytokine dysregulation promotes immune escape. This study aimed to define the splenic immunomodulatory activity of BCc1 nanomedicine in 4T1 breast tumor-bearing BALB/c mice by measuring interleukin-12 (IL-12), transforming growth factor-β1 (TGF-β1), and tumor necrosis factor-α (TNF-α), and the (TGF-β1)⁄(IL-12) balance.

Methods: Seventy female mice with palpable tumors received a 24-day regimen of intraperitoneal or oral BCc1, cyclophosphamide, or phosphate-buffered saline (PBS). Splenic cytokines were quantified by ELISA, and the (TGF-β1)⁄(IL-12)   ratio was calculated as an index of cytokine polarization.

Results: BCc1 reshaped splenic cytokine patterns in a dose- and route-dependent manner. High-dose intraperitoneal BCc1 produced the strongest effects, markedly reducing  and , inducing controlled modulation of , and substantially lowering the  ratio. These changes indicate reduced immunoregulatory dominance and a shift toward an antitumor-permissive cytokine milieu. For several cytokine endpoints, high-dose BCc1 showed effects comparable to or greater than cyclophosphamide. Oral BCc1 elicited milder dose-dependent responses, with stronger immunomodulation at the higher oral dose.

Conclusion: BCc1 therefore mediates route- and dose-dependent splenic cytokine remodeling, supporting further evaluation as a multifunctional immunomodulatory nanotherapeutic; cellular phenotyping and functional antitumor assays are required to determine whether these cytokine shifts translate into immune-mediated tumor control

Background and Aim: Breast cancer remains a major cause of cancer mortality in women, and tumor-driven cytokine dysregulation promotes immune escape. This study aimed to define the splenic immunomodulatory activity of BCc1 nanomedicine in 4T1 breast tumor-bearing BALB/c mice by measuring interleukin-12 (IL-12), transforming growth factor-β1 (TGF-β1), and tumor necrosis factor-α (TNF-α), and the (TGF-β1)⁄(IL-12) balance.

Methods: Seventy female mice with palpable tumors received a 24-day regimen of intraperitoneal or oral BCc1, cyclophosphamide, or phosphate-buffered saline (PBS). Splenic cytokines were quantified by ELISA, and the (TGF-β1)⁄(IL-12)   ratio was calculated as an index of cytokine polarization.

Results: BCc1 reshaped splenic cytokine patterns in a dose- and route-dependent manner. High-dose intraperitoneal BCc1 produced the strongest effects, markedly reducing  and , inducing controlled modulation of , and substantially lowering the  ratio. These changes indicate reduced immunoregulatory dominance and a shift toward an antitumor-permissive cytokine milieu. For several cytokine endpoints, high-dose BCc1 showed effects comparable to or greater than cyclophosphamide. Oral BCc1 elicited milder dose-dependent responses, with stronger immunomodulation at the higher oral dose.

Conclusion: BCc1 therefore mediates route- and dose-dependent splenic cytokine remodeling, supporting further evaluation as a multifunctional immunomodulatory nanotherapeutic; cellular phenotyping and functional antitumor assays are required to determine whether these cytokine shifts translate into immune-mediated tumor control

Background and Aim: Hepatocellular carcinoma (HCC) is an aggressive malignancy with limited response to conventional immunotherapies. Multi-epitope vaccines targeting multiple tumor-associated antigens (TAAs) such as alpha-fetoprotein (AFP), glypican-3 (GPC3), and telomerase reverse transcriptase (TERT) offer a promising strategy to overcome immune evasion. However, peptide-based vaccines suffer from rapid degradation and poor delivery to antigen-presenting cells. This study aimed to develop a nanoliposomal vaccine encapsulating a bioinformatics-designed merged multi-epitope peptide derived from AFP, GPC3, and TERT, and evaluate its ability to modulate inflammatory gene expression in the spleen of immunized mice.

