Bibtex references for my publications.

references.bib

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@article{mignogna:2019aa,
	Abstract = {Genome-wide association studies on alcohol dependence, by themselves, have yet to account for the estimated heritability of the disorder and provide incomplete mechanistic understanding of this complex trait. Integrating brain ethanol-responsive gene expression networks from model organisms with human genetic data on alcohol dependence could aid in identifying dependence-associated genes and functional networks in which they are involved. This study used a modification of the Edge-Weighted Dense Module Searching for genome-wide association studies (EW-dmGWAS) approach to co-analyze whole-genome gene expression data from ethanol-exposed mouse brain tissue, human protein-protein interaction databases and alcohol dependence-related genome-wide association studies. Results revealed novel ethanol-responsive and alcohol dependence-associated gene networks in prefrontal cortex, nucleus accumbens, and ventral tegmental area. Three of these networks were overrepresented with genome-wide association signals from an independent dataset. These networks were significantly overrepresented for gene ontology categories involving several mechanisms, including actin filament-based activity, transcript regulation, Wnt and Syndecan-mediated signaling, and ubiquitination. Together, these studies provide novel insight for brain mechanisms contributing to alcohol dependence.},
	Author = {Mignogna, Kristin M and Bacanu, Silviu A and Riley, Brien P and Wolen, Aaron R and Miles, Michael F},
	Date-Added = {2019-11-29 14:08:59 -0600},
	Date-Modified = {2019-11-29 14:10:06 -0600},
	Doi = {10.1371/journal.pone.0202063},
	Journal = {PLoS One},
	Journal-Full = {PloS one},
	Number = {4},
	Pages = {e0202063},
	Pmc = {PMC6481773},
	Pmid = {31017905},
	Pst = {epublish},
	Title = {Cross-species alcohol dependence-associated gene networks: Co-analysis of mouse brain gene expression and human genome-wide association data},
	Volume = {14},
	Year = {2019},
	Bdsk-Url-1 = {https://doi.org/10.1371/journal.pone.0202063}}

@article{lechuga:2019aa,
	Abstract = {Cell migration is a critical mechanism controlling tissue morphogenesis, epithelial wound healing and tumor metastasis. Migrating cells depend on orchestrated remodeling of the plasma membrane and the underlying actin cytoskeleton, which is regulated by the spectrin-adducin-based membrane skeleton. Expression of adducins is altered during tumorigenesis, however, their involvement in metastatic dissemination of tumor cells remains poorly characterized. This study investigated the roles of α-adducin (ADD1) and γ-adducin (ADD3) in regulating migration and invasion of non-small cell lung cancer (NSCLC) cells. ADD1 was mislocalized, whereas ADD3 was markedly downregulated in NSCLC cells with the invasive mesenchymal phenotype. CRISPR/Cas9-mediated knockout of ADD1 and ADD3 in epithelial-type NSCLC and normal bronchial epithelial cells promoted their Boyden chamber migration and Matrigel invasion. Furthermore, overexpression of ADD1, but not ADD3, in mesenchymal-type NSCLC cells decreased cell migration and invasion. ADD1-overexpressing NSCLC cells demonstrated increased adhesion to the extracellular matrix (ECM), accompanied by enhanced assembly of focal adhesions and hyperphosphorylation of Src and paxillin. The increased adhesiveness and decreased motility of ADD1-overexpressing cells were reversed by siRNA-mediated knockdown of Src. By contrast, the accelerated migration of ADD1 and ADD3-depleted NSCLC cells was ECM adhesion-independent and was driven by the upregulated expression of pro-motile cadherin-11. Overall, our findings reveal a novel function of adducins as negative regulators of NSCLC cell migration and invasion, which could be essential for limiting lung cancer progression and metastasis.},
	Author = {Lechuga, Susana and Amin, Parth H and Wolen, Aaron R and Ivanov, Andrei I},
	Date-Added = {2019-11-29 14:08:55 -0600},
	Date-Modified = {2019-11-29 14:10:11 -0600},
	Doi = {10.1016/j.bbamcr.2018.10.001},
	Journal = {Biochim Biophys Acta Mol Cell Res},
	Journal-Full = {Biochimica et biophysica acta. Molecular cell research},
	Keywords = {Actin cytoskeleton; Focal adhesions; Invasion; Membrane skeleton; Src},
	Mesh = {Cadherins; Calmodulin-Binding Proteins; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Cell Movement; Cell-Matrix Junctions; Cytoskeletal Proteins; Down-Regulation; Epithelial Cells; Focal Adhesions; Humans; Lung Neoplasms; Neoplasm Invasiveness; RNA, Small Interfering; Signal Transduction},
	Month = {March},
	Number = {3},
	Pages = {395-408},
	Pmc = {PMC6311435},
	Pmid = {30290240},
	Pst = {ppublish},
	Title = {Adducins inhibit lung cancer cell migration through mechanisms involving regulation of cell-matrix adhesion and cadherin-11 expression},
	Volume = {1866},
	Year = {2019},
	Bdsk-Url-1 = {https://doi.org/10.1016/j.bbamcr.2018.10.001}}

@article{salvatore:2018aa,
	Abstract = {BACKGROUND: Characterizing aggregate genetic risk for alcohol misuse and identifying variants involved in gene-by-environment (G × E) interaction effects has so far been a major challenge. We hypothesized that functional genomic information could be used to enhance detection of polygenic signal underlying alcohol misuse and to prioritize identification of single nucleotide polymorphisms (SNPs) most likely to exhibit G × E effects.
METHODS: We examined these questions in the young adult FinnTwin12 sample (n = 1,170). We used genomewide association estimates from an independent sample to derive 2 types of polygenic scores for alcohol problems in FinnTwin12. Genomewide polygenic scores included all SNPs surpassing a designated p-value threshold. DNase polygenic scores were a subset of the genomewide polygenic scores including only variants in DNase I hypersensitive sites (DHSs), which are open chromatin marks likely to index regions with a regulatory function. We conducted parallel analyses using height as a nonpsychiatric model phenotype to evaluate the consistency of effects. For the G × E analyses, we examined whether SNPs in DHSs were overrepresented among SNPs demonstrating significant G × E effects in an interaction between romantic relationship status and intoxication frequency.
RESULTS: Contrary to our expectations, we found that DNase polygenic scores were not more strongly predictive of alcohol problems than conventional polygenic scores. However, variants in DNase polygenic scores had per-SNP effects that were up to 1.4 times larger than variants in conventional polygenic scores. This same pattern of effects was also observed in supplementary analyses with height. In G × E models, SNPs in DHSs were modestly overrepresented among SNPs with significant interaction effects for intoxication frequency.
CONCLUSIONS: These findings highlight the potential utility of integrating functional genomic annotation information to increase the signal-to-noise ratio in polygenic scores and identify genetic variants that may be most susceptible to environmental modification.},
	Author = {Salvatore, Jessica E and Savage, Jeanne E and Barr, Peter and Wolen, Aaron R and Aliev, Fazil and Vuoksimaa, Eero and Latvala, Antti and Pulkkinen, Lea and Rose, Richard J and Kaprio, Jaakko and Dick, Danielle M},
	Date-Added = {2019-11-29 14:08:49 -0600},
	Date-Modified = {2019-11-29 14:10:01 -0600},
	Doi = {10.1111/acer.13551},
	Journal = {Alcohol Clin Exp Res},
	Journal-Full = {Alcoholism, clinical and experimental research},
	Keywords = {Alcohol; Functional Genomics; Gene-Environment Interplay; Polygenic Scores},
	Mesh = {Adult; Alcoholism; Female; Finland; Gene-Environment Interaction; Genetic Predisposition to Disease; Genetic Variation; Genome-Wide Association Study; Genomics; Humans; Male; Multifactorial Inheritance; Polymorphism, Single Nucleotide; Twins; Young Adult},
	Month = {Feb},
	Number = {2},
	Pages = {413-423},
	Pmc = {PMC5785466},
	Pmid = {29121402},
	Pst = {ppublish},
	Title = {Incorporating Functional Genomic Information to Enhance Polygenic Signal and Identify Variants Involved in Gene-by-Environment Interaction for Young Adult Alcohol Problems},
	Volume = {42},
	Year = {2018},
	Bdsk-Url-1 = {https://doi.org/10.1111/acer.13551}}

@misc{wolen:2013uq,
	Abstract = {It seems likely that the genetic contribution of common variants to the risk of major psychiatric disorders is distributed across at least hundreds of variants of very small effect. Even very large studies are under-powered to detect a large number of such effects, without being overwhelmed by false positives. We think that variants that carry these modest risks are mostly in exons or in functional non-coding DNA. If we can combine several sources of information to identify functional DNA, we may be able to identify these risk SNPs better. We propose here an Empirical Bayes approach to combining genomic information with association information from Genome-wide Association Studies (GWAS), to identify individual SNPs and genes that are implicated in Schizophrenia.
},
	Author = {Wolen, Aaron R and Kendler, Kenneth S and Reimers, Mark A},
	Date-Added = {2017-08-21 15:37:09 +0000},
	Date-Modified = {2017-08-21 15:37:09 +0000},
	Howpublished = {Presented at the 30th annual Daniel T. Watts Research Symposium},
	Month = {Oct},
	Title = {Integrating genomic and genetic data suggests circuit development abnormalities in schizophrenia},
	Year = {2013}}

