Background: Major depressive disorder (MDD) is a mental health and emotional disorder that affects children and adolescents worldwide. This study aimed to evaluate serum nesfatin-1, ghrelin, and lipid levels as biological markers of adolescent MDD and their relationship with the severity of depression-anxiety and suicide risk in MDD. Methods:This study included 37 drug naïve adolescents between the ages of 12 and 18 who were diagnosed with a first episode MDD according to the Kiddie Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version (K-SADS-PL) and DSM-V diagnostic criteria. Thirty-three healthy adolescents between the ages of 12 and 18 were included as the control group. The Children’s Depression Inventory (CDI), Screen for Child Anxiety Related Disorders (SCARED), and Suicide Probability Scale (SPS) were used to evaluate the subjects in the MDD and control groups. In the first stage, serum nesfatin-1, ghrelin, and lipid levels were compared between the adolescents diagnosed with MDD and the control group. Next, the correlations between these levels and the CDI, SCARED, and SPS scores were evaluated. Results: Nesfatin-1 levels were significantly lower in the MDD group than the control group (p < 0.001) A positive correlation was found between the nesfatin-1 levels and the SPS scores. Conclusions: This is the first study to evaluate nesfatin-1 levels in adolescent depression, suggesting that nesfatin-1, ghrelin, total cholesterol, and low-density lipoprotein cholesterol (LDL) levels can be used as biomarkers in child-adolescent MDD. However, it is evident that further studies with larger samples and post-treatment measurements are needed.

Objective: To compare the maternal serum catestatin (CST) levels in pregnant women with preeclampsia (PE) and with normal blood pressure and evaluate the relationship between the maternal serum CST levels and fetal cardiac functions Materials and Methods: This cross-sectional study was conducted on 27 women with early-onset PE (EOPE), 28 women with late-onset PE (LOPE), and 28 healthy pregnant women. Maternal serum CST levels were measured using the enzyme-linked immunosorbent assay kits. Fetal cardiac functions were evaluated using the cardiac Doppler. Results: Maternal serum CST levels were lower in the EOPE group; however, no statistically significant difference was found between the groups. Compared with the other two groups, a statistically significant difference was found in the fetal E/A ratio and myocardial performance index (MPI) values of the EOPE group (p=0.013, p=0.002, p=0.005, p<0.001, respectively). The fetal E/A ratio was positively correlated with the maternal serum CST levels in both the PE and control groups (p<0.001, p<0.001). The fetal isovolumetric relaxation time and MPI values were negatively correlated with maternal serum CST levels in both the PE and control groups (p<0.001, p=0.001, p<0.001, and p=0.002, respectively). Conclusion: Lower CST levels are associated with fetal cardiovascular dysfunction, thus CST can be a critical biochemical marker in fetal cardiac function evaluation.

Hyperbaric oxygen therapy (HBOT) causes insulin sensitivity, but the reason for this is not yet known. The aim of the present study was to investigate the effect of HBOT on insulin sensitivity via resistin, plasminogen activator inhibitor-I (PAI-I), and adiponectin. The study was designed using HBOT and control groups, with eight rats in each group. After 20 days of HBOT under 2.5 atmospheres for 90 minutes, the fasting insulin (FI), resistin, PAI-I, homeostatic model assessment of insulin resistance scores (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), fasting plasma glucose (FPG), triglyceride, and high-density lipoprotein cholesterol (HDL-C) in the plasma were measured. The resistin, PAI-I, and adiponectin mRNA expression levels were also measured in the adipose tissue. Compared to the control group, the FI, FPG, and HOMA-IR scores were significantly lower in the HBOT group, whereas the HDL-C and QUICKI scores were found to be higher. In addition, the resistin, adiponectin, and PAI-I mRNA expression levels were also higher in the HBOT group. The present study demonstrated that the HBOT had regulated the FI, FPG, and HDL-C associated with metabolic syndrome and diabetes mellitus. Moreover, the study showed that HBOT causes insulin sensitivity by raising adiponectin.

The use of measurement uncertainty among clinical laboratories becomes widespread. Measurement uncertainty can be reported with the result, as well as be used in certain reference change value (RCV) calculation equations. RCV is especially recommended for use in tests with a low individuality index. In our study, we calculated the measurement uncertainty of AFP, CA 125, CA 15-3, CA 19-9, CEA tumor markers with the ISO TS 20914:2019. We compared results with limits. Two Beckman Coulter DXI-800 (Minnesota, USA) autoanalysers’ results were used. We calculated the RCV values using the classical Fraser method, logarithmic Lund Method, and Clinical Laboratory Standards Institute (CLSI) method as Minimal Difference (MD). We found the same permissible measurement uncertainty limit as 15.97% for all five tumor markers. The highest RCV value was found as 90% upstream for AFP test with Lund logarithmic approach, the lowest RCV value was found as 12% for CEA with MD, all other RCV results were between these two values. We do not recommend the use of MD, as values for Biological variation are not used in the MD approach. We also recommend using the logarithmic approach, although it gives higher results. There are also clinical studies on the significance of tumor markers in a follow-up that show different results. These differences may be because the studies are conducted with different systems. Therefore, each laboratory needs to calculate its own RCV values. We also recommend informing the clinicians about the tests with high measurement uncertainty.

To evaluate the serum sortilin levels in pregnant women with gestational diabetes mellitus (GDM) and to compare the results with normoglycemic healthy pregnant women and observe the relationship be...

Study Objectives: This study aimed to evaluate and compare the effects of high and low-intensity expiratory muscle strength training (EMST) on disease severity, systemic inflammation, oxidative stress, respiratory muscle strength, exercise capacity, symptoms, daytime sleepiness, fatigue severity, and sleep quality in male patients with obstructive sleep apnea syndrome (OSAS). Methods: Thirty-one male patients diagnosed with moderate OSAS were included in this double-blind, randomized, parallel study. Patients were randomized into two groups: High-EMST and Low-EMST groups. EMST was used at home 7 days/week, once a day, for 25 breaths, 12 weeks. Respiratory muscle strength was measured using a mouth pressure device. Disease severity (Apnea–Hypopnea Index [AHI]) and, respiratory sleep events by polysomnography, total oxidant level(TOS), total antioxidant level(TAS), oxidative stress index (OSI), C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10) levels by blood serum were evaluated. Results: The percentage of AHI change in the high-EMST group(50.8%) was significantly higher than in the low-EMST group(6.3%; p = .002, d = 1.31). In general, as MEP increased by one unit, AHI decreased by 0.149 points (b = −0.149; CR = −3.065; p = .002), and as AHI increased by one unit, ODI increased by 0.746 points (b = 0.746; CR = 10.604; p < .001). TOS, OSI, TNF-α and IL-6 levels decreased at similar rates in both groups. Conclusions: EMST significantly reduces systemic inflammation and oxidative stress while improving expiratory muscle strength in male patients with moderate OSAS. High-EMST is more effective in enhancing the severity of disease than low-EMST. EMST is a practical, effective, and promising treatment for pulmonary rehabilitation in patients with moderate OSAS. Clinical Trials: Effect of EMST systemic inflammation and oxidative stress in patients with moderate OSAS, https://clinicaltrials.gov/study/NCT05242406, with the number NCT05242406.