Eurasian Journal of Chemical, Medicinal and Petroleum Research

Abstract Macrophages, as central components of the innate immune system, play a pivotal role in orchestrating inflammatory responses. Recent evidence highlights that macrophage function is closely governed by metabolic reprogramming, a process in which shifts in cellular metabolism modulate immune phenotypes and effector functions. During chronic inflammation, macrophages exhibit altered utilization of glycolysis, oxidative phosphorylation (OXPHOS), fatty acid oxidation, and glutamine metabolism. These metabolic shifts determine the polarization state of macrophages, driving pro-inflammatory (M1-like) or anti-inflammatory (M2-like) phenotypes. Persistent metabolic dysregulation contributes to uncontrolled inflammation and tissue damage in chronic diseases such as atherosclerosis, diabetes, rheumatoid arthritis, and cancer. In atherosclerosis, macrophages accumulate lipids and undergo metabolic stress that sustains inflammatory activation. In diabetes, hyperglycemia-induced metabolic reprogramming enhances macrophage glycolysis and inflammatory cytokine production. In tumors, the hypoxic microenvironment reshapes macrophage metabolism to support immunosuppressive and pro-tumorigenic activity. Understanding how metabolic pathways regulate macrophage function reveals therapeutic opportunities. Targeting key enzymes such as hexokinase 2, isocitrate dehydrogenase, or AMP-activated protein kinase (AMPK) offers potential to reprogram macrophages toward inflammation resolution. This review integrates findings from immunometabolism and pathophysiology to demonstrate that macrophage metabolic reprogramming acts as a central mechanism linking cellular metabolism to chronic inflammation and disease progression. Therapeutic strategies that correct macrophage metabolic imbalance may provide novel approaches for managing chronic inflammatory disorders and improving patient outcomes.

Abstract Regenerative endodontics is evolving rapidly as an alternative to conventional root canal therapy, aiming not merely to disinfect and fill root canals, but to restore viable pulp tissue with physiological functions such as immune defense, innervation, and dentinogenesis. Central to this paradigm are stem cell–based therapies, which, in concert with scaffolds and signaling factors, offer potential to regenerate the pulp–dentin complex in teeth with necrotic or damaged pulps. This review summarizes the latest progress in the field, focusing on (1) sources of stem cells (e.g. dental pulp stem cells, stem cells from the apical papilla, mesenchymal stem cells of non dental origin, and induced pluripotent stem cells), (2) scaffold design and biomaterial strategies, (3) delivery of growth factors and bioactive cues, (4) cell transplantation vs. cell homing approaches, (5) in vitro, in vivo, and early clinical evidence, and (6) major challenges and future directions. Evidence from animal studies and limited human trials shows promise in root maturation, vascularization, and functional tissue formation. However, full regeneration of the native pulp–dentin architecture — particularly with true odontoblast layer, innervation, and predictable function — remains elusive. Key hurdles include controlling stem cell differentiation and proliferation, immune compatibility, standardized protocols, safety (e.g. tumorigenesis risk), and regulatory issues. Emerging innovations such as cell-free secretomes or exosomes, 3D bioprinting of scaffolds, gene engineering for guided differentiation, and smart biomaterials responsive to microenvironment cues may help overcome current limitations. To accelerate translation toward routine clinical use, rigorous multicenter trials with long-term follow-up, development of GMP grade cell banks, and interdisciplinary collaboration are essential.

