Prenatal immobility stress: Relationship with oxidative stress, inflammation, apoptosis, and intrauterine growth restriction in rats.

BACKGROUND: Prenatal stress is a significant risk factor affecting pregnant women and fetal health. In the present study, we aimed to investigate the effect of immobility stress at different periods of pregnancy on oxidative stress, inflammation, placental apoptosis and intrauterine growth retardation in rats. METHODS: Fifty adult virgin female Wistar albino rats were used. Pregnant rats were exposed to 6 h/day immobilization stress in a wire cage at different stages of pregnancy. Groups I and II (Day 1-10 stress group) were sacrificed on the 10th day of pregnancy, and Group III, Group IV (10-19th-day stress group), and Group V (1-19th-day stress group) were sacrificed on the 19th day of pregnancy. Inflammatory cytokines, including interleukin-6 (IL-6) and interleukin-10 (IL-10), serum corticotropin-releasing hormone (CRH), and corticosterone levels were measured by enzyme-linked immunosorbent assay. Malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) levels in the placenta were spectrophotometrically measured. Histopathological analyses of the placenta were evaluated by hematoxylin and eosin staining. Tumor necrosis factor-alpha (TNF-α) and caspase-3 immunoreactivity in placenta tissues were determined by the indirect immunohistochemical method. Placental apoptosis was determined by the TUNEL staining method. RESULTS: We found that the immobility stress during pregnancy significantly increased serum corticosterone levels. Our results showed that the immobility stress diminished the number and weight of fetuses in rats compared to the non-stress group. The immobility stress caused significant histopathological changes in the connection zone and labyrinth zone and increased placental TNF-α and caspase-3 immunoreactivity and placental apoptosis. In addition, immobility stress significantly increased the levels of pro-inflammatory IL-6 and MDA and caused a significant decrease in the levels of antioxidant enzymes such as SOD, CAT, and anti-inflammatory IL-10. CONCLUSIONS: Our data suggest that immobility stress causes intrauterine growth retardation by activating the hypothalamic-pituitary-adrenal axis and deteriorating placental histomorphology and deregulating inflammatory and oxidative processes.

Serum chromogranin A levels are associated with the SYNTAX score in coronary artery disease.

OBJECTIVE: In this article, we investigated the association of chromogranin A with coronary artery disease. METHODS: Biochemical parameters and chromogranin A levels obtained from peripheral blood samples during coronary angiography were analyzed in 90 patients. Patients were classified into two groups, namely, SYNergy between PCI with TAXUS and Cardiac Surgery score ≥1 (n=45) and SYNergy between PCI with TAXUS and Cardiac Surgery score=0 (n=45). This is a cross-sectional, prospective study. RESULTS: Serum chromogranin A levels were significantly higher in the group with SYNergy between PCI with TAXUS and Cardiac Surgery score ≥1 compared to the group with SYNergy between PCI with TAXUS and Cardiac Surgery score=0 (1381.5±418.9 ng/mL and 1121.2±290.7 ng/mL, respectively; p=0.002). Serum chromogranin A levels were correlated with SYNergy between PCI with TAXUS and Cardiac Surgery score (r=0.556, p<0.04). ROC analysis showed that the area under the curve for serum chromogranin A levels was 0.687 (p=0.007), and the best cutoff value of 1,131 ng/mL had a sensitivity of 67% and a specificity of 65% for the prediction of coronary artery disease. CONCLUSION: Serum chromogranin A levels were increased in coronary artery disease patients with SYNergy between PCI with TAXUS and Cardiac Surgery score ≥1. Increasing serum chromogranin A levels are proportional to the SYNergy between PCI with TAXUS and Cardiac Surgery score.

Is meteorin-like (Metrnl) a novel biomarker to distinguish patients with obstructive sleep apnea (OSA) and patients with OSA at vascular risk.

