Fjölmiðlagreining á afbrotum fyrir og eftir hrun

Í ritgerðinni verður skoðað hvernig fjölmiðlar endurspegla afbrot í samfélaginu og gerður samanburður á fjölda afbrota fyrir og eftir hrun. Leitast verður við að skoða hvort tegund afbrota hafi breyst og þá sérstaklega hvort fjöldi efnahagsbrota hafi aukist. Notast er við Morgunblaðið þar sem afbrotafréttir eru skoðaðar árin 2003 og 2009 frá tímabilinu 1. janúar til 31. júní. Árið 2003 var valið vegna þess að þá voru liðin tíu ár frá því að sams konar rannsókn var gerð þar sem Helgi Gunnlaugsson skoðaði fréttir um afbrot. Árið 2009 var valið vegna þess að þá var eitt ár síðan efnahagshrunið átti sér stað

Nrf2 mediates redox adaptations to exercise

The primary aim of this review is to summarize the current literature on the effects of acute exercise and regular exercise on nuclear factor erythroid 2-related factor 2 (Nrf2) activity and downstream targets of Nrf2 signaling. Nrf2 (encoded in humans by the NFE2L2 gene) is the master regulator of antioxidant defenses, a transcription factor that regulates expression of more than 200 cytoprotective genes. Increasing evidence indicates that Nrf2 signaling plays a key role in how oxidative stress mediates the beneficial effects of exercise. Episodic increases in oxidative stress induced through bouts of acute exercise stimulate Nrf2 activation and when applied repeatedly, as with regular exercise, leads to upregulation of endogenous antioxidant defenses and overall greater ability to counteract the damaging effects of oxidative stress. The evidence of Nrf2 activation in response to exercise across variety of tissues may be an important mechanism of how exercise exerts its well-known systemic effects that are not limited to skeletal muscle and myocardium. Additionally there are emerging data that results from animal studies translate to humans

Exercise Training Is Not Associated With Improved Levels of C-Reactive Protein or Adiponectin

The purpose of this study was to determine the effect of exercise training on the levels of C-reactive protein (CRP) and adiponectin, and to assess whether exercise-induced changes in insulin resistance could be explained in part by changes in these inflammation markers. Study participants included 51 middle-aged (45.3 +/- 8.3 years; mean +/- SD), overweight (33.7 +/- 4.8 BMI), insulin-resistant, nondiabetic individuals. Subjects had their insulin sensitivity, body fat, CRP, and adiponectin levels measured, and their predicted maximal fitness calculated before and after 16 weeks of moderate, intense, or no exercise training. Modest improvements in fitness, body composition, and insulin sensitivity were observed, but these changes were not associated with decreased CRP or increased adiponectin levels, even when subjects were stratified by their change in fitness or obesity. Regression analysis demonstrated that the change in percentage of body fat was significantly related to changes in insulin sensitivity, whereas changes in VO2 MAX, CRP, and adiponectin were not. Participation in moderate to intense exercise was not associated with improved measures of chronic inflammation markers, as measured by CRP and adiponectin. Moreover, improvements in insulin sensitivity resulting from exercise or modest weight loss did not appear to be related to changes in these markers. (c) 2005 Elsevier Inc. All rights reserved