359 research outputs found
Genetic polymorphisms of the SHBG gene can be the effect on SHBG and HDL-cholesterol levels in Coronary Heart Disease: a case-control study
No full textAkadam Teker, Aysegul Basak/0000-0003-3618-0560WOS: 000478684300060PubMed: 31111369Sex hormone binding globulin (SHBG) level is positively associated with the high-density lipoprotein cholesterol (HDL-C) levels. The aim of this study was to investigate the effects of the SHBG gene variations (D356N, rs1799941, and P156L) on SHBG and HDL-C levels and Coronary Heart Disease (CHD) risk. The SHBG D356N (rs6259,G>A), P156L (rs6258,C>T), and rs1799941(G>A) polymorphisms were determined in 131 male CHD patients and 55 male controls by PCR-RFLP and real-time PCR techniques. SHGB levels were measured by Electro-chemiluminescence immunoassay (ECLIA). In the patients who had SHBG levels lower than threshold 35nmol/l value, the risk of being HDL-C levels lower than threshold 0.90mmol/l value was observed statistically significant (p=0.017; OR 2.522, 95% CI 1.170-5.438). The rs1799941 GG was associated with increased CHD risk when compared with the A allele carriers (GA+AA) (p=0.019, OR 2.222, 95% CI 1.130-4.371). In addition, the rs1799941 GG genotype and D356NN allele were associated with lower SHBG in the CHD group (p<0.01). The logistic regression analysis also revealed the rs1799941 GG genotype was significantly associated with low SHBG in CHD patients. It was observed that Haplotype-1(rs1799941 G allele-P156L P allele-D356N D allele) was associated with increased CHD risk, while Haplotype-2 (rs1799941 rare A allele-P156L C allele- D356N G allele) was correlated with the decreased CHD risk (p=0.0167). Our findings suggest that there is a positive correlation between SHBG and HDL-C levels in CHD patients, and this association might be affected by SHBG gene variations.Research Fund of Istanbul UniversityIstanbul University [12104]The present work was supported by the Research Fund of Istanbul University. Project No. 12104. The authors would like to thank Professor Oguz Ozturk and Associate Professor Ozlem Kucukhuseyin for their statistical contribution and valuable comments and suggestions, which were helpful in improving the paper
BMP1 5'UTR+104 T/C gene variation: can be a predictive marker for serum HDL and apoprotein A1 levels in male patients with coronary heart disease
No full textAkadam Teker, Aysegul Basak/0000-0003-3618-0560; Ozturk, Oguz/0000-0002-2439-9269WOS: 000444752900058PubMed: 30062502Apolipoprotein A1 (Apo A1), the major protein of HDL, is secreted as a proprotein and then is cleaved by C-terminal procollagen endoproteinase/bone morphogenetic protein-1 (BMP1). BMP1 stimulates the conversion of newly secreted proapo A1 to its phospholipid-binding form. Therefore, genetic variations of BMP1 gene may affect serum ApoA1 and HDL levels. We aimed to investigate the effects of the functional 5'UTR + 104 (T/C) variant of BMP1 on serum ApoA1 and HDL levels and risk of coronary heart disease (CHD) in this study. The BMP1 5'UTR + 104 (T/C) (rs143383) variation was determined in 131 male patients with CHD and 51 male controls by real-time polymerase chain reaction technique. ApoA1 levels were measured by immunoturbidimetry. The serum Apo-A1 levels were found higher in controls with the BMP1-CC genotype than those with the T-allele (p < 0.001). Our findings show the association of this variation with serum ApoA1 and HDL-C levels which increase in the order of CT < TT < CC in the controls. No effect was found on ApoA1 and HDL-C levels in CHD patients, as it was observed in the controls. However, the BMP1-TT genotype was associated with higher triglyceride (TG) levels as compared to C-allele (p = 0.009). These discrepancies could be due to statin therapy which has dominant effects on lowering cholesterol levels comparing to TG levels. Our results indicated that the BMP1 5'UTR + 104 (T/C) variation may affect the serum ApoA1 and lipoprotein levels depending on statin therapy so that contributes to the development of CHD.Scientific Research Projects Coordination Unit of Istanbul UniversityIstanbul University [11304]The present study was supported by a grant from the Scientific Research Projects Coordination Unit of Istanbul University (Project No: 11304)
The effects of age and gender on the relationship between HMGCR promoter-911 SNP (rs33761740) and serum lipids in patients with coronary heart disease
