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class="c-pagination__item">11</a></li><li class="c-pagination__next"><a href="" aria-label="go to Next result set">Next</a></li></ul></nav></div><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/30t3n9z8"><div class="c-clientmarkup">Insulin-Like Growth Factor, Inflammation, and MRI Markers of Alzheimer’s Disease in Predominantly Middle-Aged Adults</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AWittfeld%2C%20Katharina">Wittfeld, Katharina</a>; </li><li><a href="/search/?q=author%3ARaman%2C%20Mekala%20R">Raman, Mekala R</a>; </li><li><a href="/search/?q=author%3AConner%2C%20Sarah%20C">Conner, Sarah C</a>; </li><li><a href="/search/?q=author%3AAslam%2C%20Asra">Aslam, Asra</a>; </li><li><a href="/search/?q=author%3ATeumer%2C%20Alexander">Teumer, Alexander</a>; </li><li><a href="/search/?q=author%3ANauck%2C%20Matthias">Nauck, Matthias</a>; </li><li><a href="/search/?q=author%3AHosten%2C%20Norbert">Hosten, Norbert</a>; </li><li><a href="/search/?q=author%3AHabes%2C%20Mohamad">Habes, Mohamad</a>; </li><li><a href="/search/?q=author%3ADeCarli%2C%20Charles">DeCarli, Charles</a>; </li><li><a href="/search/?q=author%3AVasan%2C%20Ramachandran%20S">Vasan, Ramachandran S</a>; </li><li><a href="/search/?q=author%3ABeiser%2C%20Alexa%20S">Beiser, Alexa S</a>; </li><li><a href="/search/?q=author%3AHimali%2C%20Jayandra%20J">Himali, Jayandra J</a>; </li><li><a href="/search/?q=author%3ASeshadri%2C%20Sudha">Seshadri, Sudha</a>; </li><li><a href="/search/?q=author%3AGrabe%2C%20Hans%20J">Grabe, Hans J</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ASatizabal%2C%20Claudia%20L">Satizabal, Claudia L</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucd_postprints">UC Davis Previously Published Works</a> (<!-- -->2022<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Background</h3>Insulin-like growth factor 1 (IGF-1) signaling has been implicated in Alzheimer's disease pathogenesis, and further evidence suggests inflammation can be a moderator of this association. However, most research to date has been conducted on older adults.<h3>Objective</h3>To investigate the association of serum IGF-1 and IGF binding protein 3 (IGFBP-3) concentrations with MRI markers of Alzheimer's disease in predominantly middle-aged adults, and further assess moderation by chronic inflammation.<h3>Methods</h3>We included participants from the Framingham Heart Study (n = 1,852, mean age 46±8, 46% men) and the Study of Health in Pomerania (n = 674, mean age 50±13, 42% men) with available serum IGF-1, IFGBP-3, as well as brain MRI. IGF-1 and IFGBP-3 were related to MRI outcomes (i.e., total brain, cortical gray matter, white matter, white matter hyperintensities (WMH), and hippocampal volumes) using multivariable regression models adjusting for potential confounders. Subgroup analyses by C-reactive protein (CRP) concentrations were also performed. Cohort-specific summary statistics were meta-analyzed using random-effects models and corrected for multiple comparisons.<h3>Results</h3>Meta-analysis results revealed that higher IGF-1 concentrations were associated with lower WMH (estimate [β] [95% CI], -0.05 [-0.09, -0.02], p = 0.006) and larger hippocampal volumes (0.07 [0.02, 0.12], p = 0.01), independent of vascular risk factors. These associations occurred predominantly in individuals with CRP concentrations < 75th percentile. We did not observe associations between IGFBP-3 and MRI outcomes.<h3>Conclusion</h3>Our findings suggest that IGF-1-related signaling may be implicated in brain health as early as midlife.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/30t3n9z8"><img src="/cms-assets/eb157c1711c8831e564c8b5e30e04871f5782b645a05bf8164259f2d0c5f700a" alt="Cover page: Insulin-Like Growth Factor, Inflammation, and MRI Markers of Alzheimer’s Disease in Predominantly Middle-Aged Adults"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/2sz5n70h"><div class="c-clientmarkup">Neandertal Introgression Sheds Light on Modern Human Endocranial Globularity.</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AGunz%2C%20Philipp">Gunz, Philipp</a>; </li><li><a href="/search/?q=author%3ATilot%2C%20Amanda">Tilot, Amanda</a>; </li><li><a href="/search/?q=author%3AWittfeld%2C%20Katharina">Wittfeld, Katharina</a>; </li><li><a href="/search/?q=author%3ATeumer%2C%20Alexander">Teumer, Alexander</a>; </li><li><a href="/search/?q=author%3AShapland%2C%20Chin">Shapland, Chin</a>; </li><li><a href="/search/?q=author%3ADannemann%2C%20Michael">Dannemann, Michael</a>; </li><li><a href="/search/?q=author%3AVernot%2C%20Benjamin">Vernot, Benjamin</a>; </li><li><a href="/search/?q=author%3ANeubauer%2C%20Simon">Neubauer, Simon</a>; </li><li><a href="/search/?q=author%3AGuadalupe%2C%20Tulio">Guadalupe, Tulio</a>; </li><li><a