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mypubs.bib
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@article{Kurian2014,
abstract = {There are no minimally invasive diagnostic metrics for acute kidney transplant rejection (AR), especially in the setting of the common confounding diagnosis, acute dysfunction with no rejection (ADNR). Thus, though kidney transplant biopsies remain the gold standard, they are invasive, have substantial risks, sampling error issues and significant costs and are not suitable for serial monitoring. Global gene expression profiles of 148 peripheral blood samples from transplant patients with excellent function and normal histology (TX; n = 46), AR (n = 63) and ADNR (n = 39), from two independent cohorts were analyzed with DNA microarrays. We applied a new normalization tool, frozen robust multi-array analysis, particularly suitable for clinical diagnostics, multiple prediction tools to discover, refine and validate robust molecular classifiers and we tested a novel one-by-one analysis strategy to model the real clinical application of this test. Multiple three-way classifier tools identified 200 highest value probesets with sensitivity, specificity, positive predictive value, negative predictive value and area under the curve for the validation cohort ranging from 82\% to 100\%, 76\% to 95\%, 76\% to 95\%, 79\% to 100\%, 84\% to 100\% and 0.817 to 0.968, respectively. We conclude that peripheral blood gene expression profiling can be used as a minimally invasive tool to accurately reveal TX, AR and ADNR in the setting of acute kidney transplant dysfunction.},
author = {Kurian, S M and Williams, a N and Gelbart, T and Campbell, D and Mondala, T S and Head, S R and Horvath, S and Gaber, L and Thompson, R and Whisenant, T and Lin, W and Langfelder, P and Robison, E H and Schaffer, R L and Fisher, J S and Friedewald, J and Flechner, S M and Chan, L K and Wiseman, A C and Shidban, H and Mendez, R and Heilman, R and Abecassis, M M and Marsh, C L and Salomon, D R},
doi = {10/f5xswg},
file = {/Users/ryan/Zotero/storage/BS947RZT/Kurian et al_2014_Molecular Classifiers for Acute Kidney Transplant Rejection in Peripheral Blood.pdf},
issn = {16006135},
journal = {American Journal of Transplantation},
keywords = {abbreviations,abmr,acute,acute dysfunction with no,antibody-mediated rejection,arrays,gene expression profiling,kidney rejection,micro-,molecular classifiers,rejection},
month = may,
number = {5},
pages = {1164-1172},
pmid = {24725967},
title = {Molecular {{Classifiers}} for {{Acute Kidney Transplant Rejection}} in {{Peripheral Blood}} by {{Whole Genome Gene Expression Profiling}}},
volume = {14},
year = {2014}
}
@article{Kurian2017,
abstract = {We performed orthogonal technology comparisons of concurrent peripheral blood and biopsy tissue samples from 69 kidney transplant recipients who underwent comprehensive algorithm-driven clinical phenotyping. The sample cohort included patients with normal protocol biopsies and stable transplant (sTx) function (n = 25), subclinical acute rejection (subAR, n = 23), and clinical acute rejection (cAR, n = 21). Comparisons between microarray and RNA sequencing (RNA-seq) signatures were performed and demonstrated a strong correlation between the blood and tissue compartments for both technology platforms. A number of shared differentially expressed genes and pathways between subAR and cAR in both platforms strongly suggest that these two clinical phenotypes form a continuum of alloimmune activation. SubAR is associated with fewer or less expressed genes than cAR in blood, whereas in biopsy tissues, this clinical phenotype demonstrates a more robust molecular signature for both platforms. The discovery work done in this study confirms a clear ability to detect gene expression profiles for sTx, subAR, and cAR in both blood and biopsy tissue, yielding equivalent predictive performance that is agnostic to both technology and platform. Our data also provide strong biological insights into the molecular mechanisms underlying these signatures, underscoring their logistical potential as molecular diagnostics to improve clinical outcomes following kidney transplantation.},
