Numerical ability predicts mortgage default

Unprecedented levels of US subprime mortgage defaults precipitated a severe global financial crisis in late 2008, plunging much of the industrialized world into a deep recession. However, the fundamental reasons for why US mortgages defaulted at such spectacular rates remain largely unknown. This paper presents empirical evidence showing that the ability to perform basic mathematical calculations is negatively associated with the propensity to default on one’s mortgage. We measure several aspects of financial literacy and cognitive ability in a survey of subprime mortgage borrowers who took out loans in 2006 and 2007, and match them to objective, detailed administrative data on mortgage characteristics and payment histories. The relationship between numerical ability and mortgage default is robust to controlling for a broad set of sociodemographic variables, and is not driven by other aspects of cognitive ability. We find no support for the hypothesis that numerical ability impacts mortgage outcomes through the choice of the mortgage contract. Rather, our results suggest that individuals with limited numerical ability default on their mortgage due to behavior unrelated to the initial choice of their mortgage.     

Interactions between fibrin and the plasminogen activators produced by cultured endothelial cells

Serum-free conditioned medium (CM) from cultured bovine aortic endothelial cells (BAEs) was fractionated by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate and analyzed for plasminogen activator (PA) activity by fibrin autography. Distinct size forms of PA with molecular weights (mol wt) of 100,000, 74,000, and 52,000 were readily identified by this approach. When fibrinogen and thrombin were added to CM containing these forms, approximately 55% of the total activity was found to associate with the resultant fibrin clot. The other 45% remained free in the supernatant. This relationship did not change at higher fibrin concentrations. Subsequent analysis revealed that only the larger PA forms (mol wt 74,000-100,000) were recovered in the clot. The 52,000 form did not bind to the polymerizing fibrin under these conditions. The fibrin-binding forms also bound to immobilized concanavalin-A and could be separated from those forms that did not interact with fibrin by concanavalin-A affinity chromatography. The PA activity of the separated forms was then compared by assessing their ability to cleave 125I-plasminogen. Although cleavage by the 52,000 mol wt form was apparent, little if any cleavage was initiated by the mixture containing the 74,000-100,000 forms. The addition of fibrin to this sample resulted in the generation of a potent PA activity. These results indicate that cultured BAEs produce multiple forms of PA that differ both in size and in behavior toward fibrin and concanavalin-A. These forms include molecules that functionally and immunochemically resemble human urokinase, and others that resemble human tissue-type PA.     

Intraoperatives Neuromonitoring bei Schilddrüsenoperationen

Intraoperative neuromonitoring (IONM) was introduced into thyroid surgery approximately 10 years ago for better identification of recurrent laryngeal nerve palsy. Since then several studies have been performed for evaluation of this new technology. IONM is superior to visual nerve identification alone for prediction of postoperative local cord function. Therefore, in bilateral procedures IONM enables intraoperative decision-making concerning resection of the second side. To avoid misinterpretation of the results of IONM a standardized approach including preoperative and postoperative laryngoscopy and preresection and postresection vagus stimulation is recommended. Trouble-shooting requires systematic checking of the device including control of electrode position (needle or tube electrodes). For expert assessment purposes documentation of the standardized application of IONM is of utmost importance.     

Genetic influences on fibrinogen, tissue plasminogen activator-antigen and von Willebrand factor in males and females

Differences in genetic influence on death from CHD between males and females have been reported. Haemostatic factors have consistently been associated with risk for coronary heart disease (CHD), but sex differences in genetic architecture have not been studied. This study in middle-aged twins investigates whether there are sex differences in means and in genetic and/or environmental variance components of haemostatic risk factors for CHD. A total of 93 monozygotic twin pairs (44 male and 49 female) and 116 dizygotic twin pairs (36 male, 40 female and 40 opposite sex) were available for this study. Structural equation modelling was used to estimate the relative influence of genetic and environmental factors on variation in levels of fibrinogen, tissue plasminogen activator (tPA) antigen and von Willebrand factor (vWF). Mean levels of tPA and vWF increased with age. Oral contraceptive pill (OCP) and menopause had significant influences on levels of fibrinogen and tPA. Genetic influences explained 39, 66 and 72% of the variation in levels of fibrinogen, tPA and vWF, respectively. No quantitative or qualitative differences of genetic influences on haemostatic levels were seen between males and females. Haemostatic factors may account for a significant part of the genetic risk for cardiovascular disease. No difference in genetic architecture for levels of fibrinogen, tPA or vWF was observed between males and females.