Bosnian Journal of Basic Medical Sciences
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Vitamin D and calcium status in preeclampsia and pregnancy-induced hypertension
Full text linkHypertensive disorders of pregnancy are major causes of maternal and perinatal morbidity and mortality, and nutritional factors such as vitamin D and calcium have been proposed as modifiable risks; therefore, we investigated the association between maternal vitamin D and calcium status and pregnancy-induced hypertension (PIH) and pre-eclampsia (PE) and explored the relation with supplementation. In this observational cross-sectional study, 84 third-trimester women were enrolled from two hospitals in Lublin, Poland (41 PIH/PE, 43 controls). Serum total and ionised calcium, 25-hydroxyvitamin D [25(OH)D], and 1,25-dihydroxyvitamin D₃ were measured using standardised immunoassays, and group differences, correlations, and multivariable logistic regression were applied with adjustment for body mass index (BMI), maternal age, gestational age, calcium fractions, and gestational diabetes. PIH/PE cases had lower 25(OH)D than controls (27.8 vs 35.7 ng/mL; p = 0.012) and higher BMI (33.0 vs 27.5 kg/m²; p < 0.001), while total and ionised calcium and 1,25-dihydroxyvitamin D₃ were similar (all p ≥ 0.40); supplement use was more frequent among controls (84% vs 73%). In adjusted models, higher BMI increased the odds of PIH/PE (OR 1.19 per kg/m²) and higher 25(OH)D was protective (OR 0.92 per ng/mL); discrimination was fair (AUC 0.78). These findings support an association between vitamin D insufficiency and obesity with hypertensive pregnancy disorders and suggest preserved calcium homeostasis, but given the cross-sectional design, third-trimester sampling, small sample size, and non-standardised supplementation, causal inference and preventive recommendations cannot be made; larger prospective studies beginning in early pregnancy are warranted to test whether optimising vitamin D and calcium can reduce hypertensive complications
Circulating organokines in coronary artery disease and metabolic syndrome: FABP4, adiponectin, irisin, FSTL1
Full text linkCardiovascular disorders are closely linked to metabolic syndrome and remain a leading cause of mortality worldwide, despite advances in early detection and treatment. Adipokines, cardiokines, and myokines play critical roles in maintaining systemic metabolic homeostasis. In this study, we measured serum levels of fatty acid binding protein 4 (FABP4), follistatin-like 1 (FSTL1), irisin, and adiponectin in 243 male patients undergoing elective coronary angiography. We investigated the associations of these biomarkers with coronary artery disease (CAD) and their correlation with metabolic syndrome status. FSTL1 levels were predicted using a Particle Swarm Optimization-enhanced Adaptive Neuro-Fuzzy Inference System (PSO-ANFIS) based on artificial intelligence. Patients with CAD exhibited significantly lower FABP4 levels (p<0.0001), and low FABP4 levels emerged as an independent predictor of CAD in logistic regression analysis (odds ratio 0.903, 95% CI 0.825-0.987, p=0.025). The combination of adiponectin, FSTL1, and irisin as a biomarker strategy demonstrated high sensitivity and specificity for diagnosing metabolic syndrome (AUC = 0.92, 95% CI 0.88-0.96). Both FSTL1 and adiponectin independently correlated with metabolic syndrome (p<0.001, odds ratio 1.039, 95% CI 1.025-1.054; p<0.001, odds ratio 0.979, 95% CI 0.971-0.988, respectively). The prediction of FSTL1 levels using PSO-ANFIS supports the concept of harmonization among metabolic messengers. These findings underscore the potential of FABP4 and FSTL1 as valuable biomarkers for diagnosing metabolic and cardiovascular diseases, thereby facilitating personalized interventions targeting organokine pathways
Platelet-rich plasma and hyaluronic acid in the treatment of acute ankle sprains: A review
Full text linkAnkle sprains are prevalent musculoskeletal injuries commonly encountered in the general population, particularly among athletes. While conventional treatments are widely practiced, regenerative therapies have emerged as potential adjunctive options. This narrative review aims to assess the role of regenerative therapy in the management of acute ankle sprains and evaluate its efficacy through an analysis of the literature. We focused on studies available in PubMed, restricting our search to English-language articles published between January 2005 and December 2024. Our review identified five studies on platelet-rich plasma (PRP) and one on hyaluronic acid (HA). The PRP studies included four clinical trials and one case report. PRP injections demonstrated short-term benefits in pain reduction and functional recovery, particularly when administered early and in multiple doses. However, long-term outcomes were often comparable to standard treatments or placebo. The study on HA indicated consistent and sustained advantages over placebo in alleviating pain, expediting the return to sport, and reducing recurrence rates. Based on the current evidence, PRP and HA may function as adjunctive therapies for acute ankle sprains, especially for short-term symptom relief and functional recovery. Treatment efficacy appears to be influenced by factors such as injection timing, volume, immobilization protocols, and the concurrent use of nonsteroidal anti-inflammatory drugs. Nonetheless, the evidence base remains constrained by small sample sizes, heterogeneous protocols, and a lack of long-term follow-up. Therefore, further high-quality randomized controlled trials are essential to establish standardized protocols and ascertain the long-term efficacy of these regenerative therapies
Response to the Letter regarding “Sugammadex vs neostigmine in post-anesthesia recovery: A systematic review and meta-analysis”
