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Julianne S. Collins Lindy E. Harrell Ronald T. Acton Rodney C.P. Go 《American journal of medical genetics. Part A》2001,105(4):332-342
Alzheimer disease (AD) is an emotionally devastating and exceptionally costly disease. Apolipoprotein E (APOE) is a major risk factor gene for AD regardless of age of onset or family history. However, this association may not be as strong or consistent in ethnic groups such as African Americans, raising the possibility of other modifier gene(s). In a group of African American AD patients, a significantly increased risk of AD was associated with two E4 alleles (OR = 5.6; 95% CI = 1.5–21.0) or one E4 allele (OR = 2.5; 95% CI = 1.3–5.0) when compared to E3/E3 genotype, and there was a significant lowering of age of onset for affecteds with E4/E4 genotype as compared to one E2 allele (P = 0.02) or all others (P = 0.03). We also found a significant increase in age of onset with the ?308 #2 (A) allele of TNF when compared to AD cases with no #2 allele. A significant increase in age was also demonstrated with the #2 allele (99 base pairs) of the microsatellite TNFa, located ~ 10.5 kb upstream of TNF. When these two alleles were combined with the TNF ?238G (#1) allele to give a haplotype, the significant increase in age was still demonstrated. Polymorphisms in the APOE promoter and six other candidate genes did not appear to demonstrate any significant association with our African American AD patients. Our results confirm the established association of APOE4 to AD observed in several ethnic groups, including African Americans. In addition, TNF appears to have some modifying effect in AD, primarily on age of onset, or it could be in linkage disequilibrium with a modifier locus nearby. © 2001 Wiley‐Liss, Inc. 相似文献
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Blacker D Bertram L Saunders AJ Moscarillo TJ Albert MS Wiener H Perry RT Collins JS Harrell LE Go RC Mahoney A Beaty T Fallin MD Avramopoulos D Chase GA Folstein MF McInnis MG Bassett SS Doheny KJ Pugh EW Tanzi RE;NIMH Genetics Initiative Alzheimer's Disease Study Group 《Human molecular genetics》2003,12(1):23-32
Alzheimer's disease (AD) is a devastating neurodegenerative disorder of late life with complex inheritance. Mutations in three known genes lead to the rare early-onset autosomal dominant form of AD, while a common polymorphism (epsilon 4) in the gene encoding apolipoprotein E (APOE ) is a risk factor for more typical late-onset (>60 years) AD. A recent study concluded that there are up to four additional genes with an equal or greater contribution to the disease. We performed a 9 cM genome screen of 437 families with AD, the full National Institute of Mental Health (NIMH) sample, which has been carefully ascertained, evaluated and followed by our group over the last decade. Performing standard parametric and non-parametric linkage analyses, we observed a 'highly significant' linkage peak by Lander and Kruglyak criteria on chromosome 19q13, which probably represents APOE. Twelve additional locations-on 1q23, 3p26, 4q32, 5p14, 6p21, 6q27, 9q22, 10q24, 11q25, 14q22, 15q26 and 21q22-met criteria for 'suggestive' linkage [i.e. two-point lod score (TLS) >/=1.9 and/or multipoint lod score (MLS) >/=2.2] in at least one of our analyses. Although some of these will surely prove to be false positives, these linkage signals should provide a valuable framework for future studies aimed at identifying additional susceptibility genes for late-onset AD. 相似文献
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Franks CJ Pemberton D Vinogradova I Cook A Walker RJ Holden-Dye L 《Journal of neurophysiology》2002,87(2):954-961