PURPOSE: Metrnl, a newly discovered adipokine with significant expression in white adipose tissue, promotes energy expenditure and contributes to the development of cardiovascular disorders. Endocan is a surrogate marker for endothelial dysfunction and is linked to cardiovascular risk factors. Higher cardiovascular morbidity and mortality have been linked to obstructive sleep apnea (OSA). In this study, we investigated the potential of serum Metrnl and endocan as biomarkers to identify patients with OSA who are at increased cardiovascular risk and differentiate them from healthy controls. METHODS: The study included the evaluation of serum levels of endocan and Metrnl in individuals with OSA and healthy controls. All participants underwent full polysomnography to evaluate their sleep, and carotid intima-media thickness (CIMT) was measured in each of them. RESULTS: Patients with OSA (n = 117) had considerably lower levels of Metrnl and significantly higher levels of endocan than controls (n = 59). Once confounding factors were taken into account, both Metrnl and endocan were effective predictors of OSA. Additionally, the severity of OSA, as determined by the apnea-hypopnea index (AHI), was linked to Metrnl and endocan levels. The study also found a significant and independent inverse association between CIMT and Metrnl, along with a positive association with endocan after making multiple adjustments. Furthermore, there was a significant and independent connection between CIMT and AHI. CONCLUSION: Based on these findings, Metrnl and endocan have the potential to be valuable markers for identifying patients with OSA who are at increased risk of early vascular damage.

Cardiovascular disease risk prediction in scleroderma.

OBJECTIVE: Cardiovascular disease risk prediction in scleroderma is important. In this study of scleroderma patients, the aim was to investigate the relationship between cardiac myosin-binding protein-C, sensitive troponin T, and trimethylamine N-oxide and cardiovascular disease risk with the Systematic COronary Risk Evaluation 2 model of the European Society of Cardiology. METHODS: Systematic COronary Risk Evaluation 2 risk groups of 38 healthy controls and 52 women with scleroderma were evaluated. Cardiac myosin-binding protein-C, sensitive troponin T, and trimethylamine N-oxide levels were analyzed with commercial ELISA kits. RESULTS: In scleroderma patients, cardiac myosin-binding protein-C and trimethylamine N-oxide levels were higher than healthy controls but sensitive troponin T was not (p<0.001, p<0.001, and p=0.274, respectively). Out of 52 patients, 36 (69.2%) were at low risk, and the other 16 (30.8%) patients were at high-moderate risk with the Systematic COronary Risk Evaluation 2 model. At the optimal cutoff values, trimethylamine N-oxide could discriminate high-moderate risk with sensitivity 76%, specificity 86% and cardiac myosin-binding protein-C with sensitivity 75%, specificity 83%. Patients with high trimethylamine N-oxide levels (≥10.28 ng/mL) could predict high-moderate- Systematic COronary Risk Evaluation 2 risk 15 times higher than those with low trimethylamine N-oxide (<10.28 ng/mL) levels (odds ratio [OR]: 15.00, 95%CI 3.585-62.765, p<0.001). Similarly, high cardiac myosin-binding protein-C (≥8.29 ng/mL) levels could predict significantly higher Systematic COronary Risk Evaluation 2 risk than low cardiac myosin-binding protein-C (<8.29 ng/mL) levels (OR: 11.00, 95%CI 2.786-43.430). CONCLUSION: Noninvasive cardiovascular disease risk prediction indicators in scleroderma, cardiac myosin-binding protein-C, and trimethylamine N-oxide could be recommended to distinguish between high-moderate risk and low risk with the Systematic COronary Risk Evaluation 2 model.

Investigation of serum E-Cadherin, VEGF121, Survivin, Tenascin C and Tetraspanin 8 levels in patients with glioblastoma.

OBJECTIVE: The aim of this study is to determine biomarkers, which may be used in order to understand the pathophysiology, the diagnosis, progression surveillance/monitoring, and treatment efficacy of high graded glial tumors. BACKGROUND: Radiological imaging in the diagnosis and relapse surveillance of glial tumors is sometimes insufficient. There is need for additional methods of diagnosis and surveillance in order to rule out contradictory circumstances. METHOD: Using enzyme like immune sorbent assay method, E-Cadherin, Tenascin C, Tetraspanin 8, Survivin and VEGF121 levels were investigated in serum and tumor tissues of 28 patients diagnosed with pathological glioblastoma, and in the serum of 26 healthy individuals. Correlation between tumor tissue values and Ki67 percentage, and P53 mutation, and difference between unhealthy and healthy serum levels were sought. RESULTS: It was found out that E-Cadherin and VEGF 121 levels in the unhealthy serum were high in comparison to the control group (p 0.05). CONCLUSION: EC and VEGF121 are biomarkers, which have the potential to be used in the diagnosis, recurrence and treatment follow-up in high graded glial tumors (Tab. 2, Fig. 1, Ref. 37). Text in PDF www.elis.sk Keywords: E-Cadherin, VEGF, Survivin, Tenascin-C, Tetraspanin, glioblastoma.