Abstract Microbiome dysbiosis, an alteration in the composition, diversity, or function of host-associated microbial communities, is increasingly implicated in both gastrointestinal (GI) disorders (e.g., IBS, IBD, colorectal cancer) and systemic metabolic diseases. This study evaluates dysbiosis as a predictive biomarker for incident GI and metabolic disease using integrative multi-omics profiling (16S/shotgun metagenomics, metabolomics, host markers) and machine-learning risk models. We will recruit a prospective cohort (n ≈ 1,000) with baseline stool, blood, and clinical phenotyping and follow participants 3–5 years for disease incidence and progression. Primary outcomes are new diagnoses of IBD, IBS, colorectal neoplasia, NAFLD, and NAFLD; secondary outcomes include changes in glycemic markers, liver enzymes, and bowel-symptom scores. Predictors include alpha/beta diversity, taxon-level signatures (e.g., depletion of butyrate-producers), functional gene modules (SCFA synthesis, bile-acid metabolism, LPS biosynthesis), and metabolite markers (SCFAs, secondary bile acids, trimethylamine N-oxide). Models will adjust for diet, medications (antibiotics, PPIs), BMI, age, and socioeconomic factors. We will validate models internally (cross-validation) and externally (independent cohort). If successful, the work will (1) quantify predictive power of microbiome-derived features beyond traditional risk factors, (2) identify mechanistic microbe–metabolite pathways linking dysbiosis to disease, and (3) provide candidate targets for early intervention. However, clinical translation must consider variability in sampling and current limits of commercial testing; robust standardization and prospective validation are required.

Abstract This study explores the effects of temperature and pressure variations on catalyst degradation mechanisms—specifically catalyst crushing and catalyst cake formation—in a light naphtha isomerization unit. Operating conditions within the range of 200–280°C and 10–35 bar were simulated to evaluate mechanical and physical stress on the catalyst bed. Two performance indices were defined: the Catalyst Crushing Index (CCI) and Catalyst Cake Thickness (CCT). Results revealed that both CCI and CCT increase significantly with rising temperature and pressure, with pressure having a more pronounced impact. Elevated pressure intensified catalyst compaction, while temperature contributed to structural weakening and sintering. The analysis showed that high-pressure environments above 25 bar and temperatures exceeding 260°C led to accelerated crushing and cake buildup, contributing to pressure drop, pore blockage, and reduced hydrogen diffusion. These degradation mechanisms ultimately reduce catalytic activity and operational efficiency. The findings suggest that maintaining optimal reactor conditions and incorporating real-time monitoring systems are essential for preventing early catalyst failure. This research provides a predictive framework for improving catalyst performance and life cycle in isomerization processes and can support operational decision-making in refinery settings.

Abstract Introduction: Acute myocardial infarction remains a leading cause of morbidity and mortality, with impaired myocardial reperfusion and electrical instability playing key roles in adverse outcomes. Atrial conduction abnormalities may reflect ischemic burden and microvascular dysfunction. This study aimed to evaluate the clinical and prognostic significance of atrial electrical indices in relation to reperfusion quality and coronary disease severity.

Material and methods: This retrospective cross‑sectional study included 315 consecutive patients admitted to Shahid Madani Hospital, Tabriz, between March 2023 and March 2024. Clinical, laboratory, electrocardiographic, and angiographic data were extracted from medical records. Standardized ECG measurements, angiographic assessment, and post‑PCI outcomes were analyzed to evaluate electrophysiological and clinical associations.

Results: Among 315 cardiomyopathy patients, ischemic etiology was associated with a significantly higher prevalence of isoelectric T waves in lead aVR compared with non‑ischemic cardiomyopathy (P=0.004 and P=0.030). Other T‑wave amplitude categories showed no significant differences between etiologic groups, nor any significant association with the severity of left ventricular systolic dysfunction (all P>0.05).

Conclusion: This study demonstrates that while traditional cardiovascular risk factors are highly prevalent in patients with cardiomyopathy, T‑wave amplitude in lead aVR provides limited functional insight into left ventricular systolic impairment.

Abstract Introduction: Right ventricular pacing is critical for managing bradyarrhythmia but can impair left ventricular function due to dyssynchrony. This study examines the impact of septal versus apical pacing on left ventricular ejection fraction (LVEF) using three-dimensional echocardiography, aiming to determine which approach better preserves cardiac function by maintaining more physiologic ventricular activation.

