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given at an infusion rate of 0 6 ml/hour for periods ranging from 30 minutes to 12 hours. During infusion the rats had free access to pelleted food and water. After the infusion blood was sampled for plasma amylase and lipase measurements and pancreatic tissue samples were excised for light and electron microscopic 1138 on 10 May 2018 by guest. Protected by copyright.

Low back pain (LBP) in children was considered for many years to be a rare condition revealing a serious disease, but in the last two decades, epidemiological studies have shown that the prevalence of nonspecific LBP in children is high. This study was aimed at analyzing the prevalence, severity, consequences and associated factors of LBP in children. A cross-sectional study was undertaken in two preparatory schools in the city of Monastir, Tunisia, in April 2002. This study included a total of 622 children and adolescents--326 females and 296 males--with a mean age of 14 years (range: 11-19 years). They completed the questionnaire in the presence of the physician. For the first 201 questionnaires collected, the corresponding children and adolescents underwent a spine medical examination, with evaluation of pain by visual analog scale if LBP was present. A stepwise logistic regression analysis was carried out to determine the risk factors associated with LBP and chronic LBP. The cumulative lifetime prevalence of LBP was 28.4%. Eight percent of the subjects suffered from chronic LBP. LBP was responsible for 23% of school absenteeism and 29% for sports absenteeism. Medical care requirement was observed in 32.2% and psychological symptoms in 75%. Stepwise logistic regression analysis showed that three factors were associated with LBP: school failure (held back 1 year), odds ratio (OR) =2.6 (95% confidence interval [CI], 1.96-3.44), family history of LBP (parental or sibling LBP), OR=3.80 (95% CI, 2.94-5.92), dissatisfaction with school chair (in height and comfort), OR=3.40 (95% CI, 2.24-5.29). Two factors were associated with chronic LBP: dissatisfaction with school chair, OR=1.62 (95% CI, 1.46-3.32) and football playing, OR=3.07 (95% CI, 2.15-5.10). The prevalence of LBP among Tunisian schoolchildren and adolescents is high. This requires preventive measures and longitudinal studies, which are very important from the standpoint of public health.

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Haemorrhagic mucosal lesions are produced during intestinal ischaemia and after reperfusion probably mediated by oxygen radicals. Oxygen radicals react with cell membrane lipids and induce cell damage by peroxidation and induce accumulation of polymorphonuclear leucocytes in the tissue. The aim ofthe study was to elucidate the involvement of polymorphonuclear leucocytes in postischaemic intestinal damage. Intestinal ischaemia was induced in cats by partial occlusion of the superior mesenteric artery. Samples from the small intestine were excised before and at the end of the two hour hypotensive period as well as 10 minutes and 60 minutes after reperfusion. Conjugated dienes, myeloperoxidase, and the purine metabolites were determined in the samples. The tissue was also examined histologically. Seven cats were treated before reperfusion with a monoclonal antibody (IB4) which inhibits leucocyte adherence to endothelial cells and its subsequent activation. After reperfusion myeloperoxidase activity increased and the ischaemic mucosal lesions worsened significantly. IB4 treatment prevented an increase in posthypotensive myeloperoxidase activity and attenuated the normally observed severe mucosal lesions. We conclude that the severe postischaemic lesions are induced by polymorphonuclear leucocytes. Such mucosal injury may be appreciably reduced by blocking leucocyte adherence with IB4.

Characteristic mucosal lesions develop in the small intestine during ischaemia and hypotension. This tissue damage can be further aggravated in the immediate reperfusion phase, presumably secondary to the generation of oxygen free radicals which have been proposed to be generated in this situation through the hypoxanthine-xanthine oxidase system. This was further investigated in the cat small intestine using a standardized regional intestinal hypotension model in which the effects of allopurinol (a xanthine oxidase inhibitor) were compared to those of an exogenous supply of inosine. The grade of mucosal damage, the nucleotide levels, the concentrations of hypoxanthine, total and oxidized glutathione, and of conjugated dienes were measured in the intestinal tissue. The results indicate that oxygen radicals generated by xanthine oxidase are very important, but not the only significant factor in the small intestinal reperfusion damage.