author = {Kurian, S. M. and Velazquez, E. and Thompson, R. and Whisenant, T. and Rose, S. and Riley, N. and Harrison, F. and Gelbart, T. and Friedewald, J. J. and Charette, J. and Brietigam, S. and Peysakhovich, J. and First, M. R. and Abecassis, M. M. and Salomon, D. R.},
doi = {10/gbp6vr},
file = {/Users/ryan/Zotero/storage/HXYJV6V2/Kurian et al_2017_Orthogonal Comparison of Molecular Signatures of Kidney Transplants With.pdf},
issn = {16006135},
journal = {American Journal of Transplantation},
keywords = {clinical research/practice,diagnostic techniques and imaging,genomics,kidney (allograft) function/dysfunction,kidney transplantation/nephrology,microarray/gene array,rejection: acute,translational research/science},
month = aug,
number = {8},
pages = {2103-2116},
title = {Orthogonal {{Comparison}} of {{Molecular Signatures}} of {{Kidney Transplants With Subclinical}} and {{Clinical Acute Rejection}}: {{Equivalent Performance Is Agnostic}} to {{Both Technology}} and {{Platform}}},
volume = {17},
year = {2017}
}
@article{LaMere2016,
abstract = {The epigenetic determinants driving the responses of CD4 T cells to antigen are currently an area of active research. Much has been done to characterize helper T-cell subsets and their associated genome-wide epigenetic patterns. In contrast, little is known about the dynamics of histone modifications during CD4 T-cell activation and the differential kinetics of these epigenetic marks between naive and memory T cells. In this study, we have detailed the dynamics of genome-wide promoter H3K4me2 and H3K4me3 over a time course during activation of human naive and memory CD4 T cells. Our results demonstrate that changes to H3K4 methylation occur relatively late after activation (5 days) and reinforce activation-induced upregulation of gene expression, affecting multiple pathways important to T-cell activation, differentiation and function. The dynamics and mapped pathways of H3K4 methylation are distinctly different in memory cells, which have substantially more promoters marked by H3K4me3 alone, reinforcing their more differentiated state. Our study provides the first data examining genome-wide histone modification dynamics during CD4 T-cell activation, providing insight into the cross talk between H3K4 methylation and gene expression, and underscoring the impact of these marks upon key pathways integral to CD4 T-cell activation and function.},
author = {LaMere, S. A. and Thompson, R. C. and Komori, H. K. and Mark, A. and Salomon, D. R.},
doi = {10/f97x85},
file = {/Users/ryan/Documents/Mendeley Desktop/LaMere et al. - 2016 - Promoter H3K4 methylation dynamically reinforces a.ppt;/Users/ryan/Zotero/storage/5XP7MAP5/LaMere et al_2016_Promoter H3K4 methylation dynamically reinforces activation-induced pathways in.pdf},
issn = {1466-4879},
journal = {Genes \& Immunity},
month = jul,
number = {5},
pages = {283-297},
pmid = {27170561},
title = {Promoter {{H3K4}} Methylation Dynamically Reinforces Activation-Induced Pathways in Human {{CD4 T}} Cells},
volume = {17},
year = {2016}
}
@article{LaMere2017,
abstract = {The changes to the epigenetic landscape in response to Ag during CD4 T cell activation have not been well characterized. Although CD4 T cell subsets have been mapped globally for numerous epigenetic marks, little has been done to study their dynamics early after activation. We have studied changes to promoter H3K27me3 during activation of human naive and memory CD4 T cells. Our results show that these changes occur relatively early (1 d) after activation of naive and memory cells and that demethylation is the predominant change to H3K27me3 at this time point, reinforcing high expression of target genes. Additionally, inhibition of the H3K27 demethylase JMJD3 in naive CD4 T cells demonstrates how critically important molecules required for T cell differentiation, such as JAK2 and IL12RB2, are regulated by H3K27me3. Our results show that H3K27me3 is a dynamic and important epigenetic modification during CD4 T cell activation and that JMJD3-driven H3K27 demethylation is critical for CD4 T cell function.},
author = {LaMere, Sarah A. and Thompson, Ryan C. and Meng, Xiangzhi and Komori, H. Kiyomi and Mark, Adam and Salomon, Daniel R.},
doi = {10/gchc9x},
