Influence of Microstructure and Sintering Routes on Transport Properties of Apatite Materials for Fuel Cells

1 Results Oxy-apatite materials are thought as zirconia-substitutes in Solid Oxide Fuel Cells due to their fast ionic conduction. However, the well known difficulties related to their densification prevent them from being used as such. This study presents strategies to obtain oxy-apatite dense materials and the influence of elaboration route on transport properties. Particular emphasis is put on the microstructure effect on ion conduction. By the combined use of freeze-drying and conventional or spark p...     

Experimental gout from alloxan in pigeons. Findings in the joints and serous membranes

Zusammenfassung Bei Tauben erzeugt intravenös gegebenes Alloxan bekanntlich Läsionen, die denen der Eingeweidegicht ähneln. Chemische und mikroskopische Untersuchungen zeigten eine große Menge von Uraten auf Perikardium, Peritoneum und Pleura. Die große Zunahme der Harnsäure im Blute, die von anderen Autoren kolorimetrisch festgestellt wurde, wird durch die Urikasemethode bestätigt. In der vorliegenden Mitteilung wird weiterhin über ein der Gelenkgicht ähnliches Bild bei alloxanbehandelten Tauben berichtet. Verschiedene Tierarten mit einem «ureotelic-proteic metabolism» zeigen nach Alloxan weder eine nennenswerte Harnsäurezunahme im Blut noch eine Gicht der Eingeweide oder der Gelenke.     

The serini reaction

Zusammenfassung Der Mechanismus der Serini-Reaktion wird kurz erörtert und ein 17, 20-Oxyd als Zwischenprodukt vorgeschlagen. Das stereochemische Ergebnis der Reaktion soll von zwei Faktoren abhängig sein, und zwar: 1. von der Geometrie des « transition state » und 2. von der Konfiguration des Oxydrings. Ausgehend von diesen Überlegungen, kann vorausgesagt werden, daßReichsteins Substanz 0-Diacetat durch die Serini-Reaktion in ein 17-Iso-20-keton und nicht in ein 17-Normal-20-keton umgewandelt werden soll. Tatsächlich ist das 17-Isoallopregnanol-(3)-on-20 als einziges Produkt experimentell aufgefunden worden.     

Regulation of insulin receptor function

Resistance to the biological actions of insulin contributes to the development of type 2 diabetes and risk of cardiovascular disease. A reduced biological response to insulin by tissues results from an impairment in the cascade of phosphorylation events within cells that regulate the activity of enzymes comprising the insulin signaling pathway. In most models of insulin resistance, there is evidence that this decrement in insulin signaling begins with either the activation or substrate kinase activity of the insulin receptor (IR), which is the only component of the pathway that is unique to insulin action. Activation of the IR can be impaired by post-translational modifications of the protein involving serine phosphorylation, or by binding to inhibiting proteins such as PC-1 or members of the SOCS or Grb protein families. The impact of these processes on the conformational changes and phosphorylation events required for full signaling activity, as well as the role of these mechanisms in human disease, is reviewed in this article. Received 3 August 2006; received after revision 1 December 2006; accepted 8 January 2007     

A genome-wide association study for celiac disease identifies risk variants in the region harboring IL2 and IL21

We tested 310,605 SNPs for association in 778 individuals with celiac disease and 1,422 controls. Outside the HLA region, the most significant finding (rs13119723; P = 2.0 x 10(-7)) was in the KIAA1109-TENR-IL2-IL21 linkage disequilibrium block. We independently confirmed association in two further collections (strongest association at rs6822844, 24 kb 5' of IL21; meta-analysis P = 1.3 x 10(-14), odds ratio = 0.63), suggesting that genetic variation in this region predisposes to celiac disease.     

The human genome and understanding of common disease: present and future technologies

The study of candidate genes over the past three decades has yielded notable successes in common-disease genetics. During this time, however, interpretation of genetic association studies has been hampered by the use of clinical cohorts of inadequate power and insufficient information on genetic variation in candidate genes. The unavailability of highthroughput and low-cost genotyping technologies has also limited the scope of complex-disease genetic studies. More recently, however, the sequencing and characterization of variation within the human genome has revolutionized genetic studies and enabled full genome-wide scans for genes associated with disease. The identification of disease-associated (causative) genes has illuminated disease mechanisms. The translation of this knowledge into direct clinical benefit in diagnosis, prognosis and therapy for an individual’s disease still remains a challenge. Received 11 September 2006; received after revision 17 December 2006; accepted 18 January 2007     

Pierre Duhem’s virtue epistemology

Duhem’s concept of ‘good sense’ is central to his philosophy of science, given that it is what allows scientists to decide between competing theories. Scientists must use good sense and have intellectual and moral virtues in order to be neutral arbiters of scientific theories, especially when choosing between empirically adequate theories. I discuss the parallels in Duhem’s views to those of virtue epistemologists, who understand justified belief as that arrived at by a cognitive agent with intellectual and moral virtues, showing how consideration of Duhem as a virtue epistemologist offers insights into his views, as well as providing possible answers to some puzzles about virtue epistemology. The extent to which Duhem holds that the intellectual and moral virtues of the scientist determine scientific knowledge has not been generally noticed.     

Genetic studies of diseases

Pancreatitis is usually inflammation of the pancreas without infection. Our understanding of pancreatitis has been built on autopsy studies, surgical biopsies and surrogate markers of inflammation and fibroses, including abdominal imaging techniques and pancreatic functional studies. However, the discovery that a number of different environmental factors and various genetic abnormalities are seen in patients with similar appearing pancreatitis phenotypes teaches us that end-stage pathology is not the disorder. Understanding complex associations and interactions requires that the components and their interactions be organized, stratified and functionally defined. Systems biology, in the broad sense, provides the approach and tools to define the complex mechanisms driving pathology. As the mathematics behind these pathways and mechanisms are defined and calibrated, the potential pathology of patients with early signs of disease can be predicted, and a number of patient-specific targets for intervention can be defined.