ND was considered present if the patient misread or omitted the left portion of the word in three or more of the 25 target words. CN was noted in 80/138 (58.0%) patients while ND was found in 31/138 (22.5%) patients. Of the 80 patients with CN, the frequency of neglect based on ND test was only 37.5% while the frequency of neglect based on other neglect tasks ranged from 51.3% to 86.3%. The severity of neglect
was a significant predictor for ND. VFD was also a significant predictor for the occurrence of ND but this effect disappeared when the severity of neglect was controlled. Patients with CN had lesions in the superior and middle temporal gyri, inferior parietal lobule, and posterior insular cortex; patients with ND had additional lesions in the lingual and fusiform gyri. In summary, ND was dissociated from other AZD1480 price types of neglect and was most often associated with severe neglect. VFD contributed to the occurrence of ND. ND resulted
from lesions of temporoparietal junction areas (inferior parietal/superior temporal gyri) combined with those of lingual/fusiform gyri. (C) 2008 Elsevier Ltd. All rights reserved.”
“Background Hyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric acid concentration and gout.
Methods Genome-wide association studies were done for serum uric acid in 7699 participants in the Framingham cohort and in 4148 participants in the Rotterdam cohort. Genome-wide significant selleck compound single selleck kinase inhibitor nucleotide polymorphisms (SNPs) were replicated in white (n=11024) and black (n=3843) individuals who took part in the study of Atherosclerosis Risk in Communities (ARIC). The SNPs that reached genome-wide significant association with uric acid in either the Framingham cohort (p<5.0×10(-8))
or the Rotterdam cohort (p<1.0×10(-7)) were evaluated with gout. The results obtained in white participants were combined using meta-analysis.
Findings Three loci in the Framingham cohort and two in the Rotterdam cohort showed genome-wide association with uric acid. Top SNPs in each locus were: missense rs16890979 in SLC2A9 (p=7.0×10(-168) and 2.9×10(-18) for white and black participants, respectively); missense rs2231142 in ABCG2 (p=2.5×10(-60) and 9.8×10(-4)), and rs17.65205 in SLC17A3 (p=3.3×10(-26) and 0.33). All SNPs were direction-consistent with gout in white participants: rs16890979 (OR 0.59 per T allele, 95% CI 0.52-0.68, p=7.0×10(-14)), rs2231.142 (1.74, 1.51-1.99, p=3.3×10(-15)), and rs1165205 (0.85, 0.77-0.94, p=0.002). In black participants of the ARIC study, rs2231142 was direction-consistent with gout (1.71, 1.06-2.77, p=0.028).