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.

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.

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.

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.

α-Lipoic Acid Ameliorates The Changes in Prooxidant-Antioxidant Balance in Liver and Brain Tissues of Propylthiouracil-Induced Hypothyroid Rats.

OBJECTIVE: There are controversial data about the prooxidant-antioxidant balance in hypothyroidism. We aimed to investigate the effect of α-lipoic acid (ALA) on oxidative stress parameters in the liver and brain of propylthiouracil (PTU)-induced hypothyroid rats. MATERIALS AND METHODS: In this experimental study, PTU (500 mg/L) was given to rats in drinking water for 10 weeks. ALA (0.2% in diet) alone and together with thyroxine (T4, 20 µg/kg body weight, s.c) were given to hypothyroid rats in the last 5 weeks of the experimental period. The levels of reactive oxygen species, malondialdehyde, protein carbonyl, ferric reducing antioxidant power (FRAP) and glutathione (GSH) levels, superoxide dismutase, and GSH peroxidase activities were determined in the liver and brain of rats. Histopathological examinations were also performed. RESULTS: Prooxidant parameters were increased in the brain but not liver in hypothyroid rats. ALA treatment alone lowered enhanced brain oxidative stress in hypothyroid rats. Also, ALA was found to ameliorate the changes as a result of oxidative stress arising from T4 replacement therapy. CONCLUSION: Our results indicate that ALA alone and together with T4 may be useful in reducing oxidative stress in thyroid dysfunctions.

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.

Association of Leukotrichia in Vitiligo and Asp148Glu Polymorphism of Apurinic/Apyrimidinic Endonuclease 1.

BACKGROUND: Oxidative stress and increased DNA damage have been implicated in the etiopathogenesis of vitiligo. Oxidative DNA damage is mainly repaired by the base excision repair (BER) pathway. AIM: We sought to determine whether polymorphisms in DNA repair genes may have a role in the pathogenesis of vitiligo. MATERIALS AND METHODS: We conducted a study including 100 patients with vitiligo and age- and sex-matched 193 control subjects to examine the role of single-nucleotide polymorphisms of BER genes, human 8-oxoG DNA N-glycosylase 1 (codon 326), apurinic/apyrimidinic endonuclease 1 (APE1) (codon 148), and X-ray repair cross-complementing group 1 (codon 399) as risk factors for vitiligo. These polymorphisms were determined by quantitative real-time polymerase chain reaction and melting curve analysis. RESULTS: No significant association was observed between the variant alleles of studied genes and vitiligo. CONCLUSION: However, we showed that the presence of APE1 148Glu variant allele is associated with leukotrichia. This preliminary study suggests that APE1 (codon 148) polymorphism may play a role in vitiligo pathogenesis.

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.

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.

Fibroblast Growth Factor 23 and Placental Growth Factor in Patients with Psoriasis and their Relation to Disease Severity.

PURPOSE: Psoriasis is an immune-mediated skin disease characterised by accentuated keratinocyte proliferation, hyperkeratinisation, leukocyte and T-lymphocyte chemotaxis, and neoangiogenesis. Chronic inflammation, imbalance between pro- and anti-inflammatory cytokines, and many angiogenic mediators has been implicated in the disease etiopathogenesis. The aim of this study was to investigate whether psoriasis is related to fibroblast growth factor 23 (FGF23) and placental growth factor (PLGF) - mediators related to insulin resistance (IR), metabolic syndrome, and atherosclerosis. MATERIALS AND METHODS: Forty five patients with plaque type psoriasis and forty five healthy controls were included in the study. Serum FGF23 and PLGF concentrations were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: Mean homeostasis model assessment (HOMA-IR) values and serum levels of insulin, FGF23 and PLGF, in patients with psoriasis were found to be higher than those of in healthy controls (p= 0.001, p=0.001, p=0.001 and p=0.003 respectively). Psoriasis area and severity index (PASI) score correlated significantly with PLGF levels (p=0.039). There was a significant positive correlation between FGF23 and PLGF (p<0.001). CRP was significantly correlated with BMI (p=0.019), glucose (p=0.017), TC (p=0.043), TG (p=0.003), and VLDL-C (p=0.004) in patients with psoriasis. CONCLUSIONS: Increased serum FGF23 and PLGF levels and the presence of positive correlation between PLGF and PASI score probably reflects the inflammatory state and IR seen in psoriasis. Above mentioned correlations provide rationale for possible application of serum FGF23 and especially of PLGF measurements as biomarkers of disease severity, which could be useful for management of treatment efficacy.

