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This study investigates the impact of hybrid nanoparticles on the temperature of nuclear reactor coolant, with a focus on graphene nanoplatelet (GNP)‐based hybrid nanoparticles. Sixteen different hybrid nanofluids were analyzed, and their performance was compared with a standard water‐based coolant. The criticality values were obtained through MCNP modeling, revealing that higher nanoparticle ratios led to increased criticality, with the highest value of 1.3239 observed in GNP‐Fe3O4 + Al2O3 nanofluids (0.05 wt%) and the lowest value of 1.2935 in GNP–Fe3O4 + SiO2 nanofluids (0.001 wt%). Temperature variations showed that increasing nanoparticle concentrations resulted in slightly higher temperatures, with a maximum of 611.97 K for 0.05 vol.% GNP nanoparticles. Additionally, the departure from nucleate boiling ratio values were consistently above the safety threshold of 2.08, with the lowest value of 3.657 for GNP–Fe3O4 + SiO2 nanofluids (0.05 vol.%). These findings suggest that hybrid nanofluids, particularly those with higher nanoparticle ratios, can enhance the thermal performance and safety margins of nuclear reactor coolants, offering a promising avenue for future research and application. Exploring thermal flow dynamics in pressurized water reactors using hybrid graphene nanoplatelet coolants.

This study examines the potential of nanofluids to enhance the thermal efficiency of flat-plate solar water heating systems (SDHW) through numerical modeling using TRNSYS software. Improving the efficiency of such systems is critical for increasing the viability and sustainability of solar thermal technologies, particularly in regions with high solar potential like Türkiye. Three different nanofluids (Al 2 O 3 , TiO 2 , and CuO) were evaluated for their ability to improve heat transfer and system performance. Simulation results revealed that incorporating 0.1% Al 2 O 3 into the working fluid increased the collector outlet temperature from 97 °C (with pure water) to 120 °C, indicating a 23% improvement. Comparable enhancements were observed with TiO 2 and CuO nanofluids. Furthermore, collector efficiency, which typically ranges between 35 and 40% under peak solar conditions, was elevated to approximately 45% with the use of nanofluids. These findings suggest that nanofluids significantly improve thermal performance and energy conversion efficiency in SDHW systems. The results highlight the practical potential of nanofluids in advancing solar thermal technology and promoting cleaner, more efficient renewable energy solutions.

Nuclear energy sustainability and deployment flexibility can be significantly enhanced through Small Modular Reactors (SMRs) technology. Critical to their operational success is the thorough assessment of thermal-hydraulic characteristics, especially when incorporating advanced fuel design concepts. This research conducts an extensive thermal-hydraulic analysis examining various thorium-based fuel formulations, including (Th- 235 U)O 2 , (Th- 233 U)O 2 , and an innovative (Th- 233 U- 235 U)O 2 composition, benchmarked against standard UO 2 fuel. The investigation encompasses both solid fuel arrangements and dual-cooled annular assembly designs, focusing on safety optimization and operational efficiency enhancement. The analysis focuses on key safety parameters, including pressure drop, coolant enthalpy, fuel centerline temperature, and Departure from Nucleate Boiling Ratio (DNBR). Results for solid fuel configurations reveal that thorium-based fuels exhibit reduced pressure drop, more efficient enthalpy distribution, lower peak fuel temperatures, and higher DNBR values compared to conventional UO 2 , highlighting improved thermal stability and safety margins. The (Th- 233 U- 235 U)O 2 mixture demonstrates a balanced performance by mitigating the limitations of other thorium compositions. In annular configurations, all fuel types benefit from enhanced heat removal due to the dual cooling surfaces, resulting in further reductions in pressure drop and peak temperatures, as well as a significant increase in DNBR values. The highest DNBR, reaching up to 3.051, confirms the annular geometry’s superior safety performance against boiling crises.