Serum Calprotectin Level as an Inflammatory Marker in Newly Diagnosed Hypertensive Patients.

BACKGROUND: Hypertension is one of the leading causes of cardiovascular mortality. Although the pathogenetic process involved is not yet fully understood, the disease involves endothelial damage and inflammation. Calprotectin is an inflammatory marker that rises in parallel with disease activity in conditions such as systemic inflammatory diseases, infection, and atherosclerosis. The purpose of this study was to evaluate inflammation through serum calprotectin levels in newly diagnosed primary hypertension patients. METHODS: Forty-nine newly diagnosed hypertensive patients and 38 healthy adults were included in the study. Patients' office blood pressure values, biochemical findings, and demographic characteristics were recorded. Serum calprotectin levels were measured using ELISA. Parameters affecting serum calprotectin levels and determinants of hypertension were evaluated. RESULTS: Serum calprotectin levels were 242.8 (72.4-524) ng/mL in the control group and 112.6 (67.4-389.8) ng/mL in the hypertensive patient group, the difference being statistically significant (p=0.001). There was no correlation between serum calprotectin levels and other parameters (blood pressure values, age, gender, serum creatinine, uric acid, and calcium levels) in the hypertensive group. A lower serum calprotectin level was found to be independently related to hypertension (ß = -0.009, p=0.005). Serum calprotectin at a cutoff level of 128.6 ng/mL differentiated hypertensives from healthy controls with a sensitivity of 69.4% and specificity of 68.4% (AUC = 0.767). CONCLUSIONS: The results of this study were the opposite of our hypothesis that a higher calprotectin level may reflect subclinical endothelial damage in newly diagnosed hypertensive patients. Further comparative studies involving patients at different stages of hypertension may contribute to clarifying the relationship between calprotectin and hypertension. We conclude that molecular studies seem essential for understanding the place of calprotectin in hypertension-associated inflammation, a complex process.

Toxicological assessment of low-dose bisphenol A, lead and endosulfan combination: chronic toxicity study in male rats.

In the present study, toxic effects, both alone and combined, of bisphenol A (BPA), lead (Pb) and endosulfan (ES) in the low doses were investigated in rat liver and kidney functions. In the study, bisphenol A (BPA), lead (Pb) and endosulfan (ES) were chosen because although they are the chemicals people are most frequently exposed to, no combined toxic effect studies were conducted with these chemicals. Sixty-four male Wistar albino rats were used in the study, and they were randomly divided into eight groups (n = 8 per group); control, BPA (5 mg/kg), Pb (100 ppm), ES (0.61 mg/kg), BPA+Pb, BPA+ES, Pb+ES and BPA+P+ES. The rats were sacrificed after 65 days of treatment. Severe histopathological changes in the liver and kidney tissues were observed in the rats exposed to BPA+Pb+ES combination. Elevated malondialdehyde (MDA) in the liver and decreased superoxide dismutase activity (SOD) in the kidney tissue were detected in the BPA+Pb+ES group compared to those of the control group. It was found that serum alanine aminotransferase (ALT) and blood urea nitrogen (BUN) and creatinine (CREA) levels were higher in the BPA+Pb+ES combination group than the control group. Also, combined exposure of BPA, Pb and ES caused apoptotic cell numbers and inducible nitric oxide (iNOS) to increase in the liver and kidney tissues. The results of the present study suggested that the BPA, Pb and ES caused more dramatic changes to both histological architecture and cell apoptosis in the liver and kidney tissues when there was a combined exposure.

