Effect of chronic intoxication with (+)-amphetamine on its concentration in liver and brain and on (14C) leucine incorporation into microsomal and cytoplasmic proteins of rat liver

Rats were treated with increasing concentrations of (+)-amphetamine sulphate in drinking water for 90 days. The ingested dose of amphetamine was found to increase from 16 mg kg^?1 on the first day up to 90 mg kg^?1 on the 32nd day of treatment. The rats were maintained on the highest dose regime for a further 58 days without any deaths, which showed that tolerance to the overall toxicity of the drug developed. The concentrations of [³H]amphetamine in liver and brain of chronically treated rats were significantly higher than those of controls. Chronic treatment with amphetamine significantly reduced body and liver weight of rats, but did not influence the relative liver to body weight. A marked inhibition of [¹⁴C]leucine incorporation into liver microsomal and cytoplasmic proteins was observed after 90 days of treatment with amphetamine. The relation between inhibition of microsomal protein synthesis and the increase of amphetamine concentrations in liver and brain is discussed.     

The role of gluten, milk, and other dietary proteins in chronic or intermittent dyspepsia

In twenty-seven patients with chronic or intermittent dyspepsia raised levels of the gamma-M-globulin and of the α₁- and of the α₂-globulin were encountered. Malabsorption, present in about three-quarters of the cases, was usually mild. Various degrees of villous abnormalities were seen but no flat mucosa. Eight patients also had dermatitis. During dietary treatment with the elimination of gluten, milk, or other food elements the dyspepsia and the malabsorption subsided in all but two, and the dermatitis in all but one. In nearly all the investigated cases the raised levels of the gamma-M-globulin and of the α₁- and of the α₂-globulin decreased. During challenge feeding with the offending food the dyspepsia and the dermatitis reappeared. Also the faecal fat excretion increased again, and a rise was noticed in the α₁- and in the α₂-globulins and in the gamma-M-globulins. The findings suggest that gluten, milk and other dietary proteins may play a role in some chronic dyspepsias by exerting an antigenic stimulus on the small intestinal mucosa, and thus inducing a state of hypersensitivity towards these foods. The clinical and laboratory findings favour the view that the condition is different from coeliac disease     

Timing of surgery following spinal cord injury

BACKGROUND: The optimal timing for surgical intervention after traumatic spinal injuries with spinal cord injury remains unclear. DESIGN: Literature review. FINDINGS: Multiple laboratory investigations (in animal models) and many clinical studies suggest better neurological outcomes with early surgical intervention. Conclusive evidence (well-designed randomized, controlled studies), however, is lacking, partly due to the logistics involved in executing such an investigation. Early surgery also appears to decrease the incidence of complications, reduces hospital stay, and helps reduce costs associated with acute management. CONCLUSION: Early surgical treatment is beneficial in terms of reducing complications, length of stay, and hospital costs. Further studies are needed to clearly demonstrate the impact of operative timing on neurological outcome.     

New haplotype for the Glu104Asp mutation in triose-phosphate isomerase deficiency and prenatal diagnosis in a Spanish family

Summary First-trimester prenatal diagnosis was undertaken by chorionic villus DNA analysis in a Spanish family with the inherited Glu104Asp triose-phosphate isomerase deficiency. The fetus was heterozygous for the mutation and therefore predicted to be clinically unaffected. To investigate the evolutionary origin of this mutation, studies were conducted on the intragenic 2262A/G polymorphism and the CD4 pentameric tandem repeat marker. A different haplotype was found to the one previously described, suggesting a different origin of the Spanish mutation.