A preliminary study about neurofilament light chain and tau protein levels in psoriasis: Correlation with disease severity.

BACKGROUND: Studies investigating cognitive dysfunction in psoriatic patients remain inconclusive. OBJECTIVE: To investigate the risk of cognitive decline in plaque-type psoriasis patients. METHODS: Serum neurofilament light chain (NFL) and tau protein concentrations in 45 patients with plaque-type psoriasis and forty-five healthy controls were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: Mean homeostasis model assessment (HOMA-IR) values (6.82 vs 3.25) and serum levels of insulin (28.19 vs 15.71), NFL (5.74 vs 1.98), and tau (348.17 vs 207.30) in patients with psoriasis were found to be significantly higher than those of in healthy controls. There was a significant positive correlation between NFL and tau (r = .257, P = .015). There was significant correlation between NFL, tau and PASI (r = .310, P = .040) and (r = .383, P = .010), respectively. Significant correlations between NFL and insulin, TC, HDL-C, TG, VLDL-C, and BMI were found. NFL (9.38 vs 3.08) and tau (439.28 vs 281.58) concentrations and PASI values (23.94 vs 14.18) in patients with disease onset before 40 years were significantly higher than that of the patients with disease onset after 40 years. C-reactive protein (CRP) was significantly correlated with BMI (r = .449, P < .001), LDL-C (r = .240, P = .026), TG (r = .244, P = .024), and VLDL-C (r = .241, P = .025) in patients with psoriasis. CONCLUSIONS: Increased serum NFL and tau protein levels and the presence of positive correlations between NFL, tau protein and PASI score show cognitive decline risk may be higher in moderate-to-severe psoriasis.

The endothelin 1 and endothelin receptor A gene polymorphisms increase the risk of developing papillary thyroid cancer.

The endothelin (EDN) axis (EDN1 and EDN1 receptor A, EDNRA) is involved in cellular growth, differentiation, invasiveness, and tumor progression in several cancers. We wanted to examine the possible impact of single nucleotide polymorphisms (SNPs) of EDN1 and EDNRA genes on papillary thyroid cancer (PTC) development and general characteristics of PTC. Study population consist of 113 PTC patients and 185 controls. EDN1 (G5665T, T-1370G) and EDNRA (C TT70G, G-231A) SNPs were investigated by real-time PCR. The GG genotype of EDNRA + 70 SNP was associated with threefold increased PTC risk (p = 0.01), and the combined CG + GG genotype was 2.48 fold higher among PTC patients compared to controls. The variant EDNRA - 231 allele was overrepresented in PTC patients according to controls (p = 0.05). The combined GT + TT genotype of EDN1 5665 SNP was related with late (age after 40 years) PTC onset (p = 0.04), and was more prominent among male patients with PTC according to females (p = 0.03). No significant associations between PTC and - 1370 SNP were found. There were no relationships between laboratory parameters and investigated polymorphisms. The EDNRA + 70 SNP was associated with PTC development. The EDN1 5665 SNP was linked with increased risk for late PTC onset and was more prominent among male patients with PTC.

Vascular endothelial growth factor G+405C polymorphism may contribute to the risk of developing papillary thyroid carcinoma.

BACKGROUND: Papillary thyroid carcinoma (PTC) is the most common endocrine malignancy. Vascular endothelial growth factor (VEGF) is a mediator implicated with cell proliferation, differentiation and migration, and monocyte/macrophage chemotaxis. In present study, we aimed to investigate the relationship between VEGF gene polymorphisms (G+405C, T-460C, and A-2578C) and PTC susceptibility. METHODS: DNA was isolated from peripheral blood leukocytes of 127 patients with PTC and 203 healthy controls. Genotyping was performed by real-time PCR. Association of genotypes with susceptibility of PTC was analyzed with multivariate logistic regression adjusted for age, gender and smoking status. RESULTS AND CONCLUSION: In G+405C polymorphism, the frequencies of C allele (related with increased VEGF production) and combined CG+CC genotype were found to be higher (3.5 and 5-fold, respectively) among patients with PTC than controls (P<.001). However, VEGF T-460C and A-2578C polymorphisms are not associated with PTC risk. There was no relationship between VEGF polymorphisms and clinical/laboratory parameters of PTC. Haplotype analysis demonstrated that there was a strong linkage disequilibrium (LD) between -460/-2578 (D'=.89, r2 =.79), weak LD between +405/-460 (D'=.422, r2 =.035), and +405/-2578 (D'=.43, r2 =.038) locuses. Additionally, the +405/-460/-2578 GTA haplotype was found to be protective, whereas CTA haplotype to be related with increased PTC risk. As a conclusion, we suggest that VEGF G+405C polymorphism is associated with increased risk of PTC.