Serum Neudesin Levels in Obese Adolescents

Objective: Advances in knowledge of neurotrophic factors are now revealing the complex control of energy homeostasis and appetite, as well as the crucial role these factors play in nervous system function. The aim of this study was to assess serum levels of neudesin in adolescents with obesity and to examine the relationship between these levels and metabolic outcomes. Methods: Adolescents, aged 10-17 years were enrolled. Subjects were divided into normal weight, obese and morbidly obese subgroups. Serum neudesin concentrations were compared between the groups. Results: In total, 88 adolescents were recruited, of whom 30 (34.1%) were normal weight, 15 (17.0%) were obese and 43 (48.9%) were morbidly obese. Neudesin levels were significantly lower in obese adolescents than in the control group (p=0.013). A correlation analysis applied to the whole study group revealed a negative correlation between serum neudesin concentration and body mass index (BMI) z scores (r=-0.40, p<0.001). Serum neudesin levels tended to increase in adolescents with metabolic syndrome, insulin resistance, dyslipidaemia, and hypertension but the differences were not significant (p=0.259, p=0.246, p=0.259, and p=0.523, respectively). Conclusion: Serum neudesin levels were significantly correlated with BMI z score in obese adolescents. Generally, serum neudesin levels were low in obese and morbidly obese adolescents and tended to increase with the appearance of metabolic disorders. Both obesity and associated metabolic disorders have multifactorial causes. Therefore, we suggest that the role of the neudesin molecule in the regulatory mechanisms of obesity and metabolic disorders should be further investigated with well-designed studies enrolling larger groups.

MicroRNA 21 and microRNA 155 levels in resistant hypertension, and their relationships with aldosterone.

AIM: MicroRNAs (miRNAs) are non-coding RNA molecules that serve as regulators following gene expression transcription. While studies have investigated the role of miRNAs in the pathogenesis of essential hypertension (HT), very few have considered their place in the pathogenesis of resistant hypertension (RH). The purpose of this study was to investigate levels of miRNA 21 and miRNA 155 in RH and their relationships with aldosterone. METHOD: Thirty-two normotensive patients, 30 newly diagnosed HT patients, and 20 RH patients were included in the study. Patients' demographic data were recorded, and office blood pressure measurement and 24-h ambulatory blood pressure monitoring (24-h ABPM) were performed. Blood specimens were collected for miRNA 21, miRNA 155 and aldosterone measurement. MiRNA 21 and miRNA 155 levels in the control and patient groups and their relations with other demographic and biochemical parameters were then subjected to analysis. RESULTS: No difference was determined in miRNA 155 levels between the groups, but miRNA 21 and aldosterone levels were significantly higher in the RH group (p < 0.001 and <0.05, respectively). At correlation analysis, miRNA 21 exhibited positive correlation with aldosterone, age, office SBP, 24-h ABPM all-day SBP. A 9.6 copy/uL level for miRNA 21 predicted presence or absence of RH with 95% sensitivity and 71% specificity (AUC:0.823, 95% CI (0.72-0.92). CONCLUSION: The study results revealed significantly higher miRNA 21 and aldosterone in RH patients than in healthy individuals and newly diagnosed hypertensives.

Increased Carotid Intima-Media Thickness and Endothelial Cell-Specific Molecule-1 (Endocan) Levels in Obese Children.

Obesity in children appears to be associated with increased risk of cardiovascular and metabolic diseases later in life. Early development of insulin resistance (IR) may lead to endothelial dysfunction and increased carotid intima-media thickness (cIMT) even in childhood. We compared endothelial cell-specific molecule-1 (endocan) levels in pediatric obese patients with those in healthy controls to determine whether endocan could be used as a biological marker of complications caused by endothelial damage. In 80 obese pubertal children (44 males [M] and 36 females [F], mean age: 12.8 ± 2.5 years), anthropometric measurements, cIMT, endocan levels, and IR indices (homeostasis model assessment of insulin resistance [HOMA-IR]) were evaluated and compared with 80 healthy pubertal patients (42M/38F, mean age: 12.3 ± 3.2 years). High-resolution ultrasound was used to measure the cIMT. Obese children had higher levels of endocan compared with the controls (P < .001). Fasting insulin levels and HOMA-IR were also higher in obese children (P < .001 for both). In addition, obese children had an increased cIMT (P < .001). In obese children, there was a significant correlation between cIMT and HOMA-IR (ß = -1.314, P = .002) and between cIMT and endocan (ß = .483, P = .004). Measuring cIMT and endocan levels (noninvasive investigations) in obese children, together with early preventive measures, could significantly decrease morbidity and mortality in adulthood.

Association of lower serum irisin levels with diabetes mellitus: Irrespective of coronary collateral circulation, and syntax score.

