Biomarkers最新文献

Background: Acute carbon monoxide poisoning triggers complex metabolic derangements including acidosis and alkalosis, but their correlation with neurological injury severity remains insufficiently characterized clinically.

Methods: Consecutive poisoning patients (age ≥14) admitted between January 2019 and February 2025 were classified by neurological impairment severity. Acid-base parameters were analysed using Kruskal-Wallis tests, Spearman's correlation, and principal component analysis with varimax rotation.

Results: Among 940 patients (37.2% male), participants were categorized into three groups by neurological impairment severity: Mild (n = 597), moderate (n = 225), and severe (n = 118). Severe cases showed lower pH (7.39 vs. 7.41), reduced PaCO₂ (34.5 vs. 38.2 mmHg), greater base excess deficit -3.3 vs. 0.4), and higher lactate (3.7 vs. 1.6 mmol/L) (all p < 0.001). Neurological severity positively correlated with lactate (rho = 0.338) and inversely with base excess (rho = -0.268). Principal component analysis identified two components: Factor Component 1 (FAC1) (metabolic compensation, 47-65% variance) and FAC2 (respiratory regulation, 26-41% variance), with FAC1 inversely correlating with severity (rho = -0.319, p < 0.001).

Conclusions: Neurological impairment severity shows dose-dependent correlation with metabolic dysfunction (lactate accumulation, mixed metabolic acidosis-respiratory alkalosis). FAC1 (metabolic compensation) is a strong prognostic biomarker in acute carbon monoxide poisoning.

Objective: C-reactive protein (CRP) levels are generally not correlated with systemic lupus erythematosus (SLE) disease activity. We aimed to develop an algorithm to evaluate juvenile SLE (JSLE) patients with elevated CRP.

Methods: JSLE patients diagnosed at <18 years were included. Each episode of CRP elevation was evaluated separately.

Results: Of 190 JSLE patients (F/M:4/1), 88 (46.3%) never had an elevated CRP, while 102 (53.7%) had 174 episodes of CRP elevation. Causes were infection (n = 139), arthritis (n = 15), macrophage activation syndrome (MAS) (n = 9), MAS and infection (n = 3), serositis (n = 6), and vasculitis (n = 2). MAS was more common in the SLE disease activity index (SLEDAI)>4 group, while infections were more frequent in the SLEDAI ≤ 4 group. MAS episodes were more prevalent among patients with CRP >2x the upper limit of normal. We developed an algorithm to prioritize etiology in JSLE patients with elevated CRP. It led to the correct etiology in 164 of 165 episodes (99.4%) in the primary cohort. In an external JSLE cohort including 37 patients with 68 elevated CRP episodes, the algorithm led to the correct etiology in 67 (98.5%).

Conclusion: Our algorithm could assist physicians evaluating elevated CRP episodes in JSLE patients. Validation in larger cohorts may improve its performance.

Heavy metals have been reported to induce neurotoxicity associated with neurodegenerative disorders. However, there is a dearth of information on Al, Pb and Mn mixture exposure on cerebral cortex functions. This study is aimed at evaluating the effects of Al, Pb and Mn mixture on the cerebral cortex functions. Rats were exposed to Pb 20 mg/kg, Al 35 mg/kg and Mn 0.564 mg/kg body weight singly or in combination for 90 d. Our results showed that Al, Pb and Mn singly or in combination exposure significantly (p ≤ 0.05) decreased antioxidant enzymes activities, glutathione level and increased oxidative stress and neuroinflammation biomarkers in the cerebral cortex of the exposed rats. Moreover, induction of inflammation maker, i.e. COX-2 was associated with increases in apoptotic induction. Furthermore, Al, Pb and Mn singling or in combination exposure significantly (p ≤ 0.05) increased Nrf-2 and decreased BDNF and HO-1 induction as well as increased amyloid precursor proteins and decreased occludin level. Taken together, our result indicates that Al, Pb and Mn mixture exacerbates oxidative stress, neuroinflammation, and apoptosis via downregulation of Nrf2/HO-1/BDNF signalling pathway.

