Biomolecules & biomedicine最新文献

{"title":"ESAT-6-specific antibody features and Fcγ receptor expression during pulmonary tuberculosis treatment: Implications for therapeutic monitoring.","authors":"Christian Elugo, Sandra Palma Albornoz, Yomara Romero, Sandra Delgado-Málaga, Iskra Tuero","doi":"10.17305/bb.2026.14489","DOIUrl":"https://doi.org/10.17305/bb.2026.14489","url":null,"abstract":"<p><p>Tuberculosis (TB) remains a leading cause of global mortality, yet the long-term dynamics of antibody-mediated immunity during successful treatment are not fully understood. This study aimed to characterize how ESAT-6-specific antibody profiles, Fc gamma receptor (FcγR) expression, and antibody effector functions change in pulmonary TB patients undergoing treatment. In this exploratory longitudinal study, 21 adults with active pulmonary TB, who completed standard six-month therapy and achieved microbiological cure, were sampled at three time points: before treatment, after two months, and at treatment completion. We quantified ESAT-6-specific immunoglobulin G (IgG) and its subclasses using enzyme-linked immunosorbent assay (ELISA). FcγR expression was assessed via flow cytometry, and antibody-dependent cellular phagocytosis (ADCP) and antibody-dependent cellular cytotoxicity (ADCC) were evaluated with cell-based assays. Upon treatment completion, ESAT-6-specific total IgG and IgG4 significantly decreased from baseline in 85.7% and 81.0% of participants, respectively (both q < 0.001). Conversely, ADCP and ADCC increased in 76.2% of participants (q = 0.0017 and q = 0.0014, respectively). Activating FcγR expression also declined, most consistently for CD64 on granulocytes and monocytes, with additional reductions in CD16 and CD32 on monocytes. These findings reveal a coordinated remodeling of ESAT-6-specific humoral immunity during successful TB treatment. We identify IgG4 levels, FcγR expression, ADCP, and ADCC as potential correlates of treatment response. Further validation in larger prospective cohorts, including patients experiencing treatment failure and relapse, is necessary.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148820327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reduced E-cadherin, claudin-1, and claudin-6 expression and compartment-specific lymphocyte distribution in recurrent aphthous ulceration.","authors":"Efe Yetişgin, Çiğdem Sercan, Ertuğrul Çelik, Eda Yılmaz Akçay, Ömer Günhan","doi":"10.17305/bb.2026.14856","DOIUrl":"https://doi.org/10.17305/bb.2026.14856","url":null,"abstract":"<p><p>Recurrent aphthous ulceration (RAU) is a prevalent inflammatory condition affecting the oral mucosa. However, the localized epithelial junctional changes and their connection to immune cell distribution are not well understood. This study sought to characterize junction-associated protein expression and compartment-specific lymphocyte distribution in RAU. This retrospective, multicenter, paired tissue study included 56 consecutive patients with clinically and histopathologically confirmed RAU. Semiquantitative immunohistochemistry was employed to compare E-cadherin, claudin-1, and claudin-6 expression. Comparisons were made between ulcer-adjacent non-ulcerated regenerative epithelium and morphologically preserved distant mucosa from the same patient. The study also evaluated cluster of differentiation 4 (CD4)-, cluster of differentiation 8 (CD8)-, and cluster of differentiation 20 (CD20)-positive lymphocytes in both intraepithelial and subepithelial/ulcer-base compartments. All distant mucosal samples exhibited strong expression of the three junctional proteins. In contrast, within the ulcer-adjacent epithelium, E-cadherin expression was weak in 35.7% and moderate in 64.3% of cases. Claudin-1 was absent in 17.9% and weak in 82.1%, while claudin-6 was absent in 71.4% and weak in 28.6%. Each marker demonstrated significantly lower expression in all paired cases (p < 0.001). Descriptively, CD8-positive lymphocytes were consistently present intraepithelially in all cases, whereas CD20-positive lymphocytes were absent. The ulcer base and adjacent subepithelial tissue contained CD4-, CD8-, and CD20-positive lymphocytes in all cases. RAU is consistently linked to a localized reduction of epithelial junctional proteins and distinct compartmental lymphocyte patterns. These findings suggest epithelial junctional remodeling within the RAU microenvironment, though they do not confirm functional barrier impairment or causality.