Objective: Irisin is a myokine thought to be involved in the pathophysiological process of atherosclerosis with its' cardiovascular protective effects. Patients with diabetes mellitus (DM) have lower levels of irisin. Therefore, we investigated whether there is a connection between irisin, DM, coronary collateral circulation (CCC), and SYNTAX scores representing coronary artery disease (CAD) severity. Methods: This study evaluated 86 patients who have at least one epicardial coronary artery with chronic total occlusion. We included Rentrop 0-1 into the poor CCC group (n=45) and Rentrop 2-3 into the good CCC group (n=41) and measured serum irisin levels. Results: Irisin levels did not differ (17585 [882-37741] pg/ml and (17504 [813-47683] pg/ml, p=0.772) between the two groups. Irisin levels were lower in patients with diabetes (n=41; 14485 [813-29398] pg/ml) than those without diabetes (n=45; 19724 [865-47683] pg/ml (p=0.002). Irisin was not correlated with SYNTAX scores. In multivariate analysis, DM (OR=0.463; CI: 0.184-0.783; p=0.012) was a negative predictor of good CCC development. Conclusion: Although its level is decreased in patients with diabetes, serum irisin levels have no role in the pathophysiology of collateral development and CAD severity.

Assessment of salusin alpha and salusin beta levels in patients with newly diagnosed dipper and non-dipper hypertension.

OBJECTIVE: The pathophysiology of non-dipper hypertension has not been clarified. The relationship between salusins with atherosclerosis and hypertension has gained attention in recent years. The aim of this paper is to investigate whether salusins are associated with circadian blood pressure, left ventricular mass index, and diastolic functions in newly diagnosed hypertensives. METHODS: The study included 88 newly diagnosed hypertensive individuals. Twenty-four-hour ambulatory blood pressure monitoring and echocardiographic examinations were performed. The patients were assigned to dipper hypertension (n = 41) and non-dipper hypertension (n = 47) groups based on the ambulatory blood pressure monitoring results according to the presence of ≥ a 10% decrease in nighttime blood pressure values or not. Serum salusin α and ß levels were determined by electrochemiluminescence immunological test method. RESULTS: Compared to dipper hypertension, non-dipper hypertension group demonstrated lower salusin α levels (1818.71 ± 221.67 vs 1963 ± 200.75 pg/mL, p = .002), mitral E/A, septal E'/A' and higher salusin ß levels (576.24 ± 68.15 vs 516.13 ± 90.7 pg/ml, p = .001) and left ventricular mass index. Multivariate logistic regression analysis revealed salusin-α (OR 0.474, 95% CI 0.262 to 0.986, p = .001), salusin-ß (OR 2.550, 95% CI 2.123 to 2.991, p = .018), and left ventricular mass index (OR 2.620, 95% CI 2.124 to 2.860, p = .011) as independent predictors of non-dipper hypertension. As candidate markers to predict non-dipper hypertension, decreased salusin α, and increased salusin ß levels may mediate crosstalk between sympathetic and parasympathetic systems and indicate poor cardiovascular prognosis in hypertension.

Relationship between Microfibrillar-Associated Protein 4 Levels and Subclinical Myocardial Damage in Chronic Kidney Disease.

INTRODUCTION: Chronic kidney disease (CKD) is a widespread health problem, in which mortality is most frequently due to cardiovascular diseases. Microfibrillar-associated protein 4 (MFAP4) is an extracellular matrix protein. MFAP4 is involved in several biological processes, particularly the maintenance of vascular integrity and extracellular matrix remodeling. Our review of the literature revealed no data concerning MFAP4 levels in CKD and its relationship with myocardial functions. OBJECTIVE: The purpose of this study was therefore to investigate MFAP4 levels in CKD, parameters affecting these, and the relationship with myocardial functions. MATERIALS AND METHODS: Seventy-nine CKD patients and 30 healthy controls were included in the study. Routine biochemical tests and echocardiography were performed once demographic data had been recorded. Blood specimens were collected for MFAP4 analysis, and the results were subjected to statistical analysis. RESULTS: MFAP4 levels were significantly higher in the patient group than in the control group (p< 0.001). Doppler parameters revealed more frequent LV diastolic impairment in the patient group. Tissue Doppler systolic velocity and global longitudinal strain were significantly impaired, revealing the subclinical LV systolic dysfunction in CKD patients. MFAP4 elevation in the patient group was positively correlated with aortic root (AR), global circumferential strain (GCS), and GCS rate. CONCLUSION: Our results showed MFAP4 elevation in CKD for the first time in the literature, and that this elevation may be related to GCS and AR dilation. We think that, once supported by further studies, MFAP4 may constitute a marker in the evaluation of myocardial functions in CKD.