@misc{gau:2016,
	Abstract = {It seems likely that the genetic contribution of common variants to the risk of major psychiatric disorders is distributed across at least hundreds of variants of very small effect. Even very large studies are under-powered to detect a large number of such effects, without being overwhelmed by false positives. We think that variants that carry these modest risks are mostly in exons or in functional non-coding DNA. If we can combine several sources of information to identify functional DNA, we may be able to identify these risk SNPs better. We propose here an Empirical Bayes approach to combining genomic information with association information from Genome-wide Association Studies (GWAS), to identify individual SNPs and genes that are implicated in Schizophrenia.
},
	Author = {Gau, Karen H and Arendt, Julie A and Olex, Amy L and Wolen, Aaron R},
	Date-Added = {2017-08-21 15:26:32 +0000},
	Date-Modified = {2017-08-21 15:42:04 +0000},
	Howpublished = {Presented at the annual Tri-Chapter Meeting of the Medical Library Association},
	Month = {September},
	Title = {Providing Hands-on Training with Bioinformatics Databases: A Collaboration Between {VCU Libraries} & {Wright Center for Clinical and Translational Research}},
	Year = {2016}}

@misc{costin:2012,
	Address = {111 RIVER ST, HOBOKEN 07030-5774, NJ},
	Affiliation = {{Costin, B. N.; Wolen, A. R.; Fitting, S.; Shelton, K. L.; Miles, M. F., Virginia Commonwealth Univ, Dept Pharmacol, Richmond, VA 23298 USA.}},
	Author = {Costin, B. N. and Wolen, A. R. and Fitting, S. and Shelton, K. L. and Miles, M. F.},
	Da = {2017-08-21},
	Date-Added = {2017-08-21 15:14:57 +0000},
	Date-Modified = {2017-08-21 15:18:05 +0000},
	Doc-Delivery-Number = {{952QA}},
	Howpublished = {Presented at the 35th Annual Scientific Meeting of the Research Society on Alcoholism},
	Issn = {{0145-6008}},
	Journal = {Alcoholism-Clinical and Experimental Research},
	Journal-Iso = {Alcoholism},
	Language = {English},
	Month = {Jun},
	Note = {{35th Annual Scientific Meeting of the Research-Society-on-Alcoholism (RSA), San Francisco, CA, JUN 23-27, 2012}},
	Number = {{1, SI}},
	Number-Of-Cited-References = {{0}},
	Oa = {{No}},
	Orcid-Numbers = {{Wolen, Aaron/0000-0003-2542-2202}},
	Organization = {{Res Soc Alcoholism (RSA)}},
	Pages = {{25A}},
	Publisher = {{WILEY-BLACKWELL}},
	Research-Areas = {{Substance Abuse}},
	Researcherid-Numbers = {{Wolen, Aaron/H-9545-2014}},
	Times-Cited = {{0}},
	Title = {Role of Adrenal Glucocorticoid Signaling in Prefrontal Cortex Gene Expression and Acute Behavioral Responses to Ethanol},
	Type = {{Meeting Abstract}},
	Unique-Id = {{ISI:000304806000057}},
	Usage-Count-Last-180-Days = {{0}},
	Usage-Count-Since-2013 = {{0}},
	Volume = {{36}},
	Web-Of-Science-Categories = {{Substance Abuse}},
	Year = {2012}}

@misc{fernandez:2015a,
	Address = {233 SPRING ST, NEW YORK, NY 10013},
	Affiliation = {{Fernandez, L. J.; Wolen, A. R.; Olex, A. L.; Dozmorov, M.; Fenstermacher, D. A.; Takabe, K., Virginia Commonwealth Univ, Richmond, VA USA.}},
	Author = {Fernandez, L. J. and Wolen, A. R. and Olex, A. L. and Dozmorov, M. and Fenstermacher, D. A. and Takabe, K.},
	Da = {{2017-08-21}},
	Date-Added = {2017-08-21 15:07:30 +0000},
	Date-Modified = {2017-08-21 15:08:55 +0000},
	Doc-Delivery-Number = {{CQ9MZ}},
	Eissn = {{1534-4681}},
	Howpublished = {Presented at the 68th Annual Cancer Symposium of the Society of Surgical Oncology},
	Issn = {{1068-9265}},
	Journal = {Annals of Surgical Oncology},
	Journal-Iso = {{Ann. Surg. Oncol.}},
	Language = {{English}},
	Meeting = {{P120}},
	Month = {Feb},
	Note = {{68th Annual Cancer Symposium of the Society-of-Surgical-Oncology, Houston, TX, MAR 25-28, 2015}},
	Number = {1},
	Number-Of-Cited-References = {{0}},
	Oa = {{No}},
	Organization = {{Soc Surg Oncol}},
	Pages = {S81},
	Publisher = {{SPRINGER}},
	Research-Areas = {{Oncology; Surgery}},
	Times-Cited = {{0}},
	Title = {Is Patient Derived Xenograft Model Appropriate for Colon Cancer Preclinical Drug Development?},
	Type = {{Meeting Abstract}},
	Unique-Id = {{ISI:000360940500220}},
	Usage-Count-Last-180-Days = {{0}},
	Usage-Count-Since-2013 = {{0}},
	Volume = {22},
	Web-Of-Science-Categories = {{Oncology; Surgery}},
	Year = {2015}}

@misc{fernandez:2015,
	Address = {615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404},
	Affiliation = {{Fernandez, Leopoldo J.; Wolen, Aaron R.; Olex, Amy L.; Dozmorov, Mikhail; Fenstermacher, David A.; Takabe, Kazuaki, Virginia Commonwealth Univ, Richmond, VA USA.}},
	Author = {Fernandez, Leopoldo J. and Wolen, Aaron R. and Olex, Amy L. and Dozmorov, Mikhail and Fenstermacher, David A. and Takabe, Kazuaki},
	Da = {2017-08-21},
	Date-Added = {2017-08-21 14:53:00 +0000},
	Date-Modified = {2017-08-21 14:58:29 +0000},
	Doc-Delivery-Number = {DF8AH},
	Doi = {10.1158/1538-7445.AM2015-1473},
	Eissn = {1538-7445},
	Howpublished = {Presented at the 106th Annual Meeting of the American Association for Cancer Research},
	Issn = {0008-5472},
	Journal = {Cancer Research},
	Journal-Iso = {Cancer Res.},
	Language = {{English}},
	Meeting = {{1473}},
	Month = {Aug},
	Note = {{106th Annual Meeting of the American-Association-for-Cancer-Research (AACR), Philadelphia, PA, APR 18-22, 2015}},
	Number = {15},
	Number-Of-Cited-References = {{0}},
	Oa = {{No}},
	Organization = {{Amer Assoc Canc Res}},
	Publisher = {{AMER ASSOC CANCER RESEARCH}},
	Research-Areas = {{Oncology}},
	Times-Cited = {{0}},
	Title = {Are the genomic gene expression profiles maintained between the original donor and patient-derived xenograft tumors},
	Type = {{Meeting Abstract}},
	Unique-Id = {{ISI:000371578502511}},
	Usage-Count-Last-180-Days = {{0}},
	Usage-Count-Since-2013 = {{0}},
	Volume = {75},
	Web-Of-Science-Categories = {{Oncology}},
	Year = {2015},
	Bdsk-Url-1 = {http://dx.doi.org/10.1158/1538-7445.AM2015-1473%7D}}

@article{webb:2017,
	Abstract = {Background: Genetic factors impact alcohol use behaviors and these factors may become increasingly evident during emerging adulthood. Examination of the effects of individual variants as well as aggregate genetic variation can clarify mechanisms underlying risk. Methods: We conducted genome-wide association studies (GWAS) in an ethnically diverse sample of college students for three quantitative outcomes including typical monthly alcohol consumption, alcohol problems, and maximum number of drinks in 24 h. Heritability based on common genetic variants (h(2)SNP) was assessed. We also evaluated whether risk variants in aggregate were associated with alcohol use outcomes in an independent sample of young adults. Results: Two genome-wide significant markers were observed: rs11201929 in GRID1 for maximum drinks in 24 h, with supportive evidence across all ancestry groups; and rs73317305 in SAMD12 (alcohol problems), tested only in the African ancestry group. The h(2)SNP estimate was 0.19 (SE = 0.11) for consumption, and was non-significant for other outcomes. Genome-wide polygenic scores were significantly associated with alcohol outcomes in an independent sample. Conclusions: These results robustly identify genetic risk for alcohol use outcomes at the variant level and in aggregate. We confirm prior evidence that genetic variation in GRID1 impacts alcohol use, and identify novel loci of interest for multiple alcohol outcomes in emerging adults. These findings indicate that genetic variation influencing normative and problematic alcohol use is, to some extent, convergent across ancestry groups. Studying college populations represents a promising avenue by which to obtain large, diverse samples for gene identification.},
	Author = {Webb, Bradley T and Edwards, Alexis C and Wolen, Aaron R and Salvatore, Jessica E and Aliev, Fazil and Riley, Brien P and Sun, Cuie and Williamson, Vernell S and Kitchens, James N and Pedersen, Kimberly and Adkins, Amy and Cooke, Megan E and Savage, Jeanne E and Neale, Zoe and Cho, Seung B and Dick, Danielle M and Kendler, Kenneth S},
	Date-Added = {2017-04-25 18:26:36 +0000},
	Date-Modified = {2017-04-25 18:26:36 +0000},
	Doi = {10.3389/fgene.2017.00030},
	Journal = {Front Genet},
	Journal-Full = {Frontiers in genetics},
	Keywords = {GWAS; alcohol consumption; alcohol problems; genetic ancestry; genome-wide polygenic score; heritability},
	Pages = {30},
	Pmc = {PMC5350109},
	Pmid = {28360924},
	Pst = {epublish},
	Title = {Molecular Genetic Influences on Normative and Problematic Alcohol Use in a Population-Based Sample of College Students},
	Url = {http://journal.frontiersin.org/article/10.3389/fgene.2017.00030/full},
	Volume = {8},
	Year = {2017},
	Bdsk-Url-1 = {http://dx.doi.org/10.3389/fgene.2017.00030}}