High circulating levels of sICAM-1 and sVCAM-1 in the patients with Hashimoto's thyroiditis.

OBJECTIVE: To investigate whether soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) levels are increased in euthyroid patients with Hashimoto's thyroiditis (HT) and whether they are associated with thyroid autoimmunity and metabolic parameters. DESIGN: Cross-sectional. SUBJECTS AND METHODS: In total, 80 euthyroid patients with HT and 80 age- and body mass index (BMI)-matched control participants were included. Serum sICAM-1, sVCAM-1, free triiodothyronine (fT3), free thyroxine (fT4), thyroid-stimulating hormone (TSH), thyroid peroxidase antibody (anti-TPO), thyroglobulin antibody (anti-TG), fasting blood glucose (FBG), insulin, and lipid levels and homeostasis model assessment for insulin resistance (HOMA-IR) were assessed in all participants. RESULTS: The patients with HT had significantly higher levels of sICAM-1 and sVCAM-1 than controls (both p < 0.001). The difference was sustained after adjustment for TSH and levothyroxine use. Regression analysis demonstrated that sICAM-1 was related to anti-TPO (p < 0.001), and sVCAM-1 was related to both anti-TPO and-TG (p < 0.001 and p = 0.03, respectively); this relationship was sustained after adjustment for age and BMI. Although FBG and HOMA-IR were higher in the HT group, logistic regression analysis revealed that there was no effect of anti-TPO, anti-TG, sICAM-1, sVCAM-1, and C-reactive protein (CRP) on the occurrence of high FBG and high HOMA-IR. CONCLUSION: sICAM-1 and sVCAM-1 levels were significantly elevated in the patients with euthyroid HT and correlated closely with thyroid autoimmunity. However, soluble adhesion molecules had no relation with glucose metabolism parameters in the HT patients.

Serum Visfatin, Fetuin-A, and Pentraxin 3 Levels in Patients With Psoriasis and Their Relation to Disease Severity.

BACKGROUND: Psoriasis is a chronic immune-mediated inflammatory skin disease associated with increase of some pro-inflammatory mediators. We wanted to investigate whether there is a relationship between psoriasis and visfatin, fetuin-A and pentraxin 3 (PTX3)-pro-inflammatory mediators implicated in the development of insulin resistance (IR), metabolic syndrome, and atherosclerosis. METHODS: Visfatin, fetuin-A, and PTX3 concentrations were measured in 45 patients with plaque-type psoriasis and 45 healthy controls using enzyme-linked immunosorbent assay (ELISA). RESULTS: Serum levels of visfatin, fetuin-A, and PTX3 in patients with psoriasis were found to be higher than in healthy controls (P = 0.002, P = 0.009, P < 0.001, respectively). Psoriasis area and severity index (PASI) score correlated significantly with visfatin and fetuin-A levels (P = 0.011, P = 0.040, respectively). There was a significant positive correlation between visfatin and fetuin-A (P < 0.001). PTX3 levels were correlated positively with homeostasis model assessment (HOMA-IR), insulin, triglyceride (TG), and very low density lipoprotein cholesterol (VLDL; P = 0.009, P = 0.007, P = 0.023, P = 0.024, respectively). CONCLUSIONS: Increased serum visfatin, fetuin-A, and PTX3 levels, and the presence of positive correlation between visfatin, fetuin-A, and PASI score, probably reflect the inflammatory state and IR seen in psoriasis.

Interleukin-10-1082 gene polymorphism is associated with papillary thyroid cancer.

