Dysfunctional personality beliefs and psychopathology in patients with central serous chorioretinopathy.

OBJECTIVES: To assess dysfunctional personality beliefs associated with specific personality disorders (PD), as well as psychopathological symptoms and psychological distress levels in central serous chorioretinopathy (CSC) patients. MATERIAL AND METHODS: This cross-sectional study included acute and chronic CSC patients and age- and sex-matched healthy volunteers. Dysfunctional personality beliefs and psychopathological symptoms assessed with Personality Belief Questionnaire-Short Form and Symptom Check List-90 Revised (SCL-90-R), respectively, were compared between CSC patients and healthy volunteers and between acute and chronic CSC patients. MAIN RESULTS: Of the 55 CSC patients included in the study analysis, 21 (38.2%) had acute and 34 (61.8%) chronic CSC. Avoidant PD (13.92±3.79 vs. 12.03±3.98, P=0.012) and obsessive-compulsive PD (13.94±3.95 vs. 12.27±3.75, P=0.025) scores on the PBQ-SF were significantly higher in CSC patients than in healthy volunteers. The PBQ-SF scores were similar between acute and chronic CSC patients. CSC patients scored significantly higher on the general severity index (GSI) and all symptom dimensions except phobic anxiety and psychoticism on the SCL-90-R. In addition, scores for obsessive-compulsive, depression, interpersonal sensitivity, paranoid ideation, and GSI were significantly higher in acute than in chronic CSC patients. CONCLUSIONS: This first study investigating the relationship between CSC and dysfunctional personality beliefs indicates that CSC patients have higher levels of dysfunctional beliefs related to avoidant and obsessive-compulsive PD than healthy volunteers. These findings present a new aspect of the personality profile of CSC patients and point to a target for intervention, i.e., dysfunctional beliefs, through a cognitive-psychiatric approach.

Chronic tinnitus and BDNF/GDNF CpG promoter methylations: a case-control study.

Brain-derived neurotrophic factor (BDNF) and Glial-derived neurotrophic factor (GDNF) are neurotrophic factors that play key roles in the auditory pathway. While the relationship between serum levels and polymorphisms of BDNF/GDNF and chronic tinnitus is emphasized in the literature, there is no study showing the link between the promoter methylations of these genes and tinnitus. For this purpose, the relationship between chronic tinnitus and peripheral blood derived BDNF/GDNF promoter methylations was investigated to identify their role in the pathophysiology of tinnitus. In this case-control study, we examined the possible effects of BDNF/GDNF methylations in the blood samples of patients with tinnitus complaints for more than 3 months. Sixty tinnitus subjects between the ages of 18-55 and 50 healthy control subjects in the same age group who were free of any otorhinolaryngology and systemic disease were selected for examination. Methylation of total 12 CpG sites in BDNF and GDNF promoter regions were determined by the bisulfite-pyrosequencing method. Statistically significant differences were detected between BDNF CpG6 and GDNF CpG3-5-6 methylation ratios in the comparison of control group and the chronic tinnitus patients (P = 0.002, 0.0005, 0.00003, and 0.0029, respectively). To our knowledge, this is the first study in the literature investigating the relationship between chronic tinnitus and peripheral blood derived BDNF/GDNF promoter methylations. It is believed that the current results might be supported by investigating the relationships between BDNF/GDNF methylations and genotypes in future research using higher sample sizes.

Dairy Attenuates Weight Gain to a Similar Extent as Exercise in Rats Fed a High-Fat, High-Sugar Diet.

OBJECTIVE: To compare the individual and combined effects of dairy and endurance exercise training in reducing weight gain and adiposity in a rodent model of diet-induced obesity. METHODS: An 8-week feeding intervention of a high-fat, high-sugar diet was used to induce obesity in male Sprague-Dawley rats. Rats were then assigned to one of four groups for 6 weeks: (1) casein sedentary (casein-S), (2) casein exercise (casein-E), (3) dairy sedentary (dairy-S), and (4) dairy exercise (dairy-E). Rats were exercise trained by treadmill running 5 d/wk. RESULTS: Dairy-E prevented weight gain to a greater extent than either dairy or exercise alone. Adipose tissue and liver mass were reduced to a similar extent in dairy-S, casein-E, and dairy-E groups. Differences in weight gain were not explained by food intake or total energy expenditure. The total amount of lipid excreted was greater in the dairy-S compared to casein-S and dairy-E groups. CONCLUSIONS: This study provides evidence that dairy limits weight gain to a similar extent as exercise training and the combined effects are greater than either intervention alone. While exercise training reduces weight gain through increases in energy expenditure, dairy appears to increase lipid excretion in the feces.