@article{huang:2016,
	Abstract = {The bioactive sphingolipid sphingosine-1-phosphate (S1P) and the kinase that produces it have been implicated in inflammatory bowel diseases in mice and humans; however, little is known about the role of the 2 S1P-specific phosphohydrolase isoforms, SGPP1 and SGPP2, which catalyze dephosphorylation of S1P to sphingosine. To elucidate their functions, we generated specific knockout mice. Deletion of Sgpp2, which is mainly expressed in the gastrointestinal tract, significantly reduced dextran sodium sulfate (DSS)-induced colitis severity, whereas deletion of ubiquitously expressed Sgpp1 slightly worsened colitis. Moreover, Sgpp1 deletion enhanced expression of multifunctional proinflammatory cytokines, IL-6, TNF-α, and IL-1β, activation of the transcription factor signal transducer and activator of transcription 3, and immune cell infiltration into the colon. Conversely, Sgpp2-null mice failed to mount a DSS-induced systemic inflammatory response. Of interest, Sgpp2 deficiency suppressed DSS-induced intestinal epithelial cell apoptosis and improved mucosal barrier integrity. Furthermore, down-regulation of Sgpp2 attenuated LPS-induced paracellular permeability in cultured cells and enhanced expression of the adherens junction protein E-cadherin. Finally, in patients with ulcerative colitis, SGPP2 expression was elevated in colitis tissues relative to that in uninvolved tissues. These results indicate that induction of SGPP2 expression contributes to the pathogenesis of colitis by promoting disruption of the mucosal barrier function. SGPP2 may represent a novel therapeutic target in inflammatory bowel disease.-Huang, W.-C., Liang, J., Nagahashi, M., Avni, D., Yamada, A., Maceyka, M., Wolen, A. R., Kordula, T., Milstien, S., Takabe, K., Oravecz, T., Spiegel, S. Sphingosine-1-phosphate phosphatase 2 promotes disruption of mucosal integrity, and contributes to ulcerative colitis in mice and humans.},
	Author = {Huang, Wei-Ching and Liang, Jie and Nagahashi, Masayuki and Avni, Dorit and Yamada, Akimitsu and Maceyka, Michael and Wolen, Aaron R and Kordula, Tomasz and Milstien, Sheldon and Takabe, Kazuaki and Oravecz, Tamas and Spiegel, Sarah},
	Date-Added = {2017-02-01 15:46:45 +0000},
	Date-Modified = {2017-02-01 15:46:45 +0000},
	Doi = {10.1096/fj.201600394R},
	Journal = {FASEB J},
	Journal-Full = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
	Keywords = {S1P; SGPP1; SGPP2; inflammatory bowel disease},
	Month = {Aug},
	Number = {8},
	Pages = {2945-58},
	Pmc = {PMC4970610},
	Pmid = {27130484},
	Pst = {ppublish},
	Title = {Sphingosine-1-phosphate phosphatase 2 promotes disruption of mucosal integrity, and contributes to ulcerative colitis in mice and humans},
	Url = {http://dx.doi.org/10.1096/fj.201600394R},
	Volume = {30},
	Year = {2016},
	Bdsk-Url-1 = {http://dx.doi.org/10.1096/fj.201600394R}}

@article{vaart:2017,
	Abstract = {The transition from acute to chronic ethanol exposure leads to lasting behavioral and physiological changes such as increased consumption, dependence, and withdrawal. Changes in brain gene expression are hypothesized to underlie these adaptive responses to ethanol. Previous studies on acute ethanol identified genetic variation in brain gene expression networks and behavioral responses to ethanol across the BXD panel of recombinant inbred mice. In this work, we have performed the first joint genetic and genomic analysis of transcriptome shifts in response to chronic intermittent ethanol (CIE) by vapor chamber exposure in a BXD cohort. CIE treatment is known to produce significant and sustained changes in ethanol consumption with repeated cycles of ethanol vapor. Using Affymetrix microarray analysis of prefrontal cortex (PFC) and nucleus accumbens (NAC) RNA, we compared CIE expression responses to those seen following acute ethanol treatment, and to voluntary ethanol consumption. Gene expression changes in PFC and NAC after CIE overlapped significantly across brain regions and with previously published expression following acute ethanol. Genes highly modulated by CIE were enriched for specific biological processes including synaptic transmission, neuron ensheathment, intracellular signaling, and neuronal projection development. Expression quantitative trait locus (eQTL) analyses identified genomic loci associated with ethanol-induced transcriptional changes with largely distinct loci identified between brain regions. Correlating CIE-regulated genes to ethanol consumption data identified specific genes highly associated with variation in the increase in drinking seen with repeated cycles of CIE. In particular, multiple myelin-related genes were identified. Furthermore, genetic variance in or near dynamin3 (Dnm3) on Chr1 at ∼164 Mb may have a major regulatory role in CIE-responsive gene expression. Dnm3 expression correlates significantly with ethanol consumption, is contained in a highly ranked functional group of CIE-regulated genes in the NAC, and has a cis-eQTL within a genomic region linked with multiple CIE-responsive genes.},
	Author = {{van der Vaart}, Andrew D and Wolstenholme, Jennifer T and Smith, Maren L and Harris, Guy M and Lopez, Marcelo F and Wolen, Aaron R and Becker, Howard C and Williams, Robert W and Miles, Michael F},
	Date-Added = {2017-02-01 15:34:28 +0000},
	Date-Modified = {2017-02-01 15:37:22 +0000},
	Doi = {10.1016/j.alcohol.2016.07.010},
	Journal = {Alcohol},
	Journal-Full = {Alcohol (Fayetteville, N.Y.)},
	Keywords = {Bioinformatics; Chronic intermittent ethanol; Genomics},
	Month = {Feb},
	Pages = {93-106},
	Pmc = {PMC5253248},
	Pmid = {27838001},
	Pst = {ppublish},
	Title = {The allostatic impact of chronic ethanol on gene expression: A genetic analysis of chronic intermittent ethanol treatment in the BXD cohort},
	Url = {http://dx.doi.org/10.1016/j.alcohol.2016.07.010},
	Volume = {58},
	Year = {2017},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/j.alcohol.2016.07.010}}

@article{edwards:2017,
	Abstract = {BACKGROUND: Alcohol use typically begins during adolescence and escalates into young adulthood. This represents an important period for the establishment of alcohol use and misuse patterns, which can have psychosocial and medical consequences. Although changes in alcohol use during this time have been phenotypically characterized, their genetic nature is poorly understood.
METHODS: Participants of the Avon Longitudinal Study of Parents and Children completed the Alcohol Use Disorders Identification Test (AUDIT) 4 times from age 16 to 20. We used Mplus to construct a growth model characterizing changes in AUDIT scores across time (N = 4,545, where data were available for at least 2 time points). The slope of the model was used as the phenotype in a genomewide association study (N = 3,380), followed by secondary genetic analyses.
RESULTS: No individual marker met genomewide significance criteria. Top markers mapped to biologically plausible candidate genes. The slope term was moderately heritable (h(2)SNP = 0.26, p = 0.009), and replication attempts using a meta-analysis of independent samples provided support for implicated variants at the aggregate level. Nominally significant (p < 0.00001) markers mapped to putatively active genomic regions in brain tissue more frequently than expected by chance.
CONCLUSIONS: These results build on prior studies by demonstrating that common genetic variation impacts alcohol misuse trajectories. Influential loci map to genes that merit additional research, as well as to intergenic regions with regulatory functions in the central nervous system. These findings underscore the complex biological nature of alcohol misuse across development.},
	Author = {Edwards, Alexis C and Heron, Jon and Vladimirov, Vladimir and Wolen, Aaron R and Adkins, Daniel E and Aliev, Fazil and Hickman, Matthew and Kendler, Kenneth S},
	Date-Added = {2017-02-01 15:33:53 +0000},
	Date-Modified = {2017-02-01 15:33:53 +0000},
	Doi = {10.1111/acer.13262},
	Journal = {Alcohol Clin Exp Res},
	Journal-Full = {Alcoholism, clinical and experimental research},
	Keywords = {ALSPAC; Alcohol Problems; Genetic Influences; Heritability; Longitudinal Model},
	Month = {Jan},
	Number = {1},
	Pages = {57-64},
	Pmc = {PMC5205550},
	Pmid = {27892595},
	Pst = {ppublish},
	Title = {The Rate of Change in Alcohol Misuse Across Adolescence is Heritable},
	Url = {http://dx.doi.org/10.1111/acer.13262},
	Volume = {41},
	Year = {2017},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/acer.13262}}

