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Background Childhood obesity leads to an increased inflammatory response, which in the long term can lead to serious health problems such as metabolic syndrome, diabetes, cancer and cardiovascular disease, and may also increase the risk of obesity in adulthood. Our aim was to evaluate inflammatory markers associated with pediatric obesity in 30 healthy children (BMI between the 15th–85th percentiles) and 30 obese children (BMI > 95th percentile) and to determine the possible associations of these markers. Methods Anthropometric measurements of the children were obtained. The serum preptin, peroxisome proliferator activated receptor gamma (PPARγ), nod-like receptor pyrin domain-containing 3 (NLRP3), and interleukin-18 (IL-18) levels of thirty children with obesity and thirty healthy children were determined using ELISA. Results NLPR3, preptin, and PPARγ levels were greater obese children than in healthy children ( p  < 0.05). We have shown that high PPARγ levels may have an inhibitory effect on the inflammatory activation of NLRP3. Conclusions In our study, the changes observed in preptin, NLRP3 and PPARγ parameters were found to be closely associated with pediatric obesity. These molecules may play an important role in understanding the relationship between pediatric obesity and inflammation and may be used as biomarkers in determining obesity treatment and complications in future studies.

Background/Objectives: Obesity is associated with cardiovascular disease worldwide. An increased lipoprotein A (LpA) level is an independent risk factor for cardiovascular disease in children. Genetic polymorphisms of the LPA gene may play an important role in susceptibility to obesity. The aim of this study was to investigate the association of LPA rs10455872 polymorphism with the risk and clinical phenotypes of childhood obesity. Methods: This study included 103 children with obesity and 77 healthy controls. Genotyping of the LPA rs10455872 polymorphism was performed using real-time PCR. Results: The genotype distributions of the LPA rs10455872 polymorphism did not differ significantly between children with obesity and healthy children (p = 0.563). A marked difference in insulin levels was observed between children with obesity carrying the AG (16.90 IU/mL) and AA (25.57 IU/mL) genotypes. A marked difference was also observed in CRP levels between children with obesity with the AG (2.31 mg/L) and AA (4.25 mg/L) genotypes. After correcting for multiple comparisons using the false discovery rate (FDR), significant differences were found between AG and AA genotypes in vitamin B12 (adjusted p = 0.024). Serum iron showed a borderline association (adjusted p = 0.072). A statistically significant correlation was found between the metabolic syndrome index and body fat ratio among children with obesity with the AA genotype (p = 0.028). Conclusions: Although limited by the small number of children with obesity with the AG genotype, some differences were noted between the AG and AA genotypes. These exploratory findings require further investigation in adequately powered studies. In children with obesity with the AA genotype, the metabolic syndrome index increases as the body fat ratio increases.

Infertility is a problem concerning 10-15% of the individuals in the fertile period. This study investigated effects of proinflammatory factors as well as lipid hydroperoxides (LPO) levels upon in vitro fertilization (IVF) success. In this prospective, non-randomized, controlled clinical study, sera obtained from 26 fertile (group-1), 26 infertile women before (group-2) and after (group-3) IVF treatment were analyzed. Leptin, leptin receptor, resistin, tumor necrosis factor-alpha (TNF-α), and C-reactive protein (CRP) were analyzed using enzyme-linked immunosorbent assay (ELISA). LPO was determined spectrophotometrically. Mann- Whitney U test, paired samples t test, Wilcoxon signed-rank test as well as Pearson correlation analysis by SPSS were performed for statistical analysis. TNF-α, resistin and LPO levels increased (P=0.020, P=0.003, P=0.001, respectively) in group-3 compared to group-2. A significant increase in LPO was noted both in group-2 and -3 compared to controls (P=0.000). LPO were higher in non-pregnants than pregnants in group-2. For pregnants, significant correlations were observed between leptin and resistin in group-2 and TNF-α and leptin in group-3. None of these correlations were found for the women, who could not conceive. LPO, leptin-resistin correlation, associations with TNF-α may be helpful during the interpretation of IVF success rates.

Background Childhood obesity leads to an increased inflammatory response, which in the long term can lead to serious health problems such as metabolic syndrome, diabetes, cancer and cardiovascular disease, and may also increase the risk of obesity in adulthood. Our aim was to evaluate inflammatory markers associated with pediatric obesity in 30 healthy children (BMI between the 15th-85th percentiles) and 30 obese children (BMI > 95th percentile) and to determine the possible associations of these markers. Methods Anthropometric measurements of the children were obtained. The serum preptin, peroxisome proliferator activated receptor gamma (PPAR[gamma]), nod-like receptor pyrin domain-containing 3 (NLRP3), and interleukin-18 (IL-18) levels of thirty children with obesity and thirty healthy children were determined using ELISA. Results NLPR3, preptin, and PPAR[gamma] levels were greater obese children than in healthy children (p < 0.05). We have shown that high PPAR[gamma] levels may have an inhibitory effect on the inflammatory activation of NLRP3. Conclusions In our study, the changes observed in preptin, NLRP3 and PPAR[gamma] parameters were found to be closely associated with pediatric obesity. These molecules may play an important role in understanding the relationship between pediatric obesity and inflammation and may be used as biomarkers in determining obesity treatment and complications in future studies. Keywords: Child, Obesity, Preptin, NLRP3, PPAR[gamma]

