No abstract

We examined the influence of dietary stable fish oil on aortic thrombosis, platelet aggregation, and superoxide dismutase (SOD) activity in a rat model. Twenty-nine Sprague-Dawley rats were fed regular chow supplemented with stable fish oil preparation (for 1 or 3 weeks), and 37 rats fed regular chow served as controls. The abdominal cavity was opened, and the abdominal aorta isolated. Whatman paper impregnated with 35% FeCl3 was wrapped around the surface of the aorta, and aortic flow was continuously recorded. In control rats, an occlusive platelet-fibrin-rich thrombus was formed in 21 +/- 3 min. Dietary fish oil in a time-dependent fashion delayed time to thrombus formation (24 +/- 2 min in rats fed fish oil for 1 week and 31 +/- 2 min in rats fed fish oil for 3 weeks), inhibited platelet aggregation (21 +/- 5% vs. 45 +/- 6%; p < 0.01) and increased SOD activity (p < 0.01). We conclude that dietary supplementation with stable fish oil delays formation of arterial thrombus, probably by reducing platelet aggregation and oxidative stress-associated arterial injury.

Background: Excessive exposure to club drug gamma-hydroxybutyric acid (GHB) would cause cognitive dysfunction in which impaired Ca 2+ -mediated neuroplasticity in hippocampus may play an essential role in the pathogenesis of this deficiency. Considering melatonin is positive for neuroplastic regulation, the present study aims to determine whether melatonin would exert a neuro-protective effect on cognitive function following GHB. Materials and Methods: Adolescent rats subjected to ten days of GHB (500 mg/kg) and received 10 or 100 mg/kg of melatonin were processed for time-of-flight secondary ion mass spectrometry (TOF-SIMS), quantitative immunohistochemistry, biochemical and radiographic assay, together with Morris water maze to analyze the ionic, neurochemical, bio-energetic, and behavioral effects of melatonin on GHB-induced cognitive dysfunction, respectively. Results: In GHB intoxicated rats, decreased Ca 2+ imaging and depressed Ca 2+ -mediated signaling were detected in hippocampal neurons. The diminished expression of these signaling molecules corresponded well with intense oxidative stress, reduced bio-energetics, and poor performances in cognitive activities. However, in rats received different doses of melatonin during GHB intoxication, all above parameters were gradually returned to nearly normal levels in which the maximal change was detected in animals given the dose of 100 mg/kg. Conclusion:As melatonin effectively preserves cognitive function by saving the hippocampal bio-energetics through maintaining the Ca 2+ -mediated neuroplasticity, therapeutic use of melatonin may thus serve as a promising strategy to improve or counteract cognitive dysfunction induced by drug addiction prevailing in our society nowadays.

On main line railways, bottleneck sections in urban area usually have high intensity traffic flows because of trains converging from different origins through portal junctions. As a result, a small delay to one train can cause long knock-on delays to following trains because of the limit margin time and recovery time in the nominal timetable in bottleneck sections. This paper proposes a cooperative strategy framework for train rescheduling of portal junctions leading into bottleneck sections to decrease the overall delay and recovery from the unpredictable event of disturbances. The strategy is mainly based on an improved Differential Evolution algorithm for the Junction Rescheduling Model (DE-JRM), which is proved to be suitable for solving train rescheduling problems for both individual fly-over junctions and flat junctions.