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blood urea nitrogen-to-albumin ratio and in-hospital mortality in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention.","authors":"Şükriye Uslu, Ahmet Genç, Gülsüm Meral Yılmaz Öztekin, Görkem Kuş, Şakir Arslan","doi":"10.17305/bb.2026.14730","DOIUrl":"https://doi.org/10.17305/bb.2026.14730","url":null,"abstract":"<p><p>In-hospital mortality remains an important concern in patients with ST-elevation myocardial infarction (STEMI), highlighting the need for simple and readily available markers for early risk stratification. This study investigated the prognostic value of the blood urea nitrogen-to-serum albumin ratio (BAR) for in-hospital mortality in patients with STEMI undergoing primary percutaneous coronary intervention (pPCI). This single-center retrospective cohort study included 388 consecutive patients who underwent pPCI in 2024. Admission BAR was calculated using blood urea nitrogen (mg/dL) and serum albumin (g/L). Its association with in-hospital mortality was evaluated using receiver operating characteristic analysis and exploratory multivariable logistic regression, with Firth-penalized regression and bootstrap validation performed as sensitivity analyses. In-hospital death occurred in 18 patients (4.6%). Patients who died had significantly higher BAR values than survivors (0.7 vs. 0.4, p < 0.001). BAR showed good discrimination for in-hospital mortality, with an area under the curve of 0.869 (p < 0.001); the bootstrap-corrected area under the curve was also 0.869. An exploratory cut-off of 0.475 yielded 83.3% sensitivity and 75.4% specificity. In the multivariable model, each 0.1-unit increase in BAR was associated with higher odds of in-hospital mortality (odds ratio 1.412, 95% confidence interval 1.161-1.718; p = 0.0006), with a similar estimate in the Firth-penalized analysis (odds ratio 1.346, 95% confidence interval 1.121-1.616; p = 0.0008). Admission BAR may represent a simple candidate marker for early mortality risk stratification in STEMI patients undergoing pPCI; however, its prognostic performance and clinical utility require validation in larger prospective multicenter cohorts.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148802208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Post-translational modifications in sepsis-induced myocardial dysfunction - Molecular mechanisms and therapeutic targets: A review.","authors":"Xuan Liu, Haihua Pan, Jun Cha, Ruochen Sun, Chaojie He","doi":"10.17305/bb.2026.14517","DOIUrl":"https://doi.org/10.17305/bb.2026.14517","url":null,"abstract":"<p><p>Sepsis-induced myocardial dysfunction (SIMD) is a frequent and life-threatening complication of sepsis driven by interconnected inflammatory, oxidative, metabolic, and mitochondrial disturbances. Post-translational modifications (PTMs) have emerged as key regulators of these processes by dynamically altering protein activity, stability, localization, and signaling. This narrative review aimed to summarize the roles of major PTMs in SIMD and evaluate their potential as therapeutic targets. Relevant original studies and authoritative reviews published predominantly within the past decade were identified through targeted searches of PubMed and Web of Science and qualitatively synthesized. Current evidence indicates that phosphorylation, acetylation, ubiquitination, protein methylation, ADP-ribosylation, and palmitoylation regulate major pathways involved in myocardial inflammation, oxidative stress, mitochondrial dysfunction, metabolic reprogramming, apoptosis, and impaired contractility. Crosstalk among these modifications further integrates signaling networks, while upstream epigenetic mechanisms, including DNA methylation and N6-methyladenosine RNA modification, can influence PTM-related enzymes and downstream signaling. Experimental studies also suggest that pharmacological modulation of PTM-regulated pathways may attenuate myocardial injury; however, most mechanistic and therapeutic evidence derives from animal models and cultured cells, with limited validation in human septic myocardium. PTMs therefore represent promising mechanistic and therapeutic targets in SIMD, but systematic characterization of PTM crosstalk and rigorous human translational studies are required before PTM-directed strategies can be incorporated into clinical practice.