No full textKucukhuseyin, Ozlem/0000-0001-6298-5026; Ozturk, Oguz/0000-0002-2439-9269; Daglar Aday, Aynur/0000-0001-8072-0646WOS: 000324565600005PubMed: 23933271Background: Hydroxymethylglutaryl-Coenzyme A Reductase (HMGCR) catalyzes the rate-limiting step of cholesterol biosynthesis. This enzyme is the target of the widely available cholesterol lowering statins. In this population-based case-control study, the frequencies of -911 C>A polymorphism (rs3761740) of the HMGCR gene in patients with coronary heart disease (CHD) and healthy subjects were investigated and the correlations between the different genotypes and hypercholesterolemia with cardiovascular risk factors were analyzed. Methods: The HMGCR genotypes were determined in 365 patients with CHD and 365 controls by PCR-RFLP assay. Anthropometric measurements were measured in all participants. Results: There was no significant difference in the genotype frequencies of the HMGCR polymorphism between the male subjects of both patient and control groups, however, the HMGCR-CC genotype was found to be more frequent in female patients with CHD than female controls (p = 0.002). The HMGCR-CC genotype showed higher total-cholesterol (TC) and LDL-cholesterol (LDL-C) levels than the CA + AA genotypes in male CHD patients (p = 0.018). Due to this significant sex interaction, a multivariate analysis was conducted on the patient group. In the multivariate logistic regression analysis, the HMGCR-CC genotype was significantly associated with age = 5.18 mmol/L (OR = 1.970, p = 0.027) in male subjects. However, this association was not observed in female patients (p > 0.05). This analysis confirmed that the HMGCR-CC genotype was associated with elevated TC levels in male CHD patients with age < 55 years. Conclusion: These results suggest that age and sex modify the contribution of the HMGCR-911 polymorphism to fasting serum TC, LDL-C levels and risk of CHD. (C) 2013 Elsevier B.V. All rights reserved.Scientific Research Projects Coordination Unit of Istanbul UniversityIstanbul University [1707]The present work was supported by a grant from the Scientific Research Projects Coordination Unit of Istanbul University (Project No: 1707). The authors would like to thank Prof. Dr. Rian Disci, Director at the Department of Biostatistics, Istanbul Medical Faculty, Istanbul University for his statistical contribution. M.Sc. Allison P. Eronat and Mrs. Helen Sue Eronat for their understanding and suggestions in English grammar of our article and the Editor and anonymous reviewers for their valuable comments and suggestions, which were helpful in improving the paper
Glycoprotein Ib alpha Kozak polymorphism in patients presenting with early-onset acute coronary syndrome
No full texthancer, veysel sabri/0000-0003-2994-1077WOS: 000436361500011PubMed: 30013602Introduction: Glycoprotein Ib alpha (GPIb alpha) receptor is the chief molecule responsible for initial platelet adhesion to the subendothelium. A thymidine to cytosine single nucleotide substitution at position -5 from the ATG start codon characterizes the Kozak sequence polymorphism. The Kozak sequence polymorphism may increase the surface expression of GPIb alpha and contribute to thrombogenesis. We evaluated the allele frequencies of GPIb alpha Kozak sequence polymorphism in the Turkish population and examined the relationship between GPIb alpha Kozak sequence polymorphism and early-onset acute coronary syndrome (ACS). Material and methods: This study enrolled 200 patients (122 male, 78 female, mean age: 39 +/- 5 years) and 200 healthy control subjects (110 male, 90 female, 41 +/- 4 years). The patient group was composed of patients admitted to our coronary care unit with early-onset ACS and patients who attended to our cardiology outpatient clinic after hospital discharge with a diagnosis of early-onset ACS. Results: Kozak polymorphism frequencies in patients and control subjects did not differ significantly (23% versus 22.5%, p = 0.812, respectively). In patients who presented with non-ST elevation myocardial infarction (NSTEMI), the frequency of GPIb alpha Kozak polymorphism was borderline significantly higher when compared with patients who presented with ST elevation myocardial infarction (STEMI) (35% vs. 20%, p = 0.05, respectively). Allele frequencies of T and C were calculated to be 0.873 and 0.128. Conclusions: Although the frequency of GPIb alpha Kozak polymorphism did not differ significantly in early-onset ACS patients versus control subjects, Kozak polymorphism frequency was borderline significantly higher in patients who presented with NSTEMI when compared to patients with STEMI
Effects of the Variants of Activin Receptor-like Kinase-1 and 2 on the Lipid Profile of Patients with Coronary Heart Disease
No full textIntroduction: Coronary heart disease (CHD) due to atherosclerosis is a multifactorial disease with high morbidity caused by interaction of various genetic and environmental factors. Hyperlipidemia which is accepted as the most important risk factor for atherosclerosis; characterized by high concentration of low density lipoprotein (LDL)-cholesterol (LDL-C) and low concentration of high density lipoprotein (HDL)-cholesterol (HDL-C). Epidemiological studies prove the inverse relationship between HDL-C levels and CHD. Apolipoprotein A1, the major protein of HDL, is secreted as proprotein and then cleaved by C-terminal procollagen endoproteinase/bone morphogenetic protein-1 (BMP-1). Reporting of the role of BMP receptors in lipoprotein metabolism indicates that variations in these genes may be important. However, there are no studies in the literature about the variations in type I receptors for activin receptor-like kinase (ALK) 1 and ALK2 and its effects on lipid profile. In this study, it was aimed to determine the role of the gene variants of ALK1 (Q292P ve S333G) and ALK2 (R206H) receptors in the development of CHD and their effects on serum lipoprotein levels.
