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Purpose: In previous studies, higher levels of oxidized low-density lipoprotein (ox-LDL) have been reported to increase the risk of cardiovascular disease. Furthermore, the anti-oxidative properties of red wine have been invoked to explain the paradox of low cardiovascular mortality, in spite of high-fat intake, in the French population. However, the distribution of ox-LDL-antibodies (ox-LDL-Ab) in the unselected population and its relationship with red wine consumption are unknown. This study was carried out to identify factors associated with ox-LDL-Ab, with particular emphasis on the association with wine consumption.Methods: We performed a cross-sectional study of 551 unselected, community-dwelling older adults (aged 65 to 94 years) living in Dicomano (Italy). Ox-LDL-Ab titre was measured with an ELISA method.Results: In the whole study sample, ox-LDL-Ab increased with age and was unrelated to blood lipids, HbA(1c), and smoking habit. A significant inverse relationship was found between ox-LDL-Ab titre and daily wine intake, which persisted after adjusting for possible confounders or in subgroup analyses of participants who reported to drink wine or were free from significant morbidity.Conclusions: These results suggest that wine affects ox-LDL-Ab titre in older populations, possibly because of its antioxidant properties. [ABSTRACT FROM AUTHOR]

Previous findings demonstrated that haplotype B of CST3, the gene coding for cystatin C, is a recessive risk factor for late-onset Alzheimer's disease (AD; Finckh, U., von der Kammer, H., Velden, J., Michel, T., Andresen, B., Deng, A., Zhang, J., Muller-Thomsen, T., Zuchowski, K., Menzer, G., Mann, U., Papassotiropoulos, A., Heun, R., Zurdel, J., Holst, F., Benussi, L., Stoppe, G., Reiss, J., Miserez, A.R., Staehelin, H.B., Rebeck, G.W., Hyman, B.T., Binetti, G., Hock, C., Growdon, J.H., Nitsch, R.M., 2000. Genetic association of the cystatin C gene with late-onset Alzheimer disease. Arch. Neurol. 57, 1579-1583). In the present multicentric electroencephalographic (EEG) study, we analyzed the effects of CST3 haplotypes on resting cortical rhythmicity in subjects with AD and mild cognitive impairment (MCI) with the hypothesis that sources of resting EEG rhythms are more impaired in carriers of the CST3 B haplotype than non-carriers. We enrolled a population of 84 MCI subjects (42% with the B haplotype) and 65 AD patients (40% with the B haplotype). Resting eyes-closed EEG data were recorded in all subjects. EEG rhythms of interest were delta (2-4 Hz), theta (4-8 Hz), alpha 1 (8-10.5 Hz), alpha 2 (10.5-13 Hz), beta 1 (13-20 Hz), and beta 2 (20-30 Hz). EEG cortical sources were estimated by low-resolution brain electromagnetic tomography (LORETA). Results showed that the amplitude of alpha 1 (parietal, occipital, temporal areas) and alpha 2 (occipital area) was statistically lower in CST3 B carriers than non-carriers (P < 0.01). Whereas there was a trend towards statistical significance that amplitude of occipital delta sources was stronger in CST3 B carriers than in non-carriers. This was true for both MCI and AD subjects. The present findings represent the first demonstration of relationships between the AD genetic risk factor CST3 B and global neurophysiological phenotype (i.e., cortical delta and alpha rhythmicity) in MCI and AD subjects, prompting future genotype-EEG phenotype studies for the early prediction of AD conversion in individual MCI subjects.

Objective: To evaluate the correlation between antinucleosome antibodies and disease activity in patients with systemic lupus erythematosus (SLE)., Methods: We evaluated antinucleosome antibodies (by ELISA) in 48 SLE patients. They were divided in 2 groups: positive (Group A, nr = 18) and negative (Group B, nr=30). The groups were evaluated for antinucleosome antibodies and for clinical, humoral parameters (hemoglobin, blood cell count, urinanalysis, ESR, ANA, anti-dsDNA, anticardiolipin antibodies, LAC), and ECLAM., Results: C3,C4, and hemoglobin were lower in Group A than (vs) group B (C3: 0.61 +/- 0.16 g/L vs 0.88 +/- 0.08 g/L, p < 0.001; C4: 0.086 +/- 0.03 g/L vs 0.18 +/- 0.07 g/L, p < 0.05; hemoglobin: 8.7 +/- 5.8 g/dL vs 12.7 +/- 1.44 g/dL; p < 0.02). ECLAM was higher in group A 7.56 +/- 2.19 vs group B 4.67 +/- 1.35 (p < 0.001). Urinary sediment was more altered in group A (88.8%) vs group B (33.3%; p < 0.001)., Conclusion: We found a correlation between antinucleosome antibodies and SLE disease activity as expressed by the higher ECLAM score in group A.

Serum substance P was assayed in rheumatoid arthritis patients and healthy controls to evaluate whether neurogenic inflammation with substance P release is significant in rheumatoid arthritis. A very sensitive competitive immunoenzymetric assay was used. Mean serum substance P level was significantly higher in rheumatoid arthritis patients than in controls and was not correlated with disease duration, morning stiffness duration, Thompson's articular index, Larsen's radiographic score, or the following laboratory indices of inflammation: erythrocyte sedimentation rate, C-reactive protein, and alpha 1-acid glycoprotein. Neurogenic inflammation with substance P release may contribute significantly to the pathogenesis of rheumatoid arthritis. The absence of correlations between serum substance P and clinical or laboratory indices of inflammation may reflect complex interactions between neurogenic inflammation and other pathogenic mechanisms, which may influence clinical features and laboratory tests in rheumatoid arthritis patients.