@article{putman:2016,
	Abstract = {Genetic differences in acute behavioral responses to ethanol contribute to the susceptibility to alcohol use disorder and the reduction of anxiety is a commonly reported motive underlying ethanol consumption among alcoholics. Therefore, we studied the genetic variance in anxiolytic-like responses to ethanol across the BXD recombinant inbred (RI) mouse panel using the light-dark transition model of anxiety. Strain-mean genetic mapping and a mixed-model quantitative trait loci (QTL) analysis replicated several previously published QTL for locomotor activity and identified several novel anxiety-related loci. Significant loci included a chromosome 11 saline anxiety-like QTL (Salanq1) and a chromosome 12 locus (Etanq1) influencing the anxiolytic-like response to ethanol. Etanq1 was successfully validated by studies with BXD advanced intercross strains and fine-mapped to a region comprising less than 3.5 Mb. Through integration of genome-wide mRNA expression profiles of the mesocorticolimbic reward circuit (prefrontal cortex, nucleus accumbens and ventral midbrain) across the BXD RI panel, we identified high priority candidate genes within Etanq1, the strongest of which was Ninein (Nin), a Gsk3β-interacting protein that is highly expressed in the brain.},
	Author = {Putman, A H and Wolen, A R and Harenza, J L and Yordanova, R K and Webb, B T and Chesler, E J and Miles, M F},
	Date-Added = {2017-02-01 15:31:16 +0000},
	Date-Modified = {2017-02-01 15:31:44 +0000},
	Doi = {10.1111/gbb.12289},
	Journal = {Genes Brain Behav},
	Journal-Full = {Genes, brain, and behavior},
	Keywords = {Anxiety; BXD recombinant inbred; Ninein; QTL; ethanol; microarray},
	Mesh = {Alcohol Drinking; Alcohol-Related Disorders; Animals; Anti-Anxiety Agents; Chromosome Mapping; Ethanol; Genetic Association Studies; Genetic Variation; Male; Mice; Quantitative Trait Loci},
	Month = {Apr},
	Number = {4},
	Pages = {367-81},
	Pmc = {PMC4852167},
	Pmid = {26948279},
	Pst = {ppublish},
	Title = {Identification of quantitative trait loci and candidate genes for an anxiolytic-like response to ethanol in BXD recombinant inbred strains},
	Url = {http://dx.doi.org/10.1111/gbb.12289},
	Volume = {15},
	Year = {2016},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/gbb.12289}}

@article{wright:2016,
	Abstract = {The need for research investigating DNA methylation (DNAm) in clinical studies has increased, leading to the evolution of new analytic methods to improve accuracy and reproducibility of the interpretation of results from these studies. The purpose of this article is to provide clinical researchers with a summary of the major data processing steps routinely applied in clinical studies investigating genome-wide DNAm using the Illumina HumanMethylation 450K BeadChip. In most studies, the primary goal of employing DNAm analysis is to identify differential methylation at CpG sites among phenotypic groups. Experimental design considerations are crucial at the onset to minimize bias from factors related to sample processing and avoid confounding experimental variables with non-biological batch effects. Although there are currently no de facto standard methods for analyzing these data, we review the major steps in processing DNAm data recommended by several research studies. We describe several variations available for clinical researchers to process, analyze, and interpret DNAm data. These insights are applicable to most types of genome-wide DNAm array platforms and will be applicable for the next generation of DNAm array technologies (e.g., the 850K array). Selection of the DNAm analytic pipeline followed by investigators should be guided by the research question and supported by recently published methods.},
	Author = {Wright, Michelle L and Dozmorov, Mikhail G and Wolen, Aaron R and Jackson-Cook, Colleen and Starkweather, Angela R and Lyon, Debra E and York, Timothy P},
	Date-Added = {2017-02-01 15:29:02 +0000},
	Date-Modified = {2017-02-01 15:29:27 +0000},
	Doi = {10.1186/s13148-016-0212-7},
	Journal = {Clin Epigenetics},
	Journal-Full = {Clinical epigenetics},
	Keywords = {DNA methylation; Epigenomics; Microarray analysis},
	Mesh = {CpG Islands; DNA Methylation; Epigenesis, Genetic; Genome, Human; Humans; Oligonucleotide Array Sequence Analysis; Reproducibility of Results},
	Pages = {45},
	Pmc = {PMC4848848},
	Pmid = {27127542},
	Pst = {epublish},
	Title = {Establishing an analytic pipeline for genome-wide DNA methylation},
	Url = {http://dx.doi.org/10.1186/s13148-016-0212-7},
	Volume = {8},
	Year = {2016},
	Bdsk-Url-1 = {http://dx.doi.org/10.1186/s13148-016-0212-7}}

@article{smith:2016,
	Abstract = {Long lasting abusive consumption, dependence, and withdrawal are characteristic features of alcohol use disorders (AUD). Mechanistically, persistent changes in gene expression are hypothesized to contribute to brain adaptations leading to ethanol toxicity and AUD. We employed repeated chronic intermittent ethanol (CIE) exposure by vapor chamber as a mouse model to simulate the cycles of ethanol exposure and withdrawal commonly seen with AUD. This model has been shown to induce progressive ethanol consumption in rodents. Brain CIE-responsive expression networks were identified by microarray analysis across five regions of the mesolimbic dopamine system and extended amygdala with tissue harvested from 0-hours to 7-days following CIE. Weighted Gene Correlated Network Analysis (WGCNA) was used to identify gene networks over-represented for CIE-induced temporal expression changes across brain regions. Differential gene expression analysis showed that long-lasting gene regulation occurred 7-days after the final cycle of ethanol exposure only in prefrontal cortex (PFC) and hippocampus. Across all brain regions, however, ethanol-responsive expression changes occurred mainly within the first 8-hours after removal from ethanol. Bioinformatics analysis showed that neuroinflammatory responses were seen across multiple brain regions at early time-points, whereas co-expression modules related to neuroplasticity, chromatin remodeling, and neurodevelopment were seen at later time-points and in specific brain regions (PFC or HPC). In PFC a module containing Bdnf was identified as highly CIE responsive in a biphasic manner, with peak changes at 0 hours and 5 days following CIE, suggesting a possible role in mechanisms underlying long-term molecular and behavioral response to CIE. Bioinformatics analysis of this network and several other modules identified Let-7 family microRNAs as potential regulators of gene expression changes induced by CIE. Our results suggest a complex temporal and regional pattern of widespread gene network responses involving neuroinflammatory and neuroplasticity related genes as contributing to physiological and behavioral responses to chronic ethanol.},
	Author = {Smith, Maren L and Lopez, Marcelo F and Archer, Kellie J and Wolen, Aaron R and Becker, Howard C and Miles, Michael F},
	Date-Added = {2016-02-29 14:55:34 +0000},
	Date-Modified = {2016-02-29 14:55:34 +0000},
	Doi = {10.1371/journal.pone.0146257},
	Journal = {PLoS One},
	Journal-Full = {PloS one},
	Number = {1},
	Pages = {e0146257},
	Pmc = {PMC4701666},
	Pmid = {26730594},
	Pst = {epublish},
	Title = {Time-Course Analysis of Brain Regional Expression Network Responses to Chronic Intermittent Ethanol and Withdrawal: Implications for Mechanisms Underlying Excessive Ethanol Consumption},
	Url = {http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0146257},
	Volume = {11},
	Year = {2016},
	Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pone.0146257},
	Bdsk-Url-2 = {http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0146257}}

@article{hettema:2015,
	Author = {Hettema, John and Otowa, Takeshi and Hek, Karin and Lee, Minyoung and Byrne, Enda and Mirza, Saira and Nivard, Michel and Bigdeli, Tim and Aggen, Steven and Adkins, Daniel and Wolen, Aaron R and Fanous, Ayman and Keller, Matthew and Castelao, Enrique and Kutalik, Zoltan and Van der Auwera, Sandra and Homuth, Georg and Nauck, Matthias and Teumer, Alexander and Jouke-Jan Hottenga Direk, Nese and Hofman, Albert and Uitterlinden, Andr{\'e} and Mulder, Cornelis and Henders, Anjali and Medland, Sarah and Gordon, Scott and Heath, Andrew and madden, pamela and Pergadia, Michelle and van der Most, Peter and Nolte, Ilja and van Oort, Floor and Hartman, Catharina and Oldehinkel, Albertine and Preisig, Martin and Joergen Grabe, Hans and Middeldorp, Christel and W.J.H. Penninx, Brenda and Boomsma, Dorret and Martin, Nicholas and Montgomery, Grant and Maher, Brion and {van den Oord}, Edwin and Wray, Naomi and Tiemeier, Henning},
	Date-Added = {2015-12-07 12:54:56 +0000},
	Date-Modified = {2016-02-29 14:55:02 +0000},
	Journal = {Moleculary Psychiatry},
	Month = {January},
	Title = {Meta-analysis of genome-wide association studies of anxiety disorders},
	Url = {http://dx.doi.org/10.1038/mp.2015.197},
	Year = {2016},
	Bdsk-Url-1 = {http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2015197a.html}}

