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Background: Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders in which the underlying pathogenesis and etiologic factors are not fully understood. The blood brain barrier (BBB) ??plays a critical role in central nervous system defense by limiting access to circulating solutes, macromolecules, and cells that can negatively affect neuronal activity. The loss of BBB integrity is likely to be seen as a common pathologic finding for many psychiatric disorders such as schizophrenia, ASD, and mood disorders. In this study, we aimed to investigate whether serum Cingulin levels are associated with ASD. Subjects and Methods: A total of 40 treatment-naive children with ASD and 40 healthy controls were included in the present study. The Schedule for Affective Disorders and Schizophrenia for School-Aged Children, Present and Lifetime Version-DSM-5 (K-SADS-PL-DSM-5) has been used to screen healthy controls for psychiatric disorders by a psychiatrist after a physical examination by a paediatrician. The clinical severity of the ASD symptoms has been assessed by the Childhood Autism Rating Scale (CARS). Venous blood samples were collected and serum Cingulin levels were measured. Results: When the ASD and control groups were compared, CARS and Cingulin values of the patient group were statistically higher than the healthy group. There is a statistically positive correlation between CARS and Cingulin values. Discussion: To the best of our knowledge, this study is a first in the literature conducted about the serum Cingulin levels, which is a component of BBB, among patients with ASD. Our findings demonstrate that serum Cingulin levels are meaningfully higher in ASD group compared to the healthy control group. It has been also indicated that there has been a meaningful relationship between serum Cingulin levels and ASD symptom severity.

Introduction: A previous study has evaluated the association between serum tumour necrosis factor-like weak apoptosis inducer (TWEAK) levels and autism spectrum disorder (ASD). In line with this investigation, the present study aimed to measure serum TWEAK levels to determine whether their eventual alteration might have etiopathogenetic significance in children with ASD. Methods: A total of 40 treatment-naive children with ASD and 40 healthy children as controls were included in the present study. The Schedule for Affective Disorders and Schizophrenia for School-Aged Children--Present and Lifetime Version, DSM-5 was used by a psychiatrist to screen the healthy controls for psychiatric disorders after a physical examination by a paediatrician. The clinical severity of the ASD symptoms was assessed by the Childhood Autism Rating Scale. Venous blood samples were collected, and serum TWEAK levels were measured. Results: This study included 80 children in total, with 40 (50.0%) in the patient group and 40 (50.0%) in the healthy control group. Thirty four (85.0%) of the participants in the patient group, and 31 (77.5%) in the healthy control group, were male, and the remainder were female. The distribution of the gender ratio was statistically similar between groups (p = 0.568). The volunteers were between 36 and 59 months old. The average age in the patient group was 46.0 ± 6.5, while that in the healthy control group was 45.2 ± 6.7. The ages were also statistically similar between groups (p = 0.615). The TWEAK values of the patient group were found to be statistically higher than those of the healthy control group (p < 0.001). Discussion: This study examined whether serum TWEAK levels were related to ASD in childhood. Our findings indicate that children with ASD have higher TWEAK levels when compared to other children. The findings further indicate that serum TWEAK levels could be related to ASD etiopathogenesis independent of ASD symptom severity.

Nicotine is one of the main chemicals in the cigarettes responsible for addiction formation. Many researches investigating the effects of nicotine on coronary heart disease and atherosclerosis have been published. The robustness of endothelial cells is very important in the development of atherosclerosis. The aim of this study is to evaluate the effect of nicotine exposure on the indicators of endothelial function either by examining the vascular reactivity of aorta taken from rats exposed to nicotine during prenatal (starting by the mating period) and postnatal periods (6 weeks after delivery), or by determining the protein expression of nitric oxide synthase (NOS) enzymes, NADPH oxidase (Nox) and nitrotyrosine. Chronic nicotine exposure at 6 mg/L in drinking water produced a significant decrease in phenylephrine contractility of thoracic aortic rings compared to control and low dose exposure group (0.4 mg/L, p < 0.001). Endothelium-dependent relaxations to acetylcholine increased dose-dependently while no changes were observed in endothelium-independent relaxations to sodium nitroprusside and protein expressions in rat thoracic aorta. It has been concluded that long term nicotine exposure does not have serious effects on endothelial vasodilator response directly and does not change protein expression of NOS or Nox enzymes. However, more studies should be done for the exact mechanisms responsible for the effect of nicotine on endothelial function. [ABSTRACT FROM AUTHOR]

Background and Aim: Irisin is a newly identified myokine secreted by skeletal muscle and has significant effects on body metabolism. Thyroidal functional state has a profound influence on the metabolism of human body. Therefore. the aim of this study was to investigate the possible changes in serum irisin concentrations before and after treatment in hypothyroid subjects. Methods: The study included 26 patients with overt hypothyroidism due to Hashimoto thyroiditis and 19 healthy subjects. Baseline serum thyroid function tests. presence of thyroid autoantibodies and levels of creatine kinase (CK) and irisin were measured in both groups. All measurements in the hypothyroid group were repeated after euthyroidism was achieved. Results: Serum irisin levels were significantly lower in the hypothyroid groups than the control group (p<0.001). Negative correlation between irisin and TSH and CK levels (r=-0.623. p<0.001. r:-0.389. p:0.008. respectively) and a positive correlation between irisin and fT4 levels (r:0.570. p<0.001) was found. Serum CK levels decreased significantly after treatment(p<0.001).Serum irisin levels significantly increased (from 57.4 U/L to 99.8U/L. p<0.001) when the hypothyroid patients were treated to achieve euthyroidism. Conclusions: To the best of our knowledge this is the first study providing insight that low serum irisin levels significantly increased following treatment to euthyroid state in overt hypothyroid patients with Hashimoto thyroiditis. The negative correlation between CK and irisin levels found in our study might underline a possible relation between irisin level and muscle damage in patients with hypothyroidism due to Hashimoto's thyroiditis. The increase in irisin levels and the decrease in CK levels after treatment may indicate myopathy due to hypothyroidism. Larger scale studies are needed to confirm these results and to ensure irisin as a possible biomarker of Hashimoto's thyroiditis. [ABSTRACT FROM AUTHOR]