href="/search/?q=author%3AFern%C3%A1ndez%2C%20Guill%C3%A9n">Fernández, Guillén</a>; </li><li><a href="/search/?q=author%3ABrunner%2C%20Han">Brunner, Han</a>; </li><li><a href="/search/?q=author%3AEnard%2C%20Wolfgang">Enard, Wolfgang</a>; </li><li><a href="/search/?q=author%3AFallon%2C%20James">Fallon, James</a>; </li><li><a href="/search/?q=author%3AHosten%2C%20Norbert">Hosten, Norbert</a>; </li><li><a href="/search/?q=author%3AV%C3%B6lker%2C%20Uwe">Völker, Uwe</a>; </li><li><a href="/search/?q=author%3AProfico%2C%20Antonio">Profico, Antonio</a>; </li><li><a href="/search/?q=author%3ADi%20Vincenzo%2C%20Fabio">Di Vincenzo, Fabio</a>; </li><li><a href="/search/?q=author%3AManzi%2C%20Giorgio">Manzi, Giorgio</a>; </li><li><a href="/search/?q=author%3AKelso%2C%20Janet">Kelso, Janet</a>; </li><li><a href="/search/?q=author%3ASt%20Pourcain%2C%20Beate">St Pourcain, Beate</a>; </li><li><a href="/search/?q=author%3AHublin%2C%20Jean-Jacques">Hublin, Jean-Jacques</a>; </li><li><a href="/search/?q=author%3AFranke%2C%20Barbara">Franke, Barbara</a>; </li><li><a href="/search/?q=author%3AP%C3%A4%C3%A4bo%2C%20Svante">Pääbo, Svante</a>; </li><li><a href="/search/?q=author%3AGrabe%2C%20Hans">Grabe, Hans</a>; </li><li><a href="/search/?q=author%3AFisher%2C%20Simon">Fisher, Simon</a>; </li><li><a href="/search/?q=author%3AVan%20Erp%2C%20Theodorus">Van Erp, Theodorus</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AMacciardi%2C%20Fabio">Macciardi, Fabio</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/uci_postprints">UC Irvine Previously Published Works</a> (<!-- -->2019<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">One of the features that distinguishes modern humans from our extinct relatives and ancestors is a globular shape of the braincase [1-4]. As the endocranium closely mirrors the outer shape of the brain, these differences might reflect altered neural architecture [4, 5]. However, in the absence of fossil brain tissue, the underlying neuroanatomical changes as well as their genetic bases remain elusive. To better understand the biological foundations of modern human endocranial shape, we turn to our closest extinct relatives: the Neandertals. Interbreeding between modern humans and Neandertals has resulted in introgressed fragments of Neandertal DNA in the genomes of present-day non-Africans [6, 7]. Based on shape analyses of fossil skull endocasts, we derive a measure of endocranial globularity from structural MRI scans of thousands of modern humans and study the effects of introgressed fragments of Neandertal DNA on this phenotype. We find that Neandertal alleles on chromosomes 1 and 18 are associated with reduced endocranial globularity. These alleles influence expression of two nearby genes, UBR4 and PHLPP1, which are involved in neurogenesis and myelination, respectively. Our findings show how integration of fossil skull data with archaic genomics and neuroimaging can suggest developmental mechanisms that may contribute to the unique modern human endocranial shape.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/2sz5n70h"><img src="/cms-assets/e54c273ceba17455d4a6f58bb68146eb436f0c9acec3f6b92daba4dea81e590b" alt="Cover page: Neandertal Introgression Sheds Light on Modern Human Endocranial Globularity."/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/6jv896t8"><div class="c-clientmarkup">Investigation of the Interplay between Circulating Lipids and IGF-I and Relevance to Breast Cancer Risk: An Observational and Mendelian Randomization Study</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ATan%2C%20Vanessa%20Y">Tan, Vanessa Y</a>; </li><li><a href="/search/?q=author%3ABull%2C%20Caroline%20J">Bull, Caroline J</a>; </li><li><a href="/search/?q=author%3ABiernacka%2C%20Kalina%20M">Biernacka, Kalina M</a>; </li><li><a href="/search/?q=author%3ATeumer%2C%20Alexander">Teumer, Alexander</a>; </li><li><a href="/search/?q=author%3ARichardson%2C%20Tom%20G">Richardson, Tom G</a>; </li><li><a href="/search/?q=author%3ASanderson%2C%20Eleanor">Sanderson, Eleanor</a>; </li><li><a href="/search/?q=author%3ACorbin%2C%20Laura%20J">Corbin, Laura J</a>; </li><li><a href="/search/?q=author%3ADudding%2C%20Tom">Dudding, Tom</a>; </li><li><a href="/search/?q=author%3AQi%2C%20Qibin">Qi, Qibin</a>; </li><li><a href="/search/?q=author%3AKaplan%2C%20Robert%20C">Kaplan, Robert C</a>; </li><li><a href="/search/?q=author%3ARotter%2C%20Jerome%20I">Rotter, Jerome I</a>; </li><li><a href="/search/?q=author%3AFriedrich%2C%20Nele">Friedrich, Nele</a>; </li><li><a href="/search/?q=author%3AV%C3%B6lker%2C%20Uwe">Völker, Uwe</a>; </li><li><a href="/search/?q=author%3AMayerle%2C%20Julia">Mayerle, Julia</a>; </li><li><a href="/search/?q=author%3APerks%2C%20Claire%20M">Perks, Claire M</a>; </li><li><a href="/search/?q=author%3AHolly%2C%20Jeff%20MP">Holly, Jeff MP</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ATimpson%2C%20Nicholas%20J">Timpson, Nicholas J</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (<!