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.

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: 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.