Individual determinants of social fairness assessments : the case of Germany

In this contribution we study the determinants of how individuals assess the social fairness of a given income distribution. We propose an analytical framework distinguishing between potential impact factors related to the following fields: first fairness preferences, second beliefs on the sources of economic success and the functioning of democracy and third selfinterest. We test this framework on representative survey data for Germany for the years 1991, 2000 and 2004. Our results indicate that self-interest, beliefs and fairness preferences jointly shape fairness assessments. In addition, a number of personal characteristics are found to be important: Compared to their western fellow citizens, people born in GDR have a more critical view at social fairness. A particularly strong impact is related to the belief on the functioning of the democratic system. This points an important role of procedural fairness for the acceptance of a given distribution

Lack of activity of recombinant HIF prolyl hydroxylases (PHDs) on reported non-HIF substrates

AbstractHuman and other animal cells deploy three closely related dioxygenases (PHD 1, 2 and 3) to signal oxygen levels by catalysing oxygen regulated prolyl hydroxylation of the transcription factor HIF. The discovery of the HIF prolyl-hydroxylase (PHD) enzymes as oxygen sensors raises a key question as to the existence and nature of non-HIF substrates, potentially transducing other biological responses to hypoxia. Over 20 such substrates are reported. We therefore sought to characterise their reactivity with recombinant PHD enzymes. Unexpectedly, we did not detect prolyl-hydroxylase activity on any reported non-HIF protein or peptide, using conditions supporting robust HIF-α hydroxylation. We cannot exclude PHD-catalysed prolyl hydroxylation occurring under conditions other than those we have examined. However, our findings using recombinant enzymes provide no support for the wide range of non-HIF PHD substrates that have been reported.Abstract Human and other animal cells deploy three closely related dioxygenases (PHD 1, 2 and 3) to signal oxygen levels by catalysing oxygen regulated prolyl hydroxylation of the transcription factor HIF. The discovery of the HIF prolyl-hydroxylase (PHD) enzymes as oxygen sensors raises a key question as to the existence and nature of non-HIF substrates, potentially transducing other biological responses to hypoxia. Over 20 such substrates are reported. We therefore sought to characterise their reactivity with recombinant PHD enzymes. Unexpectedly, we did not detect prolyl-hydroxylase activity on any reported non-HIF protein or peptide, using conditions supporting robust HIF-α hydroxylation. We cannot exclude PHD-catalysed prolyl hydroxylation occurring under conditions other than those we have examined. However, our findings using recombinant enzymes provide no support for the wide range of non-HIF PHD substrates that have been reported

A causal relationship between right paraduodenal hernia and superior mesenteric artery syndrome: a case report

<p>Abstract</p> <p>Introduction</p> <p>Cases of right paraduodenal hernia and superior mesenteric artery syndrome have been reported separately, but their occurrence in combination has not been reported.</p> <p>Case presentation</p> <p>A 46-year-old Japanese man who had never undergone laparotomy was admitted to our hospital due to an acute abdomen. An enhanced multidetector-row computed tomography scan of our patient showed a cluster of small intestines with ischemic change in his right lateral abdominal cavity. Emergency surgery was subsequently performed, and strangulation of the distal jejunum along with incidental right paraduodenal hernia was found. His necrotic ileum was resected, and the jejunum encapsulated by the sac was repaired manually without reduction.</p> <p>Three days after the operation, however, our patient developed vomiting. An upper gastrointestinal series revealed a straight line cut-off sign on the third portion of his duodenum. A second enhanced multidetector-row computed tomography scan showed that he had a lower aortomesenteric angle and a shorter aortomesenteric distance compared to his condition before his right paraduodenal hernia was surgically repaired. We strongly suspected that the right paraduodenal hernia repair may have induced superior mesenteric artery syndrome. On the 21st post-operative day, duodenojejunostomy was performed because conservative management had failed.</p> <p>Conclusions</p> <p>In this case, enhanced multidetector-row computed tomography, which permits reconstructed multiplanar imaging, helped us to visually identify these diseases easily. It is important to recognize that surgical repair of a right paraduodenal hernia may cause superior mesenteric artery syndrome.</p

Hypobaric hypoxia causes body weight reduction in obese subjects.