The etiopathogenesis of thyroid cancer has not been clearly elucidated although the role of chronical inflammation and the imbalance between pro- and anti-inflammatory cytokines may play a role in the etiology. The aim of the present study was to investigate whether cytokine gene polymorphisms are associated with papillary thyroid cancer (PTC), and to evaluate the relationship between genotypes and clinical/laboratory manifestation of PTC. Tumor necrosis factorα (TNFα) G-308A (rs 1800629), interleukin-6 (IL-6) G-174C (rs 1800795) and IL-10 A-1082G (rs 1800896) single nucleotide polymorphisms in DNA from peripheral blood leukocytes of 190 patients with thyroid cancer and 216 healthy controls were investigated by real-time PCR combined with melting curve analysis. There was no notable risk for PTC afflicted by TNFα-308 and IL-6-174 alone. However, IL-10-1082 G allele frequency were higher among PTC patients than healthy controls (p=0.009). The patients with IL-10-1082 GG geotype have twofold increased risk of developing thyroid cancer according to AA genotype (OR 2.07, 95% CI 1.21-3.55). In addition, the concomitant presence of IL-10-1082 G allele (GG+AG genotypes) together with IL-6 -174 GG genotype has a nearly twofold increased risk for thyroid cancer (OR 1.75 with 95% CI 1.00-3.05, p=0.049). We suggest that IL-10-1082 G allele is associated with an increased risk of PTC. The polymorphism of IL-10 gene can improve our knowledge about the pathogenesis of PTC, and could provide to estimate people at the increased risk for PTC.

Relationship between plasma melatonin levels and the efficacy of selective serotonin reuptake inhibitors treatment on premature ejaculation.

OBJECTIVES: To examine the relationship between premature ejaculation and plasma melatonin levels, and assess the efficacy of selective serotonin reuptake inhibitors in treating premature ejaculation. METHODS: A total of 60 men with lifelong premature ejaculation and 40 healthy male controls were included in the present study. For each participant, a medical history was obtained, a physical examination was carried out, and intravaginal ejaculation latency time and melatonin levels were measured. Premature ejaculation patients were randomly categorized into three treatment groups: group 1 received fluoxetine (20 mg/day), group 2 received paroxetine (20 mg/day) and group 3 received sertraline (50 mg/day). RESULTS: The mean baseline plasma melatonin levels in men with premature ejaculation were significantly lower than in the healthy controls (5.34 vs 14.84 pg/mL). After 4 weeks of treatment, the mean intravaginal ejaculation latency time scores for all of the premature ejaculation treatment groups showed a significant improvement from the baseline values. The plasma melatonin levels were also significantly increased (P < 0.05) from baseline (5.34 pg/mL) to 9.50 pg/mL, 10.24 pg/mL or 13.30 pg/mL for groups 1, 2 and 3, respectively. CONCLUSIONS: Our findings show that premature ejaculation is associated with decreased plasma melatonin levels. After treatment with selective serotonin reuptake inhibitors, an increased plasma melatonin level can retard ejaculation, presumably by both central and peripheral mechanisms. This is the first study to evaluate the possible role of serotoninergic interactions on the melatoninergic system in premature ejaculation.

Effects of hemostatic agents on fibroblast cells.

PURPOSE: Hemostatic agents may be used topically to control hemorrhage, especially in patients with bleeding disorders. The agent used may have a negative effect on the tissue prolonging the healing time. The aim of this study was to compare the effects of 3 different hemostatic agents on fibroblast cells on a rat primary fibroblast cell culture model. MATERIALS AND METHODS: Ankaferd Blood Stopper (ABD) (Ankaferd Pharmaceuticals Cosmetics Production and Marketing Co.), fibrin glue, and tranexamic acid were the agents to be evaluated for their effects on cell proliferation, cell numbers, cell viability, and cell morphology. Also lactate dehydrogenase, basic fibroblast growth factor, and vascular endothelial growth factor C levels were measured. RESULTS: It was found that all of the agents used in the study have negative effects on fibroblasts, with ABD having the lowest values of cell proliferation, cell number, and cell viability. CONCLUSION: The results of this study indicate that ABD, fibrin glue, and tranexamic acid may negatively affect tissue healing.

