973 resultados para Neuron count


Relevância:

20.00% 20.00%

Publicador:

Resumo:

"Large paper edition."

Relevância:

20.00% 20.00%

Publicador:

Resumo:

Written in collaboration with Auguste Maquet and possibly P. A. Fiorentino. This edition is limited to one thousand copies. This copy not numbered.

Relevância:

20.00% 20.00%

Publicador:

Resumo:

Mode of access: Internet.

Relevância:

20.00% 20.00%

Publicador:

Resumo:

Reply to Louis Hue Girardin's "Pulaski vindicated from an unsupported charge inconsiderately or malignantly introduced in Judge Johnson's Sketches of the life and correspondence of Major Gen. Nathaniel Greene."

Relevância:

20.00% 20.00%

Publicador:

Resumo:

Mode of access: Internet.

Relevância:

20.00% 20.00%

Publicador:

Resumo:

Thesis (Master's)--University of Washington, 2016-06

Relevância:

20.00% 20.00%

Publicador:

Resumo:

Platelet count is a highly heritable trait with genetic factors responsible for around 80% of the phenotypic variance. We measured platelet count longitudinally in 327 monozygotic and 418 dizygotic twin pairs at 12, 14 and 16 years of age. We also performed a genome-wide linkage scan of these twins and their families in an attempt to localize QTLs that influenced variation in platelet concentrations. Suggestive linkage was observed on chromosome 19q13.13-19q13.31 at 12 (LOD=2.12, P=0.0009), 14 (LOD=2.23, P=0.0007) and 16 (LOD=1.01, P=0.016) years of age and multivariate analysis of counts at all three ages increased the LOD to 2.59 (P=0.0003). A possible candidate in this region is the gene for glycoprotein VI, a receptor involved in platelet aggregation. Smaller linkage peaks were also seen at 2p, 5p, 5q, 10p and 15q. There was little evidence for linkage to the chromosomal regions containing the genes for thrombopoietin (3q27) and the thrombopoietin receptor (1q34), suggesting that polymorphisms in these genes do not contribute substantially to variation in platelet count between healthy individuals.

Relevância:

20.00% 20.00%

Publicador:

Resumo:

Background: Eosinophils are granulocytic white blood cells implicated in asthma and atopic disease. The degree of eosinophilia in the blood of patients with asthma correlates with the severity of asthmatic symptoms. Quantitative trait loci (QTL) linkage analysis of eosinophil count may be a more powerful strategy of mapping genes involved in asthma than linkage analysis using affected relative pairs. 1 Objective: To identify QTLs responsible for variation in eosinophil count in adolescent twins. Methods: We measured eosinophil count longitudinally in 738 pairs of twins at 12, 14, and 16 years of age. We typed 757 highly polymorphic microsatellite markers at an average spacing of similar to5 centimorgans across the genome. We then used multipoint variance components linkage analysis to test for linkage between marker loci and eosinophil concentrations at each age across the genome. Results: We found highly significant linkage on chromosome 2q33 in 12-year-old twins (logarithm of the odds = 4.6; P = .000002) and suggestive evidence of linkage in the same region in 14-year-olds (logarithm of the odds = 1.0; P = .016). We also found suggestive evidence of linkage at other areas of the genome, including regions on chromosomes 2, 3, 4, 8, 9, 11, 12, 17, 20, and 22. Conclusion: A QTL for eosinophil count is present on chromosome 2q33. This QTL might represent a gene involved in asthma pathophysiology.