Methods: A merged peptide (PGLPDSALDINECLRGKKKDGARGGPPEAFTTSVRKKKKPEGLSPNLNRFLGDR) was designed using IEDB and NetMHCpan servers. Cationic nanoliposomes (DPPC:cholesterol:DSPE-PEG2000, 55:40:5 molar ratio) were prepared by thin-film hydration. Size, zeta potential, and peptide loading were characterized by DLS and BCA assay. Female BALB/c mice (n=24) were divided into four groups: PBS control, empty liposome, free peptide, and NLME vaccine. After three subcutaneous immunizations, splenic expression of IFN-γ, TNF-α, IL-6, IL-1β, and IL-10 was measured by qRT-PCR.

Results: Nanoliposomes exhibited mean size of 105±12 nm, zeta potential of +30.4±2.1 mV, and peptide loading efficiency of 89.4±3.2%. NLME vaccination significantly upregulated IFN-γ (5.67-fold, p<0.01), TNF-α (4.23-fold, p<0.01), IL-1β (2.98-fold, p<0.01), and IL-6 (2.12-fold, p<0.05), while downregulating IL-10 (0.42-fold, p<0.01) compared to controls.

Conclusion: The NLME vaccine induces a robust Th1-polarized inflammatory response in the spleen with high pro-inflammatory cytokine expression and suppressed IL-10, supporting its potential as an effective immunotherapy for HCC.

Background and Aim: Acinetobacter baumannii is a major nosocomial pathogen associated with multidrug resistance, limiting therapeutic options in hospital settings. This study aimed to investigate antimicrobial susceptibility patterns and the co-occurrence of resistance to aminoglycosides and fluoroquinolones among clinical isolates of A. baumannii recovered from a tertiary hospital in Shahroud, Iran.

Methods: In this descriptive cross-sectional study, six non-duplicate clinical isolates of A. baumannii were collected from hospitalized patients. Species identification was confirmed by phenotypic methods and PCR detection of the intrinsic blaOXA-51-like gene. Antimicrobial susceptibility testing was performed using the Kirby–Bauer disk diffusion method and interpreted according to CLSI M100 (2024) guidelines. Data were analyzed descriptively, and hierarchical clustering was used for exploratory visualization of resistance patterns.

Results: All isolates (6/6, 100%) were classified as multidrug-resistant (MDR), and two isolates (2/6, 33.3%) met the criteria for extensively drug-resistant (XDR). All isolates (6/6, 100%) were resistant to ciprofloxacin. High resistance rates were observed among aminoglycosides, including amikacin (5/6, 83.3%), gentamicin (5/6, 83.3%), and tobramycin (5/6, 83.3%). Resistance to ceftazidime was observed in 5/6 isolates (83.3%), while resistance rates for cefepime, piperacillin–tazobactam, and ampicillin–sulbactam were 3/6 (50.0%) each. Resistance to carbapenems was detected in 4/6 isolates (66.7%) for meropenem and 3/6 (50.0%) for imipenem. Concurrent resistance to fluoroquinolones and aminoglycosides was observed across all isolates, indicating co-occurrence of resistance phenotypes.

Conclusion: The present study demonstrates a high burden of multidrug resistance and frequent co-occurrence of resistance to aminoglycosides and fluoroquinolones among clinical isolates of A. baumannii. These findings highlight the need for continued regional antimicrobial resistance surveillance and strengthened infection control strategies.

Background and Aim: Haemolytic anaemia has been the bane of several blood borne diseases like malaria, and it appears intractable especially in endemic areas like the tropics and developing economies. It is characterized by decreased red blood cells, severe haemoglobinuria, jaundice, and high mortality rates in young subjects without prompt medical intervention. The potential ability of several nutraceuticals and plant extracts is being investigated as affordable haematinic in the management of the condition in different models of anaemia. Chlorogenic acid (CGA) is a phytonutrient with therapeutic capacities. This study is designed to investigate the haematinic property of chlorogenic acid, a plant-based polyphenol widely distributed in the diet, using Phenylhydrazine-induced haemolytic anaemia model in mice.