Evaluation of serum endocan levels in relation to epicardial fat tissue thickness in metabolic syndrome patients.

INTRODUCTION: Metabolic syndrome has been recognized as a predictor of cardiovascular diseases. Epicardial fat tissue (EFT) thickness has recently been shown to be a predictor of cardiovascular diseases in metabolic syndrome patients. Endocan is a novel molecule which is considered to be an early marker of endothelial dysfunction. Our aim was to evaluate endocan serum levels for the first time in metabolic syndrome patients, in relation to EFT thickness. MATERIAL AND METHODS: The study included 44 patients with metabolic syndrome who had neither chronic kidney disease nor chronic inflammation and 26 healthy controls. Fasting blood samples were obtained from the groups. The serum levels of endocan were measured with a Sunred ELISA kit. EFT thickness of patients was measured by echocardiography. RESULTS: The serum endocan levels were significantly lower in the metabolic syndrome patients compared to the healthy controls (120.71 ±90.17 pg/ml vs. 414.59 ±277.57, p < 0.001). Metabolic syndrome patients demonstrated significantly higher EFT (p = 0.042). EFT thickness had a positive correlation with age (r = 0.397, p = 0.008) and weight (r = 0.010). However, there was no correlation with serum endocan (r = -0.021, p = 0.893) or other parameters. Regression analysis revealed that waist circumference is the parameter among metabolic syndrome criteria having the strongest relationship with serum endocan levels (ß = -0.499, p = 0.21). CONCLUSIONS: EFT thickness was high in metabolic syndrome patients and can be a useful marker for cardiovascular risk assessment. However, serum endocan levels were found to be low and there was no correlation with EFT thickness. Large sample sized prospective studies are needed to clarify the relation of endocan levels with the other clinical indicators of cardiovascular risk in metabolic syndrome.

Relationship of serum salusin beta levels with coronary slow flow.

OBJECTIVE: The pathophysiology of coronary slow flow (CSF) has not been clarified. Salusin-ß is released predominantly from the atheroma plaques and influences the pathophysiologic processes of atherosclerosis. Therefore, this study aimed to determine serum salusin-ß levels in CSF and its correlation with CSF. METHODS: The study included 39 patients with CSF, and the control group (n=42) consisted of consecutive subjects with normal coronary arteriogram. We measured salusin-ß and thrombolysis in myocardial infarction frame count (TFC). RESULTS: Age, body mass index (BMI), systolic blood pressure, diabetes, hyperlipidemia, and smoking rates were similar (p values>0.05) in both groups. High sensitive C-reactive protein (2.80±1.2 vs. 2.21±1.2 mg/dL, p=0.011), salusin-ß [1205 (330-2092) vs. 162 (29-676), pg/ml, p<0.001], corrected TFC of left anterior descending coronary artery (29±9 vs. 19.7±3.7, p<0.001), circumflex artery TFC (25±10 vs. 15±3.2, p<0.001), right coronary artery TFC (28±7.1 vs. 13±3.3, p<0.001), and mean TFC (28±4.4 vs. 16±3.7, p<0.001) were significantly higher in the CSF group. In univariate and multivariate regression analysis, only BMI (unstandardized ß±SE=0.178±0.08, p=0.036) and salusin-ß levels (unstandardized ß±SE=0.006±0.01, p<0.001) were determined as predictors of CSF. There was a good correlation between serum salusin-ß and mean TFC values (r=0.564; p<0.001). CONCLUSION: There is an association between serum salusin-ß levels and CSF.

Tumour necrosis factor like cytokine 1A levels and lesion complexity in non-smoking patients with coronary artery disease.

