Sistemik sklerozda interlökin-1, interlökin-6, soluble interlökin-2 reseptörü düzeylerinin ve lenfosit subpopulasyonlarının incelenmesi

TEZ2194Tez (Uzmanlık) -- Çukurova Üniversitesi, Adana, 1996.Kaynakça (s. 65-73) var.[5] 73 s. ; 30 cm.

Myelodisplastik sendromda telomer dinamiği ve prognostik parametrelerle ilişkisi

TEZ3872Tez (Yandal Uzmanlık) -- Çukurova Üniversitesi, Adana, 2002.Kaynakça (s. 48-52) var.vı, 52 s. ; 30 cm.

Use of zoledronic acid in thalassemia-ınduced osteoporosis: Two case reports and review of the literature

Talasemi majör hastalarında, erken tanı ve uygulanan tedaviler ile yaşam süresinin uzamasıyla birlikte, osteoporozla ilişkili sorunlar belirgin şekilde artmıştır. Bu hastalarda optimal transfüzyonlarla bile kemik iliği hiperaktif kalmaktadır. Bu nedenle transfüzyonlar, demir şelasyonu ve seks hormonlarıyla optimal tedaviye rağmen jeneralize osteoporoz ve osteopeni talasemide sık görülmektedir. Talasemiye bağlı osteoporozda kemik rezorbsiyonunun artmış olması osteoklast fonksiyonunun potent inhibitörleri olan bifosfonatların kullanımını gündeme getirmiştir. Bu makalede talasemi major ve sekonder osteoporoz tanılarıyla takip edilen iki kızkardeş tartışılmakta ve 6 yıl süre ile uygulanan 4 mg aralıklı zoledronik asit tedavisinin sonuçları sunulmaktadır. Talasemide gelişen osteoporozun etyopatogenezi ve uygulanan tedavi yaklaşımları gözden geçirilmektedir.The life span of thalassemia major patients has been extended with early diagnosis and treatment modalities. This condition has resulted in an increase in osteoporosis-related problems. Even with optimal transfusions, the bone marrow of these patients remains hyperactive. For this reason, despite blood transfusion, iron chelation, and sex hormone replacement therapy, generalized osteoporosis and osteopenia are still frequent in thalassemia patients. In thalassemia-induced osteoporosis, bone resorption increases. This condition makes biphosphonates, which are potent inhibitors of osteoclast function, the drug of choice. In this article, two sisters with thalassemia major and secondary osteoporosis are discussed and the results of treatment with intermittent zoledronic acid (iv. 4 mg ) for 6 years are presented. We also performed a review of the literature on the etiopathogenesis of thalasemia-induced osteoporosis and the treatment modalities

Decreased CD44 expression and stromal hyaluronate accumulation in myxoid dermatofibroma

Background: Dermatofibroma (DF) is a common benign histiocytic tumor, which has several clinicopathological variants. Myxoid DF is one of these variants, which is characterized by a stromal mucin deposition. CD44 is a polymorphic transmembrane glycoprotein and the principal cell surface receptor of hyaluronate (HA), the major component of the extracellular matrix. In a recent study, we have observed an abnormal accumulation of HA in the superficial dermis of transgenic mice with a keratinocyte-specific CD44 expression defect. We have also shown that HA was accumulated in large amounts in the superficial dermis of lichen sclerosus et atrophicus (LSA) lesions and that the epidermal CD44 expression of LSA skin was significantly decreased or lost. In an another study, we have suggested that a decrease in CD44 expression in follicular epithelial proliferations might be correlated with an abnormal HA accumulation in perifollicular solitary cutaneous myxoma. Recently we have also demonstrated that classical DF lesions displayed a strong CD44 expression in tumor cells and a weak HA positivity in tumor stroma whereas CD44 expression was significantly reduced or absent in dermatofibrosarcoma lesions and the tumor stroma showed strong HA staining. Objective and Methods: Here we present 3 cases of myxoid DF, in which we explored the nature of the mucinous material in myxoid stroma by colloidal iron and hyaluronic acid binding protein stainings, as well as the expression of CD44 in the tumor cells by immunohistochemistry. Results: We show that HA is accumulated in the stroma of all myxoid DF lesions with a significant decrease in CD44 expression in the tumor cells. Conclusion: Our results suggest that a decrease in CD44 expression in the tumor cells may result in stromal myxoid changes characterized by an abnormal HA accumulation in myxoid DF. Copyright (C) 2003 S. Karger AG, Basel