Methods: Fifty-four adult male Swiss mice were used for the study. Forty-eight mice were administered 40 mg/kg dose of phenylhydrazine (PHZ) intraperitoneally twice at 12-hour interval to induce anaemia. Those animals that were confirmed to be anaemic were weight-matched into seven groups  (n = 6/group) as follows: Group I- untreated non-anaemic animals received distilled water only, Group II- PHZ only, Group III- PHZ + ferrous sulphate (2 mg/kg), Group IV- PHZ + CGA (3.75 mg/kg), Group V- PHZ + CGA (7.5 mg/kg), Group VI- PHZ + CGA (15 mg/kg), Group VII- PHZ + CGA (30 mg/kg). The treatment with chlorogenic acid was by oral gavage for 5 consecutive days. On day 6, blood specimens were obtained for haematological parameters. The liver and spleen were also excised, weighed and processed for antioxidant assay, oxidative stress markers and liver function test.

Results: Chlorogenic acid reversed the haemolytic anaemia, reduced oxidative stress and liver damage and elevated bilirubin associated with exposure to phenylhydrazine at doses of 15 and 30 mg/kg.

Conclusion: Chlorogenic acid possesses significant haematinic, antioxidant and hepatoprotective potential at moderate doses.

Background and Aim: 5-Fluorouracil (5-FU) is a widely used anticancer drug but suffers from severe systemic toxicity, short half-life, and low tumor selectivity. Boron nitride nanocages have emerged as promising drug delivery vehicles due to their high biocompatibility and low cytotoxicity. Transition metal doping, particularly with iron, can enhance drug binding affinity through electronic effects.

The purpose of this study was to evaluate the potential of iron-doped boron nitride nanocage (NC Fe) as a nanocarrier for targeted delivery of 5-FU using a multiscale approach combining DFT calculations, experimental adsorption studies, and in vitro cellular/molecular assays.

Methods: DFT calculations at the B3LYP/6 31G(d) level were performed to determine the interaction energy, QTAIM parameters, NBO charge transfer, and HOMO LUMO gap of the FU-NC-Fe complex. Batch adsorption experiments were conducted to optimize pH, contact time, initial drug concentration, and adsorbent dosage. MTT assay, flow cytometry (Annexin V FITC/PI staining), and qRT-PCR (Bax and Bcl-2 expression) were performed on MCF-7 breast cancer cells and normal HFF fibroblasts.

Results: DFT calculations revealed a negative interaction energy of –59.8 kJ/mol with positive ∇²ρ(r) (0.098 a.u.), confirming spontaneous noncovalent binding. Bidirectional charge transfer of 0.29 electrons and an 11.8% reduction in HOMO LUMO gap were observed. Optimal adsorption conditions (pH 7.0, 30 min, 20 mg/L, 0.10 g NC Fe) yielded 76.5% adsorption efficiency. FU-NC-Fe exhibited significantly enhanced cytotoxicity against MCF- 7 cells (IC₅₀ = 8.7 µg/mL) compared to free 5-FU (18.4 µg/mL), with a selectivity index of 4.86. The complex induced 52.7% total apoptosis (vs. 28.4% for free drug) and increased the Bax/Bcl-2 ratio 4.5 fold (21.3 vs. 4.7). Pristine NC-Fe showed excellent biocompatibility (IC₅₀ > 200 µg/mL).

Conclusion: Iron-doped boron nitride nanocage is a highly promising nanocarrier for targeted 5-FU delivery, offering enhanced anticancer efficacy, high cancer cell selectivity, and potent apoptosis induction through the mitochondrial pathway.

Background and Objective: Cancer is a genetically heterogeneous disease and remains one of the leading causes of mortality worldwide. Colorectal cancer (CRC) is the third most common cancer globally and accounts for approximately 38% of gastrointestinal malignancies. It is the most prevalent cancer of the gastrointestinal tract. In men, colorectal cancer ranks third after lung and prostate cancers, while in women it ranks second after breast cancer. The present study aimed to evaluate the expression levels of MUC17 and MUC13 genes in tissue samples from patients with colorectal cancer.

Methods: In this study, tumor tissues and adjacent normal colorectal tissues were analyzed. A total of 30 tumor samples from patients with colorectal cancer and 30 adjacent normal tissue samples were collected from the tumor bank of the Cancer Institute at the Imam Khomeini Hospital Complex from patients undergoing surgical resection. All tissue samples were preserved in liquid nitrogen tanks. After collection, 100 mg of each tissue sample was finely minced using a surgical scalpel and subsequently homogenized using a tissue homogenizer. Total RNA was extracted, and complementary DNA (cDNA) was synthesized. Gene expression levels of MUC17 and MUC13 were then quantified using real‑time PCR. The obtained data were analyzed along with patients’ clinical information using SPSS software and the t‑test statistical method.