-- -->2021<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Background</h3>Circulating lipids and insulin-like growth factor 1 (IGF-I) have been reliably associated with breast cancer. Observational studies suggest an interplay between lipids and IGF-I, however, whether these relationships are causal and if pathways from these phenotypes to breast cancer overlap is unclear.<h3>Methods</h3>Mendelian randomization (MR) was conducted to estimate the relationship between lipids or IGF-I and breast cancer risk using genetic summary statistics for lipids (low-density lipoprotein cholesterol, LDL-C; high-density lipoprotein cholesterol, HDL-C; triglycerides, TGs), IGF-I and breast cancer from GLGC/UKBB (<i>N</i> = 239,119), CHARGE/UKBB (<i>N</i> = 252,547), and Breast Cancer Association Consortium (<i>N</i> = 247,173), respectively. Cross-sectional observational and MR analyses were conducted to assess the bi-directional relationship between lipids and IGF-I in SHIP (<i>N</i> = 3,812) and UKBB (<i>N</i> = 422,389), and using genetic summary statistics from GLGC (<i>N</i> = 188,577) and CHARGE/UKBB (<i>N</i> = 469,872).<h3>Results</h3>In multivariable MR (MVMR) analyses, the OR for breast cancer per 1-SD increase in HDL-C and TG was 1.08 [95% confidence interval (CI), 1.04-1.13] and 0.94 (95% CI, 0.89-0.98), respectively. The OR for breast cancer per 1-SD increase in IGF-I was 1.09 (95% CI, 1.04-1.15). MR analyses suggested a bi-directional TG-IGF-I relationship (TG-IGF-I <i>β</i> per 1-SD: -0.13; 95% CI, -0.23 to -0.04; and IGF-I-TG <i>β</i> per 1-SD: -0.11; 95% CI, -0.18 to -0.05). There was little evidence for a causal relationship between HDL-C and LDL-C with IGF-I. In MVMR analyses, associations of TG or IGF-I with breast cancer were robust to adjustment for IGF-I or TG, respectively.<h3>Conclusions</h3>Our findings suggest a causal role of HDL-C, TG, and IGF-I in breast cancer. Observational and MR analyses support an interplay between IGF-I and TG; however, MVMR estimates suggest that TG and IGF-I may act independently to influence breast cancer.<h3>Impact</h3>Our findings should be considered in the development of prevention strategies for breast cancer, where interventions are known to modify circulating lipids and IGF-I.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/6jv896t8"><img src="/cms-assets/4909efe3874be8739b695323e9e21ad738d1920672a0c152dda28b1f5c7a8afa" alt="Cover page: Investigation of the Interplay between Circulating Lipids and IGF-I and Relevance to Breast Cancer Risk: An Observational and Mendelian Randomization Study"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/2xz868qv"><div class="c-clientmarkup">Full exploitation of high dimensionality in brain imaging: The JPND working group statement and findings</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AAdams%2C%20Hieab%20HH">Adams, Hieab HH</a>; </li><li><a href="/search/?q=author%3ARoshchupkin%2C%20Gennady%20V">Roshchupkin, Gennady V</a>; </li><li><a href="/search/?q=author%3ADeCarli%2C%20Charles">DeCarli, Charles</a>; </li><li><a href="/search/?q=author%3AFranke%2C%20Barbara">Franke, Barbara</a>; </li><li><a href="/search/?q=author%3AGrabe%2C%20Hans%20J">Grabe, Hans J</a>; </li><li><a href="/search/?q=author%3AHabes%2C%20Mohamad">Habes, Mohamad</a>; </li><li><a href="/search/?q=author%3AJahanshad%2C%20Neda">Jahanshad, Neda</a>; </li><li><a href="/search/?q=author%3AMedland%2C%20Sarah%20E">Medland, Sarah E</a>; </li><li><a href="/search/?q=author%3ANiessen%2C%20Wiro">Niessen, Wiro</a>; </li><li><a href="/search/?q=author%3ASatizabal%2C%20Claudia%20L">Satizabal, Claudia L</a>; </li><li><a href="/search/?q=author%3ASchmidt%2C%20Reinhold">Schmidt, Reinhold</a>; </li><li><a href="/search/?q=author%3ASeshadri%2C%20Sudha">Seshadri, Sudha</a>; </li><li><a href="/search/?q=author%3ATeumer%2C%20Alexander">Teumer, Alexander</a>; </li><li><a href="/search/?q=author%3AThompson%2C%20Paul%20M">Thompson, Paul M</a>; </li><li><a href="/search/?q=author%3AVernooij%2C%20Meike%20W">Vernooij, Meike W</a>; </li><li><a href="/search/?q=author%3AWittfeld%2C%20Katharina">Wittfeld, Katharina</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AIkram%2C%20M%20Arfan">Ikram, M Arfan</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Editor(s):</span> <a href="/search/?q=author%3AJovicich%2C%20Jorge">Jovicich, Jorge</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AFrisoni%2C%20Giovanni%20B">Frisoni, Giovanni B</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucd_postprints">UC Davis Previously Published Works</a> (<!