Background and Objectives: In this study, we aimed to investigate the effects of bosentan, an endothelin receptor antagonist, on endothelin-1 (ET-1), hypoxia-inducible factor-1 (HIF-1), nuclear factor-kappa B (NF-κB), and tumor necrosis factor (TNF)-α as inflammation markers, pro-oxidant antioxidant balance (PAB), and total antioxidant capacity (TAC) levels as oxidative stress parameters in lung tissues of rats in an experimental model of pulmonary contusion (PC) induced by blunt thoracic trauma. Materials and Methods: Thirty-seven male Sprague-Dawley rats were divided into five groups. C: The control group (n = 6) consisted of unprocessed and untreated rats. PC3 (n = 8) underwent 3 days of PC. PC-B3 (n = 8) received 100 mg/kg bosentan and was given orally once a day for 3 days. The PC7 group (n = 7) underwent 7 days of PC, and PC-B7 (n = 8) received 100 mg/kg bosentan and was given orally once a day for 7 days. Results: ET-1, NF-κB, TNF-α, HIF-1α, and PAB levels were higher, while TAC activity was lower in all groups compared with the control (p < 0.05). There was no significant difference in ET-1 and TNF-α levels between the PC-B3 and PC-B7 groups and the control group (p < 0.05), while NF-κB, HIF-1α, and PAB levels were still higher in both the PC-B3 and PC-B7 groups than in the control group. Bosentan decreased ET-1, NF-κB, TNF-α, HIF-1α, and PAB and increased TAC levels in comparison to the nontreated groups (p < 0.05). Conclusions: Bosentan decreased the severity of oxidative stress in the lungs and reduced the inflammatory reaction in rats with PC induced by blunt thoracic trauma. This suggests that bosentan may have protective effects on lung injury mechanisms by reducing hypoxia, inflammation, and oxidative stress. If supported by similar studies, bosentan can be used in both pulmonary and emergency clinics to reduce ischemic complications, inflammation, and oxidative stress in some diseases that may be accompanied by ischemia.

Objectives: HbA1c is the most widely used test as an indicator of glucoregulation in patients with type 2 diabetes mellitus (T2DM). Asprosin and oxidative stress levels can be reduced with good glycemic control (GC) and thus prevented or delayed micro/macro complications in patients with T2DM. The relationship between asprosin, which is thought to affect GC, and oxidative stress parameters such as lipid hydroperoxides (LOOHs), glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (Cu,Zn-SOD), and total antioxidant capacity (TAC) was evaluated in T2DM patients. Materials and Methods: The study was conducted prospectively in 75 healthy people admitted to the hospital for a general health check-up and 150 T2DM patients treated in the diabetes outpatient clinic. The patient’s glycemic status measurements were categorized as good glycemic control group (GGC) is defined as HbA1c < 7 and poor glycemic control (PGC) group is defined as HbA1c ≥ 7. Results: The study found a consistent increase in LOOH and MDA levels across the control, GGC, and PGC groups, while GSH, Cu/Zn-SOD, and TAC levels decreased in these respective groups. Additionally, asprosin levels showed a gradual rise in all groups. Positive correlations were observed between asprosin levels and various metabolic and oxidative stress markers, including BMI, WC, FBG, insulin, homeostasis model assessment for insulin resistance (HOMA-IR), DM duration, LOOH, and MDA, while negative correlations were noted with GSH, Cu/Zn-SOD, and TAC specifically in the PGC group. Furthermore, multivariate regression analysis identified HOMA-IR as the primary influencing factor on asprosin levels in PGC patients. Conclusions: Current glycemic dysregulation may lead to increased circulating asprosin and oxidative stress, which cause complications. Since asprosin levels may be an important hormonal factor in determining GC in T2DM, the use of this hormone may be recommended in the future to accelerate therapeutic approaches in T2DM. Early diagnosis and appropriate treatment may delay the development and progression of diabetic complications.

Adropin is a peptide involved in the regulation of glycolipid metabolism, contributing to improved glucose homeostasis and the mitigation of dyslipidemia. The objective of this study is to ascertain whether there is a discrepancy in the expression of microRNA-21 (miRNA-21) and adropin levels in Type 2 diabetes mellitus (T2DM) patients who also exhibit macro- and micro-vascular complications (nephropathy, neuropathy, retinopathy) were also observed to uncomplicated diabetes patients and healthy individuals; to explore the relationship between serum adropin and miR-21, endothelial dysfunction, and carotid intima-media thickness (CIMT). The present study comprised 89 patients with T2DM (microvascular n  = 24, macrovascular n  = 20, uncomplicated type 2 n  = 45) and 19 non-diabetic coronary artery disease (CAD). The control group was composed of 20 healthy individuals. Expression of miRNA-21 in all diabetic patients was significantly higher than control group, while adropin levels were found to be significantly lower. No significant difference was observed between the diabetic patient groups with microvascular complications and those without complications regarding miRNA-21 and adropin levels. The miR-21 expression and adropin levels of the non-complicated diabetic group and only the coronary disease group were significantly higher and lower than the control group. CIMT was significantly higher in patients with macrovascular complications and non-diabetic CAD than in the other groups. A positive correlation was found between miR-21 and CIMT, whereas a moderate negative correlation was detected between miR-21 and adropin levels. The present study indicated that adropin and miR-21 can be equally good markers both in separating diabetic patients with macrovascular complications from the healthy group. In the meantime, the endothelial cell is an important target, and endothelial dysfunction is important in diabetic vasculature. Increased miR-21 expression and decreased adropin levels can be explained by the damage that hyperglycemia causes to the endothelium in diabetic patients.