Results: Statistical analysis revealed a significant association between the expression levels of the MUC13 and MUC17 genes and the degree of tumor cell differentiation. Additionally, a significant positive correlation was observed between the expression levels of these genes and patient age. A significant difference in the expression levels of MUC13 and MUC17 was also observed between tumor tissues and adjacent normal tissues.

Conclusion: The findings indicate that MUC13 and MUC17 exhibit altered expression patterns between colorectal tumor tissues and adjacent normal tissues, suggesting a potential role for these mucins in colorectal cancer development and progression.

Background and Aim: The green biological synthesis of nanomaterials has attracted increasing attention due to its environmentally friendly nature and potential biomedical applications. This study aimed to comparatively evaluate the antibacterial and antibiofilm activities of aqueous Urtica dioica extract, its biosynthesized silver nanoparticles (AgNPs), and chlorhexidine against Streptococcus mutans PTCC 1683.

Methods: Silver nanoparticles were synthesized by adding aqueous U. dioica extract to a silver nitrate solution under controlled conditions. Key synthesis parameters, including extract volume, silver nitrate concentration, pH, and reaction time, were optimized to obtain stable nanoparticle formation. The resulting nanoparticles were characterized using UV–visible spectroscopy, FTIR, XRD, and SEM. Antimicrobial activity was assessed using agar well diffusion assay, while minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) were determined using standard broth dilution methods.

Results: Optimal synthesis conditions were achieved under neutral pH using 2 mL of plant extract and 4 mM silver nitrate. Characterization confirmed the formation of predominantly spherical nanoparticles with sizes in the range of 200–300 nm. In antibacterial assays, U. dioica aqueous extract showed the smallest inhibition zones, whereas AgNPs and chlorhexidine exhibited significantly stronger antibacterial activity. In biofilm assays, the aqueous extract demonstrated the lowest optical density (OD), indicating the strongest antibiofilm effect, while AgNPs and chlorhexidine showed comparable inhibitory effects on biofilm formation.

Conclusion: These findings suggest that Urtica dioica aqueous extract and its green-synthesized silver nanoparticles may serve as promising natural candidates for oral-care applications aimed at controlling S. mutans and dental caries. The results highlight their potential as alternative antimicrobial agents for biomedical and dental applications.

Introduction: Microgravity can affect gene expression in cancerous cells. The objective of this study is to evaluate the changes in the expression of CDK1, MCM6, FBXO5, and EXO1 genes in the LS180 colon cancer cell line under simulated microgravity.

Materials and Methods: The cells were incubated in control and simulated microgravity conditions in two time points – 24 hours and 72 hours. Then RNA was isolated from cells, converted into cDNA and amplified using real-time PCR technique in the presence of primers, while GAPDH served as a reference gene. All procedures were conducted in triplicates.

Results: The study's results demonstrated very clear differences in gene expression between the 24- and 72-hour incubation periods. There were upregulations (2.16-fold) of CDK1 at 24 hrs, and downregulations (0.08, 0.06, and 0.09-fold respectively) of MCM6, FBXO5, and EXO1. At 72 hrs, CDK1, MCM6, and FBXO5 all had increased levels of expression, with MCM6 and FBXO5 having the highest levels of upregulation (3.53). However, EXO1 remained downregulated (0.63-fold) at both time points.

Conclusion: The results indicate that microgravity has time-dependent effects on cell cycle and DNA replication gene expression in colon cancer cells. At 24 hours, the down regulation of MCM6 and FBXO5 would indicate an initial proliferative shock, and the subsequent up regulation of these two genes would indicate that cells are beginning to engage in compensatory adaptive responses at 72 hours. The continuation of EXO1 being downregulated could lead to potential increases in genomic instability. Thus, these results will provide new insight into cancer cell behavior under microgravity conditions, which may also aid in developing future therapeutic strategies.