Background: Tumour necrosis factor like cytokine 1A (TL1A), which is a member of tumour necrosis factor alpha superfamily (TNF-α), is a novel indicator of atherosclerosis.Objective: Smoking is an established stimulant of TNF-α. We aimed to investigate whether TLA1 plays a role in the presence and complexity of coronary artery atherosclerosis, exclusively in non-smoking patients with CAD.Methods: We enrolled 103 participants in the study, who underwent coronary angiography for stable angina pectoris. We divided the study population into 2 groups: The CAD group consisted of 62 patients with CAD and the control group consisted of 41 subjects with non-CAD. SYNTAX and Gensini scores, indicating CAD severity and complexity, were analysed as well as TLA1 levels.Results: TLA1 levels was higher in patients with CAD than those in controls (228[119-824] vs 178[15-418]pg/ml, p < 0.001). Presence of CAD (ß ± SE = 106.29 ± 33.11, p = 0.002), Syntax score (ß ± SE= 6.57 ± 1.75, p = 0.012), and Gensini score (ß ± SE = 2.30 ± 0.65, p = 0.001) were found to be predictors of TL1A levels. Gensini score and Syntax score were positively correlated with TL1A levels (r = 0.420, p < 0.001, and r = 0.402, p < 0.001, respectively).Conclusions: Non-smoker CAD patients have higher TLA1 levels that are promising biomarker for diagnosing CAD and indicating CAD lesion complexity.

Decreased serum orexin A levels in drug-naive children with attention deficit and hyperactivity disorder.

Attention deficit/hyperactivity disorder (ADHD) is one of the most common psychiatric disorders of childhood and characterized by inattention, hyperactivity, and impulsivity. ADHD is a neurodevelopmental disorder, and its etiology has not yet been determined precisely. Orexin A is thought to play an important role in different forms of learning, memory, and attention. Despite its importance in attention and learning, no study has investigated serum orexin levels in patients with ADHD. In the present study, we aimed to compare serum orexigenic neuropeptides such as orexin A and orexin B, neuropeptide Y, and ghrelin between drug naive children with ADHD and healthy children. Fifty-six drug-naive children with ADHD and 40 healthy controls were enrolled in the study. After comparison of serum orexin A and orexin B, neuropeptide Y, and ghrelin, we found that serum orexin A levels were significantly lower in the ADHD group (p = 0.001). Furthermore, serum orexin A levels were compared between ADHD subgroups. Orexin A levels were significantly lower in the inattentive subtype compared with the hyperactive subtype and combined subtype (p = 0.009). Our results indicate that orexin A might be a neurobiological etiological factor in ADHD, particularly associated with attention symptoms. The present study is the first to demonstrate decreased serum orexin A levels in drug-naive children with ADHD. Further studies are needed to confirm our results and to show the effects of treatments involving orexin A in patients with ADHD.

Soluble endothelial protein C is associated with blood pressure variability and salt consumption but not mean blood pressure in patients with newly diagnosed primary hypertension.

BACKGROUND: Hypertension is a widespread disease involving frequent thrombotic complications. Blood pressure variability (BPV) has recently been shown to be associated with end-organ damage and cardiovascular events. However, the pathogenesis of the relation between BPV and cardiovascular events has not yet been explained. Soluble endothelial protein C (sEPCR) exhibits a procoagulant effect by reducing the anticoagulant and anti-inflammatory effects of protein C and activated protein C. The purpose of this study was to evaluate sEPCR levels in hypertensive individuals and the parameters affecting that level, particularly BPV. METHODS: Fifty-one newly diagnosed hypertensive subjects and 31 healthy individuals were included in the study. Twenty-four-hour ambulatory blood pressure monitoring (ABPM) was performed after office control, and simultaneous 24-h urine was collected. BPV was calculated with average real variability (ARV) from ABPM data. Blood specimens were collected under appropriate conditions for sEPCR levels and biochemical tests. sEPCR levels were compared between the patient and healthy groups, after which parameters affecting sEPCR elevation in the hypertensive group were evaluated. RESULTS: sEPCR levels were significantly high in the hypertensive group (p < 0.05). At multivariate regression analysis in the hypertensive group, sEPCR was determined to be independently associated with 24-h systolic ARV (ß = 0.572, p < 0.05) and 24-h urine Na (ß = 0.428, p < 0.05). CONCLUSION: In our study, sEPCR was high in hypertensive individuals, and this elevation was related to ARV and urine Na excretion independently of mean blood pressure.