Methods: This study was carried out using a sample of 131 patients with CHD and 51 controls. ALK1 and ALK2 genotypes were determined by real-time polymerase chain reaction and technique.
Results: Genotype distributions of ALK1 and ALK2 were the same between the study groups (p>0.05). Mutations in ALK1 and ALK2 were observed only in the patient group. ALK1 Q292P mutation and ALK2 R206H mutation exerted positive effects on the serum lipid profile.
Conclusion: The findings of our study suggested that mutations of ALK1 and ALK2 genes may contribute to antiatherogenic lipid profile and may protect against the development of CHD.Supported by Istanbul University Scientific Research Projects Unit (no: 11304)
Association between the interferon gamma 874 T/A polymorphism and the severity of valvular damage in patients with rheumatic heart disease
No full textOzturk, Oguz/0000-0002-2439-9269WOS: 000433521500005PubMed: 29332266Interferon gamma (IFN-gamma) is a multifunctional cytokine that plays an important role in modulating almost all phases of the immune response and may be responsible for the increased valvular fibrosis and calcification in the pathogenesis of rheumatic heart disease (RHD). The aim of this study was to investigate the possible relationship between the IFN-gamma +874 T/A polymorphism and the severity of valvular damage in the Turkish population. The IFN-gamma genotypes were determined in 152 RHD patients and 151 healthy controls by ARMS-PCR. Differences in genotype distribution between patients with RHD and control were evaluated by the chi (2) test. All statistical analyses were performed with SPSS 15.0 Software program. Frequency of the AA genotype was found to be significantly lower and the TT genotype significantly higher in the RHD group compared to controls (p = 0.002 and p = 0.018, respectively). The TT genotype was found to be significantly higher (26.8% vs. 9.1%, p = 0.009) and the AA genotype significantly lower (29.1% vs. 8.2%, p = 0.001) in the severe valvular disease (SVD) group compared to mild valvular disease group. In the SVD group, 79 patients had mitral balloon valvotomy and/or mitral valve replacement and had significantly higher TT genotype compared to patients with medical follow-up (30.4% vs. 19%, p = 0.001). The data demonstrated that TT genotype is associated with both RHD and the severity of RHD.Scientific Research Projects Coordination Unit of the Istanbul UniversityIstanbul University [6963]This study was supported by a grant from the Scientific Research Projects Coordination Unit of the Istanbul University (Project No. 6963)
Can a Two-Sector Business Cycle Model Account for the 2001 Recession of Turkey?