@misc{miles:2015uq,
	Abstract = {Mouse genomic studies on acute or chronic ethanol exposure models have been previously used to identify gene networks and cognate hub genes as targets for intervention in human alcohol use disorder (AUD).  Similarly, multiple human genome wide association studies (GWAS) have been reported to identify genetic loci or genes conferring risk for AUD. However, neither of these approaches has, as yet, led to confirmed targets for development of future therapeutic approaches. This difficulty likely stems from the complexity of data produced by such high-throughput approaches and the small contribution that individual genes add to variance in ethanol behaviors. Our laboratory has therefore explored an approach for integrating genomic and genetic data across animal models and human GWAS results. Two approaches have been used to date. First, targeted mouse gene expression networks from acute ethanol exposure or chronic ethanol consumption models were assessed for over-representation of human GWAS signals. This verified a highly ethanol-responsive gene network as statistically associated with alcohol dependence at a network level. In a second approach, we directly integrated human GWAS data with mouse genomic data from acute or chronic ethanol exposure models in the BXD recombinant inbred panel. Using protein-protein interactions as a background matrix and a modified form of the dmGWAS program for network derivation, we identified several novel networks containing a high density of GWAS signals and ethanol-responsive genes. IGF signaling and extracellular matrix-related genes were particularly over-represented in two high scoring networks. Together, these studies hold promise for identifying new targets for experimental or therapeutic targeting, respectively, in animal models or human AUD. Supported by NIAAA grants U01AA016667, P50AA022537 AND R01AA020634 TO MFM.
},
	Author = {Miles, Michael F and Mignogna, Kristin M and Wolen, Aaron R and Riley, Brien P},
	Date-Added = {2015-11-30 16:23:08 +0000},
	Date-Modified = {2015-11-30 16:23:08 +0000},
	Howpublished = {Presented at the 38th annual conference of the Research Society on Alcoholism},
	Title = {Integrating Genomic and Genetic Data Across Species to Identify Gene Networks Contributing to Ethanol Behaviors and Alcohol Use Disorder},
	Year = {2015}}

@misc{salvatore:2015uq,
	Abstract = {PURPOSE. Genome-wide association studies (GWAS) of alcohol dependence and genetically correlated externalizing disorders have produced a number of significant and suggestive findings. Now attention is shifting from cataloging these genetic associations to understanding their functional role in disease pathogenesis. The purpose of these studies is to illustrate how bioinformatics information can elucidate the biology underlying alcohol-related GWAS findings; and to examine whether incorporating bioinformatics information improves predictive power in tests of polygenic association.

METHODS. Single nucleotide variants (SNVs) identified in a GWAS of an externalizing factor score in the Collaborative Study on the Genetics of Alcoholism (COGA) case-control GWAS sample (n = 1905) were tested for overrepresentation in genomic regions with putative regulatory functions. Polygenic risk scores derived from a GWAS of an alcohol problems factor score (in an independent discovery sample) were used to predict alcohol frequency and intoxication phenotypes in the FinnTwin 12 sample (n = 1128). Epigenomic annotations came from the ENCODE and RoadMap Epigenetics public access databases.

RESULTS. Variants with smaller p-values for the COGA externalizing factor score were enriched for multiple histone modification marks and transcription factor binding sites across multiple cell types, showing up to 20-fold enrichment. Additionally, there was brain-specific enrichment in two histone modification marks associated with gene activation across multiple cell types (e.g., for H3K79me2 p-values ranged from 3.29e-03 to 7.83e-07). In tests of polygenic association in FinnTwin12, preferentially weighting variants that met nominal p-value thresholds of p < 0.01 and p < 0.05 in the discovery sample that were also located under a DNase I peak (i.e., in an open chromatin region and likely to have a regulatory function) resulted in a stronger association signal compared to traditional polygenic scoring methods that use all variants meeting these nominal p-value thresholds. Additional analyses indicate that the per-SNV effect is larger for the variants under a DNase I peak compared SNVs filtered by p-value only.

CONCLUSIONS. The results add to emerging evidence that disease-associated variants are stratified, underscoring the importance of incorporating genomic annotation information in the interpretation of GWAS results. Discussion will focus on future direction in this area, including the use of bioinformatics information to improve polygenic risk prediction and identify new genetic signals, and the implications of this biological understanding for studies of gene-environment interplay for alcohol use disorder.
},
	Author = {Salvatore, Jessica and Savage, Jeanne and Barr, P. and Dozmorov, Mikhail and Wolen, Aaron R and Aliev, Fazil and FinnTwin12 and COGA Collaborators and Dick, Danielle},
	Date-Added = {2015-11-30 16:23:08 +0000},
	Date-Modified = {2017-08-21 14:32:20 +0000},
	Howpublished = {Presented at the 38th annual conference of the Research Society on Alcoholism},
	Month = {June},
	Title = {Incorporating Bioinformatics Data to Understand Alcohol-related GWAS Results},
	Year = {2016}}

@article{scz-group:2014,
	Abstract = {Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles, including common alleles of small effect that might be detected by genome-wide association studies. Here we report a multi-stage schizophrenia genome-wide association study of up to 36,989 cases and 113,075 controls. We identify 128 independent associations spanning 108 conservatively defined loci that meet genome-wide significance, 83 of which have not been previously reported. Associations were enriched among genes expressed in brain, providing biological plausibility for the findings. Many findings have the potential to provide entirely new insights into aetiology, but associations at DRD2 and several genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses. Independent of genes expressed in brain, associations were enriched among genes expressed in tissues that have important roles in immunity, providing support for the speculated link between the immune system and schizophrenia.},
	Author = {{Schizophrenia Working Group of the Psychiatric Genomics Consortium}},
	Date-Added = {2014-12-09 02:28:45 +0000},
	Date-Modified = {2014-12-09 02:28:45 +0000},
	Doi = {10.1038/nature13595},
	Journal = {Nature},
	Journal-Full = {Nature},
	Mesh = {Alleles; Brain; Enhancer Elements, Genetic; Genetic Loci; Genetic Predisposition to Disease; Genome-Wide Association Study; Glutamic Acid; Humans; Immunity; Multifactorial Inheritance; Mutation; Odds Ratio; Polymorphism, Single Nucleotide; Schizophrenia; Synaptic Transmission},
	Month = {Jul},
	Number = {7510},
	Pages = {421-7},
	Pdf = {http://onlinelibrary.wiley.com/doi/10.1111/add.12822/pdf},
	Pmc = {PMC4112379},
	Pmid = {25056061},
	Pst = {ppublish},
	Title = {Biological insights from 108 schizophrenia-associated genetic loci},
	Url = {http://onlinelibrary.wiley.com/doi/10.1111/add.12822/abstract},
	Volume = {511},
	Year = {2014},
	Bdsk-Url-1 = {http://dx.doi.org/10.1038/nature13595},
	Bdsk-Url-2 = {http://onlinelibrary.wiley.com/doi/10.1111/add.12822/abstract}}

@article{edwards:2014,
	Abstract = {AIMS: Alcohol problems (AP) contribute substantially to the global disease burden. Twin and family studies suggest that AP are genetically influenced, though few studies have identified variants or genes that are robustly associated with risk. This study identifies genetic and genomic influences on AP during young adulthood, which is often when drinking habits are established.
DESIGN: We conducted a genome-wide association study of AP. We further conducted gene-based tests, gene ontology analyses, and functional genomic enrichment analyses to assess genomic factors beyond single variants that are relevant to AP.
SETTING: The Avon Longitudinal Study of Parents and Children, a large population-based study of a UK birth cohort.
PARTICIPANTS: Genetic and phenotypic data were available for 4304 participants.
MEASUREMENTS: The AP phenotype was a factor score derived from items from the Alcohol Use Disorders Identification Test, symptoms of DSM-IV alcohol dependence, and three additional problem-related items.
FINDINGS: One variant met genome-wide significance criteria. Four out of 22,880 genes subjected to gene-based analyses survived a stringent significance threshold (q < .05); none of these have been previously implicated in alcohol-related phenotypes. Several biologically plausible gene ontologies were statistically over-represented among implicated SNPs. SNPs on the Illumina 550 K SNP chip accounted for ~5\% of the phenotypic variance in AP.
CONCLUSIONS: Genetic and genomic factors appear to play a role in alcohol problems in young adults. Genes involved in nervous system-related processes, such as signal transduction and neurogenesis, potentially contribute to liability to alcohol problems, as do genes expressed in non-brain tissues. This article is protected by copyright. All rights reserved.},
	Author = {Edwards, Alexis C and Aliev, Fazil and Wolen, Aaron R and Salvatore, Jessica E and Gardner, Charles O and McMahon, George and Evans, David M and Macleod, John and Hickman, Matt and Dick, Danielle M and Kendler, Kenneth S},
	Date-Added = {2014-12-09 02:26:57 +0000},
	Date-Modified = {2014-12-09 02:26:57 +0000},
	Doi = {10.1111/add.12822},
	Journal = {Addiction},
	Journal-Full = {Addiction},
	Keywords = {ALSPAC; Alcohol problems; GWAS; polygenic},
	Month = {Dec},
	Pmid = {25439982},
	Pst = {aheadofprint},
	Title = {Genomic influences on alcohol problems in a population-based sample of young adults},
	Url = {http://dx.doi.org/10.1111/add.12822},
	Year = {2014},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/add.12822}}

