Tıp Fakültesi / Faculty of Medicine

Permanent URI for this collectionhttps://hdl.handle.net/11727/1403

Browse

Search Results

Now showing 1 - 10 of 17
  • Item
    The Effects of Niacin on Inflammation in Patients with Non-ST Elevated Acute Coronary Syndrome
    (2015) Karacaglar, Emir; Atar, Ilyas; Altin, Cihan; Yetis, Begum; Cakmak, Abdulkadir; Bayraktar, Nilufer; Coner, Ali; Ozin, Bulent; Muderrisoglu, Haldun; 0000-0002-2538-1642; 0000-0002-5711-8873; 0000-0003-3821-412X; 0000-0002-7886-3688; 0000-0002-9635-6313; 27122858; ABI-6723-2020; ABD-7321-2021; AAD-9938-2021; Y-8758-2018; AAG-8233-2020
    Background: In this study, we aimed to evaluate the effects of niacin on high sensitivity C reactive protein (hs-CRP) and cholesterol levels in non-ST elevated acute coronary syndrome (NSTE-ACS) patients. Methods: In this prospective, open label study, 48 NSTE-ACS were randomized to niacin or control group. Patients continued their optimal medical therapy in the control group. In the niacin group patients were assigned to receive extended-release niacin 500 mg/day. Patients were contacted 1 month later to assess compliance and side effects. Blood samples for hs-CRP were obtained upon admittance to the coronary care unit, in the third day and in the first month of the treatment. Fasting blood samples for cholesterol levels were obtained before and 30 days after the treatment. The primary end point of the study was to evaluate changes in hs-CRP, cholesterol levels, short-term cardiovascular events, and the safety of niacin in NSTE-ACS. Results: Baseline demographic, clinical and laboratory characteristics were similar between the two groups. Logarithmic transformation of baseline and 3rd day hs-CRP levels were similar between the groups; but 1 month later, logarithmic transformation of hs-CRP level was significantly lower in the niacin group (0.43 +/- 0.39 to 0.83 +/- 0.91, p = 0.04). HDL-C level was significantly increased in the niacin group during follow-up. Drug related side effects were seen in 7 patients in the niacin group but no patients discontinued niacin. Conclusions: Our findings demonstrate that lower dose extended release niacin can be used safely and decreases hs-CRP and lipid parameters successfully in NSTE-ACS patients.
  • Item
    The Notch Pathway Is A Critical Regulator of Angiogenesis in A Skin Model of Ischemia
    (2015) Abbas, Ozan L.; Borman, Huseyin; Terzi, Yunus K.; Terzi, Aysen; Bayraktar, Nilufer; Yazici, Ayse C.; 0000-0002-1225-1320; 0000-0002-7886-3688; 0000-0001-5612-9696; 0000-0002-3132-242X; 25834117; F-7546-2013; Y-8758-2018; B-4372-2018; AAS-6810-2021
    The Notch pathway is definitely required for normal vascular development. Although the contribution of Notch in postnatal angiogenesis is the focus of intense investigation, the implication of Notch in reparative neovascularization in the skin remains unexplored. In this study, we investigated Notch changes using a skin model of ischemia. Thirty Sprague-Dawley rats were divided into two groups. In the surgery group (n = 24), a caudally based dorsal skin flap was raised and sutured back into its initial position. In the control group, no surgical procedure was performed. Tissue biopsies were obtained at different time intervals. Tissue specimens were assessed for Delta-like ligand 4 (DLL4) and vascular endothelial growth factor (VEGF) gene expression by real-time polymerase chain reaction (PCR). Immunohistochemical staining was used for detection of DLL4 in tissue materials. Quantitative assessment of skin flap microvasculature was made. Compared with normoperfused tissue, VEGF and DLL4 expressions increased significantly (p < 0.01). Immunohistochemical analysis revealed weak and patchy expression of DLL4 in microvascular endothelial cells of normoperfused tissues. Conversely, DLL4 expression was upregulated in capillary endothelial cells after ischemia. In conclusion, in this study we have shown that the Notch ligand DLL4 is upregulated in skin tissue after ischemia. A deeper understanding of these fundamental principles will aid in the development of new avenues for the treatment of blood vessel-related skin pathologies.