Assessment of left ventricular systolic and diastolic dyssynchrony with tissue Doppler echocardiography in patients with heart failure and narrow QRS complex.

AIM: Cardiac dyssynchrony is a well known entity in patients with wide QRS complex (>120 ms). Dyssynchrony may also cause ventricular dysfunction in heart failure patients with narrow QRS complexes. In the study, the presence and extent of cardiac dyssynchrony were investigated in patients with heart failure both with narrow and wide QRS complexes using tissue Doppler echocardiography (TDE). METHODS: Forty-nine patients with heart failure, were included to the study. The first group of 30 patients with a QRS duration of <120 ms (23M; mean age, 64±10.1 years) and the second group consisted of 19 patients with a QRS duration of >120 ms (12M; mean age, 65±11.6 years). In order to examine cardiac synchronization, TDE was performed. Systolic and diastolic intraventricular dyssynchrony and interventricular dyssynchrony were calculated. In order to define systolic and diastolic dyssynchrony, intraventricular delay was accepted as >60 ms, and interventricular delay was accepted as >40 ms. RESULTS: Left ventricular systolic dyssynchrony was detected in 18 patients (60%) within the narrow QRS group and in 18 patients (94%) within the wide QRS group. Interventricular dyssynchrony was detected in 17 patients (56%) within the narrow QRS group and in 18 patients (94%) within the wide QRS group. For systolic dyssynchrony, correlations existed between intraventricular delay and QRS duration (r=0.48), left ventricular end diastolic diameter (r=0.62), left ventricular end systolic diameter (r=0.61), and EF (r=-0.63). Similarly, correlations existed between interventricular delay and QRS duration (r=0.58), left ventricular end diastolic diameter (r=0.65), left ventricle end systolic diameter (r=0.64), and EF (r=-0.64). CONCLUSION: The present study suggested that systolic or diastolic dyssynchrony exists despite normal levels of QRS duration.

Prevalence of the angiotensin I converting enzyme gene insertion/deletion polymorphism in a healthy Turkish population.

Angiotensin converting enzyme (ACE) plays an essential role in the renin-angiotensin system. It converts angiotensin I to angiotensin II and inactivates bradykinin and tachykinins. Numerous studies have been published investigating associations of the ACE gene I/D polymorphism with various pathophysiological conditions. We examined the prevalence of the ACE I/D polymorphism in a sample of healthy volunteers from western Turkey, including 1063 healthy Turkish controls. Analysis of the ACE I/D gene polymorphisms by polymerase chain reaction found frequencies of 16.1% for the II genotype, 47.7% for the ID genotype, and 36.2% for the DD genotype. The allele frequency was 39.9% for the I alleles and 60.1% for the D allele. This study demonstrates that the allele and genotype frequency values for the Turkish population are similar to previously published frequencies for Caucasian populations.

G protein beta3 subunit gene polymorphism in Turkish hypertensives.

OBJECTIVE: G protein is one of the most important regulators of intracellular signaling pathways. C825T polymorphism of G protein b3 subunit is associated with increased intracellular signal transduction. The 825T allele has been found associated with a variety of cardiovascular risk factors, including hypertension. The aim of the present study was to investigate the association between the C825T polymorphism of the G protein b3 subunit and essential hypertension in Turkish population. METHODS: This cross-sectional, case-controlled study included 209 patients with essential hypertension (Patient group) and 82 subjects with normal blood pressure (Control group). The G protein b3 subunit C825T gene polymorphism was determined by polymerase chain reaction. Hypertension was defined according to JNC VII criteria. Statistical analysis was performed using Chi square and unpaired t tests. Logistic regression analysis was used to study association between hypertension and genotypes. RESULTS: We found that the frequencies of the G protein b3 subunit C825T polymorphism in hypertensive and control groups were 17.7%, 59.3%, 23.0% and 32.9%, 48.8%, 18.3%, (CC, CT, TT) respectively (chi2=7.963, p=0.019). In the multivariate logistic regression analysis CT genotype had 2.2 (OR=2.262, 95% CI 1.228-4.167, p=0.009), and TT genotype had 2.3 times (OR=2.335, 95% CI 1.089-5.008, p=0.029) greater risk of hypertension compared to CC genotype. CONCLUSION: It seems that the G protein b3 subunit C825T gene polymorphism is associated with systolic and diastolic blood pressure. Furthermore, the study indicates that the G protein b3 subunit may be a susceptible gene to essential hypertension.

