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J Pediatr Endocr Met 2011;24(5-6):361–367 © 2011 by Walter de Gruyter • Berlin • Boston. DOI 10.1515/JPEM.2011.015 Childhood obesity: evidence of an association between plasminogen activator inhibitor-1 levels and visceral adiposity Rafael M. Mantovani 1 , Danyelle R.A. Rios 2 , Let í cia C.R. Moura 1 , Juliana M. Oliveira 1 , Fl á via F. Carvalho 1 , Sarah B. Cunha 1 , Maria de F á tima S. Viana 1 , Joel A. Lamounier 1 , Juni C. Castro 1 , Luci Maria S. Dusse 2 and Ana Cristina Sim õ es e Silva 1, * 1 Department of Pediatrics

2003; 9: 1529-43. 7. Look MP, van Putten WLJ, Duffy MJ, Harbeck N, Christensen IJ, Thomssen C, et al. Pooled analysis of prognostic impact of uPA and PAI-1 in 8377 breast cancer patients. J Natl Cancer Inst 2002; 94: 116-28. 8. Jänicke F, Prechtl A, Thomssen C, Harbeck N, Meisner C, Untch M, et al. for the German chemo N0 study group. Randomyzed adjuvant chemotherapy trial in high-risk, lymph node-negative breast cancer patients identified by urokinase-type plasminogen activator and plasminogen activator inhibitor type 1. J Natl Cancer Inst 2001; 93: 913

considered as an inert organ, functioning just as a storage organ for energy in the form of triacylglycerol. However, in recent studies it has been shown that adipocytes are active endocrine organs, which release various biologically active substances. These substances are known as adipocytokines or adipokines such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), adiponectin, plasminogen activator inhibitor-1 (PAI-1) [ 1 ]. These mediators actively participate in regulating body energy metabolism mainly by endocrine, paracrine and autocrine pathways. PAI-1 is

stroke in the Han Chinese population. Cerebrovasc Dis. 2008; 26:48-62. 10.1159/000135653 4. Yu W, Gwinn M, Clyne M, Yesupriya A, Khoury MJ. A navigator for human genome epidemiology. Nat Genet. 2008; 40:124-5. 10.1038/ng0208-124 5. Van Goor ML, Garcia EG, Leebeek F, Brouwers GJ, Koudstaal P, Dippel D. The plasminogen activator inhibitor (PAI-1) 4G/5G promoter polymorphism and PAI-1 levels in ischemic stroke. A case-control study. Thromb Haemost. 2005; 93:92-6. 6. Tsantes AE, Nikolopoulos GK, Bagos PG, Tsiara CG, Kapsimali V, Travlou A, et al. Plasminogen activator

Introduction Myocardial infarction (MI) is usually associated with thrombosis at the site of a ruptured atherosclerotic plaque. The dynamic balance between coagulation and fibrinolysis is an important determinant of the thrombotic response, which, in the setting of atherosclerosis, may influence the development of acute MI [1]. An important factor in the regulation of endogenous fibrinolysis seems to be the plasminogen activator inhibitor type 1 (PAI-1), which blocks both tissue-type plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA) [2

mouse macrophages: analysis by fluorescence ratio imaging. J. Cell Sci. 113 , 3329 –3340. Arroyo de Prada , N., Schroeck, F., Sinner, E.-K., Muehlenweg, B., Twellmeyer, J., Sperl, S., Wilhelm, O.G., Schmitt, M., and Magdolen, V. ( 2002 ). Interaction of plasminogen activator inhibitor type-1 (PAI-1) with vitronectin: characterization of different PAI-1 mutants. Eur. J. Biochem. 269 , 184 –192. Binder , B.R., Christ, G., Gruber, F., Grubic, N., Hufnagl, P., Krebs, M., Mihaly, J., and Prager G.W. ( 2002 ). Plasminogen activator inhibitor 1: physiological and

References 1. Loskutoff DJ. A slice of PAI. J Clin Invest 1993 ; 92 : 2563 . 2. Kruithof EKO. Plasminogen activator inhibitors – a review. Enzyme 1988 ; 40 : 13 –121. 3. Brakman P, Astrup T. Selective inhibition in human pregnancy blood of urokinase induced fibrinolysis. Scand J Clin Lab Invest 1963 ; 15 : 603 . 4. Lecander I, Åstedt B. Isolation of a new specific plasminogen activator inhibitor from pregnancy plasma. Br J Haemat 1986 ; 62 : 221 –8. 5. Stump DC, Thienpont M, Collen D. Purification and characterization of a novel inhibitor of urokinase

in genes coding for coagulation factors and enzymes included in fibrinolysis ( 5 , 6 ). Proper placental formation is necessary for successful pregnancy outcome. Several studies have proposed association between adverse pregnancy outcome and inherited thrombophilia, as it is shown that they can induce placental insufficiency due to vascular thrombosis ( 3 , 7 ). Gene variants in factor V gene (FV), prothrombin (FII), methylene tetrahydrofolate reductase (MTHFR) and plasminogen activator inhibitor-1 (PAI-1) are the most extensively studied in association with RPL

Koelbl et al, Changes of the fibrinolytic system before and after delivery 107 J. Perinat. Med. 17 (1989) 107 Influence of delivery on plasminogen activator inhibitor activity Heinz Koelbl1, Johannes Kirchheimer2, and Gerhart Tatra1 *2nd Department of Obstetrics and Gynecology and laboratory for Clinical- Experimental Physiology at the Department of Medical Physiology, University of Vienna, Austria 1 Introduction Plasminogen activators are serine proteases which initiate the fibrinolytic system by conversion of the proenzyme plasminogen to the active fibrin

, Klinikum rechts der Isar, Ismaninger Str. 22, D-81675 München, Germany 2 Wilex AG, Grillparzer Str. 10, D-81675 München, Germany * Corresponding author The serpin plasminogen activator inhibitor type-1 (PAI-1), as the primary physiological inhibitor of both urokinase-type (uPA) and tissue-type (tPA) plasmino- gen activator, plays an important role in the regulation of the fibrinolytic system as well as in extracellular remodeling in both physiological and pathophysio- logical processes. In plasma as well as in the extra- cellular matrix PAI-1 binds to vitronectin (Vn