The Evaluation of Endothelin-1 and Endothelin Receptor Type A Gene Polymorphisms in Patients with Vitiligo.

BACKGROUND: Endothelin-1 (EDN1) and EDN receptor type A (EDNRA) are implicated in melanocyte functions. AIM AND OBJECTIVES: This study examines the role of EDN1 (G5665T and T-1370G) and EDNRA (C + 70G and G-231A) polymorphisms as a risk factor for vitiligo, and evaluates the relationship between genotypes and clinical characteristics of vitiligo patients. MATERIALS AND METHODS: We analyzed genotype/allele distributions of EDN1 and EDNRA polymorphisms in 100 patients with vitiligo and 185 healthy controls by real-time polymerase chain reaction. RESULTS: There was no notable risk for vitiligo afflicted by studied polymorphisms. However, the presence of EDNRA +70 variant G allele was found to be related with decreased risk for development of generalized type of vitiligo (odds ratio [OR]: 0.42, 95% confidence interval [CI] = 0.21-0.86, pcorr = 0.03) and showed protective effect against associated diseases seen in vitiligo (OR: 0.49, 95% CI = 0.27-0.88, pcorr = 0.034). Haplotype analysis demonstrated a strong (disequilibrium coefficient = 0.73, r (2) = 0.405) linkage disequilibrium between EDN1 G5665T and T-1370G polymorphisms. The EDN1 5665/-1330 TT haplotype was over represented significantly in controls than in patients (P = 0.04). CONCLUSION: The studied polymorphisms do not seem to be a major risk for vitiligo. Haplotype analysis denoting protective effects against vitiligo may indicate an indirect interaction in the course of vitiligo. In addition, EDNRA + 70 polymorphism is protective against generalized type of vitiligo and associated diseases.

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.

Arg25Pro (c.915G>C) polymorphism of transforming growth factor ß1 gene suggests an association with increased risk for Hashimoto's thyroiditis.

BACKGROUND: The etiopathogenesis of Hashimoto's thyroiditis (HT) - has not been clearly elucidated although the role of chronic inflammation, endothelial dysfunction, and imbalance between pro- and anti-inflammatory cytokines has been established. Transforming growth factor ß1 (TGFß1) is required to maintain immune homeostasis, and is implicated in lymphocyte infiltration, production of autoantibodies and thyrocyte destruction seen in patients with HT. AIM: The aim of the present study was to investigate the possible association of Leu10Pro (c.869T>C) and Arg25Pro (c.915G>C) single nucleotide polymorphisms (SNPs) of TGFß1 gene with the occurrence of HT. METHODS: We analyzed the genotype and allele frequencies of polymorphisms at codon 10 and 25 in 178 patients who had been diagnosed as having HT and 197 healthy controls using PCR-restriction fragment length polymorphism (RFLP). RESULTS: There was no notable risk for HT afflicted by Leu10Pro (c.869T>C) polymorphism of TGFß1 gene. However, there was a significant increase of Arg25Pro (c.915G>C) C allele frequency in patients with HT compared with healthy controls (p=0.003, OR=1.87, 95% CI=1.23-2.84). Moreover, heterozygous (CG) subjects had a 2.53-fold increased risk for developing HT with respect to wild (GG) homozygotes (p<0.001, 95% CI=1.57-4.05). TSH levels in CG heterozygous patients were increased in comparison with wild homozygotes (p=0.006). CONCLUSION: This study indicates that the Arg25Pro (c.915G>C) polymorphism of TGFß1 gene may be related to increased risk for HT.