Association of platelet-activating factor acetylhydrolase gene polymorphism with premature coronary artery disease in Turkish patients.

OBJECTIVE: Platelet-activating factor (PAF) is a phospholipid with multiple actions that is involved in inflammatory diseases as well as in atherogenesis. It is inactivated by a plasma enzyme, PAF-acetylhydrolase (PAF-AH). Deficiency of this enzyme in plasma is caused by a missense mutation in the gene (G994T). The aim of this study was to investigate association of this mutation with premature coronary artery disease (CAD). METHODS: One hundred and fifteen unrelated Turkish patients with a diagnosis of premature CAD and 128 unrelated healthy subjects were enrolled in this study. Genotyping was performed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). RESULTS: The prevalence of the G994T mutation in the patients was 2.60 % (heterozygote), and 0 % in the controls. There was no significant difference in allele frequency and genotype distribution among the study groups. CONCLUSION: The G9943T mutation in the plasma PAF acetylhydrolase gene is not associated with premature CAD in Turkish subjects.

Renin-angiotensin system gene polymorphisms and premature coronary heart disease.

INTRODUCTION: Experimental and clinical studies demonstrated that the renin-angiotensin system (RAS) affects the pathogenesis of atherosclerosis and prognosis of coronary heart disease (CHD). The aim of this study was to investigate the genotype distribution and the allele frequencies of three RAS genes polymorphisms and their effects on premature CHD in a Turkish population. MATERIALS AND METHODS: One-hundred and fifteen Turkish patients with premature CHD and 128 controls were included into the study. Angiotensin-converting enzyme (ACE), angiotensin II type 1 (AT1) receptor and angiotensinogen (AGT) gene polymorphisms were analysed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). RESULTS: The patients group showed an increased frequency of the ACE D allele compared with controls (65% vs. 35%, p = 0.0001). There was a significant association between the DD genotype and premature CHD (ACE DD vs. ID and II; odds ratio [OR] = 2.82 [CI 95% 1.33 2.91, p = 0.002]). Also, we observed increased premature CHD risk associated with higher frequencies of the AGT MM genotype in patients when compared with controls (AGT MM vs. TT and MT, OR = 1.92 [CI 95% 1.11-3.33, p = 0.018]). We found a significant association between AT1-receptor AA genotype and decreased risk of premature CHD (AT1R AA vs. AC and CC, OR = 0.57[CI 95% 0.34-0.95, p = 0.03]). CONCLUSIONS: We demonstrated that increased premature CHD risk is associated with higher frequencies of the ACE DD and AGT MM genotypes. These findings indicate a synergistic contribution of ACE DD and AGT MM polymorphisms to the development of premature CHD. Also, our results suggest that family history, smoking, diabetes, hypertension, obesity and ACE DD genotype were independent risk factors for premature CHD.

ACE genotype may have an effect on single versus multiple set preferences in strength training.