  • Item
    Relationship Between Inflammation, Sex Hormone Profile and Sexual Dysfunction in Female Patients Receiving Different Types of Renal Replacement Therapy
    (2014) Altunoglu, Alpaslan; Yavuz, Demet; Canoz, Mujdat Batur; Yavuz, Rahman; Karakas, Latife Atasoy; Bayraktar, Nilufer; Colak, Turan; Sezer, Siren; Ozdemir, Fatma Nurhan; Haberal, Mehmet; https://orcid.org/0000-0002-4082-6320; https://orcid.org/0000-0001-7369-5470; https://orcid.org/0000-0002-7886-3688; https://orcid.org/0000-0002-8372-7840; https://orcid.org/0000-0002-7326-8388; https://orcid.org/0000-0002-5682-0943; https://orcid.org/0000-0002-3462-7632; ABG-9980-2021; AEY-5060-2022; Y-8758-2018; AAJ-8554-2021; JYQ-2550-2024; AAK-1697-2021; AAJ-8097-2021
  • Item
    Oxidative Stress in Maintenance Hemodialysis Patients
    (2014) Uyar, Mehtap Erkmen; Bal, Zeynep; Bayraktar, Nilufer; Demirci, Bahar Gurlek; Sayin, Burak; Sezer, Siren; https://orcid.org/0000-0002-7886-3688; https://orcid.org/0000-0001-8287-6572; https://orcid.org/0000-0002-7326-8388; IAO-2608-2023; AAZ-5795-2021; Y-8758-2018; J-3707-2015; JYQ-2550-2024
  • Item
    Inhibition of the Notch Pathway Promotes Flap Survival by Inducing Functional Neoangiogenesis
    (2015) Abbas, Ozan Luay; Borman, Huseyin; Terzi, Yunus K.; Terzi, Aysen; Bayraktar, Nilufer; Ozkan, Burak; Yazici, Ayse C.; 0000-0002-7886-3688; 0000-0003-3093-8369; 0000-0002-1225-1320; 0000-0002-3132-242X; 0000-0001-5612-9696; 25180956; Y-8758-2018; AAI-5063-2020; F-7546-2013; AAS-6810-2021; B-4372-2018
    Objective The Notch pathway seems to function as an antiangiogenic factor, negatively regulating the sprouting effect of vascular endothelial growth factor (VEGF). This function is well defined in embryonic and tumor vasculature. However, little is known about its function in ischemia-induced angiogenesis. In the first part of this study, we investigated the role of Notch in reparative angiogenesis after ischemia. In the second part, we hypothesized that anti-Notch therapy will result in increased angiogenic sprouting. We analyzed the effect of Notch inhibition in the induction of angiogenic sprouting. Methods In the first part, we investigated the effect of ischemia on the Notch ligand delta-like ligand 4 (DLL4). Twenty rats were divided equally into 2 groups. In the surgery group, dorsal skin flap was used as model of ischemia. In the control group, no surgical procedure was performed. DLL4 and VEGF gene expressions were assessed. Immunohistochemical staining was used for detection of DLL4 in tissue materials. Plasma levels of VEGF and DLL4 were measured. In the second part, we investigated the effect of Notch inhibition using a gamma-secretase inhibitor (GSI) on inducing neoangiogenesis. Twenty rats were assigned to 2 equal groups. In all animals, dorsal skin flap was raised and sutured back into its bed. Animals in the GSI-treated group received GSI intravenously after surgery for 3 days. Saline was administered in the control group. Necrotic area measurements, microangiography, and histologic evaluations were performed to compare groups. Results In the first part, VEGF and DLL expressions increased in ischemic tissues (P < 0.01). Immunohistochemical analysis revealed that DLL4 expression was upregulated in capillary endothelial cells after ischemia. Plasma levels for VEGF and DLL4 were higher in the animals that underwent surgery (P < 0.01). In the second part, GSI treatment resulted in higher flap survival rates (P < 0.05). Microscopic analysis exhibited increase in the number of microvascular structures after GSI treatment (P < 0.05). Microangiographic evaluation showed that neovascularization increased in the GSI-applied flaps. Conclusions We present an evidence for the importance of the Notch pathway in the regulation of ischemia-induced angiogenesis. Notch inhibition promotes flap survival by creating a neovasculature that has an increase in vascular density.