-- -->2019<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Advances in technology enable increasing amounts of data collection from individuals for biomedical research. Such technologies, for example, in genetics and medical imaging, have also led to important scientific discoveries about health and disease. The combination of multiple types of high-throughput data for complex analyses, however, has been limited by analytical and logistic resources to handle high-dimensional data sets. In our previous EU Joint Programme-Neurodegenerative Disease Research (JPND) Working Group, called HD-READY, we developed methods that allowed successful combination of omics data with neuroimaging. Still, several issues remained to fully leverage high-dimensional multimodality data. For instance, high-dimensional features, such as voxels and vertices, which are common in neuroimaging, remain difficult to harmonize. In this Full-HD Working Group, we focused on such harmonization of high-dimensional neuroimaging phenotypes in combination with other omics data and how to make the resulting ultra-high-dimensional data easily accessible in neurodegeneration research.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/2xz868qv"><img src="/cms-assets/be8c8909d5c60fe7091a9f9ea91bcc82055595544906ec19d6181dab0511b34c" alt="Cover page: Full exploitation of high dimensionality in brain imaging: The JPND working group statement and findings"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/0mx5k9z3"><div class="c-clientmarkup">Neandertal Introgression Sheds Light on Modern Human Endocranial Globularity</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AGunz%2C%20Philipp">Gunz, Philipp</a>; </li><li><a href="/search/?q=author%3ATilot%2C%20Amanda%20K">Tilot, Amanda K</a>; </li><li><a href="/search/?q=author%3AWittfeld%2C%20Katharina">Wittfeld, Katharina</a>; </li><li><a href="/search/?q=author%3ATeumer%2C%20Alexander">Teumer, Alexander</a>; </li><li><a href="/search/?q=author%3AShapland%2C%20Chin%20Yang">Shapland, Chin Yang</a>; </li><li><a href="/search/?q=author%3Avan%20Erp%2C%20Theo%20GM">van Erp, Theo GM</a>; </li><li><a href="/search/?q=author%3ADannemann%2C%20Michael">Dannemann, Michael</a>; </li><li><a href="/search/?q=author%3AVernot%2C%20Benjamin">Vernot, Benjamin</a>; </li><li><a href="/search/?q=author%3ANeubauer%2C%20Simon">Neubauer, Simon</a>; </li><li><a href="/search/?q=author%3AGuadalupe%2C%20Tulio">Guadalupe, Tulio</a>; </li><li><a href="/search/?q=author%3AFern%C3%A1ndez%2C%20Guill%C3%A9n">Fernández, Guillén</a>; </li><li><a href="/search/?q=author%3ABrunner%2C%20Han%20G">Brunner, Han G</a>; </li><li><a href="/search/?q=author%3AEnard%2C%20Wolfgang">Enard, Wolfgang</a>; </li><li><a href="/search/?q=author%3AFallon%2C%20James">Fallon, James</a>; </li><li><a href="/search/?q=author%3AHosten%2C%20Norbert">Hosten, Norbert</a>; </li><li><a href="/search/?q=author%3AV%C3%B6lker%2C%20Uwe">Völker, Uwe</a>; </li><li><a href="/search/?q=author%3AProfico%2C%20Antonio">Profico, Antonio</a>; </li><li><a href="/search/?q=author%3ADi%20Vincenzo%2C%20Fabio">Di Vincenzo, Fabio</a>; </li><li><a href="/search/?q=author%3AManzi%2C%20Giorgio">Manzi, Giorgio</a>; </li><li><a href="/search/?q=author%3AKelso%2C%20Janet">Kelso, Janet</a>; </li><li><a href="/search/?q=author%3ASt.%20Pourcain%2C%20Beate">St. Pourcain, Beate</a>; </li><li><a href="/search/?q=author%3AHublin%2C%20Jean-Jacques">Hublin, Jean-Jacques</a>; </li><li><a href="/search/?q=author%3AFranke%2C%20Barbara">Franke, Barbara</a>; </li><li><a href="/search/?q=author%3AP%C3%A4%C3%A4bo%2C%20Svante">Pääbo, Svante</a>; </li><li><a href="/search/?q=author%3AMacciardi%2C%20Fabio">Macciardi, Fabio</a>; </li><li><a href="/search/?q=author%3AGrabe%2C%20Hans%20J">Grabe, Hans J</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AFisher%2C%20Simon%20E">Fisher, Simon E</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/uci_postprints">UC Irvine Previously Published Works</a> (<!-- -->2019<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">One of the features that distinguishes modern humans from our extinct relatives and ancestors is a globular shape of the braincase [1-4]. As the endocranium closely mirrors the outer shape of the brain, these differences might reflect altered neural architecture [4, 5]. However, in the absence of fossil brain tissue, the underlying neuroanatomical changes as well as their genetic bases remain elusive. To better understand the biological foundations of modern human endocranial shape, we turn to our closest extinct relatives: the Neandertals. Interbreeding between modern humans and Neandertals has resulted in introgressed fragments of Neandertal DNA in the genomes of present-day non-Africans [6, 7]. Based on shape analyses of fossil skull endocasts, we derive a measure of endocranial globularity from structural MRI scans of thousands of modern humans and study the effects of introgressed fragments of Neandertal DNA on this phenotype. We find that Neandertal alleles on chromosomes 1 and 18 are associated with reduced endocranial globularity. These alleles influence expression of two nearby genes, UBR4 and PHLPP1, which are involved in neurogenesis and myelination, respectively. Our findings show how integration of fossil skull data with archaic genomics and neuroimaging can suggest developmental mechanisms that may contribute to the unique modern human endocranial shape.