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Öğe BRUTON DISEASE DIAGNOSED WITH CERVICAL ABSCESS IN EARLY INFANCY(Springer/Plenum Publishers, 2014) Guner, Sukru Nail; Sayar, Esra Hazar; Ng, Yuk Yin; Reisli, Ismail[Abstract Not Availabe]Öğe EDUCATION AND PID AWARENESS AMONG MEDICAL STUDENTS(Springer/Plenum Publishers, 2014) Reisli, Nesrin; Guner, Sukru; Sayar, Esra Hazar; Reisli, Ismail[Abstract Not Availabe]Öğe How effective are the 6 European Society of Immunodeficiency warning signs for primary immunodeficiency disease?(Elsevier Science Inc, 2016) Arslan, Sevket; Ucar, Ramazan; Caliskaner, Ahmet Zafer; Reisli, Ismail; Guner, Sukru Nail; Sayar, Esra Hazar; Baloglu, IsmailBackground: The European Society of Immunodeficiency (ESID) developed 6 warning signs to promote the awareness of adult primary immunodeficiency disease (PID). Objective: To screen adult patients for the presence of PID using these 6 warning signs to determine the effectiveness of this protocol. Methods: Questions related to the ESID warning signs for adult PID were added to the standard outpatient clinic file system and asked of 3,510 patients who were admitted to our clinic for any reason. Patients with signs and/or suspicion of PID based on their medical history underwent immunologic investigation. Results: In total, 24 patients were diagnosed as having a PID. The most common reason that patients with PID were admitted was frequent infection (n = 18 [75%]), and the most common PID subgroup was common variable immunodeficiency (n = 12 [50%]). Twenty patients with PID had at least one positive finding according to the ESID warning signs. Two patients with gastrointestinal concerns and 2 with dermatologic symptoms were also diagnosed as having a PID, although they did not have any of the ESID warning signs. Conclusion: The ESID warning signs do not specify the need for symptoms to diagnose a PIDs and do not include a comprehensive list of all signs and symptoms of PIDs. As a result, more than infection-centric questions are needed to identify adult patients with immunodeficiencies. (C) 2016 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.Öğe The Ineffectiveness of Tacrolimus in an Infant With a Mutation in the IL-10 Receptor(Lippincott Williams & Wilkins, 2016) Sayar, Ersin; Yucel, Aylin; Eisele, Bianca; Sayar, Esra Hazar; Glocker, Erik; Yuksekkaya, Hasan Ali[Abstract Not Availabe]Öğe Ocular Findings in Children With 22q11.2 Deletion Syndrome(Slack Inc, 2016) Gokturk, Bahar; Topcu-Yilmaz, Pinar; Bozkurt, Banu; Yildirim, Mahmut Selman; Guner, Sukru Nail; Sayar, Esra Hazar; Reisli, IsmailPurpose: To identify the ocular features of children diagnosed as having 22q11.2 deletion syndrome in a Turkish population, which is the most common microdeletion syndrome with a wide range of facial and ocular abnormalities. Methods: Sixteen children aged between 4 months and 18 years with a microdeletion in chromosome 22q11.2 underwent a detailed ophthalmological examination including uncorrected and best corrected visual acuity testing, stereoscopic vision examination, biomicroscopic and indirect fundus examination, and ocular motility testing. Results: All patients had at least one ocular abnormality. The major abnormalities were eyelid abnormalities (eye hooding, narrow palpebral fissure, telecanthus, hypertelorism, sparse and thin eyebrows and eyelashes, blepharitis, and distichiasis), posterior embryotoxon, and tortuous retinal vessels in at least half of the patients. Other ophthalmological disorders were refractive errors, iris remnants, and strabismus. Conclusions: The chromosome 22q11.2 deletion syndrome is associated with a wide range of ocular disorders, which necessitates a comprehensive eye examination for appropriate treatment and follow-up. Ocular findings sometimes can provide a clue to the diagnosis of 22q11.2 deletion.Öğe Type I IFN-related NETosis in ataxia telangiectasia and Artemis deficiency(Mosby-Elsevier, 2018) Gul, Ersin; Sayar, Esra Hazar; Gungor, Bilgi; Eroglu, Fehime Kara; Surucu, Naz; Keles, Sevgi; Guner, Sukru NailBackground: Pathological inflammatory syndromes of unknown etiology are commonly observed in ataxia telangiectasia (AT) and Artemis deficiency. Similar inflammatory manifestations also exist in patients with STING-associated vasculopathy in infancy (SAVI). Objective: We sought to test the hypothesis that the inflammation-associated manifestations observed in patients with AT and Artemis deficiency stem from increased type I IFN signature leading to neutrophil-mediated pathological damage. Methods: Cytokine/protein signatures were determined by ELISA, cytometric bead array, or quantitative PCR. Stat1 phosphorylation levels were determined by flow cytometry. DNA species accumulating in the cytosol of patients' cells were quantified microscopically and flow cytometrically. Propensity of isolated polymorhonuclear granulocytes to form neutrophil extracellular traps (NETs) was determined using fluorescence microscopy and picogreen assay. Neutrophil reactive oxygen species levels and mitochondrial stress were assayed using fluorogenic probes, microscopy, and flow cytometry. Results: Type I and III IFNsignatures were elevated in plasma and peripheral blood cells of patients with AT, Artemis deficiency, and SAVI. Chronic IFN production stemmed fromthe accumulation of DNA in the cytoplasm of ATand Artemis-deficient cells. Neutrophils isolated from patients spontaneously produced NETs and displayed indicators of oxidative and mitochondrial stress, supportive of theirNETotic tendencies. Asimilar phenomenonwas also observed in neutrophils from healthy controls exposed to patient plasma samples or exogeneous IFN-alpha. Conclusions: Type I IFN-mediated neutrophil activation and NET formation may contribute to inflammatory manifestations observed in patients with AT, Artemis deficiency, and SAVI. Thus, neutrophils represent a promising target to manage inflammatory syndromes in diseases with active type I IFN signature.