Introduction: The mechanism of cell death during pulsed-field ablation (PFA) appears distinct from thermal energy sources like radiofrequency ablation (RFA), with apoptosis often cited as the primary cause in PFA. This study aimed to clarify the mechanism by comparing markers of necrosis and apoptosis after PFA and RFA.

Methods and results: Patients undergoing pulmonary vein isolation (PVI) for atrial fibrillation were randomized to receive either PFA (Farapulse, Boston Scientific) or RFA (CARTO Smart Touch, Biosense Webster). Myocardial necrosis was assessed via troponin I, and apoptosis via soluble cleaved caspase-3 and Fas ligand, measured pre- and one day post-ablation.

Results: Sixty-five patients were enrolled (PFA: n = 33; RFA: n = 32), with comparable baseline characteristics. One day post-procedure, troponin I levels were significantly higher in the PFA group (median 10,102 ng/L; IQR 8,272-14,207) versus the RFA group (1,006 ng/L; IQR 603-1,433). No post-procedure increase in caspase-3 or Fas ligand was observed in the PFA group, and no differences in apoptotic markers were found between groups.

Conclusion: In vivo, apoptosis does not appear to be the predominant mechanism of cardiomyocyte death following PFA for atrial fibrillation.

Introduction: Early cancer detection significantly improves treatment outcomes; however, many cancers remain undiagnosed until advanced stages. This highlights the urgent need for rapid and precise diagnostic tools. Biosensors offer a transformative approach in cancer diagnostics by enabling early detection and continuous monitoring through the identification of molecular biomarkers.

Methods: Biosensors function by converting biological elements-such as proteins, RNA, or genetic material-into measurable electrical signals. These devices are tailored to detect specific biomarkers, including proteins, peptides, gene mutations, or abnormal gene expression levels associated with various cancers.

Results: Biosensors provide high sensitivity and specificity in identifying cancer cells. They enable real-time monitoring of tumour progression, angiogenesis, and treatment responses. These tools also facilitate accurate imaging of cancer cells and help evaluate the effectiveness of targeted therapies such as chemotherapy.

Conclusion: The integration of biosensors into clinical practice could revolutionize cancer diagnostics by offering early, accurate, and minimally invasive detection methods. This review explores recent advances in biosensor development, the evolving landscape of cancer biomarkers, and the application of different biosensor technologies in cancer detection. Additionally, it addresses current limitations and challenges in clinical implementation, emphasizing the potential of biosensors to enhance patient outcomes through early intervention.

Background: Mitochondria play a crucial role in cellular processes, such as energy metabolism, reactive oxygen species (ROS) generation and apoptosis. Mitochondrial dysfunction induced by stress has been implicated in various health conditions. Circulating cell-free mitochondrial DNA (CFC-MT-DNA) has emerged as a potential biomarker reflecting mitochondrial damage under stress.

Methods: To evaluate the association between CFC-MT-DNA levels and human stress through a systematic review and meta-analysis of case-control studies. A comprehensive literature search was conducted across PubMed, Web of Science and ScienceDirect databases up to September 2023. Eight eligible studies assessing CFC-MT-DNA levels in stressed vs. control individuals were included. Data were analysed using RevMan version 5.4 software.

Results: The meta-analysis revealed significantly elevated CFC-MT-DNA levels in individuals experiencing stress (p = 0.03), particularly in psychological stress-related conditions, such as bipolar disorder (BD) and major depressive disorder (MDD). However, no significant increase was observed in physiological stress conditions, including diabetes and sports training. High heterogeneity (I² = 96%) was observed across studies.

Conclusions: CFC-MT-DNA shows promise as a non-invasive biomarker for psychological stress. Further longitudinal and mechanistic studies are needed to clarify its role across different types of stress and its potential clinical utility.

Background: Breast cancer (BC) is the most common cancer in women. Taxanes are widely used, but their neurotoxicity affects patients' quality of life. Genetic polymorphisms in CYP450 enzymes influence taxane metabolism, leading to variability in toxicity risk.