Material and methods: This randomized historical control study included 60 patients undergoing permanent pacemaker implantation at Shahid Madani Hospital between 2011 and 2013. Patients were assigned to septal or apical right ventricular pacing. Three dimensional echocardiography was used to compare left ventricular volumes and ejection fraction, with blinded assessment and standard statistical analyses to evaluate functional differences between pacing strategies.

Results: Patients with septal right ventricular pacing demonstrated preserved conventional and three‑dimensional ejection fraction with no significant deviation from normal values (P > 0.05). Compared with apical pacing, septal pacing was associated with significantly higher conventional and 3D ejection fraction and less impaired septal longitudinal strain, with a clear intergroup difference in SPSS‑Sep.A (P = 0.001).

Conclusion: This study demonstrates that right ventricular septal pacing is associated with more favorable left ventricular systolic performance compared with apical pacing when assessed using both conventional and three dimensional echocardiography.

Abstract Introduction: Right ventricular pacing can alter physiological ventricular activation, potentially leading to mechanical dyssynchrony and regional myocardial dysfunction. Advanced echocardiographic techniques, particularly segmental peak systolic strain analysis, allow sensitive detection of these changes. The aim of this study was to evaluate and compare segmental peak systolic strain in patients with septal versus apical right ventricular pacing.

Material and methods: This randomized clinical study with a historical control design was conducted at Shahid Madani Hospital, Tabriz, between 2011 and 2013. Sixty patients requiring permanent pacing were enrolled by census sampling and allocated to septal or apical right ventricular pacing. Segmental peak systolic strain was assessed using speckle‑tracking echocardiography, with blinded analysis and appropriate statistical comparison between groups.

Results: In this cohort, septal right ventricular pacing demonstrated relatively preserved and homogeneous segmental peak systolic strain compared with apical pacing. Both pacing strategies significantly reduced mid and basal septal strain compared with normal values (p < 0.001), with no significant difference between RVS and RVA in Sep.M and Sep.B (p > 0.05). In contrast, anterior septal angle and motion were significantly altered in RVA compared with RVS and normal reference values (p < 0.05).

Conclusion: This study demonstrates that the site of right ventricular pacing plays a critical role in determining regional left ventricular myocardial mechanics. Although both septal and apical pacing are associated with deviations from physiological strain patterns, septal pacing consistently preserves a more uniform and coordinated deformation profile across myocardial segments.

Abstract Introduction: Right ventricular pacing can profoundly influence left ventricular mechanics, particularly when non‑physiological activation patterns induce mechanical dyssynchrony and impaired myocardial deformation. Global peak systolic strain is a sensitive marker for detecting pacing‑related alterations in ventricular function. This study aimed to evaluate and compare global peak systolic strain in patients undergoing right ventricular apical versus septal pacing to determine the pacing site associated with more preserved myocardial mechanics.

Material and methods: This randomized historical control study included 60 patients undergoing permanent right ventricular pacing at a tertiary cardiac center. Participants were equally assigned to apical or septal pacing. Standardized echocardiography with speckle tracking analysis was performed to quantify global peak systolic strain, and outcomes were compared using appropriate statistical methods under blinded assessment and ethical approval.

Results: Right ventricular pacing was associated with significant impairment of left ventricular myocardial deformation. Global longitudinal strain showed a stepwise reduction from normal subjects to septal pacing and was most severely attenuated with apical pacing (p < 0.001). Inferior and mid‑inferior segmental strain was preserved with septal pacing but significantly reduced with apical pacing compared with both normal and septal groups (p ≤ 0.01).

Conclusion: This study demonstrates that the site of right ventricular pacing is a critical determinant of left ventricular mechanical performance. Although septal pacing does not fully replicate physiological ventricular activation, it is associated with relatively preserved global and regional myocardial deformation and reduced mechanical heterogeneity compared with apical pacing.