The pharynx of C. elegans is a rhythmically active muscle that pumps bacteria into the gut of the nematode. This activity is maintained by action potentials, which qualitatively bear a resemblance to vertebrate cardiac action potentials. Here, the ionic basis of the resting membrane potential and pharyngeal action potential has been characterized using intracellular recording techniques. The resting membrane potential is largely determined by a K(+) permeability, and a ouabain-sensitive, electrogenic pump. As previously suggested, the action potential is at least partly dependent on voltage-gated Ca(2+) channels, as the amplitude was increased as extracellular Ca(2+) was increased, and decreased by L-type Ca(2+) channel blockers verapamil and nifedipine. Barium caused a marked prolongation of action potential duration, suggesting that a calcium-activated K(+) current may contribute to repolarization. Most notably, however, we found that action potentials were abolished in the absence of external Na(+). This may be due, at least in part, to a Na(+)-dependent pacemaker potential. In addition, the persistence of action potentials in nominally free Ca(2+), the inhibition by Na(+) channel blockers procaine and quinidine, and the increase in action potential frequency caused by veratridine, a toxin that alters activation of voltage-gated Na(+) channels, point to the involvement of a voltage-gated Na(+) current. Voltage-clamp analysis is required for detailed characterization of this current, and this is in progress. Nonetheless, these observations are quite surprising in view of the lack of any obvious candidate genes for voltage-gated Na(+) channels in the C. elegans genome. It would therefore be informative to re-evaluate the data from these homology searches, with the aim of identifying the gene(s) conferring this Na(+), quinidine, and veratridine sensitivity to the pharynx. 相似文献
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Extractability of Cell Wall Polysaccharide from Lactobacilli and Streptococci by Autoclaving and by Dilute Acid
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Autoclaving cell wall of Streptococcus mutans Ingbritt for 15 min under the Rantz and Randall conditions released one-tenth of the total cell wall carbohydrate, whereas two-thirds was extracted after autoclaving for 180 min. The extract contained the serotype c-specific antigen but lacked the lipoteichoic acid component extracted when whole cells were autoclaved. Autoclaving cell wall preparations from other strains of S. mutans and also Streptococcus salivarius and Streptococcus mitis in 0.85% NaCl for 180 min released the major proportion of the wall polysaccharide fraction. Approximately 50 to 90% of wall carbohydrate of Lactobacillus fermentum and Lactobacillus casei was released when cell wall preparations were autoclaved in 0.85% NaCl for 180 min. For wall preparations from several strains of S. mutans, autoclaving for 60 min at pH 3.75 released only 39 to 62% of wall carbohydrate, whereas almost total release could be achieved with the lactobacilli. Heating S. mutans Ingbritt cell wall for 24 h at 60 degrees C in 0.1 N H(2)SO(4) released only two-thirds of the wall carbohydrate; by comparison nearly all of the wall carbohydrate was released in 3 h from L. casei and L. fermentum. Autoclaving L. casei cell wall and purified soluble wall fractions hydrolyzed the phosphodiester bond between the polysaccharide and peptidoglycan. This was shown by the release of reactive N-acetylhexosamine in both cases and the presence of a phosphomonoester in the autoclaved soluble wall fractions. The results indicate that autoclaving can hydrolyze covalent linkages, and this must be considered when the Rantz and Randall procedure is used to obtain antigen preparations. 相似文献
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Induced recruitment of NK cells to lymph nodes provides IFN-gamma for T(H)1 priming 总被引:13,自引:0,他引:13
Martín-Fontecha A Thomsen LL Brett S Gerard C Lipp M Lanzavecchia A Sallusto F 《Nature immunology》2004,5(12):1260-1265
Naive T cells are stimulated by antigen-presenting dendritic cells (DCs) in secondary lymphoid organs, but whether other types of cell participate in T cell priming is unclear. Here we show in mice that natural killer (NK) cells, which are normally excluded from lymph nodes, are rapidly recruited in a CCR7-independent, CXCR3-dependent manner to lymph nodes on stimulation by the injection of mature DCs. Recruitment of NK cells is also induced by some, but not all, adjuvants and correlates with the induction of T helper cell type 1 (T(H)1) responses. NK cell depletion and reconstitution experiments show that NK cells provide an early source of interferon-gamma (IFN-gamma) that is necessary for T(H)1 polarization. Taken together, our results identify an induced pathway of NK cell migration in antigen-stimulated lymph nodes and a mechanism by which some adjuvants may facilitate T(H)1 responses. 相似文献