Affection of vascular structures is a known complication in diabetes and prediabetes. Subclinical atherosclerosis begins to develop years before both cardiovascular and cerebrovascular diseases become symptomatic. The aim of this study was to evaluate the relationship between circulating oxidized LDL (oxLDL), soluble lectin-like oxidized LDL (sLOX)-1 and proprotein convertase subtilisin/kexin type 9 (PCSK9) levels and carotid intima-media thickness (CIMT) in patients with prediabetes and T2DM. We recruited 50 T2DM patients with macrovascular complications, 50 T2DM patients with uncomplicated, 50 prediabetes patients, and 50 healthy participants. The common carotid arteries were visualized by high-resolution B-mode carotid artery ultrasonography. Measurement of serum oxLDL, sLOX-1 and PCSK9 levels were assessed by using a commercially available human enzyme-linked immunosorbent assay (ELISA) method. Homeostasis model assessment for insulin resistance (HOMA-IR) was also calculated. Circulating LDL-C, oxLDL, sLOX-1 and PCSK9 levels were significantly higher in T2DM patients with macrovascular complications compared to control group, prediabetes and uncomplicated diabetes. There was significant difference, especially between the controls and the T2DM patients with macrovascular complications. The CIMT increased progressively from control through to T2DM. Both right and left CIMT also showed significant differences between the groups of prediabetes versus uncomplicated diabetes at p  < 0.001 showing progressive increase in vascular involvement with progression of disease. There was a positive correlation between PCSK9 levels with LDL-C, oxLDL, sLOX-1, and CIMT. ROC curve analyses showed that PCSK9, as well as oxLDL and LOX-1, was a strong predictor of T2DM with high sensitivity and specificity. In this study, we found that oxLDL, sLOX-1 and PCSK9 levels were significantly associated with carotid intima-media thickness. Our findings suggest that these biomarkers may be used as potential markers for the assessment of cardiovascular risk in patients with prediabetes and type 2 diabetes.

Background and Objectives: Cardiovascular disease remains a leading cause of mortality in Diabetes mellitus (DM), where chronic hyperglycemia induces oxidative stress, mitochondrial dysfunction, and hypoxia in cardiomyocytes. Liraglutide (Lir), a glucagon-like peptide-1 receptor agonist, is widely used for type 2 DM management and has been shown to exert cardioprotective and antioxidant effects. This study aimed to evaluate whether Lir mitigates hyperglycemia-induced oxidative and hypoxic stress in H9c2 cardiomyoblasts while preserving cellular ultrastructure. Materials and Methods: H9c2 cells were cultured under normoglycemic (5.5 mM) or hyperglycemic (30 mM) conditions, with or without Lir. Cell viability was assessed using MTT assay. Ultrastructural changes were examined by transmission electron microscopy (TEM). Hypoxia-inducible factor-1α (HIF-1α), lipid peroxidation markers (LOOH, MDA), advanced oxidation protein products (AOPP), and total antioxidant capacity (TAC) were quantified by spectrophotometric assays. Results: MTT assays revealed that Lir significantly improved cell viability under hyperglycemic conditions and the EC50 was 1.05 ± 0.06 μM after 48 h of treatment. Under HG, HIF-1α, lipid hydroperoxides (LOOH), malondialdehyde (MDA) and advanced oxidation protein products (AOPP) increased and total antioxidant capacity (TAC) decreased (p < 0.001, for all); Lir significantly reversed these changes, restoring values to near-NG levels. Ultrastructural analysis of HG + Lir-treated cells revealed reduced granules, increased vacuolization, and slight rough endoplasmic reticulum dilatation, though mitochondria appeared normal. Conclusions: Lir significantly attenuated oxidative stress and cellular injury in cardiomyocytes under hyperglycemic conditions, improving viability, modulating HIF-1α expression, and restoring antioxidant balance. These findings support a dual role for Lir in diabetic cardiomyopathy: glucose-independent cytoprotection and regulation of mitochondrial and hypoxia pathways, highlighting its therapeutic potential beyond glycemic control.