Full text linkThis response addresses feedback on our systematic review and meta-analysis comparing sugammadex with neostigmine for neuromuscular block reversal. We acknowledge high heterogeneity for time-based outcomes, likely due to differences in clinical settings and anesthetic/surgical protocols, but pooled effects consistently favored sugammadex for faster and more complete reversal. We agree hypnotic depth and other perioperative factors may modify emergence and airway safety, yet these variables were inconsistently reported and could not be analyzed quantitatively. We also clarify that time outcomes were synthesized using standardized mean differences to account for different reporting units, and any presentation inconsistencies will be corrected. Overall, our findings support pharmacologic superiority of sugammadex with reductions in selected complications, while emphasizing that broader recovery quality may not uniformly improve and should be interpreted in clinical context
Andrographolide suppresses cervical cancer progression by targeting angiogenesis and inducing apoptosis in a CAM-PDX model
Full text linkCervical cancer poses significant clinical challenges, particularly in advanced stages. This study explores the therapeutic potential of andrographolide (AND), a bioactive compound derived from Andrographis paniculata, in mitigating cervical cancer progression using the chick embryo chorioallantoic membrane patient-derived xenograft (CAM-PDX) model. The model was validated through hematoxylin–eosin (H&E) staining and immunohistochemistry, which confirmed its ability to accurately replicate the histological and molecular characteristics of patient-derived xenografts (PDXs), establishing its reliability for therapeutic screening. A dose of 20 mg/kg AND was selected for further evaluation based on preliminary chorioallantoic membrane (CAM) assay findings. In the CAM-PDX model, AND significantly inhibited tumor growth, primarily by reducing angiogenesis and vessel density. Immunohistochemical analysis revealed that AND downregulated key proteins associated with cancer cell proliferation and survival, including Ki67, B-cell lymphoma 2 (BCL-2), and Erythroblast transformation-specific-related gene (ERG). These results indicate that AND not only disrupts tumor angiogenesis but also induces cell cycle arrest and promotes apoptosis in cervical cancer cells. In summary, this study successfully established a reproducible CAM-PDX model for drug evaluation and highlighted the potential of AND as a promising therapeutic candidate for cervical cancer, warranting further clinical investigation
Mesenchymal stem cell- derived exosomes as cell-free therapeutics for sensorineural hearing loss
Full text linkSensorineural hearing loss (SNHL) can result from various factors, including ototoxic drugs (such as aminoglycosides and chemotherapeutic agents), prolonged exposure to intense sound, and autoimmune or genetic disorders. In adult mammals, the loss of sensory cells in the cochlea is irreversible due to their lack of regenerative capacity. Current treatment options include hearing aids for mild to moderate hearing loss, which rely on residual hearing, and cochlear implants for severe cases, which provide limited auditory recovery while leading to the loss of any remaining natural hearing. Stem cell therapies, particularly those involving mesenchymal stem cells (MSCs), are being increasingly explored in regenerative medicine. MSCs are multipotent cells capable of differentiating into mesodermal lineage cells and possess immunomodulatory and regenerative properties, making them potential candidates for SNHL treatment. However, their administration carries risks, including unwanted differentiation, immune system activation, and potential tumorigenic effects. Exosomes, extracellular vesicles in the nanometer size range, are secreted by most eukaryotic cells. These vesicles, which have a double lipid membrane and contain genomic and proteomic material, play a crucial role in intercellular communication. Exosomes derived from MSCs exhibit similar biological functions to their parent cells but with significantly lower risks, as they do not trigger immune responses or pose oncological concerns. This paper aims to review current knowledge on the use of MSCs and MSC-derived exosomes for inner ear sensory cell regeneration and explore their potential for clinical applications
Comparison of robotic, conventional, and endoscopic nipple-sparing mastectomy with immediate prosthetic breast reconstruction for breast cancer: A systematic review and meta-analysis
Full text linkIn this network meta-analysis (NMA), we aimed to evaluate the relative efficacy of robotic nipple-sparing mastectomy (RNSM), conventional nipple-sparing mastectomy (CNSM), and endoscope-assisted nipple-sparing mastectomy (ENSM), each combined with immediate prosthetic breast reconstruction (IPBR), for the treatment of breast cancer. Relevant studies published up to June 15, 2024, were identified through searches of PubMed, Embase, the Cochrane Library, and Web of Science. Data extracted from these studies were analyzed using Stata 15.1 and the Gemtc 1.0.1 package in R 4.2.3. A Bayesian framework and a Markov Chain Monte Carlo model were employed to conduct the NMA. Additionally, a ranking chart was generated to compare the advantages and disadvantages of the surgical methods. Ten studies met the inclusion criteria and were included in the NMA. The results indicated that ENSM with immediate implant-based reconstruction was associated with a smaller incision compared to CNSM. RNSM combined with IPBR was linked to a lower incidence of total complications, Grade 3 complications, and nipple-areola complex necrosis than CNSM. Furthermore, RNSM with IPBR demonstrated a lower recurrence rate than CNSM. However, CNSM with IPBR showed better outcomes in terms of surgical time, hospital stay, and positive margin infiltration. In contrast, RNSM and ENSM, both combined with IPBR, outperformed CNSM in terms of incision length, complication rates, and recurrence outcomes