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148802256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel peptide inhibitors targeting the TGF-β receptor I/II complex modulate SMAD and ERK signaling <i>in vitro</i>.","authors":"Jacek Plichta, Michał Seweryn Karbownik, Piotr Kuna, Michał Panek","doi":"10.17305/bb.2026.14724","DOIUrl":"https://doi.org/10.17305/bb.2026.14724","url":null,"abstract":"<p><p>Transforming growth factor-β (TGF-β) contributes to fibrosis, immunosuppression, and tumor progression, but systemic TGF-β inhibition is limited by toxicity and lack of selectivity. This exploratory proof-of-concept study evaluated novel peptides designed to target the TGF-β receptor I/II complex and examined their effects on canonical and noncanonical TGF-β signaling in vitro. Peptides 2_5 and 2_6, selected by in silico docking of receptor-ligand interface-derived sequences, were tested in human embryonic kidney 293T (HEK293T) cells at 20 and 50 μM, with the TGF-β receptor I inhibitor SD-208 as a reference. Total and phosphorylated SMAD2, SMAD3, extracellular signal-regulated kinase 1/2 (ERK1/2), and c-Jun N-terminal kinase (JNK) were assessed by Western blotting and densitometry. Peptide 2_5 showed the strongest activity, reducing total ERK1/2 by 65% at 50 μM and phosphorylated ERK1/2 by 90.4% and 83.4% at 20 and 50 μM, respectively; SD-208 reduced total and phosphorylated ERK1/2 by 64.3% and 54.5%, respectively. Peptide 2_5 also reduced total SMAD2 by 81% at 50 μM, whereas its effect on SMAD2 phosphorylation was inconsistent. Peptide 2_6 showed minimal effects, JNK was largely unaffected, and SMAD3 results were inconclusive because of weak signals. These preliminary findings suggest that peptide 2_5 may differentially modulate TGF-β signaling, with a stronger effect on ERK1/2 than on SMAD2; however, receptor targeting and pathway selectivity require confirmation in fully replicated quantitative studies.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148802262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulatory and other-cause mortality after neoadjuvant versus adjuvant chemotherapy in women with stage II-III breast cancer.","authors":"Burcu Zihni, İsmail Zihni, Mehmet Zafer Sabuncuoğlu","doi":"10.17305/bb.2026.14742","DOIUrl":"https://doi.org/10.17305/bb.2026.14742","url":null,"abstract":"<p><p>Most women with operable breast cancer increasingly survive long enough for non-cancer causes to become important contributors to mortality, particularly at older ages. We investigated whether the recorded sequence of systemic therapy relative to surgery among women receiving chemotherapy was associated with circulatory mortality and examined how causes of death evolve in long-term survivors. This retrospective population-based cohort study included 74,233 women with stage II-III non-metastatic invasive breast cancer diagnosed between 2010 and 2015 in the Surveillance, Epidemiology, and End Results (SEER) database who received chemotherapy and definitive surgery. A six-month landmark was used to reduce immortal-time bias, and treatment groups were balanced using stabilized inverse-probability-of-treatment weighting. Weighted cumulative incidence, cause-specific hazard, and Fine-Gray subdistribution models were used to evaluate circulatory mortality, while mortality patterns after a five-year landmark were examined descriptively by age. Median follow-up was 10.8 years. The weighted 10-year cumulative incidence of circulatory death was 2.06% after recorded preoperative systemic therapy and 2.10% after postoperative therapy, corresponding to a risk difference of -0.05 percentage points (95% confidence interval [CI], -0.31 to 0.18). The cause-specific hazard ratio was 1.092 (95% CI, 0.968-1.231), and the subdistribution hazard ratio was 1.024 (95% CI, 0.920-1.140). Among deaths occurring after the five-year landmark, the circulatory share increased with age, reaching 25.5% in women aged ≥75 years at diagnosis; however, other non-circulatory causes remained the largest category (49.9%). In women aged ≥75 years who survived five years, circulatory mortality approached and eventually exceeded breast-cancer mortality, but the difference was not significant at the prespecified seven-year time point. The recorded systemic-therapy/surgery sequence was not associated with long-term circulatory mortality. In older long-term breast-cancer survivors, late mortality is predominantly multimorbid rather than circulatory-dominant, supporting survivorship care that addresses cardiovascular risk within a broader framework of age-related competing health risks.