👤 Bulent Bayraktar

The main objective of this study is to non-invasively investigate the relationship between metacognitive beliefs and cortisol, the primary stress output of the hypothalamic-pituitary-adrenal (HPA) axis, as well as neurotrophic factors associated with neuroplasticity brain-derived neurotrophic factor and neuron-derived neurotrophic factor (BDNF and NDNF). Within this framework, the hypotheses that negative metacognitions would be associated with increased cortisol and decreased BDNF levels, and that cortisol might play a mediating role in this relationship, were tested. The study was designed in a cross-sectional model with 60 university students. Participants' metacognitive beliefs were measured using the Metacognitions Questionnaire-30 (MCQ-30). Salivary cortisol, BDNF, and NDNF levels were analyzed using the ELISA method. Pearson correlation and hierarchical multiple regression analyses were used for data analysis. The results showed a significant positive relationship between the total metacognition score and cortisol (r = 0.589, p < 0.01) and a strong negative relationship between cortisol and BDNF (r = -0.662, p < 0.01). Hierarchical regression analysis supported a partial mediation model, indicating that dysfunctional metacognitive beliefs have both a significant direct negative association with BDNF and an indirect association mediated by cortisol. In the final model, both metacognition (β = -0.298, p < 0.05) and cortisol (β = -0.281, p < 0.05) were significant factors associated with lower BDNF levels. NDNF showed a positive relationship with BDNF (r = 0.571) but not with other variables. These findings point to a psychobiological model where dysfunctional metacognitive beliefs are linked to suppressed neuroprotective mechanisms like BDNF, both directly and indirectly through HPA axis activation. The results shed light on the potential neurobiological mechanisms underlying the effectiveness of metacognitive therapies. Show less

Carbamoyl phosphate synthetase 1 (CPS1) deficiency due to CPS1 mutations is a rare autosomal-recessive urea cycle disorder causing hyperammonemia that can lead to death or severe neurological impairment. CPS1 catalyzes carbamoyl phosphate formation from ammonia, bicarbonate and two molecules of ATP, and requires the allosteric activator N-acetyl-L-glutamate. Clinical mutations occur in the entire CPS1 coding region, but mainly in single families, with little recurrence. We characterized here the only currently known recurrent CPS1 mutation, p.Val1013del, found in eleven unrelated patients of Turkish descent using recombinant His-tagged wild type or mutant CPS1 expressed in baculovirus/insect cell system. The global CPS1 reaction and the ATPase and ATP synthesis partial reactions that reflect, respectively, the bicarbonate and the carbamate phosphorylation steps, were assayed. We found that CPS1 wild type and V1013del mutant showed comparable expression levels and purity but the mutant CPS1 exhibited no significant residual activities. In the CPS1 structural model, V1013 belongs to a highly hydrophobic β-strand at the middle of the central β-sheet of the A subdomain of the carbamate phosphorylation domain and is close to the predicted carbamate tunnel that links both phosphorylation sites. Haplotype studies suggested that p.Val1013del is a founder mutation. In conclusion, the mutation p.V1013del inactivates CPS1 but does not render the enzyme grossly unstable or insoluble. Recurrence of this particular mutation in Turkish patients is likely due to a founder effect, which is consistent with the frequent consanguinity observed in the affected population. Show less

The purpose of this study was to compare the effects of the Traditional acupuncture point ST.36 and 'Omura's ST.36 Point' ("True ST.36") needling on the isokinetic knee extension & flexion strength of young soccer players. The Bi-Digital O-Ring Test (B.D.O.R.T.) of Yoshiaki Omura, M.D.,Sc.D. was used to determine the "True ST.36". Young soccer players (N = 24) between 16-18 years of age (Mean = 16.92 +/- 0.65) were involved in the study. The extension & flexion strengths of dominant legs were measured with Cybex 350 Extremity System isokinetically. The testing velocity was 60 degrees/sec. The peak torque value in Newton meters (Nm) was evaluated. Subjects were tested 3 times. Extension & Flexion 1 (EXT1, FLEX1) without acupuncture application, EXT2 & FLEX2 after application on the traditional acupuncture point, ST.36 and EXT3 & FLEX3 after application onto the 'Omura's New Foot-point' ("True ST.36"). Before each test, subjects warmed up for 10 minutes by cycling on an isokinetic ergometer at 50 RPM, 75 Watts load followed by stretching exercises of lower extremity. Mean EXT1, EXT2, EXT3 values were 196.92 +/- 28.70: 210.00 +/- 23.00; 224.42 +/- 21.70 respectively, where FLEX1, FLEX2, FLEX3 were 140.88 +/- 22.45; 151.13 +/- 21.27; 161.00 +/- 22.23. Comparisons of EXT1-EXT2, EXT1-EXT3, EXT2-EXT3, FLEX1-FLEX2, FLEX1-FLEX3, FLEX2-FLEX3 strength values showed all very high significance (P < 0.001) in favor of 1) Needling on relevant points and 2) Omura's ST.36 Point ("True ST.36"). We conclude that B.D.O.R.T. can help to determine new (True) Acupuncture points and, both points were effective for increasing the isokinetic knee extension & flexion strength of young soccer players very significantly where as Omura's ST.36 Point ("True ST.36") was more effective than Traditional Acupuncture point, ST.36. Show less