ABSTRACT Background Although high‐dose biotin interference in automated immunoassays is now considered, there are very few studies showing biotin interference in manually operated research kits, especially with enzyme‐linked immunosorbent assay (ELISA). The aims of our study were to determine the effects of biotin interference on various parameters, including leptin, leptin receptor (LEPR), ghrelin, acylated ghrelin, deacylated ghrelin, ghrelin receptor (GHSR), kisspeptin (KISS1), kisspeptin receptor (KISS1R), preptin, peroxisome proliferator activated receptor gamma (PPARγ), nod‐like receptor pyrin domain‐containing 3 (NLRP3) and interleukin‐18 (IL‐18), which contribute to energy homeostasis in healthy and obese children. Methods Serum pools were prepared from healthy and obese individuals, and biotin concentrations in samples containing different amounts of biotin were measured via sandwich and competitive ELISA methods. In addition, possible biotin interactions were investigated by determining the concentrations of all the study parameters in serum pools containing different amounts of biotin. Results We found that the biotin‐competitive, ghrelin‐competitive, KISS1‐competitive, GHSR, leptin and LEPR ELISA kits were less affected by biotin interference and the results of these assay kits were more reliable. Unexpectedly, high levels were also measured in the biotin sandwich ELISA kit, indicating that biotin interference can also occur in manually operated assay kits. Conclusions Biotin exhibited an interference effect even in well‐functioning, qualified kits, and this negative effect was less common in competitive kits. Biotin interference was closely associated with the quality of the research kit, the parameters studied, and the presence of high biotin concentrations in the blood. In this study, we aimed for the first time to demonstrate biotin interference in ELISA research kits used in the analysis of pediatric obesity parameters other than routine testing. Our study revealed that biotin interaction may occur in manual ELISA kits and may cause erroneous test results. It will raise awareness among health professionals, researchers, and medical companies on this issue. By encouraging manufacturers developing medical products to take measures to reduce the effect of biotin interaction, it will prevent erroneous results in scientific studies and contribute to more precise measurements.

Paraoxonase (PON1) protects low and high-density lipoproteins (LDL and HDL) against oxidation induced by reactive oxygen species formation facilitated by iron (Fe) and copper (Cu) ions. Plasma PON1, arylesterase, oxidized LDL (Ox-LDL), Cu, Fe, thiobarbituric acid-reactive substances (TBARS), lipid, lipoprotein, and apolipoprotein profile in bronchial asthma were determined and the relations among these parameters in different steps of asthma were interpreted. A total of 58 individuals, 30 asthmatics and 28 controls, were included into the scope of this study. Plasma PON1, arylesterase, and TBARS levels were measured spectrophotometrically. Determination of plasma oxidized LDL, Cu, and Fe levels were performed by enzyme-linked immunosorbent assay, atomic absorption spectrophotometry, and the automated TPTZ method, respectively. Apo-A-1 and Apo-B levels were determined immunoturbidometrically. Plasma total cholesterol, triglyceride, and HDL cholesterol levels were enzymatically determined. Plasma LDL levels were estimated using the Fridewald formula. The average plasma PON1 and arylesterase activities in the group of patients were lower than those of the individuals in the control group, but there was no statistically significant difference found between them (p > 0.05). No significant difference was found in plasma Apo-A-1, Apo-B, total cholesterol, triglyceride, HDL, and LDL concentrations between the control and patient groups (p > 0.05). Plasma oxidized LDL (p < 0.05), Cu (p < 0.01), Fe (p < 0.01), and TBARS (p < 0.001) levels in patients with asthma were found to be significantly higher than for the control group. Increases in Cu, Fe, lipid peroxidation, and oxidized LDL levels supported by relative decreases in PON1 activities observed in asthmatic patients might be introduced as the striking findings as well as the possible potential indicators of this airway disease, the prevalence of which has increased dramatically over recent decades.

The aim of this prospective case control study is to determine CD4 + , CD25 + , and FoxP3 + T regulatory cells (Tregs) and T helper cells (Ths) in obese, asthmatic, asthmatic obese, and healthy children. Obese ( n  = 40), asthmatic ( n  = 40), asthmatic obese ( n  = 40), and healthy children ( n  = 40) were included in this study. Blood samples collected from children were marked with CD4, CD25, ve Foxp3 in order to detect Tregs and Ths by flow cytometric method. Statistical analyses were performed. p  ≤ 0.05 was chosen as meaningful threshold. Tregs exhibiting anti-inflammatory nature were significantly lower in obese (0.16 %; p  ≤ 0.001), asthmatic (0.25 %; p  ≤ 0.01), and asthmatic obese (0.29 %; p  ≤ 0.05) groups than control group (0.38 %). Ths were counted higher in asthma group than control ( p  ≤ 0.01) and obese ( p  ≤ 0.001) groups. T cell immunity plays important roles in chronic inflammatory diseases such as obesity and asthma pathogeneses. Decreased numbers of Tregs found in obese, asthmatic, and asthmatic obese children might represent a challenge of these cells.