Contex: RNA-binding proteins (RBPs) are key regulators of post-transcriptional gene expression and play essential roles in hematopoietic stem cell (HSC) function. Although major advances have been made in understanding transcriptional regulation in hematopoiesis, the contribution of RBPs to HSC maintenance and leukemia development remains incompletely defined.

Evidence Acquisition: Relevant literature was collected from major scientific databases and high-impact journals, including PubMed, Web of Science, Google Scholar, Nature Portfolio, Elsevier, and related peer-reviewed sources. This systematic review summarizes current findings on the roles of major RBPs and RNA-modifying factors in normal and malignant hematopoiesis, with particular focus on MUSASHI2, IGF2BP family proteins, Lin28b, METTL3, METTL14, ALKBH5, and FTO.

Results: Available studies demonstrate that RBPs regulate RNA processing, stability, translation, and modification, thereby influencing stem cell self-renewal, differentiation, and leukemic transformation. Dysregulation of these factors contributes to leukemia progression, maintenance of leukemia stem cells, and treatment resistance. Emerging evidence also highlights RBP-associated pathways as potential therapeutic targets.

Conclusion: RBPs represent a critical regulatory layer in hematopoietic stem cell biology and leukemia. An improved understanding of these post-transcriptional mechanisms may support the development of more effective therapies that target leukemia stem cells while preserving normal hematopoiesis.

Contex: Reactive oxygen species (ROS) have a contradictory function in cancer biology because they promote both oncogenic signaling and mediate cell death. At the molecular level, ROS consist of free radicals like O2•⁻, •OH and ONOO-, as well as non-radical oxidants like H2O2 and 1O2. Cytochrome P450 uncoupling, xanthine oxidase, ER oxidative protein folding (Ero1–PDI), peroxisomal β-oxidation, mitochondrial leakage (Complexes I/III), and NADPH oxidases (NOX1–5, DUOX1–2) are mechanisms that naturally produce these species. Exogenous stimuli such as photodynamic treatment, radiation, and nanoparticle-induced redox cycling further increase oxidative flux. In order to adapt, cancer cells reorganize redox homeostasis by upregulating SOD2, while glutathione peroxidases (GPX4), catalase, peroxiredoxins, and thiol buffers (GSH, thioredoxin) detoxify peroxides and maintain cysteine residues in a reduced form. Since Nrf2 hyperactivation encourages the long-term transcription of cytoprotective enzymes, the Nrf2-Keap1 axis is crucial to this network. Such hypertrophied antioxidant defenses establish a "redox setpoint" by keeping ROS levels below fatal thresholds but high enough to sustain oncogenic signaling via MAPK/ERK, JAK/STAT, NF-κB, and stability of HIF-1α.

Evidence Acquisition: A systematic search of major electronic databases was conducted through 2025 using redox-related keywords. Relevant peer-reviewed articles were selected and synthesized to evaluate ROS mechanisms and their therapeutic potential in oncology. The search integrated databases such as PubMed and Scopus, utilizing specific terms like Redox Homeostasis and Ferroptosis to ensure a comprehensive evaluation of current therapeutic vulnerabilities.

Results: The analysis highlights broad clinical applications in early cancer detection (skin, gastrointestinal, respiratory, cervical, and other organs), non-cancerous diseases (inflammation, infection, wound monitoring), and intraoperative guidance. Despite advantages like non-invasiveness and real-time diagnosis, limitations such as limited light penetration depth, complexity of data interpretation, and the inability to fully replace histopathology remain significant challenges.

Conclusion: Additional ROS amplification overwhelms defenses when GPX4 and GSH are reduced, leading to ferroptosis via lipid peroxidation, cytochrome c release, caspase activation, or mitochondrial permeability transition. A "redox vulnerability" is created as a result, which may be used therapeutically In parallel, ROS-induced DNA damages (such as 8-oxoG) activate ATM/ATR pathways, and ER stress initiates CHOP-mediated apoptosis. Crucially, immunogenic cell death brought on by oxidative damage can also release DAMPs including ATP, HMGB1, and calreticulin to boost antitumor immunity. Through the combination of redox buffering systems, antioxidant adaptations, and molecular-level ROS formation, this review reframes ROS as a biochemical language and therapeutic lever in oncology.