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148802193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Black mulberry fruit extract attenuates valproic acid-induced toxicity by enhancing antioxidant defenses in FaO cells.","authors":"Iza Oblak, Nebojša Pavlović, Saša Vukmirović, Dušan Šuput, Nebojša Stilinović, Irina Milisav","doi":"10.17305/bb.2026.14532","DOIUrl":"https://doi.org/10.17305/bb.2026.14532","url":null,"abstract":"<p><p>Valproic acid (VPA) is widely used to treat neurological and psychiatric disorders but may cause hepatotoxicity partly through oxidative stress and impaired cellular metabolism. This study investigated whether black mulberry (Morus nigra L.) fruit extract attenuates VPA-induced injury in rat FaO hepatoma cells. Cells were exposed to VPA acutely (500 μg/mL for 28 hours) or chronically (120 μg/mL for 4 weeks). Mulberry extract (0.1 mg/mL) was added 3 hours before acute VPA exposure and maintained throughout co-treatment or administered during the final 24 hours of chronic exposure. Cell viability, hydrogen peroxide production, antioxidant enzyme activities, hepatocellular injury markers, glucose concentration, and extracellular 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical-scavenging capacity were assessed. Compared with VPA alone, mulberry extract significantly increased glutathione peroxidase (GPx) activity under both acute and chronic conditions. During chronic VPA exposure, it also increased glutathione S-transferase (GST) activity and extracellular ABTS radical-scavenging capacity, improved cell viability, and reduced extracellular alanine aminotransferase (ALT) activity. During acute exposure, mulberry significantly reduced extracellular aspartate aminotransferase (AST) activity, whereas the improvement in cell viability was not statistically significant. Hydrogen peroxide production did not differ among acute treatment groups, and mulberry did not restore superoxide dismutase or catalase activity. These findings indicate that black mulberry fruit extract partially mitigates VPA-induced hepatocellular injury, primarily by enhancing glutathione-dependent antioxidant defenses. Further dose-response and in vivo studies are required to confirm its hepatoprotective potential.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148802110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leukocyte telomere length and gut microbiome profiles in pancreatic ductal adenocarcinoma and at-risk conditions.","authors":"Keti Kharazishvili, Alzbeta Hujova, Tomas Hucl, Katerina Balounova, Klara Vokacova, Michal Kroupa","doi":"10.17305/bb.2026.14506","DOIUrl":"https://doi.org/10.17305/bb.2026.14506","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is often diagnosed at an advanced stage, highlighting the need for minimally invasive biomarkers capable of distinguishing it from related risk conditions. This study evaluated relative leukocyte telomere length (LTL) and gut microbiome profiles as potential biomarkers for PDAC. The study included 244 participants with PDAC (n = 37), chronic pancreatitis (CP; n = 56), type 2 diabetes mellitus (T2DM; n = 99), or no related risk conditions (controls; n = 52). LTL was measured by monochrome multiplex quantitative polymerase chain reaction (qPCR), while gut microbiome composition was assessed by 16S ribosomal RNA (rRNA) gene sequencing in a subset of participants with PDAC (n = 12), CP (n = 13), and controls (n = 7). LTL varied with age, sex, and smoking status. After adjustment for these factors, patients with PDAC had significantly longer LTL than controls (p = 0.029), whereas differences between PDAC and CP or T2DM were not significant. LTL showed limited ability to discriminate PDAC from controls (area under the receiver operating characteristic curve = 0.651) and was not associated with overall survival. Gut microbiome diversity and taxonomic composition did not differ significantly among the analyzed groups. These findings indicate that LTL has limited utility as a standalone diagnostic or prognostic biomarker for PDAC but may warrant further evaluation as a complementary marker in larger prospective studies. The exploratory microbiome findings also require validation in adequately powered cohorts.