@unpublished{wolen:2015fk,
	Author = {Wolen, Aaron R and Kendler, Kenneth S and Reimers, Mark A},
	Date-Added = {2013-10-15 21:39:08 +0000},
	Date-Modified = {2015-12-07 12:54:31 +0000},
	Title = {Integrative use of genomic information uncovers many further loci of small effect in major psychiatric disorders},
	Year = {2015}}

@unpublished{wolen:2017,
	Author = {Wolen, Aaron R and Fernandez, Leopoldo and Fenstermacher, David and Olex, Amy and Kazuaki, Takabe and Dozmorov, Mikhail},
	Date-Added = {2013-10-15 21:37:02 +0000},
	Date-Modified = {2017-08-21 18:53:58 +0000},
	Title = {Widespread Deregulation of Cancer-related Genes in Patient Derived Colorectal Cancer Explants},
	Year = {2017}}

@misc{wolen:2013,
	Abstract = {It seems likely that the genetic contribution of common variants to the risk of major psychiatric disorders is distributed across at least hundreds of variants of very small effect. Even very large studies are under-powered to detect a large number of such effects, without being overwhelmed by false positives. We think that variants that carry these modest risks are mostly in exons or in functional non-coding DNA. If we can combine several sources of information to identify functional DNA, we may be able to identify these risk SNPs better. We propose here an Empirical Bayes approach to combining genomic information with association information from Genome-wide Association Studies (GWAS), to identify individual SNPs and genes that are implicated in Schizophrenia.
},
	Author = {Wolen, Aaron R and Kendler, Kenneth S and Reimers, Mark A},
	Date-Added = {2013-10-09 23:12:39 +0000},
	Date-Modified = {2017-08-21 15:30:43 +0000},
	Howpublished = {Presented at Gordon Research Conference on Neuroethology: Behavior, Evolution and Neurobiology},
	Month = {Aug},
	Title = {Integrative use of genomic information uncovers many further loci of small effect in major psychiatric disorders},
	Year = {2013}}

@misc{edwards:2013fk,
	Author = {Edwards, Alexis C and Wolen, Aaron R and Aliev, Fazil and Reimers, Mark A. and Hickman, Matt and Lewis, Glyn and Dick, Danielle M. and Kendler, Kenneth S},
	Date-Added = {2013-10-09 23:08:14 +0000},
	Date-Modified = {2013-10-09 23:11:48 +0000},
	Howpublished = {Presented at the 21st annual World Congress of Psychiatric Genetics},
	Month = {Oct},
	Title = {Genomic influences on alcohol problems in a population-based sample of young adults},
	Year = {2013}}

@misc{kotov:2005zr,
	Author = {Kotov, Roman and Gamez, W and Benson, Sarah and Wolen, Aaron R and Luchman, Joseph and Boldebuck, L},
	Date-Added = {2013-09-09 17:21:01 +0000},
	Date-Modified = {2013-09-09 17:21:01 +0000},
	Howpublished = {Presented at the 39th annual conference of the Association for Behavioral and Cognitive Therapies},
	Publisher = {Association for Behavioral and Cognitive Therapies},
	Title = {Personality and symptoms of anxiety and depression: A prospective study},
	Year = {2005}}

@misc{phillips:2009ys,
	Author = {Phillips, Charles A and Perkins A D and Wolen, Aaron R and Chesler, Elissa J and Miles, Michael F and Langston, Michael A},
	Date-Added = {2013-09-09 17:21:01 +0000},
	Date-Modified = {2013-09-28 21:24:48 +0000},
	Howpublished = {Presented at the 38th annual conference of the Society for Neuroscience},
	Month = {November},
	Publisher = {Society for Neuroscience},
	Title = {Graph-theoretical algorithmic analysis of microarray data for identification of murine brain ethanol-regulated gene networks},
	Year = {2008}}

@misc{wolen:2009vn,
	Author = {Wolen, Aaron R and Green, Thomas A and Miles, Michael F},
	Date-Added = {2013-09-09 17:21:01 +0000},
	Date-Modified = {2013-09-28 21:24:22 +0000},
	Howpublished = {Presented at the 38th annual conference of the Society for Neuroscience},
	Month = {November},
	Publisher = {Society for Neuroscience},
	Title = {Expression genetics analysis of responses to acute ethanol in mouse prefrontal cortex},
	Year = {2008}}

@misc{wolen:2009fk,
	Author = {Wolen, Aaron R and Putman, Alex H and Bruce, Nathan A and Miles, Michael F},
	Date-Added = {2013-09-09 17:21:01 +0000},
	Date-Modified = {2013-09-28 21:45:57 +0000},
	Howpublished = {Presented at the 32nd annual conference of the Research Society on Alcoholism},
	Month = {June},
	Pdf = {http://aaronwolen.com/portfolio/2009-wolen-poster-rsa.pdf},
	Publisher = {Alcoholism-Clinical and Experimental Research},
	Title = {Fine mapping a quantitative trait locus for the anxiolytic-like response to acute ethanol in BXD recombinant inbred strains},
	Year = {2009}}

@misc{miles:2009uq,
	Author = {Miles, Michael F and Wolen, Aaron R and Putman, Alex H and Bruce, Nathan A},
	Date-Added = {2013-09-09 17:21:01 +0000},
	Date-Modified = {2013-09-28 21:50:23 +0000},
	Howpublished = {Presented at the 32nd annual conference of the Research Society on Alcoholism},
	Month = {June},
	Publisher = {Alcoholism-Clinical and Experimental Research},
	Title = {Gene expression networks in prefrontal cortex contributing to ethanol anxiolytic effects},
	Year = {2009}}

@misc{barker:2009kx,
	Author = {Barker, Sandra B and Pandurangi, A K and Knisely, Janet S and McCain, Nancy L and Schubert, C M and Murphy, P J and Burakgazi, Erin and Dalkilic A and Wolen, Aaron R},
	Date-Added = {2013-09-09 17:21:01 +0000},
	Date-Modified = {2013-09-09 17:21:01 +0000},
	Howpublished = {Presented at the 162nd annual conference of the American Psychiatric Association},
	Publisher = {American Psychiatric Association},
	Title = {Autonomic, endocrine and neurophysiologic correlates of human-animal interaction},
	Year = {2009}}

@misc{wolen:2010jk,
	Author = {Wolen, Aaron R and Phillips, Charles A and Langston, Michael A and Putman, Alex H and Williams, Robert W and Lu, Lu and Miles, Michael F},
	Date-Added = {2013-09-09 17:21:01 +0000},
	Date-Modified = {2013-09-28 21:46:29 +0000},
	Howpublished = {Presented at the 33rd annual conference of the Research Society on Alcoholism},
	Month = {June},
	Pdf = {http://aaronwolen.com/portfolio/2010-wolen-poster-rsa.pdf},
	Publisher = {Alcoholism-Clinical and Experimental Research},
	Title = {Elucidation of ethanol responsive gene networks in {{BXD}} recombinant inbred strains},
	Year = {2010}}

@misc{harenza:2011yq,
	Author = {Harenza, JoLynne and Wolen, Aaron R and Putman, Alex H and Miles, Michael F},
	Date-Added = {2013-09-09 17:21:01 +0000},
	Date-Modified = {2013-09-28 21:50:04 +0000},
	Howpublished = {Presented at the 34th annual conference of the Research Society on Alcoholism. Alcoholism},
	Month = {June},
	Number = {6},
	Publisher = {Alcoholism-Clinical and Experimental Research},
	Title = {Genetic dissection of an acute ethanol-induced anxiolysis QTL},
	Volume = {35},
	Year = {2011}}

@misc{farris:2011uq,
	Author = {Farris, Sean P and Wolen, Aaron R and Miles, Michael F},
	Date-Added = {2013-09-09 17:21:01 +0000},
	Date-Modified = {2013-09-28 21:49:55 +0000},
	Howpublished = {Presented at the 34th annual conference of the Research Society on Alcoholism},
	Month = {June},
	Number = {6},
	Pages = {258A},
	Publisher = {Alcoholism-Clinical and Experimental Research},
	Title = {Myelin gene expression: Implications for alcohol abuse and dependence},
	Volume = {35},
	Year = {2011}}

@misc{wolen:2011jk,
	Author = {Wolen, Aaron R and Phillips, Charles A and Langston, Michael A and Putman, Alex H and Vorster, Paul J and Bruce, Nathan A and York, Timothy P and Williams, Robert W and Lu, Lu and Miles, Michael F},
	Date-Added = {2013-09-09 17:21:01 +0000},
	Date-Modified = {2013-09-28 21:48:44 +0000},
	Howpublished = {Presented at the 34th annual conference of the Research Society on Alcoholism},
	Month = {June},
	Number = {6},
	Pages = {260A},
	Pdf = {http://aaronwolen.com/portfolio/2011-wolen-poster-rsa.pdf},
	Publisher = {Alcoholism-Clinical and Experimental Research},
	Title = {Intra- and inter-regional ethanol responsive gene networks of the mesolimbocortical reward pathway},
	Volume = {35},
	Year = {2011}}

@misc{maluf:2011jk,
	Abstract = {Background. Improvement in short term outcomes in kidney transplantation (Tx) had been achieved. However, long-term outcomes have not changed. MicroRNAs (miRNAs), a recently discovered class of noncoding RNAs, have the potential of being biomarkers of allograft status.

