Bosnian Journal of Basic Medical Sciences
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Nutritional support and immunonutrition in esophageal cancer – From perioperative care to long-term survivorship: A review
Full text linkEsophageal cancer is recognized as one of the most aggressive malignancies within the digestive system, with global survival rates typically falling below 20%. Malnutrition impacts up to 80% of patients, significantly affecting treatment tolerance, postoperative outcomes, and overall quality of life. Recent advancements in clinical nutrition and immunometabolism have transformed the perception of nutrition from a mere supportive measure to a vital therapeutic component in cancer care. This review synthesizes evidence from studies published between 2010 and 2025, exploring the effects of various nutritional strategies—including enteral, elemental, parenteral, immuno-nutritional, behavioral, and prehabilitative interventions—on metabolism, immune response, and clinical outcomes in patients with esophageal cancer. The findings demonstrate that targeted approaches such as immune-enhancing enteral formulations, omega-3-enriched parenteral nutrition, and structured dietary counseling can mitigate inflammation, preserve muscle mass, enhance treatment adherence, and improve psychological well-being. Overall, the literature supports the perspective of nutrition as a precision-based, integral component of multidisciplinary cancer management. Incorporating nutritional optimization throughout all stages of care—ranging from prehabilitation and perioperative support to survivorship and palliative management—can enhance metabolic resilience, promote faster recovery, and significantly improve the quality of life for individuals diagnosed with esophageal cancer
Letter regarding “Sugammadex vs neostigmine in post-anesthesia recovery: A systematic review and meta-analysis”
Full text linkThis correspondence comments on the systematic review and meta-analysis by Zhu and Li comparing sugammadex with neostigmine for neuromuscular block reversal and postoperative outcomes. While the authors provide a useful synthesis suggesting faster recovery and less residual blockade with sugammadex, several issues may limit the validity and clinical generalizability of the pooled conclusions. Many key outcomes show extreme heterogeneity (I² frequently >90%), raising concerns that combined estimates may obscure clinically important variation in anesthetic technique, blockade depth, monitoring, and recovery protocols. In particular, emergence safety depends not only on neuromuscular indices (e.g., TOF ≥0.9) but also on hypnotic depth at the time of reversal; evidence indicates that volatile anesthetic concentration (MAC) can meaningfully modify airway obstruction risk after sugammadex. Additionally, inconsistencies in the reporting of time-based effect sizes, specifically between standardized mean differences (SMD) and mean differences (MD) with identical values, necessitate clarification to enhance interpretability. We highlight the need for more cautious interpretation, targeted subgroup analyses incorporating anesthetic depth and other effect modifiers, and more robust meta-analytic methods to strengthen precision and applicability of the findings
Pathological roles of ubiquitination and deubiquitination systems in sepsis-induced myocardial dysfunction
Full text linkSepsis-induced myocardial dysfunction (SIMD) is a severe complication of sepsis, characterized by impaired cardiac function and high mortality rates. Despite significant advances in understanding sepsis pathophysiology, the molecular mechanisms underlying SIMD remain incompletely elucidated. Ubiquitination and deubiquitination, critical post-translational modifications (PTMs) regulating protein stability, localization, and activity, play pivotal roles in cellular processes, such as inflammation, apoptosis, mitochondrial function, and calcium handling. Dysregulation of these systems has been increasingly implicated in the pathogenesis of SIMD. This review provides a comprehensive overview of the pathological mechanisms driving SIMD, with a focus on the classification and functions of E3 ubiquitin ligases and deubiquitinating enzymes (DUBs), their regulatory systems, and their involvement in SIMD. Dysfunction of the ubiquitin-proteasome system (UPS), often driven by altered activity of E3 ligases, accelerates the degradation of critical regulatory proteins, thereby exacerbating cardiac inflammation, oxidative stress, and apoptosis. Concurrently, imbalances in DUB activity disrupt protein homeostasis, further amplifying myocardial injury. Emerging research underscores the therapeutic potential of targeting these systems. Strategies aimed at modulating E3 ligase activity or restoring DUB balance have shown promise in preclinical studies. This review summarizes current findings on the roles of ubiquitination and deubiquitination in SIMD pathogenesis, highlights the key challenges in advancing this field, and proposes directions for future research
