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AKKAN, AHMET GÖKHAN

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AHMET GÖKHAN
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AKKAN
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Now showing 1 - 5 of 5
  • PublicationMetadata only
    The Effects of Potassium Channels in Human Internal Mammary Artery
    (2016-01-01T00:00:00Z) Afsar, Selim; Hemsinli, Dogus; Ozyazgan, Sibel; Akkan, Ahmet Gökhan; Arslan, Caner; AKKAN, AHMET GÖKHAN
    Background: Structural and functional changes in potassium channels of vascular smooth muscle cells may contribute to the development of diseases such as hypertension. We aim to investigate the vascular effects of potassium channel openers and blockers in human internal mammary artery (HIMA). Methods: Remaining segments of HIMA from 18 consecutive patients undergoing coronary artery bypass surgery were obtained to examine the vascular effects of various potassium channel openers (staurosporine, hydrochlorothiazide and cromakalim) and potassium channel blockers (4-aminopyridin [4-AP], charybdotoxin [CTX] and glibenclamide [GLBC]). Results: Noradrenaline (NA)-induced maximal contractions were inhibited by all 3 K+-channel blockers but only fully inhibited by 4-AP (95.6%). Only NA-induced contractions were reversed by CTX. Only K+-induced maximal contractions were significantly inhibited by 4-AP (95.6%, p < 0.05). Only acetylcholine-induced relaxation was fully inhibited by CTX. Only sodium nitroprusside-induced relaxations in potassium chloride-precontracted strips could be reversed by GLBC. Conclusions: Drugs affecting potassium channels may be useful in the treatment of hypertension and management of perioperative vasospasm during the coronary artery bypass surgery. (C) 2015 S. Karger AG, Basel
  • PublicationMetadata only
    The Anti-Inflammatory Effects of Anacardic Acid on a TNF-alpha Induced Human Saphenous Vein Endothelial Cell Culture Model
    (2020-01-01T00:00:00Z) DURSUN, Erdinç; Onal, Burak; Ozen, Deniz; Demir, Bulent; Ak, Duygu Gezen; Demir, Caner; Akkan, Ahmet Gökhan; Ozyazgan, Sibel; AKKAN, AHMET GÖKHAN
    Background and Objective: Coronary bypass operations are commonly performed for the treatment of ischemic heart diseases. Coronary artery bypass surgery with autologous human saphenous vein maintains its importance as a commonly used therapy for advanced atherosclerosis. Vascular inflammation-related intimal hyperplasia and atherosclerotic progress have major roles in the pathogenesis of saphenous vein graft disease.
  • PublicationMetadata only
    Does Inflammation Have a Role in the Pathogenesis of Cardiac Syndrome X? A Genetic-Based Clinical Study With Assessment of Multiple Cytokine Levels
    (2016-04-01T00:00:00Z) Demir, Bulent; Onal, Burak; Ozyazgan, Sibel; Kandaz, Cemre; UZUN, Hafize; Aciksari, Gonul; Uygun, Turgut; Opan, Selcuk; Karakaya, Osman; Akkan, Ahmet Gökhan; AKKAN, AHMET GÖKHAN
    We compared Turkish patients with cardiac syndrome X (CSX) and controls with respect to serum pro- and anti-inflammatory cytokine levels, as well as the single-nucleotide polymorphisms located in the promoter regions of their related genes. This study included 111 consecutive patients angiographically diagnosed with CSX and 111 healthy controls with similar demographic characteristics. Serum interleukin (IL) 6, tumor necrosis factor (TNF-), and IL-10 levels were measured, and the genotypes of the patients and controls were determined using standard methods. Serum IL-6 and IL-10 levels were significantly higher in the CSX group than in the control group (P < .01, respectively). Serum TNF- level was lower in the CSX group than in the control group (P < .001). On the other hand, participants with CSX and healthy controls were not significantly different with respect to the genotype distributions of IL-6, TNF-, and IL-10 genes. As a result of our study, both pro-inflammatory and anti-inflammatory cytokines may play a role in the pathogenesis of CSX. In contrast, the studied gene polymorphisms did not influence CSX pathogenesis.
  • PublicationMetadata only
    Effect of Three PDEIs on Neuroprotective and Autophagy Proteins in vitro AD Model
    (2021-01-01T00:00:00Z) Saygisever-Faikoglu, Kubra; Faikoglu, Gokhan; Celik, Hande; Ugur, Sedat Askin; AKKAN, Ahmet Gökhan; Kelicen-Ugur, Pelin; Ozyazgan, Sibel; AKKAN, AHMET GÖKHAN
    Background and Objective: The effects of PDEIs on neuroprotective SIRT1 and SESN2, on the autophagy-related proteins, are unknown but neuroprotective enzymes (sirtuins and sestrins) with autophagy genes are involved in the pathogenesis of Alzheimer-s disease. In this study, we aimed to elucidate the effect of three PDE Inhibitors (PDEIs) as autophagy enhancers and provide insights into their neuroprotective effects. Materials and Methods: HT-22 cells were exposed to A$ 25-35 with or without PDEIs for 32 hrs. qRT-PCR was performed for SIRT1, SESN2, ATG5 and BECN1 genes. Western blot analysis was performed for neuroprotective SIRT1, SESN2 proteins and autophagy proteins such as p-mTOR/mTOR, p-AMPK/AMPK and LC3. Results: A$ 25-35 exposure decreased SIRT1, ATG5 and BECN1 expression, while PDEIs prevented these genes from the A$ 25-35 induced decrease. Increased SESN2 gene expression by A$ 25-35 exposure was decreased by PDEIs treatment. Western blot experiment has also shown that SIRT1, p-AMPK and autophagy marker LC3II were decreased, whereas SESN2 and p-mTOR were elevated in the A$ 25-35 exposed HT-22 cells. Co administration of three PDEIs with A$ 25-35 recovered SIRT1, p-AMPK and LC3II decline and compensated SESN2 increase by elevating SIRT1, p-AMPK and LC3II expression and decreasing p-mTOR expression. Conclusion: The present study revealed the significant neuroprotective and autophagy stimulating potential of three PDEIs in A$-induced in vitro AD model. SIRT1 is a novel candidate for determining new, safe and effective treatment strategies and PDEI-mediated SIRT1 increase may advocate autophagy activation through different autophagy components.
  • PublicationMetadata only
    Investigation of MTHFR gene C677T polymorphism in cardiac syndrome X patients
    (2018-02-01T00:00:00Z) Kandaz, Cemre; Onal, Burak; Ozen, Deniz; Demir, Bulent; Akkan, Ahmet Gökhan; Ozyazgan, Sibel; AKKAN, AHMET GÖKHAN
    BackgroundDefinition of Cardiac Syndrome X (CSX) refers to groups of patients with positive exercise stress test and normal epicardial coronary arteries on coronary angiography accompanied by chest pain. Although the etiology of CSX is not completely understood, there is a common consensus that its pathophysiology may be associated with endothelial dysfunction resulting in impaired coronary flow. Some polymorphisms observed on the MTHFR gene cause inactivation of the MTHFR enzyme, leading to hyperhomocysteinemia and homocysteinuria, which are prominent risk factors of cardiovascular and cerebrovascular diseases. It was aimed to explain the association of the endothelial dysfunction, which is thought to play a role in the pathophysiology of CSX, with C677T polymorphism on MTHFR gene based on genetic basis.