Your search: "author:"Nelson, B""
Peer-reviewed only (35)
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Scholarly Works (38 results)
HIGH-LEVEL SPILL AT THE HILAC
Garden, Nelson B.
Dailey, Carroll.
THE FABRICATION OF RADIOACTIVE SOURCES
Salo, Albert E.
A genome-wide survey of segmental duplications that mediate common human genetic variation of chromosomal architecture
Mehan, Michael R
Freimer, Nelson B
Ophoff, Roel A
Abstract Recent studies have identified a small number of genomic rearrangements that occur frequently in the general population. Bioinformatics tools are now available for systematic genome-wide surveys of higher-order structures predisposing to such common variations in genomic architecture. Segmental duplications (SDs) constitute up to 5 per cent of the genome and play an important role in generating additional rearrangements and in disease aetiology. We conducted a genome-wide database search for a form of SD, palindromic segmental duplications (PSDs), which consist of paired, inverted duplications, and which predispose to inversions, duplications and deletions. The survey was complemented by a search for SDs in tandem orientation (TSDs) that can mediate duplications and deletions but not inversions. We found more than 230 distinct loci with higher-order genomic structure that can mediate genomic variation, of these about 180 contained a PSD. A number of these sites were previously identified as harbouring common inversions or as being associated with specific genomic diseases characterised by duplication, deletions or inversions. Most of the regions, however, were previously unidentified; their characterisation should identify further common rearrangements and may indicate localisations for additional genomic disorders. The widespread distribution of complex chromosomal architecture suggests a potentially high degree of plasticity of the human genome and could uncover another level of genetic variation within human populations.
Phenomenological aspects of heterotic orbifold models at one loop
Birkedal-Hansen, A.
Binetruy, P.
Mambrini, Y.
Nelson, B.
Lawrence Berkeley National Laboratory (2003)
INVESTIGATION OF WINDOWS AND SHIELDS FOR NEUTRON POINT SOURCES
Browne, Howard J.
Kaufmann, John A.
The molecular signatures of bipolar disorder and lithium treatment
Krebs, Catharine Elizabeth
UCLA Electronic Theses and Dissertations (2018)
Bipolar disorder (BD) is a highly heritable mood disorder with a complex genetic architecture. It is commonly treated prophylactically with the mood stabilizer lithium, although treatment responses vary widely across patients. Both how BD genetic variants confer risk and the molecular mechanisms underlying lithium's therapeutic effects remain poorly understood. This dissertation begins with a review of recent findings from BD and lithium-response genetic studies and from BD and lithium treatment transcriptomic studies. This review will show that while presenting an opportunity to learn valuable information about underlying biology, gene expression studies investigating these phenotypes have had low sample sizes and inconsistent findings. Then, an original study attempting to fill this gap by exploring the whole blood transcriptome in a large BD case-control RNA sequencing sample is reported on. In this study, strong effects of lithium treatment and cell-type composition were revealed, pointing to potential therapeutic mechanisms of lithium, and underlining the importance of carefully correcting for these variables. To put these findings in the context of the current understanding of BD etiology and lithium treatment mechanisms, a comparison was made with findings previously reported highlighting a list of high-confidence lithium-associated genes. A gene-set analysis comparing genes with differential expression to genes implicated from major psychiatric genome-wide association studies revealed that the observed gene expression changes were unrelated to genetic risk. The findings herein contribute to the current understanding of the BD transcriptome in whole blood and provide evidence for the mechanistic actions of lithium treatment.
A comparison of echocardiography to invasive measurement in the evaluation of pulmonary arterial hypertension in a rat model
Koskenvuo, Juha W.
Mirsky, Rachel
Angeli, Franca S.
Jahn, Sarah
Alastalo, Tero-Pekka
Schiller, Nelson B.
Boyle, Andrew J.
Chatterjee, Kanu
Marco, Teresa
Yeghiazarians, Yerem
Pulmonary arterial hypertension (PAH) is a life-threatening condition characterized by progressive elevation in pulmonary artery pressure (PAP) and total pulmonary vascular resistance (TPVR). Recent advances in imaging techniques have allowed the development of new echocardiographic parameters to evaluate disease progression. However, there are no reports comparing the diagnostic performance of these non-invasive parameters to each other and to invasive measurements. Therefore, we investigated the diagnostic yield of echocardiographically derived TPVR and Doppler parameters of PAP in screening and measuring the severity of PAH in a rat model. Serial echocardiographic and invasive measurements were performed at baseline, 21 and 35 days after monocrotaline-induction of PAH. The most challenging echocardiographic derived TPVR measurement had good correlation with the invasive measurement (r = 0.92, P < 0.001) but also more simple and novel parameters of TPVR were found to be useful although the non-invasive TPVR measurement was feasible in only 29% of the studies due to lack of sufficient tricuspid valve regurgitation. However, echocardiographic measures of PAP, pulmonary artery flow acceleration time (PAAT) and deceleration (PAD), were measurable in all animals, and correlated with invasive PAP (r = −0.74 and r = 0.75, P < 0.001 for both). Right ventricular thickness and area correlated with invasive PAP (r = 0.59 and r = 0.64, P < 0.001 for both). Observer variability of the invasive and non-invasive parameters was low except in tissue-Doppler derived isovolumetric relaxation time. These non-invasive parameters may be used to replace invasive measurements in detecting successful disease induction and to complement invasive data in the evaluation of PAH severity in a rat model.
Whole-genome sequencing of individuals from a founder population identifies candidate genes for asthma
Burchard, Esteban
Campbell, CD
Mohajeri, K
Malig, M
Hormozdiari, F
Nelson, B
Du, G
Patterson, KM
Eng, C
Torgerson, DG
Hu, D
UC San Francisco Previously Published Works (2014)
Asthma is a complex genetic disease caused by a combination of genetic and environmental risk factors. We sought to test classes of genetic variants largely missed by genome-wide association studies (GWAS), including copy number variants (CNVs) and low-fre
Alternating hemiplegia of childhood: Retrospective genetic study and genotype-phenotype correlations in 187 subjects from the US AHCF registry
Ptacek, Louis
Viollet, L
Glusman, G
Murphy, KJ
Newcomb, TM
Reyna, SP
Sweney, M
Andermann, F
Andermann, E
Acsadi, G
© 2015 Viollet et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
Associations of Menopausal Vasomotor Symptoms with Fracture Incidence
Crandall, Carolyn J
Aragaki, Aaron
Cauley, Jane A
Manson, JoAnn E
LeBlanc, Erin
Wallace, Robert
Wactawski-Wende, Jean
LaCroix, Andrea
O'Sullivan, Mary Jo
Vitolins, Mara
Watts, Nelson B