Objective: The purpose of this study was therefore to investigate whether neuronal, axonal, and glial cell markers (Neuron-specific enolase [NSE], tau, serum 100 beta protein [S100B], respectively) and apoptosis markers (active caspase 3, M30, M65) and whether these parameters can be used as diagnostic biomarkers in autism spectrum disorders (ASD). Methods: This study measured the serum S100B, NSE, tau, active caspase 3, M30, and M65 levels in 43 patients with ASD (aged 3−12 years) and in 41 age-and sex-matched healthy controls. ASD severity was rated using the Childhood Autism Rating Scale. The serum levels were determined in the biochemistry laboratory using the ELISA technique. The receiver operator characteristics curve method was employed to evaluate the accuracy of the parameters in diagnosing ASD. Results: Serum S100B, tau, NSE, active caspase-3, M30, and M65 levels were significantly higher in the patient group than in the control group (p ＜ 0.001, p = 0.002, p = 0.002, p = 0.005, p ＜ 0.001, and p = 0.004, respectively). The cutoff value of S100B was 48.085 pg/ml (sensitivity: 74.4%, specificity: 80.5%, areas under the curve: 0.879, p ＜ 0.001). Conclusion: Apoptosis increased in children with ASD, and neuronal, axonal, and glial cell injury was observed. In addition, S100B may be an important diagnostic biomarker in patients with ASD. Apoptosis, and neuronal, axonal and astrocyte pathologies may play a significant role in the pathogenesis of ASD, and further studies are now required to confirm this.

Introduction: Psoriasis is a common, inflammatory skin disease of which etiopathogenesis is still not explained clearly, however in which trace elements and oxidative stress are considered to play a role. Aim: To evaluate the serum trace element and oxidative stress levels in patients diagnosed with psoriasis. Material and methods: A total of 87 psoriasis patients and 60 healthy subjects were included in the study. Serum sodium (Na), potassium (K), calcium (Ca), phosphorus (P), magnesium (Mg), iron (Fe), selenium (Se), zinc (Zn), copper (Cu) levels, oxidative stress parameters, ischemia-modified albumin (IMA), catalase (CAT), myeloperoxidase (MPO) and ferroxidase (FOX) activity and an inflammatory marker, C-reactive protein (CRP), were examined in all participants. Results: IMA, IMA/Albumin (IMA/Alb), CAT, Cu, FOX and CRP levels were found to be significantly higher; Se, Zn and albumin levels were significantly lower in the patient group as compared to the control group. No significant difference was found between groups with regard to Na, K, Ca, P, Mg, Fe and MPO levels. Conclusions: Some trace element levels and oxidant-antioxidant balance were changed in psoriasis patients.

A b s t r a c tIntroduction: Psoriasis is a common chronic inflammatory skin disease with unknown etiopathogenesis. Aim: To examine the thiol/disulfide balance in psoriasis patients and to compare the results with a healthy control group. Material and methods: Eighty patients with psoriasis and 80 healthy individuals who were age-and gender-matched with these patients were included in this study. Serum native thiol, disulfide and total thiol levels were measured by a new automated method developed by Erel and Neselioglu. Disulphide/total thiol, disulphide/ native thiol and native thiol/total thiol were calculated. Results: While there was no statistically significant difference in terms of disulphide levels (SS) between the patient and control groups (p > 0.05), there were significant differences in terms of total thiol and native thiol (SH) levels, SS/SH, SS/total thiol and SH/total thiol ratios between the patient and control groups (p < 0.05). There was a statistically significant relationship between duration of the disease and the disulfide/native thiol ratio (p > 0.05). Conclusions: In recent years, there have been few studies on the role of oxidative stress in the etiopathogenesis of psoriasis. In this study, we investigated in psoriasis patients, thiol/disulfide balance as a new oxidative stress marker. The results were compared with a healthy control group. Our results showed that thiol/disulphide balance shifted towards disulphide in psoriasis patients. This is important as a finding that supports the role of oxidative stress in the pathogenesis of psoriasis.

This was the first study in which the ceruloplasmin and Cu levels were investigated in HELLP syndrome patients. When considering the results obtained in the present study, there were significant relationships between the Cu, CP levels which are the markers of oxidative stress and the preeclampsia severity.

Acetylcholinesterase inhibitors, including Neostigmine, have been used to reverse neuromuscular blockage for many years. Sugammadex reverses this blockage using its gamma cyclodextrin ring, a mechanism that differs from that of cholinesterases and so circumvents the side effects of Neostigmine. Although the superiority of Sugammadex to Neostigmine has been outlined in several clinical studies, to our knowledge, there is not any research into cell culture that compares the cytotoxic, genotoxic and apoptotic effects of the two drugs. Hence, this is the first study to compare the cytotoxic, genotoxic and apoptotic effects of different dosages of both drugs on human embryonic renal (HEK-293) cells. In this study, the cytotoxicity, genotoxicity and apoptotic effects of Sugammadex and Neostigmine on HEK-293 cells were analyzed with using the MTT, Comet Assay and Flow Cytometric Annexin-V methods, respectively. The results demonstrate that Neostigmine at 50, 100, 250, and 500 µg/mL is more cytotoxic than equivalent dosages of Sugammadex. Neostigmine at 500 and 1000 µg/mL was found to be more genotoxic, and Neostigmine at 500 µg/mL had a statistically higher risk of causing apoptosis and necrosis than Sugammadex (p<0.05). Neostigmine administered in-vitro in the same doses as Sugammadex had greater cytotoxic, genotoxic and apoptotic effects on HEK-293 cells.