SOX-9 as a prognostic marker in gastric adenocarcinoma
Full text linkSRY-box transcription factor 9 (SOX9) has been reported to be overexpressed in a wide variety of gastrointestinal malignancies. While its role has been studied in gastric cancer (GC), the results remain conflicting. This study aimed to evaluate the relationship between SOX9 immunohistochemistry results and the pathological and clinical characteristics of gastric adenocarcinoma, assessing its potential as a prognostic marker. Gastric tissue samples from 150 patients with gastric cancer were included in the study. Tissue sections were stained using an anti-SOX9 antibody, and relevant data were retrospectively collected from digital records. Immunostaining results were scored based on the proportion and intensity of stained nuclei throughout the tumor. A final immunostaining score was calculated by multiplying the SOX9 intensity score by the proportion score. Strong SOX9 nuclear staining was observed in 68 patients (45.3%), while moderate staining was seen in 60 patients (40%). SOX9 nuclear staining was absent in three patients (2%). A final SOX9 immunostaining score of ≥10, classified as high expression, was identified in 60 patients (40%). Patients with higher SOX9 expression or strong intensity scores exhibited significantly larger tumor sizes, higher rates of perineural and vascular invasion, more advanced T or lymph node staging, and greater likelihoods of lymphatic or distant metastases compared to those with lower SOX9 expression or intensity scores (all P < 0.05). These findings suggest that SOX9 staining intensity and expression are associated with increased tumor malignancy and disease progression. Therefore, SOX9 may serve as a prognostic pathological indicator in GC patients
Adipose-derived MSC extracellular vesicles ameliorate sepsis by reprogramming macrophages via miR-21-5p targeting PELI1
Full text linkSepsis is a common and life-threatening condition encountered in intensive care units (ICUs). Mesenchymal stromal cells (MSCs) and their small extracellular vesicles (EVs) have emerged as promising nanotherapeutics, particularly in the context of COVID-19. This study evaluates the efficacy and mechanisms of adipose-derived MSC EVs (ADMSC-EVs) in a lipopolysaccharide (LPS)-induced sepsis model. We quantified M2 macrophages and IL-10 in peripheral blood mononuclear cells (PBMCs) from both septic patients and healthy donors. ADMSCs and their EVs were isolated, and EVs were administered to LPS-challenged mice. Macrophage phenotypes in lung tissue were analyzed using flow cytometry and immunofluorescence. The biodistribution of EVs was traced with PKH67 green fluorescent cell linker dye (PKH-67), and the signaling pathways involved in macrophage reprogramming were examined. ADMSC-EVs efficiently entered macrophages, promoted M2 polarization, suppressed inflammation, and improved survival rates in septic mice. Biodistribution studies demonstrated widespread organ accumulation, with notable localization in the lungs, liver, and kidneys. Mechanistically, the EV cargo miR-21-5p targeted Pellino E3 ubiquitin protein ligase 1 (PELI1), driving M2 polarization in vivo, which was accompanied by increased IL-10 levels. These findings position ADMSC-EVs as a viable cell-free therapeutic approach for mitigating LPS-induced sepsis through the delivery of miR-21-5p to PELI1, thereby supporting further development of EV-based immunomodulatory strategies for sepsis management
Comprehensive analysis of angiogenesis and stemness-related genes in chemotherapy and immunotherapy of bladder cancer
