Purpose – This paper aims to determine the nutritional profile of popular takeaway meals in the UK. Fast food has a poor nutritional profile; research has focused on the major catering chains, with limited data on takeaway food from independent establishments. Design/methodology/approach – Random samples of takeaway meals were purchased from small, independent takeaway establishments. Multiple samples of 27 different takeaway meals, from Indian, Chinese, kebab, pizza and English-style establishments (n = 489), were analysed for portion size, energy, protein, carbohydrate, total fat, salt and total sugars. Findings – Takeaway meals were inconsistent with UK dietary recommendations; pizzas revealed the highest energy content, and Chinese meals were lowest in total fat. However, there was a high degree of variability between and within categories, but the majority of meals were excessive for portion size, energy, macronutrients and salt. Research limitations/implications – The present study focused on energy, macronutrients, salt and total sugars. Future research should analyse the quality of fat and carbohydrates and micronutrients to provide a more detailed nutritional profile of takeaway food. Practical implications – The nutritional variability between establishments suggests that recipe reformulation should be explored in an attempt to improve the nutritional quality of takeaway foods. In addition, portion size reduction could favour both the consumer and the industry. Social implications – Takeaway outlets do not provide nutritional information; due to the excessive nutritional profiles, regular intake may increase the risk of non-communicable disease. Therefore, there is a pressing need for this provision to help consumers make conscious food choices. Originality/value – This is the first study to analyse energy and macronutrient content of independent takeaway meals in the UK.
Analysis of seven strains designated as Rickettsia conorii for reactivity with a panel of 12 monoclonal antibodies to surface-protein epitopes of spotted fever group rickettsiae and by Western immunoblotting with standard serotyping sera revealed remarkable antigenic diversity. Rickettsial strains from France, Morocco, Ethiopia, Kenya, South Africa, India, and the USSR differed from one another in reactivity with at least one and as many as five monoclonal antibodies. Simko and Indian strains were similar to one another and differed substantially from other R. conorii strains. All seven strains reacted with three R. conorii-specific monoclonal antibodies. Western immunoblotting demonstrated a major 120-kD protein and a major 135-kD protein in all strains. The principal differences were the presence of a major undenatured 130-kD protein in all strains except Indian and Simko, which had an analogous protein of 124 kD. Immunodominant antigenically related, heat-denatured protein bands of 170 kD (Malish 7 strain), 175 kD (Manuel strain), and 190 kD (Kenya tick typhus, Indian, and Simko strains) were not detected in the M-1 and Moroccan strains. This antigenic diversity is greater than that previously reported for other spotted fever group rickettsial species, suggesting that R. conorrii is an older species than R. rickettsii with a longer period of time for evolutionary divergence.
Objective-To establish criteria for the diagnosis of medium chain acyl-CoA dehydrogenase (MCAD) deficiency in the UK population using a method in which carnitine species eluted from blood spots are butylated and analysed by electrospray ionisation tandem mass spectrometry (ESI-MS/MS). 38-1.0 µM). However, the free carnitine concentrations were reduced (< 20 µM) in the patients with MCAD deficiency but normal in the heterozygotes. Conclusions-Criteria for the diagnosis of MCAD deficiency using ESI-MS/MS must take account of age and carnitine depletion. If screening is undertaken at 7-10 days, the number of false positive and negative results should be negligible. Because there have been no instances of death or neurological damage following diagnosis of MCAD deficiency in our patient group, a strong case can be made for neonatal screening for MCAD deficiency in the UK. (Arch Dis Child 1998;79:109-115) Design-Four
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