II. Dünya Savaşı'nın Tan ve Cumhuriyet gazeteleri tarafından değerlendirilmesi

Ankara : İhsan Doğramacı Bilkent Üniversitesi İktisadi, İdari ve Sosyal Bilimler Fakültesi, Tarih Bölümü, 2012.This work is a student project of the The Department of History, Faculty of Economics, Administrative and Social Sciences, İhsan Doğramacı Bilkent University.by Hamdi Özdiş.Özdiş, Hamdi. HIST 200-11, 17, 18ÖZDİŞ HIST 200-11, 17, 18/24 2011-1

Orak hücre hastalığında karaciğer tutulumu

Amaç: Orak hücre hastalığında karaciğer tutulumu primer hastalık ya da aşırı demir yüklenmesi, viral hepatitler ve kolelithiasis nedeniyle gelişebilir. Çalışmamızda 48 orak hücre hastasında hepatik disfonksiyon sıklığını ve etyolojik faktörleri inceledik. Yöntem: Tüm hastalarda klinik bulgularla birlikte esas olarak karaciğer fonksiyon testleri olmak üzere laboratuar bulgular incelendi ve üst batın ultrasonografisi yapıldı. Ek olarak 13 hastadan karaciğer biyopsisi alındı. Bulgular: Biyopsi örneklerinin tümünde intrasinüzoidal oraklaşma ve Kupffer hücre hiperplazisi izlendi. Tüm hasta grubunda hepatomegali, %27 hastada ise karaciğer fonksiyon testlerinde bozukluk mevcuttu. Kolelithiasis sıklığı 35% olarak bulundu. Serolojik test sonuçlarına gore hepatit B yüzey antijeni üç, hepatit B antikor pozitişiği 19 ve hepatit C antikor pozitişiği ise toplam dört hastada tespit edildi. Karaciğer örneklerinin histolojik incelemesinde en sık izlenen bulgu hemosiderosis idi. Sonuç: Bulguları mız orak hücre hastalarında kronik karaciğer hasarının genellikle birden fazla nedeni olduğunu, bu faktörler arasında ise primer hastalıktan çok aşırı demir yükünün ve viral nedenlerin ön planda olduğunu düşündürmektedir.Background/aims: Liver involvement in sickle cell disease may take place due to the primary disease itself or to secondary conditions such as iron overload, viral hepatitis and cholelithiasis. In the present study we have tried to evaluate the frequency of hepatic dysfunction and etiological factors in 48 patients with sickle cell disease. Methods: Clinical and laboratory investigation including liver function tests, serological tests for viral hepatitis, and abdominal ultrasonography were performed in all of the patients. Additionally, liver biopsies were taken from 13 patients. Results: Intrasinusoidal sickling and Kupffer cell hyperplasia were consistently seen in all of the biopsy specimens. Hepatomegaly was present in all patients, whereas liver function test abnormalities were seen in 27%. The prevalence of cholelithiasis was found as 35%. Serological tests demonstrated the presence of hepatitis B surface antigen in three, antibody to hepatitis B virus in 19 and antibody to hepatitis C virus in four of the patients. The most significant contributory finding was the presence of hemosiderosis in histological examination of liver specimens. Conclusion: Our data suggest that chronic liver injury in patients with sickle cell disease seems to be a multifactorial phenomenon depending mostly on overlapping factors such as iron overload and viral damage rather than primary disease itself