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/0mx5k9z3"><img src="/cms-assets/e54c273ceba17455d4a6f58bb68146eb436f0c9acec3f6b92daba4dea81e590b" alt="Cover page: Neandertal Introgression Sheds Light on Modern Human Endocranial Globularity"/></a><a href="https://creativecommons.org/licenses/by/4.0/" class="c-scholworks__license"><img class="c-lazyimage" data-src="/images/cc-by-small.svg" alt="Creative Commons 'BY' version 4.0 license"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/8sm5d1xw"><div class="c-clientmarkup">Distinct genetic liability profiles define clinically relevant patient strata across common diseases.</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ATrastulla%2C%20Lucia">Trastulla, Lucia</a>; </li><li><a href="/search/?q=author%3ADolgalev%2C%20Georgii">Dolgalev, Georgii</a>; </li><li><a href="/search/?q=author%3AMoser%2C%20Sylvain">Moser, Sylvain</a>; </li><li><a href="/search/?q=author%3AJim%C3%A9nez-Barr%C3%B3n%2C%20Laura">Jiménez-Barrón, Laura</a>; </li><li><a href="/search/?q=author%3AAndlauer%2C%20Till">Andlauer, Till</a>; </li><li><a href="/search/?q=author%3Avon%20Scheidt%2C%20Moritz">von Scheidt, Moritz</a>; </li><li><a href="/search/?q=author%3ABudde%2C%20Monika">Budde, Monika</a>; </li><li><a href="/search/?q=author%3AHeilbronner%2C%20Urs">Heilbronner, Urs</a>; </li><li><a href="/search/?q=author%3APapiol%2C%20Sergi">Papiol, Sergi</a>; </li><li><a href="/search/?q=author%3ATeumer%2C%20Alexander">Teumer, Alexander</a>; </li><li><a href="/search/?q=author%3AHomuth%2C%20Georg">Homuth, Georg</a>; </li><li><a href="/search/?q=author%3AV%C3%B6lzke%2C%20Henry">Völzke, Henry</a>; </li><li><a href="/search/?q=author%3AD%C3%B6rr%2C%20Marcus">Dörr, Marcus</a>; </li><li><a href="/search/?q=author%3AFalkai%2C%20Peter">Falkai, Peter</a>; </li><li><a href="/search/?q=author%3ASchulze%2C%20Thomas">Schulze, Thomas</a>; </li><li><a href="/search/?q=author%3AGagneur%2C%20Julien">Gagneur, Julien</a>; </li><li><a href="/search/?q=author%3AIorio%2C%20Francesco">Iorio, Francesco</a>; </li><li><a href="/search/?q=author%3AM%C3%BCller-Myhsok%2C%20Bertram">Müller-Myhsok, Bertram</a>; </li><li><a href="/search/?q=author%3ASchunkert%2C%20Heribert">Schunkert, Heribert</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AZiller%2C%20Michael">Ziller, Michael</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (<!-- -->2024<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Stratified medicine holds great promise to tailor treatment to the needs of individual patients. While genetics holds great potential to aid patient stratification, it remains a major challenge to operationalize complex genetic risk factor profiles to deconstruct clinical heterogeneity. Contemporary approaches to this problem rely on polygenic risk scores (PRS), which provide only limited clinical utility and lack a clear biological foundation. To overcome these limitations, we develop the CASTom-iGEx approach to stratify individuals based on the aggregated impact of their genetic risk factor profiles on tissue specific gene expression levels. The paradigmatic application of this approach to coronary artery disease or schizophrenia patient cohorts identified diverse strata or biotypes. These biotypes are characterized by distinct endophenotype profiles as well as clinical parameters and are fundamentally distinct from PRS based groupings. In stark contrast to the latter, the CASTom-iGEx strategy discovers biologically meaningful and clinically actionable patient subgroups, where complex genetic liabilities are not randomly distributed across individuals but rather converge onto distinct disease relevant biological processes. These results support the notion of different patient biotypes characterized by partially distinct pathomechanisms. Thus, the universally applicable approach presented here has the potential to constitute an important component of future personalized medicine paradigms.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/8sm5d1xw"><img src="/cms-assets/2dc260d3b4c7e970982a365bd838259e0c53519a0c16b354654e60ff8b60da8d" alt="Cover page: Distinct genetic liability profiles define clinically relevant patient strata across common diseases."