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148802295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sabinene attenuates inflammation and oxidative stress in CFA-induced arthritis: <i>In vivo</i> and <i>in silico</i> evidence implicating TLR4/NLRP3/NF-κB signaling.","authors":"Kanwal Asif, Ambreen Malik Uttra, Arham Shabbir, Sumera Qasim, Saima Kalsoom, Abdulelah Alhazza, Hamoud Alotaibi, Mona Al Hamod, Saleh Alfuraih, Ali F Almutairy, Raiyan Faisal Alharbi, Ashfaq Ahmad","doi":"10.17305/bb.2026.14544","DOIUrl":"https://doi.org/10.17305/bb.2026.14544","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a chronic immune-mediated disease in which persistent inflammation and oxidative stress contribute to progressive joint damage. This study evaluated the prophylactic effects of sabinene in complete Freund's adjuvant (CFA)-induced arthritis and explored potential molecular associations using integrated in vivo and computational approaches. Rats were allocated to vehicle control, arthritic control, piroxicam, or sabinene groups (15, 30, or 60 mg/kg; n = 6/group); sabinene was administered orally beginning 30 minutes before CFA injection and continued for 28 days. Paw swelling, hematological and biochemical parameters, inflammatory and oxidative-stress markers, and gene expression were assessed, followed by network pharmacology, enrichment analysis, and molecular docking. Sabinene dose-dependently attenuated CFA-induced paw swelling and body-weight loss and improved hematological, hepatic, renal, and inflammatory parameters. Treatment also enhanced antioxidant defenses and reduced lipid peroxidation, prostaglandin E₂, 5-lipoxygenase, and anti-cyclic citrullinated peptide antibody levels. Sabinene reduced messenger RNA expression of nuclear factor kappa B (NF-κB), toll-like receptor 4 (TLR4), NOD-like receptor family pyrin domain-containing 3 (NLRP3), caspase-1, gasdermin D, and other pro-inflammatory genes while increasing interleukin-4 and interleukin-10 expression. Network pharmacology identified 133 overlapping sabinene-RA targets, and molecular docking predicted interactions with tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), signal transducer and activator of transcription 3 (STAT3), and interferon gamma (IFN-γ). These findings support a prophylactic protective effect of sabinene against CFA-induced arthritis associated with reduced inflammation, improved antioxidant status, and modulation of inflammasome-related gene expression. Further protein-level, functional, and post-induction studies are required to confirm the proposed mechanisms and therapeutic relevance.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148765751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temporal increase in the endothelial activation and stress index before brain death.","authors":"Aysen Baysan, Mehmet Tercan, Erhan Ozyurt, Nilgun Kavrut Ozturk, Kerem Inanoglu, Meltem Ceylan Delice, Sadik Ozmen","doi":"10.17305/bb.2026.14540","DOIUrl":"10.17305/bb.2026.14540","url":null,"abstract":"<p><p>Brain death (BD) is accompanied by systemic inflammation and endothelial dysfunction, but temporal changes in endothelial injury during progression to BD remain insufficiently characterized. This study aimed to evaluate serial changes in the Endothelial Activation and Stress Index (EASIX) during the clinical course leading to BD. This retrospective, single-center study included patients diagnosed with BD in the intensive care unit (ICU) between January 2019 and June 2025. EASIX, calculated from lactate dehydrogenase (LDH), serum creatinine, and platelet count, was assessed at ICU admission, 24 hours before BD, 12 hours before BD, and at BD diagnosis. Temporal differences were analyzed using the Friedman test, followed by Wilcoxon signed-rank tests with Bonferroni adjustment. Of 222 patients diagnosed with BD, 52 met the inclusion criteria. EASIX values differed significantly across the four time points (p < 0.001), with significant differences observed between ICU admission and BD diagnosis and between 24 and 12 hours before BD. These findings indicate that EASIX increases during the clinical course leading to BD and may reflect progressive systemic endothelial activation and worsening critical illness rather than a BD-specific process. Prospective comparative studies are needed to validate its clinical utility.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148723146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}