Learning may provide neuroprotection against dementia

A number of studies attempting to identify specific risk factors for dementia have noted an inverse relationship between educational background and the likelihood of developing dementia. This idea has been somewhat controversial as educational background can introduce a number of confounding factors that generally affect health and lifestyle. Despite these reservations, there is mounting evidence to support the concept of education (or increased mental activity) producing a functional reserve in the brain, a process that provides some protection against the clinical manifestation of dementia. Long-term potentiation (LTP) is a recognized neural correlate of learning and memory. We have shown recently that LTP reduces the sensitivity of hippocampal neurons to agonists of the neurotransmitter glutamate; additionally, we have reported that LTP protects the neurons from the effects of acute hypoxia. Given that the effect of hypoxia on neurons involves over-stimulation by glutamate, and hypoxia has been implicated in the aetio-pathology of some types of dementia, our observations suggest that LTP has a protective effect on neuronal tissue. Such an interaction offers a physiological basis for the epidemiological evidence that lifelong learning can protect a person from some types of dementia.

Neuroprotection by caffeine and pentoxifylline during experimental cerebral ischaemia

Cerebral ischaemia was induced in anaesthetized rats by occlusion of the ipsilateral common carotid and middle cerebral arteries. The response to ischaemia was assessed by the reduction of the amplitude of recorded somatosensory evoked potentials (SSEPs), and the rate of recovery of the SSEPs during reperfusion. Caffeine and pentoxifylline when applied at 70 mM to the cortex for 60 min prior to induction of ischaemia significantly reduced the ischaemia induced attenuation of the SSEPs and hastened recovery to control levels. In contrast, application of normal saline or of the drugs for 15 min did not reduce the effect of ischaemia on the SSEPs. These results suggest that caffeine and pentoxifylline have potential roles in the management of patients with cerebral ischaemia.

Entrance qualifications and student performance in a hybrid problem based and traditional medical programme

A hybrid problem based learning (PBL) and traditional medical programme was started at the Trinidad campus of the University of the West Indies in 1989. Analyses were carried out to determine the extent to which the entrance qualifications of the students were related to their performances at the examinations in the Phase I (preclinical and paraclinical) and Phase II (clinical) programmes. Students who were admitted on the basis of their results in the secondary school General Certificate of Examination (GCE), 'A' level scored higher at the Phase I, but not at the Phase II, level than those who already had university education. Among the 'A' level students, there was positive correlation between the total 'A' level scores and the examination marks in the medical programme, particularly at the Phase I level. Furthermore, multiple regression analyses indicated that the grades in 'A' level Chemistry and, to a lesser extent in Biology, had the most influence on performances at the Phase I examinations, with much less influence on performances at the Phase II examinations. These results suggest that good grades at 'A' level examinations are significant factors, but not the only important ones, that favour high achievement in the initial stages of this type of PBL/traditional medical programme.

Effects of ackee fruit extracts on bronchomotor tone in rats

The unripe ackee fruit, when eaten, is known to cause serious clincial manifestations, including vomitting, hypoglycaemia and acidosis. The effects, of various extracts from the arilli of the unripe ackee fruit (including hypoglycin-A) on the lungs from rats were examined in an in vitro preparation. All the extracts were found to induce moderately severe broncho-constriction, indicating a possible contribution of these effects to the observed toxicity of ackee

A re-examination of the mechanism of ackee-induced vomiting sckness

The hypoglycemia seen in ackee poisoning almost certainly results from the presence of hypoglycin A in the aril. However, the mechanisms underlying the vomiting and neurological disrders have not been properly established. We have, in thes review, re-examined the latter and proposed that the vomiting of glutamic and neurological feactures of ackee poisoning probably result from the excitotoxic properties of glutamic and aspartic acids derived directly and indirectly from ackee intake