Soluble urokinase-type plasminogen activator receptor (suPAR) in multiple respiratory diseases

Serum soluble urokinase-type plasminogen activator receptor (suPAR) is a glycoprotein secreted during infections and inflammation [1]. Urokinase-type plasminogen activator (uPA) is secreted by polymorphonuclear neutrophils (PMN) and macrophages; then uPA binds to membrane urokinase-type plasminogen activator receptor (uPAR) [2]. suPAR is formed by cleaved from the uPAR [2]. suPAR is expressed in various cell types, such as macrophages monocytes, endothelial cells and neutrophils [3]. suPAR can be potentially cause or modulate various diseases in patients with cancer, various infectious and inflammatory diseases (including infections with human immunodeficiency virus (HIV), tuberculosis, liver fibrosis and inflammatory bowel disease) [2, 3]. suPAR can convert plasminogen to plasmin, which degrades fibrin, activates matrix metalloproteases and mediates proteolysis of extracellular matrix proteins during cellular invasion [4]. suPAR modulate the functions of integrins (including activating intracellular signals, monocyte chemotaxis, cell adhesion and proliferation) [4, 5]. So suPAR contributes to cell adhesion, migration, proliferation inflammation, chemotaxis, proteolysis, immune system activation, tissue remodeling and signal transduction [5, 6]. Several studies have identified that suPAR level is a important marker in patients with various diseases and associated with a poorer outcome in a range of non-infectious and infectious diseases [2]. Biomarkers of lung disease are required to aid diagnosis, define clinical phenotypes and monitor the response to existing and new therapeutic strategies. Our review aims to explore the potential of suPAR as a general marker in the diagnosis, prognosis and follow-up of therapy of lung disease

A New Marker for Ischemia: Ischemia-modified Albumin

İskemi modifiye albumin iskemi sonucu oluşan reaktif oksijen türevlerinin yol açtığı albuminde modifikasyon ile oluşur. Albumin kobalt bağlama testi kullanılarak ölçülür. Bu test geçici olmayan kardiyak hasarın başlangıcından önce iskeminin erken saptanmasında kullanılır. Bu yazıda iskemi modifiye albuminin patofizyolojisi, analizi ve klinik uygulamalarını inceledik.Ischemia-modified albumin constitutes via a modifcation in albumin where reactive oxygen species are formed due to ischemia. Albumin is measured using the cobalt binding test, and this test is used for the determination of albumin prior to the development of permanent cardiac injuries. In this review, we investigated the pathophysiology, analysis and clinical utility of ischemia-modified albumin

Soluble urokinase-type plasminogen activator receptor (suPAR) in multiple respiratory diseases

Serum soluble urokinase-type plasminogen activator receptor (suPAR) is a glycoprotein secreted during infections and inflammation [1]. Urokinase-type plasminogen activator (uPA) is secreted by polymorphonuclear neutrophils (PMN) and macrophages; then uPA binds to membrane urokinase-type plasminogen activator receptor (uPAR) [2]. suPAR is formed by cleaved from the uPAR [2]. suPAR is expressed in various cell types, such as macrophages monocytes, endothelial cells and neutrophils [3]. suPAR can be potentially cause or modulate various diseases in patients with cancer, various infectious and inflammatory diseases (including infections with human immunodeficiency virus (HIV), tuberculosis, liver fibrosis and inflammatory bowel disease) [2, 3]. suPAR can convert plasminogen to plasmin, which degrades fibrin, activates matrix metalloproteases and mediates proteolysis of extracellular matrix proteins during cellular invasion [4]. suPAR modulate the functions of integrins (including activating intracellular signals, monocyte chemotaxis, cell adhesion and proliferation) [4, 5]. So suPAR contributes to cell adhesion, migration, proliferation inflammation, chemotaxis, proteolysis, immune system activation, tissue remodeling and signal transduction [5, 6]. Several studies have identified that suPAR level is a important marker in patients with various diseases and associated with a poorer outcome in a range of non-infectious and infectious diseases [2]. Biomarkers of lung disease are required to aid diagnosis, define clinical phenotypes and monitor the response to existing and new therapeutic strategies. Our review aims to explore the potential of suPAR as a general marker in the diagnosis, prognosis and follow-up of therapy of lung disease

Obezitede Lipid Metabolizması İle İlgili Micro RNA’lar

Obezite Metabolik Sedrom, dislipidemi, Tip 2 Diabetes Mellitus ve kardiovasküler hastalık gibi kronik hastalıklar için major risk faktörüdür. Son yıllarda obezitenin moleküler temelinin anlaşılmasında ilerlemelere rağmen, obezite’ye karşı kullanılan ilaçlar fizyolojik spesifite eksikliğine ve yan etkilere sahiptir. MicroRNA’lar (miRNA), kısa (~22 nt), kodlanamayan endojen RNA molekülleridir ve mRNA’nın 3’ untranslated bölgesine bağlanarak birçok geni transkripsiyon sonrası düzenler. Bir miRNA birçok hedeflere sahiptir. Gelecekte miRNA’lar kronik hastalıklarının erken teşhisine yardımcı olacak ve yeni terapötik hedefler sağlayacaktır. miRNA’lar obezitede lipid metabolizması düzenlenmesinde bildirilmiştir. Bu derlemede adiposit biyolojisi ve obezite ile arasındaki ilgi, miRNA biyogenezi, düzenlenmesi, fonksiyonları ve obezitede lipid metabolizmasının düzenlenmesindeki rolü incelenecektir