The reason for weight loss at high altitudes is largely unknown. To date, studies have been unable to differentiate between weight loss due to hypobaric hypoxia and that related to increased physical exercise. The aim of our study was to examine the effect of hypobaric hypoxia on body weight at high altitude in obese subjects. We investigated 20 male obese subjects (age 55.7 +/- 4.1 years, BMI 33.7 +/- 1.0 kg/m(2)). Body weight, waist circumference, basal metabolic rate (BMR), nutrition protocols, and objective activity parameters as well as metabolic and cardiovascular parameters, blood gas analysis, leptin, and ghrelin were determined at low altitude (LA) (Munich 530 m, D1), at the beginning and at the end of a 1-week stay at high altitude (2,650 m, D7 and D14) and 4 weeks after returning to LA (D42). Although daily pace counting remained stable at high altitude, at D14 and D42, participants weighed significantly less and had higher BMRs than at D1. Food intake was decreased at D7. Basal leptin levels increased significantly at high altitude despite the reduction in body weight. Diastolic blood pressure was significantly lower at D7, D14, and D42 compared to D1. This study shows that obese subjects lose weight at high altitudes. This may be due to a higher metabolic rate and reduced food intake. Interestingly, leptin levels rise in high altitude despite reduced body weight. Hypobaric hypoxia seems to play a major role, although the physiological mechanisms remain unclear. Weight loss at high altitudes was associated with clinically relevant improvements in diastolic blood pressure

Do we need gastric acid?

Evidence from comparative anatomy and physiology studies indicates that gastric acid secretion developed during the evolution of vertebrates approximately 350 million years ago. The cellular mechanisms that produce gastric acid have been conserved over the millennia and therefore proton pump inhibitors have pharmacological effects in almost all relevant species. These observations suggest that gastric acid provides an important selective advantage; however, in modern-day humans the need for gastric acid can be questioned in light of the widespread use of safe and effective pharmacologic acid suppression. The Kandahar Working Group addressed questions concerning the need, production and effects of gastric acid, specifically: (1) motility in the upper gastrointestinal (GI) tract; (2) neuroendocrine factors; (3) digestive and mucosal processes; (4) microbiology, and (5) central processes and psychological involvement. We addressed each topic with the individual models available to answer our questions including animal versus human studies, pharmacologic, surgical as well as pathophysiologic states of acid suppression

TNF-alpha induces apoptosis of parietal cells.

Helicobacter pylori infection can be associated with chronic gastric inflammation and hypochlorhydria with increased levels of the proinflammatory cytokines. The current study investigated the effects of TNF-alpha on programmed death of gastric parietal cells. TNF-alpha induced apoptosis of parietal cells in isolated perfused rat stomachs at 10 ng/mL. In isolated and highly enriched rat parietal cells, 10 ng/mL TNF-alpha induced a 2.6-fold increase in the apoptotic rate. The 55 kDa protein of TNFR-I but not the 75 kDa of TNFR-2 was detected by Western blot analysis. TNF-alpha-induced apoptosis of isolated parietal cells was inhibited by pretreatment with different NF-kappaB-inhibitors, nitric oxide synthase inhibitors and with antisense-oligodeoxynucleotides against the p65 subunit of NF-kappaB. Investigation of downstream signaling pathways of apoptosis revealed that TNF-alpha induced the expression of NOS, but failed to stimulate the activity of caspase 3. The TNF-alpha effect on gastric parietal cells may contribute to the atrophy and hypochlorhydria of the gastric mucosa observed during chronic H. pylori infection. (C) 2003 Elsevier Science Inc. All rights reserved