Monthly variation of fatty acids, lipid quality index and metal content of Pontastacus leptodactylus (Eschscholtz, 1823) in Atikhisar Dam Lake (Çanakkale, Türkiye).

This study aims to investigate the metal content, fatty acid composition, lipid quality, and potential health risks of Pontastacus leptodactylus crayfish inhabiting Atikhisar Dam Lake. The research covers a 12-month period and includes both male and female individuals. The study investigated the metal content of crayfish specimens. In female individuals, the metal concentrations were ranked as Fe > Zn > Al > Cu > Mn > Se > As > Hg > Cd > Pb, while in male individuals, the ranking was Fe > Al > Zn > Cu > Mn > Se > As > Hg > Pb > Cd. The results demonstrate that Atherogenicity Index (AI) values for both genders range between 0.21 and 0.31, and Thrombogenicity Index (TI) values fall within 0.14 and 0.20. This indicates that crayfish meat is composed of healthy and high-quality fatty acids. In male individuals, omega-3 values range from 25.28 ± 0.380% to 28.34 ± 0.430%, and in female individuals, they vary from 22.98 ± 0.195% to 28.73 ± 0.871%. These findings underscore the absence of significant health risks associated with mercury levels in crayfish meat. Monthly meal calculations reveal that consuming female crayfish at an average of 4.35 servings per month for adults and 2.24 servings per month for children presents no health hazards. Similarly, the consumption of crayfish meat at an average of 5.29 servings per month for adult males and 2.72 servings per month for male children is deemed safe for health. Based on these results, the lipid quality of both male and female individuals from this species is found to be beneficial, as confirmed by risk-benefit assessments.

The Role of Sertoli Cell Hormones in Male Preponderance Observed in Autism Spectrum Disorder.

Introduction: There is a significant, but poorly understood, male preponderance in prevalence of autism spectrum disorder (ASD). The aim of this study was to examine the relationship between male preponderance in ASD and Inhibin B (InhB) and Anti-Müllerian hormone (AMH) levels and the 2D/4D finger ratio associated with fetal androgen exposure. Methods: 42 patients with ASD and 42 neurotypical controls between the ages of 5 and 10 were included. ASD diagnosis and severity were determined using K-SADS PL (Kiddie-SADS - Present and Life Time) Version 2016 and the Childhood Autism Rating Scale (CARS). Serum InhB and AMH were measured. The 2D/4D finger length ratio was also calculated for hand anthropometric measurements. Results: Serum InhB levels were higher in children diagnosed with ASD compared to the neurotypical controls (p=0.003). Serum AMH levels were similar in both groups. Positive correlation was determined between AMH and CARS scores (r=0.315, p=0.05). 2D/4D finger ratios in the ASD group were significantly lower than in the control group (p<0.001). Conclusion: The study findings suggest that InhB, AMH, and fetal testosterone may be associated with male preponderance in ASD. More research is now required for a better understanding of this subject.

ICAM1 K469E and E-selectin S128R polymorphisms could predispose to increased autoantibody production and TSH suppression in Graves' disease.

The etiopathogenesis of Graves' disease (GD) has not been clearly elucidated although the role of chronical inflammation and endothelial dysfunction has been established. Adhesion molecules such as intercellular adhesion molecule 1 (ICAM1), vascular cell adhesion molecule 1 (VCAM1), and E-selectin are secreted from vascular endothelium and promote accumulation of leukocytes in damaged endothelial areas. This study examined the possible association of ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) single nucleotide polymorphisms (SNPs) with the occurrence of GD. ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) SNPs in DNA from peripheral blood leukocytes of 171 patients with GD and 259 healthy controls were investigated by real-time PCR combined with melting curve analysis using fluorescence-labeled hybridization probes. We did not find significant differences in the distributions of studied polymorphisms, nor in the haplotype frequencies between patients with GD and healthy control. However, the anti-TPO levels in E-selectin 128R allele carrying subjects (SR + RR) were higher than S128S genotype (p < 0.05). In addition, the decline of TSH levels was more prominent in ICAM1 469 E carrying subjects (KE + EE) in comparison with wild homozygotes (p < 0.05). Although there is not association between ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) SNPs and susceptibility to GD, higher anti-TPO in E-selectin 128 SR + RR, and lower TSH in ICAM1 469 KE + EE subjects suspect that these genotypes are prone to increased antithyroid autoantibody production with more accentuated TSH suppression in GD. Further studies with a larger cohort, analyzing other polymorphisms in ICAM, VCAM1 and E-selectin genes are necessary to support our observations.