Methods. Gene expression (mRNA) and miRNA signatures were evaluated using microarray platforms in kidney allograft biopsies that were histological defi ned as IF/TA (N=13) and normal allograft (NA, N= 5). Total RNA was isolated from urine samples collected at the biopsy time. Five miRNAs (miR142-3p, miR-32, miR-204, miR-107, miR-211) were chosen for being evaluated in urine samples from the total miRNA signature identified in the same kidney biopsies. Selection was based on in silico predicted miRNA targeting of gene products identified as differentially expressed in the mRNA signature of the same biopsies. An independent set of 20 prospectively studied kidney transplant patients, urine samples were collected and evaluated for miRNA expression at 3, 9, and 12 months post-KTx. MiRNA expression was analyzed by QPCR analysis. Expression of individual miRNAs was measured through Ct value with relative expression assessed using two endogenous controls (RNU44, RNU48) for each sample.

Results. Spearman's rank correlation indicated a good correlation between the miRNAs in IF/TA tissues and urine samples (r=0.912, p=0.0012). The prospective evaluation of the miRNA panel expression in urine samples from the independent set of patients (classified according graft function (eGFR >45 mL/min (n=11) or ≤ 45 mL/min (n=9) at 12 month post-KTx), resulted in 3 miRNAs (miR142-3p, miR-32, miR-204), being able to differentiate patients according with their graft function at every point of the analysis. Interesting, miR-107 and miR-211 were able to differentiate patients according their graft function at 3-9 months but not at 12 months post-KTx. Furthermore, these two miRNAs were differentially expressed also between patients with and without delayed graft function and they might be good markers of recovery of graft function.

Conclusions. miRNAs can be detected in urine samples and have the potential for being non-invasive biomarkers of kidney graft function. There was a correlation between tissues and urine samples at the diagnosis time (NA vs. IF/TA). Prospective evaluation of a limited panel of miRNAs was associated with graft function at 12 months post-KTx.},
	Author = {Maluf, D G and Scian, M J and Suh, J L and Wolen, Aaron R and Kapoor S and Posner, M and Cotterell, A and King, A L and Mas, V},
	Date-Added = {2013-09-09 17:21:01 +0000},
	Date-Modified = {2013-09-28 21:44:42 +0000},
	Howpublished = {Presented at the American Transplant Congress.},
	Month = {April},
	Number = {2},
	Pages = {34},
	Publisher = {American Journal of Transplantation},
	Title = {Urine miRNA panel as accurate biomarkers for monitoring kidney graft function},
	Volume = {11},
	Year = {2011}}

@article{Wolen:2011fk,
	Abstract = {For complex disorders such as alcoholism, identifying the genes linked to these diseases and their specific roles is difficult. Traditional genetic approaches, such as genetic association studies (including genome-wide association studies) and analyses of quantitative trait loci (QTLs) in both humans and laboratory aniMals already have helped identify some candidate genes. However, because of technical obstacles, such as the sMall impact of any individual gene, these approaches only have limited effectiveness in identifying specific genes that contribute to complex diseases. The emerging field of systems biology, which allows for analyses of entire gene networks, may help researchers better elucidate the genetic basis of alcoholism, both in humans and in aniMal models. Such networks can be identified using approaches such as high-throughput molecular profiling (e.g., through microarray-based gene expression analyses) or strategies referred to as genetical genomics, such as the mapping of expression QTLs (eQTLs). Characterization of gene networks can shed light on the biological pathways underlying complex traits and provide the functional context for identifying those genes that contribute to disease development.},
	Author = {Wolen, Aaron R and Miles, Michael F},
	Date-Added = {2012-10-26 18:56:52 +0000},
	Date-Modified = {2013-09-30 20:37:48 +0000},
	Editor = {Williams, Robert W and Noronha, Antonio},
	Journal = {Alcohol Research: Current Reviews},
	Number = {3},
	Pages = {306},
	Pdf = {http://pubs.niaaa.nih.gov/publications/arcr343/306-317.pdf},
	Publisher = {National Institute on Alcohol Abuse and Alcoholism},
	Series = {The Journal of the National Institute on Alcohol Abuse and Alcoholism},
	Title = {Identifying Gene Networks Underlying the Neurobiology of Ethanol and Alcoholism},
	Url = {http://pubs.niaaa.nih.gov/publications/arcr343/306-317.htm},
	Volume = {34},
	Year = {2012},
	Bdsk-Url-1 = {http://pubs.niaaa.nih.gov/publications/arcr343/306-317.htm}}

@article{Costin:2012ys,
	Abstract = {BACKGROUND: Glucocorticoid hormones modulate acute and chronic behavioral and molecular responses to drugs of abuse including psychostimulants and opioids. There is growing evidence that glucocorticoids might also modulate behavioral responses to ethanol ( EtOH ). Acute EtOH activates the hypothalamic-pituitary-adrenal axis, causing the release of adrenal glucocorticoid hormones. Our prior genomic studies suggest that glucocorticoids play a role in regulating gene expression in the prefrontal cortex (PFC) of DBA2/J (D2) mice following acute EtOH administration. However, few studies have analyzed the role of glucocorticoid signaling in behavioral responses to acute EtOH . Such work could be significant, given the predictive value for the level of response to acute EtOH in the risk for alcoholism. METHODS: We studied whether the glucocorticoid receptor (GR) antagonist, RU-486, or adrenalectomy (ADX) altered male D2 mouse behavioral responses to acute (locomotor activation, anxiolysis, or loss-of-righting reflex [LORR]) or repeated (sensitization) EtOH treatment. Whole-genome microarray analysis and bioinformatics approaches were used to identify PFC candidate genes possibly responsible for altered behavioral responses to EtOH following ADX. RESULTS: ADX and RU-486 both impaired acute EtOH (2 g/kg)-induced locomotor activation in D2 mice without affecting basal locomotor activity. However, neither ADX nor RU-486 altered the initiation of EtOH sensitization (locomotor activation or jump counts), EtOH -induced anxiolysis, or LORR. ADX mice showed microarray gene expression changes in PFC that significantly overlapped with acute EtOH -responsive gene sets derived by our prior microarray studies. Q-rtPCR analysis verified that ADX decreased PFC expression of Fkbp5 while significantly increasing Gpr6 expression. In addition, high-dose RU-486 pretreatment blunted EtOH -induced Fkbp5 expression. CONCLUSIONS: Our studies suggest that EtOH 's activation of adrenal glucocorticoid release and subsequent GR activation may partially modulate EtOH 's acute locomotor activation in male D2 mice. Furthermore, because adrenal glucocorticoid basal tone regulated PFC gene expression, including a significant set of acute EtOH -responsive genes, this suggests that glucocorticoid-regulated PFC gene expression may be an important factor modulating acute behavioral responses to EtOH .},
	Author = {Costin, Blair N and Wolen, Aaron R and Fitting, Sylvia and Shelton, Keith L and Miles, Michael F},
	Date-Added = {2012-10-25 20:46:10 +0000},
	Date-Modified = {2013-10-30 17:59:45 +0000},
	Doi = {10.1111/j.1530-0277.2012.01841.x},
	Journal = {Alcoholism, Clinical and Experimental Research},
	Journal-Full = {Alcoholism, Clinical and Experimental Research},
	Month = {January},
	Number = {1},
	Pages = {56-66},
	Pdf = {http://onlinelibrary.wiley.com/doi/10.1111/j.1530-0277.2012.01841.x/pdf},
	Pmid = {22671426},
	Pst = {aheadofprint},
	Title = {Role of Adrenal Glucocorticoid Signaling in Prefrontal Cortex Gene Expression and Acute Behavioral Responses to Ethanol},
	Url = {http://onlinelibrary.wiley.com/doi/10.1111/j.1530-0277.2012.01841.x/full},
	Volume = {37},
	Year = {2013},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1530-0277.2012.01841.x},
	Bdsk-Url-2 = {http://onlinelibrary.wiley.com/doi/10.1111/j.1530-0277.2012.01841.x/full}}