A polymorphic variant of the human angiotensin converting enzyme (ACE) gene was identified. The 'D' (rather than 'I') variant was associated with improvements in strength related to physical training. We set out to determine whether the response to different patterns of strength training might also differ. Ninty-nine Caucasian male non-elite athletes were randomly allocated into one of three groups: 31 non-training/control (CG: 31), single-set (SSG: 35) and multiple-set (MSG: 33). SSG and MSG trained three times a week for 6 weeks. Both training groups were underwent a strength-training program with two mesocycles (12-15 repetition maximum (RM) and 8-12 RM mesocycles). One RM loads in half squat and bench press were assessed before training and after the first and second mesocycles. ACE polymorphisms analysed by polymerase chain reaction (PCR) methods. Subjects with ACE II genotype in the MST group had improved strength development in 12-15 RM, while SST and MST groups had similar gains in 8-12 RM. Subjects with ACE DD genotype in both the SSG and the MSG had similar benefits from both 12-15 RM and 8-12 RM. Strength gains for subjects with ACE ID genotype in the SSG were similar to MSG gains in response to 8-12 RM loads but not with 12-15 RM loads. Additionally, subjects with DD genotype had superior strength gains in both strength training groups. Tailoring strength training programmes (single-set vs. multiple set) according to the athlete's ACE genotype may be advantageous.

Association between the ACE I/D gene polymorphism and physical performance in a homogeneous non-elite cohort.

BACKGROUND: I/D polymorphism of the ACE gene may be associated with better endurance performance and a stronger response to exercise training. The aim of this study was to investigate the association between ACE gene polymorphism and athletic performance in a homogeneous cohort. METHODS: Eighty-eight male non-elite Caucasian Turkish athletes with similar training backgrounds for at least for 6 months were studied for ACE gene polymorphisms by PCR analysis. Performance on the 60-meter sprint and middle-distance running tests were evaluated. RESULTS: The distributions of the ACE I/D genotypes were 20.5%, 40.9%, and 38.6% for II, ID, and DD polymorphisms in the whole group (N = 88), respectively. The ACE DD genotype frequency was significantly higher in the superior group (56.7%) than in the poor (37.9%) and mediocre (20.7%) group in middle-distance running performance (chi2 = 11.778; p = 0.019). CONCLUSION: The ACE DD genotype may be related to better short-duration aerobic endurance performance. Larger homogeneous cohorts may help clarify the association between ACE I/D polymorphism and physical performance.

Association between the eNOS (Glu298Asp) and the RAS genes polymorphisms and premature coronary artery disease in a Turkish population.

BACKGROUND: The renin-angiotensin system (RAS) and endothelial nitric oxide (NO) affect the pathogenesis of atherosclerosis and prognosis of coronary artery disease (CAD). Previous epidemiologic data suggested that genetic factors are more likely to affect young rather than old people. Our objective was to investigate the association between the polymorphisms of eNOS (Glu298Asp) and the RAS genes and premature CAD in a Turkish population. METHODS: A total of 115 Turkish patients with premature CAD and 83 controls were included in the study. ACE I/D, AT1R A/C, AGT T/M and eNOS Glu298Asp gene polymorphisms were analysed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). RESULTS: It was found that increased premature CAD risk is associated with higher frequencies of the ACE DD [OR: 2.600 (CI 95% 1.395-4.847, p=0.002)], AGT MM [OR=2.407 (CI 95% 1.267-4.573, p=0.007)] and eNOS 894TT [OR=17.000 (CI 95% 3.952-73.125, p<0.001)] genotypes. Carriers of ACE DD+eNOS 894TT (p=0.002), AGT MM+eNOS 894TT (p=0.001), AT1R AA+eNOS 894TT and AT1R non-AA+eNOS 894TT (p=0.002) genotypes were significantly associated with the risk of premature CAD. CONCLUSIONS: This study indicates a synergistic contribution of RAS genes (ACE I/D, AGT T/M, AT1R T/C) and eNOS Glu298Asp polymorphisms to the development of the premature CAD.

Hypertrophic cardiomyopathy: pathological features and molecular pathogenesis.

Hypertrophic cardiomyopathy (HCM) is a heterogeneous genetic cardiac disorder with various genotypic and phenotypic manifestations, and is often a diagnostic challenge. Although more than forty years have passed since the first description of HCM, a variety of mutations in genes encoding sarcomeric proteins, that cause the disease have been defined by laboratory and clinical studies over the past few years. The fact that HCM is the most common cause of sudden death in young competitive athletes and that, it is actually an important cause of morbidity and mortality in people of all ages, has made the researchers to concentrate more on the molecular basis and treatment strategies of the disease. This study aims to summarize both pathological features and rapidly evolving molecular genetics of HCM, and so to understand this not infrequently seen, complex disorder better.