Full text linkTumor angiogenesis and cancer stem cells (CSCs) are critical features of malignancies. Research has shown that CSCs promote blood vessel formation, while increased vasculature, in turn, supports CSC proliferation—creating a detrimental feedback loop that drives disease progression. However, studies investigating vascularization and stem-like properties in bladder cancer (BLCA) remain limited. In our investigation, we applied clustering techniques and LASSO methodology to assess the significance of vascularization- and stemness-related genes in predicting responses to chemotherapy and immunotherapy in BLCA. Using multivariate Cox regression analysis, we identified Von Hippel–Lindau (VHL) as the primary prognostic marker associated with both vascularization and stem-like traits. Tissue array analysis of 40 BLCA specimens, combined with molecular docking simulations, revealed interactions between HDAC6 and VHL that influence stem-like behavior and angiogenesis in BLCA. Additionally, VHL showed strong correlations with treatment responses to both chemotherapy and immunotherapy in BLCA. In conclusion, our findings highlight the critical role of vascularization- and stemness-related genes in determining therapeutic outcomes in BLCA and underscore the regulatory relationship between VHL and HDAC6 in modulating treatment response
Green synthesis of plant-derived ZnO nanoparticles: Characterization, pharmacokinetics, molecular interactions, and in-vitro antimicrobial and antifungal evaluation
Full text linkNowadays, nanoparticles (NPs) are used to counteract various medicinal and industrial problems. This study aimed to biosynthesize zinc oxide NPs (ZnONPs) from the plant species Aloe vera L., Peganum harmala L., Retama monosperma L., and Thymelaea hirsuta L. The biosynthesized ZnONPs were referred to as “Thymhirs.bio-ZnONP,” “Aloever.bio-ZnONP,” “Retam.bio-ZnONP,” and “Harm.bio-ZnONP.” A UV-visible spectrophotometer, granulometry, Fourier transform infrared spectroscopy, and electron paramagnetic resonance were used for physicochemical characterization. Pharmacokinetics and antimicrobial effects were explored using combined in vitro and computational assays. An abundance of phenolic acids and flavonoids was observed, particularly rutin, quinic acid, apigenin-7-O-glucoside, and cirsiliol, which may act as reducing, stabilizing, and capping agents in the biosynthesis. ZnONPs demonstrated strong antimicrobial activity against various bacterial, fungal, and yeast strains, highlighting their potential medicinal applications. This inhibitory activity can be attributed to the effect of the plant-based ZnO nanosized particles more than to the plant extracts or Zn salt. Computational modeling revealed that the identified phytochemicals (phenolic acids and flavonoids) bound Tyrosyl-tRNA Synthetase (TyrRS) from S. aureus (1JIJ), aspartic proteinase from C. albicans (2QZW), and wheat germ agglutinin (2UVO) with considerable affinities, which, together with molecular interactions and pharmacokinetics, satisfactorily support the in vitro antimicrobial findings. This study lays the groundwork for future research and pharmaceutical explorations aimed at harnessing the likely beneficial properties of green-synthesized ZnONPs for medicinal and therapeutic purposes, particularly their antimicrobial effects
Skin pathology in ALS: Diagnostic implications and biomarker potential
Full text linkAmyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the loss of motor neurons in the spinal cord and brain, resulting in motor deficits and muscle atrophy. Approximately 5–10% of ALS patients are familial (fALS), while the rest are sporadic (sALS). Currently, early diagnosis of ALS cannot be achieved based on clinical manifestations and electromyography due to the lack of effective and easily available biomarkers. The skin and central nervous system (CNS) share the same embryonic origin. Several skin biomarkers have been found in many neurodegenerative diseases, such as abnormal deposition of pathological α-synuclein (α-Syn) in Parkinson\u27s disease. Thus, molecular changes in the skin associated with ALS-specific pathological events could readily be detected and become biomarkers for ALS through skin testing. Here, we summarize the literature on pathological changes in the skin of ALS patients and animal models, including structural abnormalities of the skin, reduced density of skin nerve fibers, abnormal protein aggregation, altered mitochondrial morphology and function, and dysregulation of skin inflammation, which may be useful for early diagnosis and monitoring of ALS progression