@article{Wolen:2012vn,
	Abstract = {BACKGROUND: Individual differences in initial sensitivity to ethanol are strongly related to the heritable risk of alcoholism in humans. To elucidate key molecular networks that modulate ethanol sensitivity we performed the first systems genetics analysis of ethanol-responsive gene expression in brain regions of the mesocorticolimbic reward circuit (prefrontal cortex, nucleus accumbens, and ventral midbrain) across a highly diverse family of 27 isogenic mouse strains (BXD panel) before and after treatment with ethanol.
RESULTS: Acute ethanol altered the expression of ~2,750 genes in one or more regions and 400 transcripts were jointly modulated in all three. Ethanol-responsive gene networks were extracted with a powerful graph theoretical method that efficiently summarized ethanol's effects. These networks correlated with acute behavioral responses to ethanol and other drugs of abuse. As predicted, networks were heavily populated by genes controlling synaptic transmission and neuroplasticity. Several of the most densely interconnected network hubs, including Kcnma1 and Gsk3β, are known to influence behavioral or physiological responses to ethanol, validating our overall approach. Other major hub genes like Grm3, Pten and Nrg3 represent novel targets of ethanol effects. Networks were under strong genetic control by variants that we mapped to a small number of chromosomal loci. Using a novel combination of genetic, bioinformatic and network-based approaches, we identified high priority cis-regulatory candidate genes, including Scn1b, Gria1, Sncb and Nell2.
CONCLUSIONS: The ethanol-responsive gene networks identified here represent a previously uncharacterized intermediate phenotype between DNA variation and ethanol sensitivity in mice. Networks involved in synaptic transmission were strongly regulated by ethanol and could contribute to behavioral plasticity seen with chronic ethanol. Our novel finding that hub genes and a small number of loci exert major influence over the ethanol response of gene networks could have important implications for future studies regarding the mechanisms and treatment of alcohol use disorders.},
	Author = {Wolen, Aaron R and Phillips, Charles A and Langston, Michael A and Putman, Alex H and Vorster, Paul J and Bruce, Nathan A and York, Timothy P and Williams, Robert W and Miles, Michael F},
	Date-Added = {2012-10-25 20:46:09 +0000},
	Date-Modified = {2017-08-21 15:44:01 +0000},
	Doi = {10.1371/journal.pone.0033575},
	Journal = {PLoS One},
	Journal-Full = {PLoS One},
	Month = {April},
	Number = {4},
	Pages = {e33575},
	Pmc = {PMC3325236},
	Pmid = {22511924},
	Pst = {ppublish},
	Title = {Genetic dissection of acute ethanol responsive gene networks in prefrontal cortex: functional and mechanistic implications},
	Url = {http://www.plosone.org/article/info:doi/10.1371/journal.pone.0033575},
	Volume = {7},
	Year = {2012},
	Bdsk-Url-1 = {http://dx.doi.org/10.1371/journal.pone.0033575},
	Bdsk-Url-2 = {http://www.plosone.org/article/info:doi/10.1371/journal.pone.0033575}}

@article{Scian:2011kx,
	Abstract = {Despite the advances in immunosuppression, renal allograft attrition over time remains unabated due to chronic allograft dysfunction (CAD) with interstitial fibrosis (IF) and tubular atrophy (TA). We aimed to evaluate microRNA (miRNA) signatures in CAD with IF/TA and appraise correlation with paired urine samples and potential utility in prospective evaluation of graft function. MiRNA signatures were established between CAD with IF/TA versus normal allografts by microarray. Validation of the microarray results and prospective evaluation of urine samples was performed using real-time quantitative-PCR (RT-qPCR). Fifty-six miRNAs were identified in samples with CAD-IF/TA. Five miRNAs were selected for further validation based on array fold change, p-value and in silico predicted mRNA targets. We confirmed the differential expression of these five miRNAs by RT-qPCR using an independent set of samples. Differential expression was detected for miR-142-3p, miR-204, miR-107 and miR-211 (p < 0.001) and miR-32 (p < 0.05). Furthermore, differential expression of miR-142-3p (p < 0.01), miR-204 (p < 0.01) and miR-211 (p < 0.05) was also observed between patient groups in urine samples. A characteristic miRNA signature for IF/TA that correlates with paired urine samples was identified. These results support the potential use of miRNAs as noninvasive markers of IF/TA and for monitoring graft function.},
	Author = {Scian, M J and Maluf, D G and David, K G and Archer, K J and Suh, J L and Wolen, A R and Mba, M U and Massey, H D and King, A L and Gehr, T and Cotterell, A and Posner, M and Mas, V},
	Date-Added = {2012-10-25 20:46:08 +0000},
	Date-Modified = {2013-07-07 19:20:58 +0000},
	Doi = {10.1111/j.1600-6143.2011.03666.x},
	Journal = {American Journal of Transplantation},
	Journal-Full = {American journal of transplantation},
	Mesh = {Adult; Base Sequence; Creatinine; Female; Glomerular Filtration Rate; Graft Rejection; Humans; Kidney Transplantation; Male; MicroRNAs; Middle Aged; Oligonucleotide Array Sequence Analysis; Real-Time Polymerase Chain Reaction; Transplantation, Homologous; Urine},
	Month = {Oct},
	Number = {10},
	Pages = {2110-22},
	Pdf = {http://onlinelibrary.wiley.com/doi/10.1111/j.1600-6143.2011.03666.x/pdf},
	Pmc = {PMC3184368},
	Pmid = {21794090},
	Pst = {ppublish},
	Title = {{MicroRNA} profiles in allograft tissues and paired urines associate with chronic allograft dysfunction with {IF/TA}},
	Url = {http://onlinelibrary.wiley.com/doi/10.1111/j.1600-6143.2011.03666.x/full},
	Volume = {11},
	Year = {2011},
	Bdsk-Url-1 = {http://dx.doi.org/10.1111/j.1600-6143.2011.03666.x},
	Bdsk-Url-2 = {http://onlinelibrary.wiley.com/doi/10.1111/j.1600-6143.2011.03666.x/full}}

@incollection{Farris:2010uq,
	Abstract = {Recent simultaneous progress in human and animal model genetics and the advent of microarray whole genome expression profiling have produced prodigious data sets on genetic loci, potential candidate genes, and differential gene expression related to alcoholism and ethanol behaviors. Validated target genes or gene networks functioning in alcoholism are still of meager proportions. Genetical genomics, which combines genetic analysis of both traditional phenotypes and whole genome expression data, offers a potential methodology for characterizing brain gene networks functioning in alcoholism. This chapter will describe concepts, approaches, and recent findings in the field of genetical genomics as it applies to alcohol research.},
	Author = {Farris, Sean P and Wolen, Aaron R and Miles, Michael F},
	Booktitle = {Functional plasticity and genetic variation: Insights into the neurobiology of alcoholism},
	Date-Added = {2012-10-25 20:46:07 +0000},
	Date-Modified = {2012-10-26 19:11:54 +0000},
	Doi = {10.1016/S0074-7742(10)91004-0},
	Editor = {Reilly, Matthew T and Lovinger, David M},
	Issn = {0074-7742},
	Keywords = {Brain gene expression},
	Mesh = {Alcoholism; Animals; Brain; Ethanol; Gene Expression Profiling; Genome-Wide Association Study; Humans; Neurobiology; Oligonucleotide Array Sequence Analysis},
	Pages = {95-128},
	Pmc = {PMC3427772},
	Pmid = {20813241},
	Pst = {ppublish},
	Publisher = {Academic Press},
	Series = {International Review of Neurobiology},
	Title = {Using expression genetics to study the neurobiology of ethanol and alcoholism},
	Url = {http://www.sciencedirect.com/science/article/pii/S0074774210910040},
	Volume = {91},
	Year = {2010},
	Bdsk-Url-1 = {http://dx.doi.org/10.1016/S0074-7742(10)91004-0},
	Bdsk-Url-2 = {http://www.sciencedirect.com/science/article/pii/S0074774210910040}}

@article{Barker:2008fk,
	Abstract = {This article provides a review of research published since 1980 on the benefits of human-companion animal interaction. Studies focusing on the benefits of pet ownership are presented first, followed by research on the benefits of interacting with companion animals that are not owned by the subject (animal-assisted activities). While most of the published studies are descriptive and have been conducted with convenience samples, a promising number of controlled studies support the health benefits of interacting with companion animals. Future research employing more rigorous designs and systematically building upon a clearly defined line of inquiry is needed to advance our knowledge of the benefits of human-companion animal interaction.},
	Author = {Barker, Sandra B and Wolen, Aaron R},
	Date-Added = {2012-10-25 20:46:06 +0000},
	Date-Modified = {2013-09-30 20:36:02 +0000},
	Doi = {10.3138/jvme.35.4.487},
	Journal = {Journal of Veterinary Medical Education},
	Journal-Full = {Journal of Veterinary Medical Education},
	Mesh = {Animals; Animals, Domestic; Bonding, Human-Pet; Cardiovascular Diseases; Congresses as Topic; Health Status; Humans; Mental Disorders; Mental Health; Ownership; Social Support},
	Month = {February},
	Number = {4},
	Pages = {487-95},
	Pmid = {19228898},
	Pst = {ppublish},
	Title = {The benefits of human-companion animal interaction: a review},
	Url = {http://jvmeonline.metapress.com/content/k67852wh16k26267},
	Volume = {35},
	Year = {2008},
	Bdsk-Url-1 = {http://dx.doi.org/10.3138/jvme.35.4.487},
	Bdsk-Url-2 = {http://jvmeonline.metapress.com/content/k67852wh16k26267}}