Celtic languages in European Higher Education: CRAMLAP - Celtic, Regional and Minority Languages Abroad Project

The Celtic, Regional and Minority Languages Abroad
Project (CRAMLAP) is funded by the European Commission
to research the provision and pedagogy of regional
and minority languages outside their national borders in
Europe. The teaching of Celtic languages across Europe
was the focus in year one (2003-2004). This article summarizes
the qualitative data received in response to
questionnaires sent to institutions across Europe offering
Celtic Studies. Responses indicated that Celtic Studies
are quite widely available across Europe. The languages
are taught in comparative linguistics, linguistics and English
departments, with few dedicated Celtic departments
or sections outside the Celtic countries. Irish is supported
abroad by Irish government grant aid which will
become more widely available in the immediate future.
Many of the teachers have considerable experience, but
limited pedagogic training. The lack of suitable teaching
resources is the most commonly expressed concern.

Amyloid B-peptide 1-40 increases neuronal membrane fluidity: role of cholesterol and brain region

There is increasing evidence of an interaction between cholesterol dynamics and Alzheimer's disease (AD), and amyloid ß-peptide may play an important role in this interaction. Aß destabilizes brain membranes and this action of Aß may be dependent on the amount of membrane cholesterol. We tested this hypothesis by examining effects of Aß1-40 on the annular fluidity (i.e., lipid environment adjacent to proteins) and bulk fluidity of rat synaptic plasma membranes (SPM) of the cerebral cortex, cerebellum, and hippocampus using the fluorescent probe pyrene and energy transfer. Amounts of cholesterol and phospholipid of SPM from each brain region were determined. SPM of the cerebellum were significantly more fluid as compared with SPM of the cerebral cortex and hippocampus. Aß significantly increased (P 0.01) annular and bulk fluidity in SPM of cerebral cortex and hippocampus. In contrast, Aß had no effect on annular fluidity and bulk fluidity of SPM of cerebellum. The amounts of cholesterol in SPM of cerebral cortex and hippocampus were significantly higher (P 0.05) than amount of cholesterol in SPM of cerebellum. There was significantly less (P 0.05) total phospholipid in cerebellar SPM as compared with SPM of cerebral cortex. Neuronal membranes enriched in cholesterol may promote accumulation of Aß by hydrophobic interaction, and such an interpretation is consistent with recent studies showing that soluble Aß can act as a seed for fibrillogenesis in the presence of cholesterol.

Behavioural and histopathological analyses of ibuprofen treatment on the effect of aggregated AB (1-42) injections in the rat

It has been suggested that inflammatory processes may play a role in the development of Alzheimerâ??s disease (AD), and that nonsteroidal anti-inflammatory drug treatments may provide protection against the onset of AD. In the current study male Wistar rats were trained in two-lever operant chambers under an alternating lever cyclic-ratio ratio (ALCR) schedule. When responding showed no trends, subjects were divided into groups. One group was bilaterally injected into the CA3 area of the hippocampus with 5 μl of aggregated β-amyloid (Aβ) suspension, and one group was bilaterally injected into the CA3 area of the hippocampus with 5 μl of sterile saline. Subgroups were treated twice daily with 0.1 ml (40 mg/kg) ibuprofen administered orally. The results indicated that chronic administration of ibuprofen protected against detrimental behavioural effects following aggregated Aβ injections. Withdrawal of ibuprofen treatment from aggregated Aβ-injected subjects produced a decline in behavioural performance to the level of the non-treated aggregated Aβ-injected group. Ibuprofen treatment reduced the numbers of reactive astrocytes following aggregated Aβ injection, and withdrawal of ibuprofen resulted in an increase of reactive astrocytes. These results suggest that induced inflammatory processes may play a role in AD, and that ibuprofen treatment may protect against some of the symptoms seen in AD.

An operant determination of the behavioural mechanism of benzodiazepine enhancement of food intake

Rationale A recent review paper by Cooper (Appetite 44:133–150, 2005) has pointed out that a role for benzodiazepines as appetite stimulants has been largely overlooked. Cooper’s review cited several studies that suggested the putative mechanism of enhancement of food intake after benzodiazepine administration might involve increasing the perceived pleasantness of food (palatability). Objectives The present study examined the behavioral mechanism of increased food intake after benzodiazepine administration. Materials and methods The cyclic-ratio operant schedule has been proposed as a useful behavioral assay for differentiating palatability from regulatory effects on food intake (Ettinger and Staddon, Physiol Behav 29:455–458, 1982 and Behav Neurosci 97:639–653, 1983). The current study employed the cyclic-ratio schedule to determine whether the effects on food intake of chlordiazepoxide (CDP) (5.0 mg/kg), sodium pentobarbital (5.0 mg/kg), and picrotoxin (1.0 mg/kg) were mediated through palatability or regulatory processes. Results The results of this study show that both the benzodiazepine CDP and the barbiturate sodium pentobarbital increased food intake in a manner similar to increasing the palatability of the ingestant, and picrotoxin decreased food intake in a manner similar to decreasing the palatability of the ingestant. Conclusions These results suggest that the food intake enhancement properties of benzodiazepines are mediated through a mechanism affecting perceived palatability.