Story

I parked the car and started toward the house. My heart was pounding harder now, and my chest ached..

Causality between Energy Consumption and GDP: Evidence from 30 OECD and 78 Non-OECD Countries

Energy arguably plays a vital role in economic development. Hence many studies have attempted to test for causality between energy and economic growth; however, no consensus has emerged. This paper, therefore, tests for causality between energy and GDP using a consistent data set and methodology for 30 OECD and 78 non-OECD countries. Causality from aggregate energy consumption to GDP and GDP to energy consumption is found to be more prevalent in the developed OECD countries compared to the developing non-OECD countries; implying that a policy to reduce energy consumption aimed at reducing emissions is likely to have greater impact on the GDP of the developed rather than the developing world.Energy; GDP; Development; Causality; Modelling

Floor Plan by Richard M. Hunt for Ogden Goelet

https://digitalcommons.salve.edu/goelet-new-york/1060/thumbnail.jp

An examination of the effects of thalamic lesions on learning and memory in the rat

The study examined the effects of lesions of the thalamic nucleus medialis dorsalis (MD) made by neurotoxin in three cohorts ofrats to help understand the contribution of this nucleus to learning and memory. The lesions typically provided comprehensive damage to . MD, while the use of an excitotoxin helped to minimise damage to fibres of passage or adjacent fibre tracts. This excluded one confounding influence that may have been present in some previous studies. Some MD lesions also affected the anterior thalamic nuclei, and this additional damage led to spatial memory impairments, helping to confirm the value of results from rats with lesions confined to MD. Whilst the groups with MD lesions were largely unimpaired on non-spatial tests of visual recognition and discrimination, they were impaired on a configural discrimination task. The MD lesions did not impair spatial nonmatching to sample in aT-maze, nor the acquisition or performance over delay conditions of the standard radial maze task. There were impairments, however, when the radial maze was rotated during the delay, requiring a strategy shift. Similar impairment was found when a matching, rather than non-matching, strategy was required on the T-maze task and also when only some arms were rewarded on the radial arm maze task for reference memory measurement. No impairment was seen when the T-maze matching task was reversed to the non-matching variant, emphasising the lesion rats' preference for preexisting rules. In addition, some evidence was found that MD lesions brought about increased activity, but had no effect on conditioned place preference. The study concludes that MD damage in rats does not directly cause memory deficits. The influence that MD damage has on memory is, however, similar to that associated with damage to prefrontal cortex causing deficits in rule-switching ability, a higher order frontal lobe function

Medial Dorsal Thalamic Lesions and Working Memory in the Rat

Pigmented rats of the DA strain with either radio frequency or ibotenic acid lesions of the thalamic nucleus medialis dorsalis were postoperatively given non-spatial and spatial tests of working memory. In the non-spatial task, delayed non-matching to sample, rats with both types of thalamic lesions showed acquisition impairmnts. The subgroup of rats with nucleus medialis dorsalis lesions that were able to reach the acquisition criterion did, however, perform normally when the retention interval was extended to 60 seconds and when proactive interference was increased. A final, control variant of this task was included to address the possibility of a sensory deficit. In the spatial task, delayed forced alternation, rats were tested with differing retention intervals and with both spaced and massed trials. Damage to nucleus medialis dorsalis had no effect on acquisition or on spaced trials, but a slight deficit was found in the animals with radio frequency lesions under the massed trial condition. Much clearer deficits were, however, present in those animals in which the lesion extended appreciably into the anterior thalamic nuclei. The findings indicate that while cellular damage to nucleus medialis dorsalis may disrupt learning, some impairments in tests of spatial working memory attributed to this nucleus may reflect damage to the adjacent anterior thalamic nuclei