G-231A and G+70C Polymorphisms of Endothelin Receptor Type-A Gene could Affect the Psoriasis Area and Severity Index Score and Endothelin 1 Levels.

BACKGROUND: The etiopathogenesis of psoriasis has not been clearly elucidated although the role of chronic inflammation, imbalance between pro- and anti-inflammatory cytokines, and many immunological events have been established. Endothelin 1 (EDN1) and endothelin receptor type-A (EDNRA) are implicated in the inflammatory process. The relationships between EDN1 and EDNRA polymorphisms with several diseases have been found. AIMS AND OBJECTIVES: This study examined the possible association of EDN1 (G5665T and T-1370G) and EDNRA (G-231A and G + 70C) single nucleotide polymorphisms (SNPs) with the occurence of psoriasis, and evaluated the relationship between genotypes and clinical/laboratory manifestation of psoriasis. MATERIALS AND METHODS: We analyzed genotype and allele distributions of the above-mentioned polymorphisms in 151 patients with psoriasis and 152 healthy controls by real-time PCR combined with melting curve analysis. RESULTS: We did not find significant differences in the genotype and allele distributions of EDN1 T-1370G, EDNRA G-231A, and EDNRA G+70C polymorphisms between patients with psoriasis and healthy controls. Psoriasis area and severity index (PASI) score of EDNRA -231 polymorphic A allele carrying subjects (AA and AA + AG) was higher than that of wild homozygotes (P = 0.044 and P = 0.027, respectively). In addition, EDN1 levels in EDNRA+70 polymorphic C allele carriers (CC + CG) were elevated when compared with GG genotype; however, the difference was at borderline significance (P = 0.05). CONCLUSION: Although there were no associations between studied polymorphisms and psoriasis susceptibility, the PASI score and EDN1 levels seem to be affected by EDNRA G-231A and G + 70C polymorphisms.

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.

The evaluation of endothelin 1 (EDN1) and endothelin receptor type A (EDNRA) gene polymorphisms in Hashimoto's thyroiditis.

PURPOSE: Endothelin1 (EDN1) is well established marker of inflammation. The functions of EDN1 are mediated mainly by endothelin receptors type A (EDNRA). The etiopathogenesis of Hashimoto's thyroiditis (HT) remains still elusive although the role of chronic inflammation and subsequent endothelial dysfunction has been established. This study examined firstly the possible association of EDN1 (G5665Tand T-1370G) and EDNRA (C+70G and G-231A) single nucleotide polymorphisms (SNPs) with the occurrence of HT, and evaluates the relationship between genotypes and clinical/laboratory manifestation of HT. MATERIALS AND METHODS: We analyzed genotype and allele distributions of above mentioned polymorphisms in 163 patients with HT and 181 healthy controls by real-time PCR combined with melting curve analysis. RESULTS: No significant associations between HT and variant alleles of EDN1 5665 and -1370, as well as EDNRA +70 and -231 SNPs were found. Haplotype analysis demonstrated that there was a strong (D'=0.76, r(2)=0.487) and weak (D'=0.403, r(2)=0.086) linkage disequilibrium (LD) between EDN1 -1370 and 5665, and between EDNRA -231 and +70 SNPs, respectively. However, haplotype frequencies in patients were similar to those in controls. In addition, it was observed that the EDNRA +70 G allele had protective effect against early (at age before 40 years) disease onset of HT (OR: 0.51, 95% CI=0.32-0.79, p=0.003). CONCLUSION: Although no significant associations between susceptibility to HT with EDN1 5665 and -1370, as well as with EDNRA+70 and -231 SNPs were found, EDNRA +70 polymorphism was related with decreased risk for early onset HT.

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.