Molecular aspects of Angelman Syndrome: Defining the new path forward
Full text linkAs a rare neuro-genetic disease, Angelman syndrome (AS) affects about 15 to 500 thousand people worldwide. The AS is an imprinting genomic disease characterized by the loss of function of the maternal UBE3A gene, located in the 15q11-q13. This gene encodes a ~100 kDa protein, the Ubiquitin-protein ligase E3A (UBE3A), that participates in the ubiquitination process, one of the post-translational protein modifications. In the brain, under normal conditions, the paternal allele of the UBE3A gene is silenced, with only the maternal allele being active. However, in individuals with AS, the maternal loss of function of this gene leads to the complete absence of UBE3A expression, resulting in multiple pathological features. Clinically, children diagnosed with AS exhibit a characteristic behavioral phenotype, including a happy demeanor, frequent and unmotivated laughter, movement, speech impairment, severe intellectual disability, and sleep problems. Since its discovery in 1965, significant progress has been made in understanding the genetic and pathophysiological aspects of AS. However, despite these advances, the molecular mechanisms underlying the disease remain incompletely understood, and no effective treatment currently exists. Current therapies focus solely on symptom management, and no approach has yet succeeded in reactivating the silenced paternal UBE3A allele. Therefore, this review highlights the epigenetic aspects involved in the AS in order to provide a better understanding and clarification of the mechanisms, hopefully paving the way for future research to improve the treatment of affected individuals
UPP1 and AHSA1 as emerging biomarkers and targets in pancreatic cancer: A proteomic approach
Full text linkThe specific protein targets involved in pancreatic cancer (PC) pathogenesis and its varying levels of differentiation remain incompletely understood. Advanced proteomic methodologies provide a powerful means of identifying key regulatory proteins and signaling pathways central to cancer progression. In this study, proteomic analyses were performed on PC tissue samples of different differentiation grades, along with adjacent non-cancerous (para-PC) tissues. Bioinformatics techniques were used to identify differentially expressed proteins (DEPs) and their associated pathways. Key target proteins were validated using the Gene Expression Profiling Interactive Analysis (GEPIA) database, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western blotting, immunohistochemistry (IHC), and immunofluorescence (IF). A total of 431 DEPs were identified between PC and para-PC tissues, while 470 DEPs distinguished poorly differentiated (PD) from moderately differentiated (MD) PCs. Functional enrichment analysis revealed that these DEPs participate in various biological processes and signaling pathways. Five DEPs were common to both comparisons, with Uridine Phosphorylase 1 (UPP1), Lactamase Beta, and Activator of HSP90 ATPase Activity 1 (AHSA1) showing particularly notable differences. UPP1 and AHSA1 were significantly upregulated in PC tissues relative to adjacent tissues and exhibited even higher expression in PD-PCs compared to MD ones. These findings were consistently supported by GEPIA, RT-qPCR, Western blotting, IHC, and IF analyses. This study identifies UPP1 and AHSA1 as key proteins linked to PC differentiation and progression, highlighting their potential as diagnostic markers and therapeutic targets. These insights enhance our understanding of the molecular mechanisms underlying PC and open new avenues for precision treatment strategies
Machine learning integration of single-cell and bulk transcriptomics identifies fibroblast-driven prognostic markers in colorectal cancer
Full text linkSingle-cell RNA sequencing (scRNA-seq) has significantly advanced our understanding of cellular heterogeneity and the complex interplay within the tumor microenvironment (TME) of colorectal cancer (CRC). However, translating these molecular insights into clinically actionable prognostic biomarkers and therapeutic strategies remains a considerable challenge. In this study, we conducted a comprehensive scRNA-seq analysis of 306 CRC samples comprising 448,255 cells to characterize the TME in depth. By constructing intercellular communication networks based on connection counts and communication probabilities, we identified fibroblasts as central regulatory hubs within the TME. Using Wilcoxon rank-sum tests and univariate survival analyses, we initially identified 23 prognostic fibroblast markers. These were refined to a seven-gene fibroblast-related prognostic signature via an integrated machine learning approach. The signature exhibited robust predictive performance in the The Cancer Genome Atlas - Colon Adenocarcinoma (TCGA-COAD) training cohort (n=351; C-index=0.65) and was successfully validated in the GSE17536 dataset (n=177; C-index=0.63). Functional enrichment analyses revealed that this signature is involved in immune regulation and multiple tumor-associated cellular pathways. Notably, high-risk patients displayed increased macrophage and NK cell infiltration, impaired immune function, and elevated immune rejection scores, while low-risk patients demonstrated heightened sensitivity to camptothecin and irinotecan. Together, our findings underscore the prognostic value of fibroblast-derived signatures in CRC and support their potential utility in risk stratification and the development of personalized therapeutic strategies, contributing to the advancement of precision oncology