file = {/Users/ryan/Zotero/storage/BVR39DW7/LaMere et al_2017_H3K27 Methylation Dynamics during CD4 T Cell Activation.pdf},
issn = {0022-1767},
journal = {The Journal of Immunology},
keywords = {development,epigenetics,histone demethylation,kdm 4},
month = nov,
number = {9},
pages = {3158-3175},
pmid = {28947543},
title = {{{H3K27 Methylation Dynamics}} during {{CD4 T Cell Activation}}: {{Regulation}} of {{JAK}}/{{STAT}} and {{IL12RB2 Expression}} by {{JMJD3}}},
volume = {199},
year = {2017}
}
@article{Rangaraju2015a,
abstract = {Longevity mechanisms increase lifespan by counteracting the effects of aging. However, whether longevity mechanisms counteract the effects of aging continually throughout life, or whether they act during specific periods of life, preventing changes that precede mortality is unclear. Here, we uncover transcriptional drift, a phenomenon that describes how aging causes genes within functional groups to change expression in opposing directions. These changes cause a transcriptome-wide loss in mRNA stoichiometry and loss of co-expression patterns in aging animals, as compared to young adults. Using Caenorhabditis elegans as a model, we show that extending lifespan by inhibiting serotonergic signals by the antidepressant mianserin attenuates transcriptional drift, allowing the preservation of a younger transcriptome into an older age. Our data are consistent with a model in which inhibition of serotonergic signals slows age-dependent physiological decline and the associated rise in mortality levels exclusively in young adults, thereby postponing the onset of major mortality.},
author = {Rangaraju, Sunitha and Solis, Gregory M. and Thompson, Ryan C. and {Gomez-Amaro}, Rafael L. and Kurian, Leo and Encalada, Sandra E. and Niculescu, Alexander B. and Salomon, Daniel R. and Petrascheck, Michael},
doi = {10/ggcxmg},
file = {/Users/ryan/Zotero/storage/58BU429B/Rangaraju et al_2015_Suppression of transcriptional drift extends C.pdf;/Users/ryan/Zotero/storage/LUFV5VQT/Rangaraju et al_2015_Suppression of transcriptional drift extends C.pdf},
issn = {2050-084X},
journal = {eLife},
month = dec,
number = {December2015},
pages = {1-39},
pmid = {26623667},
title = {Suppression of Transcriptional Drift Extends {{C}}. Elegans Lifespan by Postponing the Onset of Mortality},
volume = {4},
year = {2015}
}
@article{VanNieuwerburgh2012,
abstract = {Standard Illumina mate-paired libraries are constructed from 3- to 5-kb DNA fragments by a blunt-end circularization. Sequencing reads that pass through the junction of the two joined ends of a 3-5-kb DNA fragment are not easy to identify and pose problems during mapping and de novo assembly. Longer read lengths increase the possibility that a read will cross the junction. To solve this problem, we developed a mate-paired protocol for use with Illumina sequencing technology that uses Cre-Lox recombination instead of blunt end circularization. In this method, a LoxP sequence is incorporated at the junction site. This sequence allows screening reads for junctions without using a reference genome. Junction reads can be trimmed or split at the junction. Moreover, the location of the LoxP sequence in the reads distinguishes mate-paired reads from spurious paired-end reads. We tested this new method by preparing and sequencing a mate-paired library with an insert size of 3\,kb from Saccharomyces cerevisiae. We present an analysis of the library quality statistics and a new bio-informatics tool called DeLoxer that can be used to analyze an IlluminaCre-Lox mate-paired data set. We also demonstrate how the resulting data significantly improves a de novo assembly of the S. cerevisiae genome.},
author = {Van Nieuwerburgh, Filip and Thompson, Ryan C and Ledesma, Jessica and Deforce, Dieter and Gaasterland, Terry and Ordoukhanian, Phillip and Head, Steven R},
doi = {10/fmzd3r},
file = {/Users/ryan/Zotero/storage/7ZLSJRA8/Van Nieuwerburgh et al_2012_Illumina mate-paired DNA sequencing-library preparation using Cre-Lox.pdf},
issn = {1362-4962},
journal = {Nucleic acids research},
month = feb,
number = {3},
pages = {e24},
pmid = {22127871},
title = {Illumina Mate-Paired {{DNA}} Sequencing-Library Preparation Using {{Cre}}-{{Lox}} Recombination.},
volume = {40},
year = {2012}
}