  • Item
    Evaluation of Serum Leptin and Adiponectin Levels in Obese and Lean Asthmatic Children
    (2015) Koksal, Burcu Tahire; Ozbek, Ozlem Yilmaz; Bayraktar, Nilufer; Kinik, Sibel Tulgar; Yazici, Ayse Canan; 0000-0003-2974-9579; 0000-0002-7886-3688; 0000-0002-3132-242X; 0000-0001-9580-7656; AAJ-2034-2021; Y-8758-2018; AAS-6810-2021; HKW-0623-2023; AAF-2109-2021
    Background: Adipokines have been claimed for the link between obesity and asthma. The aim of the present study was to evaluate the roles of leptin and adiponectin in children with asthma and/or obesity and their effect on pulmonary functions. Methods: Obese (n=71) and lean asthmatics (n=72), obese non-asthmatics (n=46), and lean healthy children (n=49) were included in the study. Serum leptin and adiponectin levels were compared according to groups and sex. Results: Mean leptin levels of obese asthmatics were higher than those of lean asthmatics (13.19.1 vs. 3.7 +/- 4.4; p<0.001). Serum adiponectin levels of lean asthmatics (16 +/- 7.1) were significantly higher than those of obese asthmatics (12.1 +/- 6.9; p<0.001) and of their lean healthy (13.2 +/- 5.9; p<0.05) counterparts. In obese asthmatics, adiponectin levels were positively correlated with the forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) ratio, and serum leptin levels were inversely correlated with forced expiratory flow (FEF25-75). Leptin/adiponectin ratio was inversely correlated with FEV1/FVC ratio in lean and obese asthmatic patients. Conclusions: The present findings suggest that adiponectin may have protective disease modifying effect(s) in asthmatic children. Anti-inflammatory mechanisms regarding adiponectin may work better in girls than in boys.
  • Item
    AMH Levels at Central Precocious Puberty and Premature Thelarche: Is It A Parameter?
    (2015) Sahin, Nursel Muratoglu; Kinik, Sibel Tulgar; Tekindal, Mustafa Agah; Bayraktar, Nilufer; 0000-0002-7886-3688; 0000-0002-4060-7048; 0000-0002-8215-0146; 26226120; Y-8758-2018; U-9270-2018; AAA-1266-2019
    Background: The possible difference of antimllrin hormone (AMH) levels at central precocious puberty (CPP) and premature thelarche (PT) has not been properly evaluated. Objective/hypothesis: By evaluating AMH levels in girls with diagnosed CPP and PT, we aim to show the change of AMH levels at the pubertal onset. Subjects: Sixty-five girls who have breast development before the age of 8 years and 25 healthy girls were enrolled in the study. Methods: The subjects were divided into two groups as CPP and PT, according to results of GnRH test. AMH levels were determined in the two groups. Results: The mean AMH levels of the CPP group were significantly lower than those in the PT group (13.57 +/- 9.85 pmol/L and 58.42 +/- 12.78 pmol/L, respectively, p=0.022). Conclusion: These results suggest that the AMH levels decrease in the duration of the hypothalamus-pituitaryovarian axis activation. We thought that AMH might/may be a marker for distinguishing between CPP and PT.
  • Item
    Evaluation of Angiopoietin 1 and 2, Vascular Endothelial Growth Factor, and Tumor Necrosis Factor Alpha Levels in Asthmatic Children
    (2014) Koksal, Burcu Tahire; Ozbek, Ozlem Yilmaz; Bayraktar, Nilufer; Yazici, Ayse Canan; https://orcid.org/0000-0001-9580-7656; https://orcid.org/0000-0003-2974-9579; https://orcid.org/0000-0002-7886-3688; https://orcid.org/0000-0002-3132-242X; 25584916; AAF-2109-2021; AAJ-2034-2021; Y-8758-2018; AAS-6810-2021
    Asthma is characterized by chronic airway inflammation that is associated with structural changes termed airway remodeling. Recently, cytokines/mediators that augment inflammation have been attracting attention in this field. The aim of this study was to evaluate serum angiopoietin (Ang)-1, Ang-2, vascular endothelial growth factor (VEGF), and tumor necrosis. factor (TNF) alpha values, which have important roles in inflammation, angiogenesis, and remodeling in astlunatic children. We also documented correlations between demographic features, duration of asthma, and pulmonary function test (PFT) parameters. Randomly selected 40 children (20 male and 20 female children, aged 6-16 years) with mild or moderate persistent asthma and 32 healthy children (15 male and 17 female children, aged 6-16 years) enrolled in the study. All asthmatic children had been using inhaled corticosteroids at least for the last 3 months. Serum Ang-1 levels were significantly lower in asthmatic children than those in normal controls. The Ang-1/Ang-2 ratio was also significantly lower in asthmatic children compared with those in normal controls (p < 0.01). However, serum Ang-2, VEGF, and TNF-alpha levels were similar in the two groups. A significant positive correlation was found between VEGF and duration of asthma. No correlation between sewn Aug-I, Ang-2, VEGF values, and PFT parameters was obtained. On the other hand, significant negative correlation was detected between serum TNF-alpha and forced expiratory volume in 1 second. We have shown that serum Aug-1 levels and Ang-1/Ang-2 ratio were significantly reduced and balance was toward Ang-2 in asthmatics children. This process may lead to inflammation, destabilization of blood vessels, and trigger remodeling.