ObjectiveJuvenile SLE (jSLE) is an autoimmune disease characterised by the presence of high levels of autoantibodies, predominantly targeting nuclear antigens, resulting in a breakdown of self-tolerance. However, its pathogenesis is multifactorial and poorly understood. The aim of this study was to evaluate the potential of nuclear factor-kappa B (NF-κB) and peroxisome proliferator-activated receptor-gamma (PPAR-γ) as biomarkers for jSLE.MethodsIn this study, serum NF-κB and PPAR-γ levels were determined by immunoassay in 42 patients with jSLE. In addition, 19 juvenile systemic sclerosis (jSSc) and 25 age-matched healthy children were selected as patient control and healthy control, respectively.ResultsSerum NF-κB levels in patients with jSLE demonstrated a positive trend towards elevation compared with the controls with no significant difference (p=0.030). In addition, serum NF-κB levels in patients with jSSc were significantly higher than that of the healthy controls (p=0.005). Serum PPAR-γ levels were tend to be lower in both patients with jSLE and jSSc compared with the controls, with no significant difference. Specifically, NF-κB levels were significantly higher in patients with jSLE with cumulative damage (PedSDI≥1) compared with those without, at p=0.044. Logistic regression showed that PPAR-γ levels lower than 2.42 ng/mL were associated with the development of jSLE (OR 7.59) and lower than 2.16 ng/mL for jSSc (OR 10.90). The combined high levels of NF-κB with low PPAR-γ increased the risk of developing jSSc by 21.33-fold.ConclusionsThe observed trend of elevated NF-κB levels and decreased PPAR-γ levels in our study suggests their potential as biomarkers associated with increased proinflammatory signalling in jSLE and jSSc. However, our findings must be regarded as hypothesis-generating and confirmed in larger datasets. Moreover, their roles in monitoring the course of a disease and guiding therapeutic strategies in juvenile systemic autoimmune diseases need to be clearly investigated. Further extension of these findings may lead to better management and improvement in the outcomes of such patients.

Background and Objectives: Type 1 Diabetes Mellitus (T1DM) is an autoimmune disease with T cell-mediated pathogenesis of pancreatic β-cell destruction, leading to insulin deficiency. MicroRNAs such as miR-223 and miR-106b, along with PTEN, have been reported to participate in the pathophysiology of diabetes and its complications. The current study has explored the expression of miR-223, miR-106b, and PTEN and their association with various clinical and biochemical parameters in subjects diagnosed with T1DM. Materials and Methods: Sixty T1DM patients (two groups as uncomplicated/ with microalbuminuria) and fifty healthy volunteers, age- and sex-matched, were enrolled in this study. The fasting venous blood samples were collected, and PTEN and miRNAs (miR-223 and miR-106b) levels were measured by ELISA and real-time PCR, respectively. Results: The PTEN levels of patients with microalbuminuria were significantly lower than those of patients without microalbuminuria, while those of miR-223 and miR-106b were significantly increased in the T1DM group compared with the healthy control group (p < 0.001). ROC analysis indicated that PTEN, miR-223, and miR-106b could be potential biomarkers for diagnosing T1DM with high specificity but with variable sensitivities. Also, PTEN and miR-223 were negatively correlated with r =−0.398 and p < 0.0001, indicating that they were interrelated in their role within the T1DM pathophysiology. Conclusions: In the current study, it has been shown that the circulating levels of PTEN, miR-223, and miR-106b are significantly changed in T1DM patients and may back their potential to be used as non-invasive biomarkers for the diagnosis and monitoring of T1DM. Low PTEN protein expression was related to high miR-223 expression, indicating involvement of these miRNA in the regulation of PTEN. Further studies should be performed to clarify the exact mechanisms and possible clinical applications of these molecules.