/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/7597c7wp"><div class="c-clientmarkup">Genome-wide association and functional studies identify a role for IGFBP3 in hip osteoarthritis</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AEvans%2C%20Daniel%20S">Evans, Daniel S</a>; </li><li><a href="/search/?q=author%3ACailotto%2C%20Frederic">Cailotto, Frederic</a>; </li><li><a href="/search/?q=author%3AParimi%2C%20Neeta">Parimi, Neeta</a>; </li><li><a href="/search/?q=author%3AValdes%2C%20Ana%20M">Valdes, Ana M</a>; </li><li><a href="/search/?q=author%3ACasta%C3%B1o-Betancourt%2C%20Martha%20C">Castaño-Betancourt, Martha C</a>; </li><li><a href="/search/?q=author%3ALiu%2C%20Youfang">Liu, Youfang</a>; </li><li><a href="/search/?q=author%3AKaplan%2C%20Robert%20C">Kaplan, Robert C</a>; </li><li><a href="/search/?q=author%3ABidlingmaier%2C%20Martin">Bidlingmaier, Martin</a>; </li><li><a href="/search/?q=author%3AVasan%2C%20Ramachandran%20S">Vasan, Ramachandran S</a>; </li><li><a href="/search/?q=author%3ATeumer%2C%20Alexander">Teumer, Alexander</a>; </li><li><a href="/search/?q=author%3ATranah%2C%20Gregory%20J">Tranah, Gregory J</a>; </li><li><a href="/search/?q=author%3ANevitt%2C%20Michael%20C">Nevitt, Michael C</a>; </li><li><a href="/search/?q=author%3ACummings%2C%20Steven%20R">Cummings, Steven R</a>; </li><li><a href="/search/?q=author%3AOrwoll%2C%20Eric%20S">Orwoll, Eric S</a>; </li><li><a href="/search/?q=author%3ABarrett-Connor%2C%20Elizabeth">Barrett-Connor, Elizabeth</a>; </li><li><a href="/search/?q=author%3ARenner%2C%20Jordan%20B">Renner, Jordan B</a>; </li><li><a href="/search/?q=author%3AJordan%2C%20Joanne%20M">Jordan, Joanne M</a>; </li><li><a href="/search/?q=author%3ADoherty%2C%20Michael">Doherty, Michael</a>; </li><li><a href="/search/?q=author%3ADoherty%2C%20Sally%20A">Doherty, Sally A</a>; </li><li><a href="/search/?q=author%3AUitterlinden%2C%20Andre%20G">Uitterlinden, Andre G</a>; </li><li><a href="/search/?q=author%3Avan%20Meurs%2C%20Joyce%20BJ">van Meurs, Joyce BJ</a>; </li><li><a href="/search/?q=author%3ASpector%2C%20Tim%20D">Spector, Tim D</a>; </li><li><a href="/search/?q=author%3ALories%2C%20Rik%20J">Lories, Rik J</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ALane%2C%20Nancy%20E">Lane, Nancy E</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucd_postprints">UC Davis Previously Published Works</a> (<!-- -->2015<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Objectives</h3>To identify genetic associations with hip osteoarthritis (HOA), we performed a meta-analysis of genome-wide association studies (GWAS) of HOA.<h3>Methods</h3>The GWAS meta-analysis included approximately 2.5 million imputed HapMap single nucleotide polymorphisms (SNPs). HOA cases and controls defined radiographically and by total hip replacement were selected from the Osteoporotic Fractures in Men (MrOS) Study and the Study of Osteoporotic Fractures (SOF) (654 cases and 4697 controls, combined). Replication of genome-wide significant SNP associations (p ≤5×10(-8)) was examined in five studies (3243 cases and 6891 controls, combined). Functional studies were performed using in vitro models of chondrogenesis and osteogenesis.<h3>Results</h3>The A allele of rs788748, located 65 kb upstream of the IGFBP3 gene, was associated with lower HOA odds at the genome-wide significance level in the discovery stage (OR 0.71, p=2×10(-8)). The association replicated in five studies (OR 0.92, p=0.020), but the joint analysis of discovery and replication results was not genome-wide significant (p=1×10(-6)). In separate study populations, the rs788748 A allele was also associated with lower circulating IGFBP3 protein levels (p=4×10(-13)), suggesting that this SNP or a variant in linkage disequilibrium could be an IGFBP3 regulatory variant. Results from functional studies were consistent with association results. Chondrocyte hypertrophy, a deleterious event in OA pathogenesis, was largely prevented upon IGFBP3 knockdown in chondrocytes. Furthermore, IGFBP3 overexpression induced cartilage catabolism and osteogenic differentiation.<h3>Conclusions</h3>Results from GWAS and functional studies provided suggestive links between IGFBP3 and HOA.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/2gp960sb"><div class="c-clientmarkup">Association of eGFR-Related Loci Identified by GWAS with Incident CKD and ESRD</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AB%C3%B6ger%2C%20Carsten%20A">Böger, Carsten A</a>; </li><li><a href="/search/?q=author%3AGorski%2C%20Mathias">Gorski, Mathias</a>; </li><li><a href="/search/?q=author%3ALi%2C%20Man">Li, Man</a>; </li><li><a href="/search/?q=author%3AHoffmann%2C%20Michael%20M">Hoffmann, Michael M</a>; </li><li><a href="/search/?q=author%3AHuang%2C%20Chunmei">Huang, Chunmei</a>; </li><li><a href="/search/?q=author%3AYang%2C%20Qiong">Yang, Qiong</a>; </li><li><a href="/search/?q=author%3ATeumer%2C%20Alexander">Teumer, Alexander</a>; </li><li><a