  • Item
    Aspirin Resistance in Cerebrovascular Disease and the Role of Glycoprotein IIIa Polymorphism in Turkish Stroke Patients
    (2016) Derle, Eda; Ocal, Ruhsen; Kibaroglu, Seda; Celikkol, Ceyda; Bayraktar, Nilufer; Verdi, Hasibe; Atac, Belgin F.; Can, Ufuk; https://orcid.org/0000-0002-3964-268X; https://orcid.org/0000-0002-7886-3688; https://orcid.org/0000-0003-0591-009X; https://orcid.org/0000-0001-6868-2165; https://orcid.org/0000-0001-8689-417X; 26809135; V-3553-2017; AAJ-2956-2021; Y-8758-2018; V-5499-2017; ABG-9966-2020; AAJ-2999-2021
    Aspirin resistance occurs in 5-45% of high-risk patients, with various mechanisms proposed for its development. This study aimed to determine the relationships among aspirin resistance, aspirin dosage, type of aspirin and glycoprotein IIIa P1A1/A2 polymorphism in patients with vascular risk factors. Two hundred and eight (75 symptomatic, 133 asymptomatic) patients with vascular risk factors who were using aspirin for primary or secondary prevention were prospectively included. The symptomatic group was further classified into two groups according to aspirin use at the time of stroke. Aspirin resistance was measured by the PFA-100 system (collagen/epinephrine cartridge) and glycoprotein IIIa P1A1/A2 polymorphism was determined by PCR. The overall prevalence of aspirin resistance was 32.2%. The mean age of patients with aspirin resistance was significantly higher than that in those who did not have resistance (P=0.009). The prevalence of aspirin resistance was similar for the symptomatic and asymptomatic under aspirin therapy groups. The resistance rate was found to be highest with 100mg enteric-coated preparation use (39.3%). Increasing the aspirin dosage and/or shifting to uncoated preparations caused a change in aspirin sensitivity of 36-60%. Repeated measurements showed development of aspirin resistance in 14% of patients who were sensitive to aspirin in previous measurements. Glycoprotein IIIaP1A1/A2 polymorphism, aspirin resistance and development of atherothrombotic stroke were not significantly related. The effect of aspirin can change by time, dosage and type of preparation used. There are no relationships among glycoprotein IIIa P1A1/A2 polymorphism, aspirin resistance and development of atherothrombotic stroke. Copyright (C) 2016 Wolters Kluwer Health, Inc. All rights reserved.
  • Item
    Is Celiac Disease an Etiological Factor in Children with Nonsyndromic Intellectual Disability?
    (2016) Sezer, Taner; Balci, Oya; Ozcay, Figen; Bayraktar, Nilufer; Alehan, Fusun; https://orcid.org/0000-0002-2278-1827; https://orcid.org/0000-0002-8402-8208; https://orcid.org/0000-0002-5214-516X; https://orcid.org/0000-0002-7886-3688; 26078418; AAJ-5931-2021; AAI-9346-2021; ABG-5684-2020; Y-8758-2018
    To determine the prevalence of celiac disease in children and adolescents with nonsyndromic intellectual disability, we investigated serum levels of tissue transglutaminase antibody and total IgA from 232 children with nonsyndromic intellectual disability and in a healthy control group of 239 children. Study participants who were positive for tissue transglutaminase antibody underwent a duodenal biopsy. A total of 3 patients in the nonsyndromic intellectual disability group (5.45%) and 1 in the control group (0.41%) had positive serum tissue transglutaminase antibody (P > .05). Duodenal biopsy confirmed celiac disease in only 1 patient who had nonsyndromic intellectual disability. In this present study, children with nonsyndromic intellectual disability did not exhibit a higher celiac disease prevalence rate compared with healthy controls. Therefore, we suggest that screening test for celiac disease should not be necessary as a part of the management of mild and moderate nonsyndromic intellectual disability. However, cases of severe nonsyndromic intellectual disability could be examined for celiac disease.