Methods: A literature search was conducted to identify studies on the association between CYP450 polymorphisms and Taxane-Induced Peripheral Neuropathy (TIPN) in BC patients. Odds ratios (OR) and hazard ratios (HR) with 95% confidence intervals (CI) were estimated using a random-effects model in RStudio.

Results: Nine studies with 3034 patients were included. Overall CYP polymorphisms showed a significant association with TIPN (OR: 1.2877, 95% CI: 1.0262-1.6157). CYP1B1 polymorphism had an inconsistent link to TIPN by OR of 1.1524 (95% CI: 0.7441-1.7849). CYP2C8 polymorphism demonstrated the strongest association (OR: 1.5532, 95% CI: 1.2013-2.0082; HR: 1.5236, 95% CI: 1.1317-2.0512). CYP3A4 showed no significant association (OR: 1.0988, 95% CI: 0.5022-2.4404).

Conclusions: CYP2C8 polymorphisms were significantly linked to TIPN. While CYP1B1 showed inconsistent results, CYP3A4 had no significant association. These findings imply that CYP2C8 genetic variations may affect taxane metabolism and neurotoxicity risk, indicating that pharmacogenomic profiling could help personalize chemotherapy and reduce adverse effects.

Background: There are hundreds of xenobiotics that can damage the respiratory system, necessitating mechanical ventilation. Therefore, acute respiratory toxicity may represent a serious condition that can be complicated by acute respiratory distress syndrome (ARDS). This study aimed to evaluate the role of Human Neutrophil Elastase (HNE) as a predictor of acute respiratory toxicity outcome and to compare it with the neutrophil lymphocyte ratio (N/L ratio) and platelet lymphocyte ratio (P/L ratio).

Methods: This prospective study was conducted on adult patients with acute respiratory toxicity admitted to Poison Control Center; Ain Shams University Hospitals from January 2022 to December 2022. Their HNE, N/L ratio, and P/L ratio levels were assessed twice: First upon admission and again 24 h later.

Results: Fifty-five patients were enrolled in the study and were classified into ARDS group and non-ARDS group. HNE levels were significantly higher in ARDS patients at both time points with excellent predictive performance. Although the N/L and P/L ratios were significantly elevated in ARDS patients at 30 h, their diagnostic performance was inferior to HNE. Combining HNE with the N/L ratio offered minimal additional benefit over HNE alone.

Conclusion: HNE Level can serve as predictor of ARDS in acutely intoxicated patients.

Background and aim: The protective effects of aqueous extract of Pistacia lentiscus leaves (AELPL) against gastric and duodenal ulcers induced by alcohol oral gavage administration in Wistar rats were investigated in this study.

Methods: The rats were divided into six groups control, ethanol single, ethanol + AEPL (25-50-100) and famotidine + ethanol.

Results: HPLC-MS analysis allowed the identification of numerous phenolic compounds in P. lentiscus leaves such as flavonoids (isoquercetin and luteolin), flavonols (catechin, rutin and kaempferol), phenolic acids (ellagic and dicaffeoylquinic) and tannins. Ethanol administration induced significant gastric and duodenal ulcerative lesions, while AELPL pretreatment (25, 50 and 100 mg/kg) provided a dose-dependent mucosal protection comparable to famotidine, a widely used drug for the treatment of gastric ulcers. AELPL like famotidine also restored gastric pH and volume, counteracting ethanol-induced acidity. Biochemical analyses demonstrated that AELPL like famotidine mitigated oxidative stress by reducing lipid peroxidation, carbonylated proteins and hydrogen peroxide levels, whereas it restored non-protein thiols content in the stomach, duodenum and plasma in a dose-dependent manner. Additionally, AELPL restored antioxidant enzyme activities including catalase, superoxide dismutase, glutathione peroxidase and glutathione-S-transferase. AELPL also reduced ethanol-induced increase in free iron, ionized calcium and interleukin-6 levels, indicating its anti-inflammatory potential.

Conclusion: These findings suggest that AELPL exhibits gastroduodenal protective effects against ethanol-induced damage, with efficacy comparable to famotidine. Protective mechanisms likely involve modulation of oxidative stress and inflammation, supporting AELPL's potential as a therapeutic agent for gastroduodenal injuries.