No full textThis paper investigates whether a two-sector small open economy real business cycle model calibrated to match Turkish data is able to account for the simultaneous sharp reversal in the current account, real exchange rate depreciation, and the severe recession observed in the aftermath of the 2001 financial and currency crisis of Turkey. Estimated shocks for the model's eight exogenous variables are used to simulate model dynamics, and the resulting time series are compared to the actual series. The model does a fairly good job in matching the output drop, while it faces difficulty in matching the sharp real exchange rate depreciation.Business cycles, Turkey
Evaluierung von sechs Fotofallenmodellen hinsichtlich der Eignung für Fang-Wiederfang Methoden beim Eurasischen Luchs (Lynx lynx)
No full textDigital outdoor cameras are increasingly used in wildlife research because they allow species inventories, population estimates, and behavior or activity observations. Which camera model is suitable and practical depends on environmental conditions, focus species and specific scientific questions posed. Here we focused on testing cameras appropriate for elusive species that can be identified visually owing to individual coat patterns. Specifically the camera should be adequate for calculating the minimum population of Eurasian Lynx (Lynx lynx) during a systematic monitoring with camera traps. Therefore we tested six digital camera models with regard to trigger speed and the image quality necessary for visual identification of pacing lynx on trails. The decision if a camera model is adequate for the scientific goal was regulated due to priority levels under laboratory conditions. Only one camera model proved to be suitable for camera-trap monitoring. Our practical camera test can be used to evaluate newer models of digital cameras as they become available. This application opens an avenue for a non-invasive population monitoring of rare and elusive species in a low mountain range area.Digitale Fotofallen werden weltweit in der Wildtierforschung eingesetzt. Die Einsatzgebiete sind vielfältig, sie reichen von Artenbestandsaufnahmen und Populationsschätzungen über die Verhaltensforschung bis hin zu Aktivitätsanalysen. Das jeweilig eingesetzte Kameramodell muss an die Aufnahmesituation und die Zielsetzung der Analyse angepasst sein. Das Ziel unseres Fotofallentests war es, ein Modell zu finden, welches für die visuelle Identifizierung von Fellmustern des Eurasischen Luchses geeignet ist. Die Fotofalle soll in einem systematischen Monitoring für die minimale Anzahl der im Gebiet vorkommenden Luchse und deren Populationsschätzung mit Fang-Wiederfang Methoden eingesetzt werden können. Bei dem Test von sechs Fotofallenmodellen, fiel das Hauptaugenmerk auf die Auslösegeschwindigkeit und die Bildqualität welche die nötigen Faktoren für die Sicherstellung der visuellen Identifikation von schreitenden Luchsen am Wildwechsel darstellen. Zur Entscheidungsfindung der Eignung eines Fotofallenmodells für die Fragestellung definierten wir Prioritätslevel unter Laborbedingungen. Es stellte sich heraus, dass nur ein Fotofallenmodell die Ansprüche erfüllte. Der praktische Fotofallentest kann für neuerscheinende Fotofallenmodelle adaptiert werden. Diese Anwendung eröffnet die Möglichkeit für ein nicht invasives Monitoring in Mittelgebirgslandschaften
Neural basis for priming of pop-out during visual search revealed with fMRI
No full textMalikovic and Nakayama first showed that visual search efficiency can be influenced by priming effects. Even "pop-out" targets (defined by unique color) are judged quicker if they appear at the same location and/or in the same color as on the preceding trial, in an unpredictable sequence. Here, we studied the potential neural correlates of such priming in human visual search using functional magnetic resonance imaging (fMRI). We found that repeating either the location or the color of a singleton target led to repetition suppression of blood oxygen level-dependent (BOLD) activity in brain regions traditionally linked with attentional control, including bilateral intraparietal sulci. This indicates that the attention system of the human brain can be "primed," in apparent analogy to repetition-suppression effects on activity in other neural systems. For repetition of target color but not location, we also found repetition suppression in inferior temporal areas that may be associated with color processing, whereas repetition of target location led to greater reduction of activation in contralateral inferior parietal and frontal areas, relative to color repetition. The frontal eye fields were also implicated, notably when both target properties (color and location) were repeated together, which also led to further BOLD decreases in anterior fusiform cortex not seen when either property was repeated alone. These findings reveal the neural correlates for priming of pop-out search, including commonalities, differences, and interactions between location and color repetition. fMRI repetition-suppression effects may arise in components of the attention network because these settle into a stable 1. attractor state" more readily when the same target property is repeated than when a different attentional state is required
Current concepts on oxidative/carbonyl stress, inflammation and epigenetics in pathogenesis of chronic obstructive pulmonary disease
No full textChronic obstructive pulmonary disease (COPD) is a global health problem. The current therapies for COPD are poorly effective and the mainstays of pharmacotherapy are bronchodilators. A better understanding of the pathobiology of COPD is critical for the development of novel therapies. In the present review, we have discussed the roles of oxidative/aldehyde stress, inflammation/immunity, and chromatin remodeling in the pathogenesis of COPD. An imbalance of oxidants/antioxidants caused by cigarette smoke and other pollutants/biomass fuels plays an important role in the pathogenesis of COPD by regulating redox-sensitive transcription factors (e.g., NF-κB), autophagy and unfolded protein response leading to chronic lung inflammatory response. Cigarette smoke also activates canonical/alternative NF-κB pathways and their upstream kinases leading to sustained inflammatory response in lungs. Recently, epigenetic regulation has been shown to be critical for the development of COPD because the expression/activity of enzymes that regulate these epigenetic modifications have been reported to be abnormal in airways of COPD patients. Hence, the significant advances made in understanding the pathophysiology of COPD as described herein will identify novel therapeutic targets for intervention in COPD
- …