Low-level laser therapy vs. pulsed electromagnetic field on neonatal rat calvarial osteoblast-like cells.

To compare the effects of pulsed electromagnetic field (PEMF) and low-level laser therapy (LLLT) on osteoblast cells in a cell culture model. Fifty thousand neonatal rat calvarial osteoblast-like cells per milliliter were seeded and 0.06 mT PEMF, 0.2 mT PEMF, and LLLT at 808 nm were applied for 24 and 96 h on the cells. To evaluate cellular proliferation and differentiation, specimens were examined for DNA synthesis, alkaline phosphatase (ALP) activity, cell numbers, and viability of the cells. Morphological appearances of the cells were observed using scanning electron microcopy after 24 and 96 h of incubation. At 24 and 96 h, the control group had a higher cell proliferation than 0.06 and 0.2 mT PEMF groups (p=0.001). At 96 h, 0.2 mT PEMF group had higher cell proliferation rate than 0.06 mT PEMF and LLLT groups (p=0.001). The cell count and cell viability in 0.2 mT PEMF group were higher than the 0.06-mT PEMF and LLLT groups, although these differences were not statistically significant at 96 h (p>0.05). At 24 and 96 h, cell viability in the control group was higher than the test groups. Alkaline phosphatase levels of the groups were comparable in both time intervals (p>0.05). 0.2 mT PEMF application on osteoblast-like cells led to cell proliferation and differentiation better than 0.06 mT PEMF and LLLT at 808 nm, although a remarkable effect of both PEMF and LLLT could not be detected. The ALP activity of 0.2 and 0.06 mT PEMF and LLLT were comparable.

Elevated Serum Galectin-1 and Galectin-3 Levels in Children With Specific Learning Disorder: A Case Control Study.

OBJECTIVE: Specific learning disorder (SLD) is a neurodevelopmental disorder in which underlying pathogenesis and etiological factors are not fully understood. Neuroinflammatory response (measured with serum levels of galectin-1 and galectin-3), which is associated with learning and memory, may play an important role in the etiopathogenesis of SLD. Aim of the present study is to examine whether serum galectin-1 and galectin-3 levels are related to SLD. METHODS: The current study consisted of 42 treatment-naive children with SLD and 42 control subjects. All of the subjects were assessed using semi-structured psychiatric examination to diagnose SLD and exclude attention-deficit hyperactivity disorder. Serum galectin-1 and galectin-3 levels were measured via venous blood samples. RESULTS: The SLD and control group did not differ significantly in terms of age, sex, and body mass index (BMI). The SLD group had significantly higher serum levels of galectin-1 (8.78±2.97 vs. 7.40±2.03, p=0.019) and galectin-3 (1.86±0.93 vs. 1.32±0.69, p=0.003) than the control group when controlled for age, sex, and BMI. CONCLUSION: Higher serum levels of galectin-1 and galectin-3 in children with SLD may indicate the role of neuroinflammatory response in the pathogenesis of SLD. Other mechanisms involving galectin-1 and galectin-3 related to learning may play a part in the etiology of SLD.

Serum Zonulin and Claudin-5 but not Interferon-Gamma and Interleukin-17A Levels Increased in Children with Specific Learning Disorder: A Case-Control Study.