href="/search/?q=author%3AKrane%2C%20Vera">Krane, Vera</a>; </li><li><a href="/search/?q=author%3AO'Seaghdha%2C%20Conall%20M">O'Seaghdha, Conall M</a>; </li><li><a href="/search/?q=author%3AKutalik%2C%20Zolt%C3%A1n">Kutalik, Zoltán</a>; </li><li><a href="/search/?q=author%3AWichmann%2C%20H-Erich">Wichmann, H-Erich</a>; </li><li><a href="/search/?q=author%3AHaak%2C%20Thomas">Haak, Thomas</a>; </li><li><a href="/search/?q=author%3ABoes%2C%20Eva">Boes, Eva</a>; </li><li><a href="/search/?q=author%3ACoassin%2C%20Stefan">Coassin, Stefan</a>; </li><li><a href="/search/?q=author%3ACoresh%2C%20Josef">Coresh, Josef</a>; </li><li><a href="/search/?q=author%3AKollerits%2C%20Barbara">Kollerits, Barbara</a>; </li><li><a href="/search/?q=author%3AHaun%2C%20Margot">Haun, Margot</a>; </li><li><a href="/search/?q=author%3APaulweber%2C%20Bernhard">Paulweber, Bernhard</a>; </li><li><a href="/search/?q=author%3AK%C3%B6ttgen%2C%20Anna">Köttgen, Anna</a>; </li><li><a href="/search/?q=author%3ALi%2C%20Guo">Li, Guo</a>; </li><li><a href="/search/?q=author%3AShlipak%2C%20Michael%20G">Shlipak, Michael G</a>; </li><li><a href="/search/?q=author%3APowe%2C%20Neil">Powe, Neil</a>; </li><li><a href="/search/?q=author%3AHwang%2C%20Shih-Jen">Hwang, Shih-Jen</a>; </li><li><a href="/search/?q=author%3ADehghan%2C%20Abbas">Dehghan, Abbas</a>; </li><li><a href="/search/?q=author%3ARivadeneira%2C%20Fernando">Rivadeneira, Fernando</a>; </li><li><a href="/search/?q=author%3AUitterlinden%2C%20Andr%C3%A9">Uitterlinden, André</a>; </li><li><a href="/search/?q=author%3AHofman%2C%20Albert">Hofman, Albert</a>; </li><li><a href="/search/?q=author%3ABeckmann%2C%20Jacques%20S">Beckmann, Jacques S</a>; </li><li><a href="/search/?q=author%3AKr%C3%A4mer%2C%20Bernhard%20K">Krämer, Bernhard K</a>; </li><li><a href="/search/?q=author%3AWitteman%2C%20Jacqueline">Witteman, Jacqueline</a>; </li><li><a href="/search/?q=author%3ABochud%2C%20Murielle">Bochud, Murielle</a>; </li><li><a href="/search/?q=author%3ASiscovick%2C%20David">Siscovick, David</a>; </li><li><a href="/search/?q=author%3ARettig%2C%20Rainer">Rettig, Rainer</a>; </li><li><a href="/search/?q=author%3AKronenberg%2C%20Florian">Kronenberg, Florian</a>; </li><li><a href="/search/?q=author%3AWanner%2C%20Christoph">Wanner, Christoph</a>; </li><li><a href="/search/?q=author%3AThadhani%2C%20Ravi%20I">Thadhani, Ravi I</a>; </li><li><a href="/search/?q=author%3AHeid%2C%20Iris%20M">Heid, Iris M</a>; </li><li><a href="/search/?q=author%3AFox%2C%20Caroline%20S">Fox, Caroline S</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AKao%2C%20WH">Kao, WH</a> </li><li class="c-authorlist__begin"><span class="c-authorlist__heading">Editor(s):</span> <a href="/search/?q=author%3AKim%2C%20Stuart%20K">Kim, Stuart K</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsf_postprints">UC San Francisco Previously Published Works</a> (<!-- -->2011<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Family studies suggest a genetic component to the etiology of chronic kidney disease (CKD) and end stage renal disease (ESRD). Previously, we identified 16 loci for eGFR in genome-wide association studies, but the associations of these single nucleotide polymorphisms (SNPs) for incident CKD or ESRD are unknown. We thus investigated the association of these loci with incident CKD in 26,308 individuals of European ancestry free of CKD at baseline drawn from eight population-based cohorts followed for a median of 7.2 years (including 2,122 incident CKD cases defined as eGFR <60ml/min/1.73m(2) at follow-up) and with ESRD in four case-control studies in subjects of European ancestry (3,775 cases, 4,577 controls). SNPs at 11 of the 16 loci (UMOD, PRKAG2, ANXA9, DAB2, SHROOM3, DACH1, STC1, SLC34A1, ALMS1/NAT8, UBE2Q2, and GCKR) were associated with incident CKD; p-values ranged from p = 4.1e-9 in UMOD to p = 0.03 in GCKR. After adjusting for baseline eGFR, six of these loci remained significantly associated with incident CKD (UMOD, PRKAG2, ANXA9, DAB2, DACH1, and STC1). SNPs in UMOD (OR = 0.92, p = 0.04) and GCKR (OR = 0.93, p = 0.03) were nominally associated with ESRD. In summary, the majority of eGFR-related loci are either associated or show a strong trend towards association with incident CKD, but have modest associations with ESRD in individuals of European descent. Additional work is required to characterize the association of genetic determinants of CKD and ESRD at different stages of disease progression.