Gut microbial metabolites and the brain–gut axis in Alzheimer’s disease: A review
Full text linkAlzheimer’s disease (AD) is increasingly recognised as a disorder that extends beyond the brain, with accumulating evidence implicating gut microbiota–derived metabolites in its onset and progression. This narrative review synthesises 92 peer-reviewed animal, human and meta-analytic studies published between 2010 and 2025 that investigated short-chain fatty acids (SCFAs), tryptophan-derived indoles and kynurenines, trimethylamine N-oxide (TMAO) and secondary bile acids in the context of AD. Collectively, the literature shows that SCFAs support blood–brain-barrier integrity, dampen microglial reactivity and enhance synaptic plasticity, yet can paradoxically amplify β-amyloid (Aβ) deposition under germ-free or supraphysiological conditions, highlighting the importance of host status and dosing. Beneficial indole metabolites such as indole-3-propionic acid counter oxidative stress, strengthen intestinal and cerebral barriers and suppress pro-inflammatory cascades, whereas a shift toward neurotoxic kynurenines correlates with cognitive decline. TMAO emerges as a consistently deleterious metabolite that aggravates endothelial dysfunction, neuroinflammation and Aβ aggregation; dietary precursor restriction and microbial enzyme inhibitors are therefore being explored as mitigation strategies. Secondary bile acids and polyphenol derivatives further modulate mitochondrial bioenergetics and NF-κB signalling, broadening the therapeutic landscape. Multi-omics profiling reveals that AD patients typically exhibit reduced SCFAs and indoles but elevated TMAO, changes that scale with Mini-Mental State Examination scores, brain atrophy and cerebrospinal Aβ₄₂ levels. Early probiotic and faecal-microbiota-transplant trials have begun to normalise these metabolite profiles and yield modest cognitive benefits, underscoring translational potential. Altogether, gut-derived metabolites are not passive by-products but active modulators of neural, immune and metabolic circuits along the microbiota–gut–brain axis; their targeted manipulation and standardised metabolomic assessment could enable earlier diagnosis and precision microbiome-based interventions for AD, a promise that now warrants validation in large, longitudinal and mechanistically informed clinical studies
Increased carotid intima-media thickness in pediatric nephrotic syndrome: A meta-analysis
Full text linkNephrotic syndrome (NS) in children has been associated with an increased risk of early atherosclerosis, as indicated by carotid intima-media thickness (cIMT). However, the existing literature on the relationship between NS and cIMT in pediatric populations presents inconsistent findings. This meta-analysis aims to compare cIMT measurements between children with NS and healthy controls. A comprehensive search of PubMed, Embase, and Web of Science was conducted through May 22, 2025. Observational studies that compared cIMT in children under 18 years with NS against controls were included. Mean differences (MDs) with 95% confidence intervals (CIs) were aggregated using a random-effects model to account for potential heterogeneity. Thirteen case-control studies involving 578 children with NS and 741 controls were analyzed. The results indicated that children with NS had significantly higher cIMT compared to controls (MD: 0.06 mm; 95% CI: 0.04–0.08; p < 0.001; I² = 68%). Subgroup analyses revealed that the difference in cIMT was notably larger in studies with ≥ 60% male participants (MD: 0.09 mm) compared to those with < 60% males (MD: 0.03 mm; p for subgroup difference = 0.01). No significant differences were observed based on age, disease duration, or adjustments for body mass index, blood pressure, or lipid profile (all p > 0.05). Meta-regression analyses suggested that the proportion of male participants and the rate of steroid-resistant nephrotic syndrome (SRNS) may contribute to observed heterogeneity (adjusted R² = 29.8% and 22.5%, respectively), although the slopes for these meta-regressions were not statistically significant (p = 0.13 and 0.87). In conclusion, children with NS exhibit increased cIMT compared to controls, indicating early vascular changes. The predominance of males and the presence of SRNS may partially account for the heterogeneity observed across studies