Background: Gut-blood and blood-brain barrier permeabilty (gut-brain axis) has been attracting increased attention in the etiology of neurodevelopmental disorders. In this study, we aimed to investigate serum levels of zonulin (a biomarker of intestinal permeability), claudin-5 (a biomarker of blood-brain barrier permeability), and interferon-gamma and interleukin-17A in children with specific learning disorder. Methods: Forty-three children with DSM-5 diagnosis of specific learning disorder and 43 healthy children were included in this study. Serum levels of zonulin, claudin-5, interferon-gamma, and interleukin-17A were measured using commercial enzyme-linked immunosorbent assay kits. Results: Serum zonulin and claudin-5 levels of the study group were significantly higher than the control group according to the multivariate analysis of covariance test while controlling for age, gender, and body mass index. However, serum interferon-gamma and interleukin-17A levels were not significantly different between the two groups. There was no correlation either between zonulin and interferon-gamma and interleukin-17A or claudin-5 and interferon-gamma and interleukin-17A. Conclusion: Gut-blood and blood-brain barrier permeability may be disrupted in subjects with special learning disorder. Further research is needed to determine whether zonulin and claudin-5 may be biomarkers, and some dietary interventions or specific agents such as zonulin or claudin-5 inhibitors could be used in the management of neurodevelopmental disorders including special learning disorder.

Effect of carnosine on prooxidant-antioxidant balance in several tissues of rats exposed to chronic cold plus immobilization stress.

In this study, we investigated the effect of L-carnosine (CAR) on prooxidant-antioxidant balance in several tissues of rats exposed to chronic stress. Both cold and immobilization stresses were applied to rats at the same time. In the stress group, rats were placed in restraint cages and kept in a cold room (+4°C) for 1 h for 21 days (5 days a week). Rats were injected with CAR (250 mg/kg, i.p.) at 30 min before stress application. Malondialdehyde, diene conjugate, protein carbonyl and nitrotyrosine levels, nonenzymatic (glutathione, vitamin E, and vitamin C), and enzymatic (catalase, superoxide dismutase and glutathione peroxidase) antioxidants were determined in the liver, heart, and brain tissues. Chronic cold plus immobilization stress was observed to affect especially the prooxidant-antioxidant status in the brain tissue of rats. This is the first report showing the beneficial effects of CAR on oxidative stress in the brain in rats exposed to stress.

G241R and K469E polymorphisms of intercellular adhesion molecule 1 (ICAM-1) could predispose to Hashimoto thyroiditis.

This study examined firstly the possible association of G241R and K469E single nucleotide polymorphisms (SNPs) of ICAM-1 gene with the occurrence of Hashimoto thyroiditis (HT). G241R and K469E SNPs in DNA from peripheral blood leukocytes of 190 HT and 247 healthy controls were investigated by real-time PCR combined with melting curve analysis using fluorescence-labeled hybridization probes. There was a significant increase of ICAM-1 241R allele frequency in patients with HT compared with healthy controls (P = 0.04, OR = 1.84, 95 % CI = 1.00-3.37). Regarding ICAM-1 K469E polymorphism, patients homozygous for E allele had 1.73-fold increased risk for developing HT according to KK homozygotes (P = 0.04, 95 % CI = 1.00-3.01). The 469E allele frequency was higher in HT patients according to controls, however the difference was at borderline significance (P = 0.05, OR = 1.30, 95 % CI = 1.00-1.70). No associations between polymorphisms and HT phenotypes were observed. We suggest that the G241R and K469E SNPs of ICAM-1 gene may be related to occurrence of HT. However, more studies with larger sample size including other loci of the ICAM-1 gene are necessary to support our findings before any definite statement can be made about the relationship between HT and ICAM-1 polymorphism.

Analysis of vitamin D receptor gene polymorphisms in vitiligo.