Purpose: To evaluate interleukin-8 (IL-8), nitric oxide (NO) and glutathione (GSH) profiles in vitreous humor and blood samples in patients with proliferative diabetic retinopathy (PDR) and in patients with proliferative vitreoretinopathy (PVR) and to compare the levels with those of controls. Patients and Methods: NO concentrations were determined by using the Greiss reaction in plasma and vitreous humor samples. GSH levels were determined in both blood and vitreous humor samples, using DTNB, a disulfide chromogen. Vitreous IL-8 were assayed by ELISA. Twenty-three patients with PDR, 18 patients with PVR and 21 cadavers as the control group were included in the study. Results: Plasma and vitreous NO levels were found to be25.6 ± 2.1 and 36.9 ± 3.0 µmol/l in patients with PDR, 27.0 ± 4.7 and 34.3 ± 2.9 µmol/l in patients with PVR and 17.4 ± 2.7 and 15.9 ± 1.4 µmol/l in controls, respectively. Vitreous humor and plasma NO levels did not show any statistically significant difference between PDR and PVR groups. However, the values for vitreous in both groups were significantly higher than those of controls (p < 0.0001). Although IL-8 levels in vitreous samples of patients with PDR were not significantly different (79.6 ± 9.7 pg/ml) from those of patients with PVR (42.2 ± 7.3 pg/ml) (p = 0.06), the levels in both groups were significantly higher than those of controls (19.0 ± 3.9 pg/ml) (p < 0.0001 and p < 0.05, respectively). Blood and vitreousGSH levels were found to be5.3 ± 0.4 µmol/g·Hb and 0.58 ± 0.16 µmol/l in patients with PDR and 8.4 ± 0.5 µmol/g·Hb and 15.7 ± 2.2 µmol/l in patients with PVR and 12.0 ± 1.1 µmol/g·Hb and 0.26 ± 0.03 mmol/l in controls, respectively. Vitreous and blood GSH levels were significantly lower in patients with PDR compared to those with PVR (p < 0.0001 for both). Conclusion: Elevated levels of vitreous and plasma NO and vitreous IL-8 in PDR and PVR implicate a role for these parameters in the proliferation in these ocular disorders. GSH concentrations both in vitreous and blood samples of the PVR and PDR patients were much less than those observed in the control group. Lower GSH concentrations detected in PDR in comparison with those in PVR in vitreous humor and to a lesser degree in blood may play an important role in pathogenesis of new retinal vessel formation in patients with PDR. This also suggests that oxidative stress may be involved in the pathogenesis of PVR and particularly that of PDR.

The aim of this prospective case control study is to determine CD4^sup +^, CD25^sup +^, and FoxP3^sup +^ T regulatory cells (Tregs) and T helper cells (Ths) in obese, asthmatic, asthmatic obese, and healthy children. Obese (n=40), asthmatic (n=40), asthmatic obese (n=40), and healthy children (n=40) were included in this study. Blood samples collected from children were marked with CD4, CD25, ve Foxp3 in order to detect Tregs and Ths by flow cytometric method. Statistical analyses were performed. p≤0.05 was chosen as meaningful threshold. Tregs exhibiting anti-inflammatory nature were significantly lower in obese (0.16 %; p≤0.001), asthmatic (0.25 %; p≤0.01), and asthmatic obese (0.29 %; p≤0.05) groups than control group (0.38 %). Ths were counted higher in asthma group than control (p≤0.01) and obese (p≤0.001) groups. T cell immunity plays important roles in chronic inflammatory diseases such as obesity and asthma pathogeneses. Decreased numbers of Tregs found in obese, asthmatic, and asthmatic obese children might represent a challenge of these cells.

The aim of this prospective case control study is to determine CD4 super(+), CD25 super(+), and FoxP3 super(+) T regulatory cells (Tregs) and T helper cells (Ths) in obese, asthmatic, asthmatic obese, and healthy children. Obese (n=40), asthmatic (n=40), asthmatic obese (n=40), and healthy children (n=40) were included in this study. Blood samples collected from children were marked with CD4, CD25, ve Foxp3 in order to detect Tregs and Ths by flow cytometric method. Statistical analyses were performed. p less than or equal to 0.05 was chosen as meaningful threshold. Tregs exhibiting anti-inflammatory nature were significantly lower in obese (0.16 %; p less than or equal to 0.001), asthmatic (0.25 %; p less than or equal to 0.01), and asthmatic obese (0.29 %; p less than or equal to 0.05) groups than control group (0.38 %). Ths were counted higher in asthma group than control (p less than or equal to 0.01) and obese (p less than or equal to 0.001) groups. T cell immunity plays important roles in chronic inflammatory diseases such as obesity and asthma pathogeneses. Decreased numbers of Tregs found in obese, asthmatic, and asthmatic obese children might represent a challenge of these cells.