Bringing Efficiency In?

The implementation of Research Training Groups (RTG) by the German Research Foundation at the beginning of the 1990 was one of the major steps towards a reform of doctoral education in Germany. A main intention of the RTG was to increase the efficiency of doctoral training. RTG aimed at a lowering of time-to-degree and age-at-graduation, also at achieving a higher degree of transparency as regards the supervision and training of doctoral students. To achieve these goals RTGs were implemented as temporary research units with a focused (interdisciplinary) research and study program at universities. Given this background the paper will compare processes, training conditions of the RTG along the following lines: • As regards efficiency we will have a closer look at the time to the doctorate. • Regards the conditions of doctoral training the RTG will be compared to other forms of doctoral training for those aspects that the RTG tried to change. • Finally, the paper will investigate in the question to what extent different conditions of training and other determinants have contributed to achieve more efficiency in terms of shortening the time to the doctorate. To answer these questions a comparative analysis will be done. The paper will be based on a survey among former doctoral students who pursued their doctorate in Germany during the 1990s. In this survey former members of RTG as well as former doctoral students who were graduating in a different, traditional setting had been integrated. These two groups will be compared. In total individual data from 1,424 doctorates from a wide range of different academic disciplines graduating from their doctoral studies between 1995 and 2000 will be analyze

Dose-dependent changes in neuroinflammatory and arachidonic acid cascade markers with synaptic marker loss in rat lipopolysaccharide infusion model of neuroinflammation

<p>Abstract</p> <p>Background</p> <p>Neuroinflammation, caused by six days of intracerebroventricular infusion of bacterial lipopolysaccharide (LPS), stimulates rat brain arachidonic acid (AA) metabolism. The molecular changes associated with increased AA metabolism are not clear. We examined effects of a six-day infusion of a low-dose (0.5 ng/h) and a high-dose (250 ng/h) of LPS on neuroinflammatory, AA cascade, and pre- and post-synaptic markers in rat brain. We used artificial cerebrospinal fluid-infused brains as controls.</p> <p>Results</p> <p>Infusion of low- or high-dose LPS increased brain protein levels of TNFα, and iNOS, without significantly changing GFAP. High-dose LPS infusion upregulated brain protein and mRNA levels of AA cascade markers (cytosolic cPLA₂-IVA, secretory sPLA₂-V, cyclooxygenase-2 and 5-lipoxygenase), and of transcription factor NF-κB p50 DNA binding activity. Both LPS doses increased cPLA₂ and p38 mitogen-activated protein kinase levels, while reducing protein levels of the pre-synaptic marker, synaptophysin. Post-synaptic markers drebrin and PSD95 protein levels were decreased with high- but not low-dose LPS.</p> <p>Conclusions</p> <p>Chronic LPS infusion has differential effects, depending on dose, on inflammatory, AA and synaptic markers in rat brain. Neuroinflammation associated with upregulated brain AA metabolism can lead to synaptic dysfunction.</p

Dietary Linoleic Acid Lowering Reduces Lipopolysaccharide-Induced Increase in Brain Arachidonic Acid Metabolism

Linoleic acid (LA, 18:2n-6) is a precursor to arachidonic acid (AA, 20:4n-6), which can be converted by brain lipoxygenase and cyclooxygenase (COX) enzymes into various lipid mediators involved in the regulation of brain immunity. Brain AA metabolism is activated in rodents by the bacterial endotoxin, lipopolysaccharide (LPS). This study tested the hypothesis that dietary LA lowering, which limits plasma supply of AA to the brain, reduces LPS-induced upregulation in brain AA metabolism. Male Fischer CDF344 rats fed an adequate LA (5.2&nbsp;% energy (en)) or low LA (0.4&nbsp;% en) diet for 15&nbsp;weeks were infused with LPS (250&nbsp;ng/h) or vehicle into the fourth ventricle for 2&nbsp;days using a mini-osmotic pump. The incorporation rate of intravenously infused unesterified 14C-AA into brain lipids, eicosanoids, and activities of phospholipase A2 and COX-1 and 2 enzymes were measured. Dietary LA lowering reduced the LPS-induced increase in prostaglandin E2 concentration and COX-2 activity (P &lt; 0.05 by two-way ANOVA)&nbsp;without altering phospholipase activity. The 14C-AA incorporation rate into brain lipids was decreased by dietary LA lowering (P &lt; 0.05 by two-way ANOVA). The present findings suggest that dietary LA lowering reduced LPS-induced increase in brain markers of AA metabolism. The clinical utility of LA lowering in brain disorders should be explored&nbsp;in future studies