BACKGROUND: Vitiligo is a progressive depigmenting disorder characterized by the loss of functional melanocytes from the epidermis. The etiopathogenesis of vitiligo is still unclear. Vitamin D has both stimulatory and protective effects on melanocytes and acts through its nuclear vitamin D receptor (VDR) on target cells. AIM: The aim of this study was to investigate the association between VDR gene polymorphisms and susceptibility to vitiligo. METHODS: 98 patients with vitiligo and 216 age- and sex-matched controls recruited from dermatology outpatients attending the same department were included in the study. Genomic DNA was extracted from peripheral blood leukocytes using a DNA isolation kit. The VDR polymorphisms of BsmI, ApaI, TaqI, FokI and Cdx2 were investigated by rapid capillary PCR with melting curve analysis. Differences in genotype distributions and allele frequencies in vitiligo cases versus controls were compared for statistical significance using χ(2) test. RESULTS: Subjects with TaqI polymorphism had a 2.23-fold increased risk of developing vitiligo. Furthermore, a haplotype analysis showed that BsmI/ApaI/TaqI/FokI/Cdx2 GCCCG was significantly overrepresented in the vitiligo patients in comparison with controls (p = 0.031). CONCLUSION: This study showed that VDR TaqI gene polymorphism and the haplotype BsmI/ApaI/ TaqI/FokI/Cdx2 GCCCG may be considered as novel risk factors in vitiligo.

The oxidant/antioxidant status and cell death mode in oral squamous cell carcinoma.

OBJECTIVE: Oxidative stress and imbalance in the oxidant/antioxidant system have a critical role in carcinogenesis by affecting necrosis and apoptosis. The aim of this study is to evaluate the oxidant/antioxidant status and cell death modes in patients with oral squamous cell carcinoma (OSCC). MATERIALS AND METHODS: Twenty-nine patients with OSCC and 29 control subjects were included in the study. The levels of malondialdehyde (MDA), advanced oxidation protein products (AOPP) and ferric reducing antioxidant power (FRAP) were determined in plasma samples of all subjects. The necrotic and apoptotic cell death modes were evaluated with M65 ELISA and M30 ELISA, respectively. RESULTS: MDA and AOPP values as oxidative stress markers were higher in patients with OSCC than in the control group. FRAP values evaluating plasma antioxidant status increased in OSCC patients. M65 and M30 levels indicating necrosis and apoptosis were significantly higher in OSCC patients compared to controls. There were significant correlations between MDA, AOPP and FRAP; M65 and M30 values. CONCLUSIONS: The elevated levels of oxidative stress markers together with the increase of antioxidant capacity and the presence of a strong correlation between MDA, AOPP and FRAP suggest an activation of antioxidant defense against accentuated oxidative stress determined in OSCC. Enhanced oxidation of lipids and proteins may cause decomposition of cell membranes with subsequent leakage of cytoskeletal cytokeratins as CK18 and caspase-cleaved CK18 (evaluated as M65 and M30, respectively) in the circulation, suggesting that both cell death modes are affected in OSCC.

Serum Levels of Brain-Derived Neurotrophic Factor, Nerve Growth Factor, Neurotrophin-3, and Glial-Derived Neurotrophic Factor in Children with Specific Learning Disorder.

Introduction: Specific learning disorder (SLD) is a neurodevelopmental disorder that involves complex interactions of genetic, neurobiological and environmental factors, but the definite mechanisms remain mostly unknown. The possible role of neurotrophins has been implicated in the pathophysiology of various neurodevelopmental disorders. This study aimed to investigate whether serum levels of brain-derived neurotrophic factor (BDNF), glial-derived neurotrophic factor (GDNF), nerve growth factor (NGF), and neurotrophin-3 (NT-3) in children with SLD deviate from those of neurotypical brains. Methods: Forty-four patients with SLD and 44 healthy controls aged 7--12 years were included. SLD diagnosis and severity was determined using DSM-5-based interviews and SLD clinical observation battery. Serum neurotrophins were measured using enzyme-linked immunosorbent assay. Results: BDNF (p=0.032), NGF (p=0.029), and NT-3 (p=0.025) serum levels were significantly higher in the SLD group compared to the control group; however, serum levels of GDNF did not show any significant difference between groups. On the other hand, GDNF serum levels were significantly different between mild and severe SLD groups (p=0.007) and were lower in severe SLD subjects than in mild cases. There was also a significant correlation between patients' reading speeds and serum levels of GDNF (p=0.025), and GDNF serum levels were lower in patients with slower reading speeds. Conclusion: These findings suggest that neurotrophins might play a role in the pathophysiology of SLD. Increased serum levels of BDNF, NGF, and NT-3 might reflect compensatory attempts at neuroprotection against neurodevelopmental impairment.