Okside-LDL ve Reseptörü Lektin Benzeri Ox-LDL Reseptör-1

Oksidatif stres fazla oksidant bileşiğin yapılması ve antioksidant koruma mekanizmasının azlığı sonucu oluşarak doku hasarlarına yol açar. Oksidatif stres sonucu oluşan okside-düşük dansiteli lipoprotein oxidized low-density lipoprotein ox-LDL , reseptörü lektin benzeri ox-LDL reseptör-1 lectin-like receptor for ox-LDL-1 LOX-1 ’e bağlanır. ox-LDL ve LOX-1 endotel disfonksiyonu, monosit adezyonu, düz kas hücre proliferasyon, migrasyon ve apoptozis, yağ hücre yapımı ve trombosit aktivasyonu ile ilgili mekanizmalarda görev alır. ox-LDL, ateroskleroz, diabetes mellitus, yaşlanma, metabolik sendrom, kardiovasküler, ve serebrovasküler, böbrek ve karaciğer hastalıklarında artarak hastalıkların patogenezlerinde aktif rol alır. Bu derlemede, ox-LDL ve reseptörü LOX-1 etkileri incelenmişti

Yeni jenerasyon Bis ve Amino Ditiyolpirol bileşenlerinin sentezi

TEZ 547.75/CANyKaynakça : 47 - 52 ss.[Özet Yok

Çocukluk Çağı Obezite ve Metabolik Sendromda Serum Heat Şok Protein 70, S100A12 ve Matriks Gla Protein

Amaç: Metabolik Sendromun primer nedeni erişkin ve çocuk popülasyonunda insülin rezistansı ile sonuçlanan düşük dereceli inflamasyon ile ilgili obezitedir. Heat şok protein 70,S100A12 ve matriks Gla protein kronik inflamatuar hastalık ile ilgilidir. Çocuk çağı obezitesi ve metabolik sendromun da bu markırları değerlendirmeyi amaçladık. Gereç ve Yöntem: Bu çalışma 10-15 yaş aralığında 45 obez çocuk ve 47 metabolik sendrom'lu çocukta yapıldı. Heat şok protein 70, S100A12 ve matriks Gla protein ELISA metodu kullanılarak ölçüldü.Bulgular: Obez çocuklarda serum matriks Gla protein ve S100A12 seviyeleri metabolik sendrom'lu gruptan anlamlı olarak yüksekti (p0.05). İlaveten, metabolik sendrom ve obez bireyler arasında serum hsCRP (p0.288) ve heat şok protein 70 (p0.960) fark yoktu. Her iki grupta S100A12, matriks Gla protein ve heat şok protein 70 seviyeleri arasında anlamlı pozitif korelasyon vardı. Sonuç: Bulgularımız S100A12, matriks Gla protein ve heat şok protein 70 biyomarkırları metabolik sendrom ve obezite ile anlamlı olarak ilgili olduğunu gösterdi. Obezite metabolik sendrom gelişiminde önemli bir risk faktörüdür. Obezitede bu proteinlerin artışı, metabolik sendrom ve diabet gibi metabolik bozuklukların gelişiminin önlenmesinde ilgi çekici olabilir.Objectives: The primary cause of the metabolic syndrome appears to be obesity that is associated with a low-grade inflammatory state resulting from insulin resistance in both adult and pediatric populations. Heat shock protein 70, S100A12 and matrix Gla protein are involved in chronic inflammatory diseases. We aimed to evaluate the association between these markers and childhood obesity and metabolic syndrome. Materials and Methods: This study was performed with 45 obese children aged 10-15 years and 47 children with metabolic syndrome aged 10-15 years. Serum heat shock protein 70, S100A12 and matrix Gla protein levels were measured by using ELISA method. Results: Serum matrix Gla protein and S100A12 levels in obese subjects were significantly higher than metabolic syndrome groups (p>0.05). However no significant differences were observed in serum high sensitivity Creactive protein (p0.288) and heat shock protein 70 (p0.960) levels between metabolic syndrome and obese subjects. There was a significant positive correlation between serum S100A12, matrix Gla protein and heat shock protein 70 levels in both groups. Conclusions: Our findings showed a significant association between heat shock protein 70, S100A12, matrix Gla protein, and obesity and metabolic syndrome. Obesity may be involved in increased risk of developing metabolic syndrome. It might be useful to focus on the roles of these proteins in obesity in accordance with the prevention of the development of metabolic syndrome and other metabolic disorders like diabetes