Recrystallisation behaviour of native and processed waxy maize starch in relation to the molecular characteristics

Molecular characteristics were determined for native waxy maize starch and maize starch modified in different way (by mechanical treatment or/and acid hydrolysis). Recrystallisation behaviour was studied. Methods used in this study were MALLS, HPAEC-PAD, NMR, DSC, SEM, light microscopy. Five starch materials were subjected to storage under the same conditions in the presence of water (70 w/w%). Molecular weight, radius of gyration, initial crystallinity, and degree of polymerisation, degree of branching, chain length distribution profiles, were related to nucleation rate during the recrystallisation process, rate of recrystallisation, thermal stability and amount of obtained crystallinity. This allowed the following connections between the molecular characteristics and kinetic of recrystallisation to be proposed: Amylopectin molecular weight appeared to affect the number of starch crystallites formed and amount of crystallinity but not the stability of the rebuilt crystallites. The stability of rebuilt crystallites can be controlled by degree of polymerization, degree of branching and unit chain length distribution, characteristics which were similar for the starches. A mixture of two starches, with and without crystalline structure in initial state but with molecular weight in same range, were stored and scanned in order to understand possible cocrystallisation effects. (C) 2004 Elsevier Ltd. All rights reserved

Association study of three polymorphisms of the TGF-β1 gene with AD

Objectives: To explore the impact of the -800 and -509 TGF-ß1 promoter polymorphisms and the +25 polymorphism on the risk of occurrence of Alzheimer's disease in a large population of sporadic cases and controls, and on the amyloid ß (Aß) load in the brains of Alzheimer patients. Methods: The TGF-ß1 genotypes of the three polymorphisms were determined in 678 sporadic Alzheimer's disease patients and 667 controls. They were also characterised, along with Aß load, in the brains of 81 necropsy confirmed Alzheimer patients. Results: No significant variations in the distribution of the genotypes and haplotypes were observed between Alzheimer patients and controls, or in the amount of Aß deposition. Conclusions: These results do not suggest an influence of genetic variability at the TGF-ß1 gene locus on the occurrence of Alzheimer's disease

A plantar flexion device exercise programme for patients with peripheral arterial disease: a randomised prospective feasibility study

Objectives: To determine if the use of a plantar flexion device (Step It pedal) in a newly developed exercise programme is of benefit to patients with peripheral arterial disease. Design: Prospective feasibility trial with patients randomised to either standard care or the Step It exercise programme plus standard care. Setting: Physiotherapy Department at Cumberland Infirmary, Carlisle, UK. Participants: Patients were identified from the vascular team's referral list. In total, 42 patients agreed to take part; 18 in the control group and 24 in the intervention group. Interventions: Eligible participants were randomised and received either standard care or took part in a plantar flexion resistance exercise programme, involving the Step It pedal, for a period of 12 weeks. Main outcome measures: Maximum walking distance, claudication distance and ankle brachial pressure index. Results: Eighty-three percent of patients completed the study. Improvements in median distance to claudication symptoms and maximum walking distance were observed in the intervention group but not in the control group. Nine out of 15 (60%) participants in the control group and 14 out of 20 (70%) participants in the intervention group improved their walking distance. Ankle brachial pressure index remained virtually unchanged in both groups. Conclusions: Due to the variability of patients' fitness in the sample, it cannot be concluded whether use of the Step It pedal has additional benefits to patients over standard care. However, the study completion rate implies that patients with peripheral arterial disease are receptive to undertaking exercise programmes

Association of 3'-UTR polymorphisms of the oxidised LDL receptor 1 (OLR1) gene with Alzheimer's disease

Although possession of the ε4 allele of the apolipoprotein E gene appears to be an important biological marker for Alzheimer's disease (AD) susceptibility, strong evidence indicates that at least one additional risk gene exists on chromosome 12. Here, we describe an association of the 3'-UTR +1073 C/T polymorphism of the OLR1 (oxidised LDL receptor 1) on chromosome 12 with AD in French sporadic (589 cases and 663 controls) and American familial (230 affected sibs and 143 unaffected sibs) populations. The age and sex adjusted odds ratio between the CC+CT genotypes versus the TT genotypes was 1.56 (p=0.001) in the French sample and 1.92 (p=0.02) in the American sample. Furthermore, we have discovered a new T/A polymorphism two bases upstream of the +1073 C/T polymorphism. This +1071 T/A polymorphism was not associated with the disease, although it may weakly modulate the impact of the +1073 C/T polymorphism. Using 3'-UTR sequence probes, we have observed specific DNA protein binding with nuclear proteins from lymphocyte, astrocytoma, and neuroblastoma cell lines, but not from the microglia cell line. This binding was modified by both the +1071 T/A and +1073 C/T polymorphisms. In addition, a trend was observed between the presence or absence of the +1073 C allele and the level of astrocytic activation in the brain of AD cases. However, Aß(40), Aß(42), Aß total, and Tau loads or the level of microglial cell activation were not modulated by the 3'-UTR OLR1 polymorphisms. Finally, we assessed the impact of these polymorphisms on the level of OLR1 expression in lymphocytes from AD cases compared with controls. The OLR1 expression was significantly lower in AD cases bearing the CC and CT genotypes compared with controls with the same genotypes. In conclusion, our data suggest that genetic variation in the OLR1 gene may modify the risk of AD