Context: Advances in genetics, genomics, and precision medicine have created unprecedented opportunities to improve population health. However, translating these scientific breakthroughs into equitable public health practice remains a major challenge, particularly in low- and middle-income countries (LMICs), where financial, organizational, policy, and workforce barriers limit implementation. This review examines how social innovation can bridge the gap between genomic discoveries and public health impact.

Evidence Acquisition: A narrative review of the literature was conducted using major scientific databases, including PubMed, Scopus, Web of Science, and Google Scholar, together with reports from international organizations. Relevant evidence on social innovation, public health genomics, precision medicine, implementation science, and health equity was identified, critically appraised, and synthesized, with particular attention to experiences from LMICs and Iran.

Results: The evidence indicates that successful translation of genomics into public health depends not only on technological advances but also on social innovation. Four complementary domains were identified: innovative service delivery, sustainable financing mechanisms, participatory governance, and supportive policy and regulatory frameworks. International case studies demonstrate that approaches such as task-shifting, tele-genetics, community engagement, and digital health platforms can substantially improve equitable access to genomic services. Iran possesses important strengths, including an extensive primary healthcare network, a nationwide newborn screening program, and established community health workers (Behvarzes). Nevertheless, workforce shortages, fragmented genomic infrastructure, financing limitations, and policy inconsistencies remain major barriers to implementation.

Conclusion: : Social innovation is a critical mechanism for translating genomic research into equitable public health practice. Integrating genomics within existing primary healthcare systems, strengthening governance, investing in workforce capacity, and promoting community participation can accelerate the implementation of precision public health, particularly in Iran and other LMICs.

Context: Metabolic dysfunction-associated steatotic liver disease (MASLD) has replaced non-alcoholic fatty liver disease in contemporary nomenclature and reframes hepatic steatosis as a multisystem cardiometabolic condition. In general medicine, the usual presentation is incidental steatosis on imaging or mildly abnormal aminotransferases in a patient with obesity, diabetes, hypertension, dyslipidemia, or cardiovascular risk.

Evidence Acquisition: This narrative review was updated through June 2026 using PubMed/MEDLINE, major society guidance, clinical care pathways, systematic reviews, randomized trials, and regulatory sources relevant to adult primary care, internal medicine, endocrinology, obesity medicine, cardiology, and hepatology.

Results: Current evidence supports a pragmatic shift from detecting steatosis alone to identifying clinically significant fibrosis and cardiometabolic risk. MASLD is diagnosed when hepatic steatosis coexists with at least one cardiometabolic risk factor after assessment of alcohol intake and alternative causes of steatosis. Clear separation of MASLD, MetALD, and alcohol-related liver disease is clinically important because alcohol exposure modifies prognosis, counseling, surveillance, and referral needs. Stepwise non-invasive testing, usually beginning with the fibrosis-4 index followed by transient elastography or serum fibrosis testing when indicated, can identify patients who need hepatology referral. Resmetirom and semaglutide have expanded the treatment landscape for selected adults with non-cirrhotic MASH and moderate-to-advanced fibrosis in the jurisdictions where they are approved, but long-term clinical outcome data remain incomplete.

Conclusion: MASLD should be approached as a cardiometabolic risk signal with liver-fibrosis implications. A structured pathway for incidental steatosis can reduce missed advanced fibrosis while improving diabetes, obesity, lipid, blood pressure, cardiovascular, and lifestyle care.

  The use of medicinal plants is increasing worldwide; however, the absence of effective quality assurance has resulted in the presence and distribution of adulterations. Adulteration appears intentionally or unintentionally, both of which lead to serious consequences for public health. The present policy note evaluates the extent of the subject and emphasizes the central role of universities in preventing and controlling adulteration in medicinal plants and herbal medicines. By conducting research, developing infrastructures for laboratories, training expert technicians, and also improving the knowledge of the public, universities can play a significant role in preventing this problem. Improving these capabilities will result in a systematic quality assurance for safe use of medicinal plants and herbal medicines.