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/2gp960sb"><img src="/cms-assets/51ff3997f26a78365d0be918eb6a2979bf552bd01682fd951cbdc4ed6a902658" alt="Cover page: Association of eGFR-Related Loci Identified by GWAS with Incident CKD and ESRD"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/8bf9j0jr"><div class="c-clientmarkup">Transcriptome-Wide Analysis Identifies Novel Associations With Blood Pressure</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AZeller%2C%20Tanja">Zeller, Tanja</a>; </li><li><a href="/search/?q=author%3ASchurmann%2C%20Claudia">Schurmann, Claudia</a>; </li><li><a href="/search/?q=author%3ASchramm%2C%20Katharina">Schramm, Katharina</a>; </li><li><a href="/search/?q=author%3AM%C3%BCller%2C%20Christian">Müller, Christian</a>; </li><li><a href="/search/?q=author%3AKwon%2C%20Soonil">Kwon, Soonil</a>; </li><li><a href="/search/?q=author%3AWild%2C%20Philipp%20S">Wild, Philipp S</a>; </li><li><a href="/search/?q=author%3ATeumer%2C%20Alexander">Teumer, Alexander</a>; </li><li><a href="/search/?q=author%3AHerrington%2C%20David">Herrington, David</a>; </li><li><a href="/search/?q=author%3ASchillert%2C%20Arne">Schillert, Arne</a>; </li><li><a href="/search/?q=author%3AIacoviello%2C%20Licia">Iacoviello, Licia</a>; </li><li><a href="/search/?q=author%3AKratzer%2C%20Adelheid">Kratzer, Adelheid</a>; </li><li><a href="/search/?q=author%3AJagodzinski%2C%20Annika">Jagodzinski, Annika</a>; </li><li><a href="/search/?q=author%3AKarakas%2C%20Mahir">Karakas, Mahir</a>; </li><li><a href="/search/?q=author%3ADing%2C%20Jingzhong">Ding, Jingzhong</a>; </li><li><a href="/search/?q=author%3ANeumann%2C%20Johannes%20T">Neumann, Johannes T</a>; </li><li><a href="/search/?q=author%3AKuulasmaa%2C%20Kari">Kuulasmaa, Kari</a>; </li><li><a href="/search/?q=author%3AGieger%2C%20Christian">Gieger, Christian</a>; </li><li><a href="/search/?q=author%3AKacprowski%2C%20Tim">Kacprowski, Tim</a>; </li><li><a href="/search/?q=author%3ASchnabel%2C%20Renate%20B">Schnabel, Renate B</a>; </li><li><a href="/search/?q=author%3ARoden%2C%20Michael">Roden, Michael</a>; </li><li><a href="/search/?q=author%3AWahl%2C%20Simone">Wahl, Simone</a>; </li><li><a href="/search/?q=author%3ARotter%2C%20Jerome%20I">Rotter, Jerome I</a>; </li><li><a href="/search/?q=author%3AOjeda%2C%20Francisco">Ojeda, Francisco</a>; </li><li><a href="/search/?q=author%3ACarstensen-Kirberg%2C%20Maren">Carstensen-Kirberg, Maren</a>; </li><li><a href="/search/?q=author%3ATregouet%2C%20David-Alexandre">Tregouet, David-Alexandre</a>; </li><li><a href="/search/?q=author%3AD%C3%B6rr%2C%20Marcus">Dörr, Marcus</a>; </li><li><a href="/search/?q=author%3AMeitinger%2C%20Thomas">Meitinger, Thomas</a>; </li><li><a href="/search/?q=author%3ALackner%2C%20Karl%20J">Lackner, Karl J</a>; </li><li><a href="/search/?q=author%3AWolf%2C%20Petra">Wolf, Petra</a>; </li><li><a href="/search/?q=author%3AFelix%2C%20Stephan%20B">Felix, Stephan B</a>; </li><li><a href="/search/?q=author%3ALandmesser%2C%20Ulf">Landmesser, Ulf</a>; </li><li><a href="/search/?q=author%3ACostanzo%2C%20Simona">Costanzo, Simona</a>; </li><li><a href="/search/?q=author%3AZiegler%2C%20Andreas">Ziegler, Andreas</a>; </li><li><a href="/search/?q=author%3ALiu%2C%20Yongmei">Liu, Yongmei</a>; </li><li><a href="/search/?q=author%3AV%C3%B6lker%2C%20Uwe">Völker, Uwe</a>; </li><li><a href="/search/?q=author%3APalmas%2C%20Walter">Palmas, Walter</a>; </li><li><a href="/search/?q=author%3AProkisch%2C%20Holger">Prokisch, Holger</a>; </li><li><a href="/search/?q=author%3AGuo%2C%20Xiuqing">Guo, Xiuqing</a>; </li><li><a href="/search/?q=author%3AHerder%2C%20Christian">Herder, Christian</a>; </li><li><a href="/search/?q=author%3ABlankenberg%2C%20Stefan">Blankenberg, Stefan</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AHomuth%2C%20Georg">Homuth, Georg</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (<!-- -->2017<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Hypertension represents a major cardiovascular risk factor. The pathophysiology of increased blood pressure (BP) is not yet completely understood. Transcriptome profiling offers possibilities to uncover genetics effects on BP. Based on 2 populations including 2549 individuals, a meta-analyses of monocytic transcriptome-wide profiles were performed to identify transcripts associated with BP. Replication was performed in 2 independent studies of whole-blood transcriptome data including 1990 individuals. For identified candidate genes, a direct link between long-term changes in BP and gene expression over time and by treatment with BP-lowering therapy was assessed. The predictive value of protein levels encoded by candidate genes for subsequent cardiovascular disease was investigated. Eight transcripts (<i>CRIP1</i>, <i>MYADM</i>, <i>TIPARP</i>, <i>TSC22D3</i>, <i>CEBPA</i>, <i>F12, LMNA</i>, and <i>TPPP3</i>) were identified jointly accounting for up to 13% (95% confidence interval, 8.7-16.2) of BP variability. Changes in <i>CRIP1</i>, <i>MYADM</i>, <i>TIPARP</i>, <i>LMNA</i>, <i>TSC22D3</i>, <i>CEBPA</i>, and <i>TPPP3</i> expression associated with BP changes-among these, <i>CRIP1</i> gene expression was additionally correlated to measures of cardiac hypertrophy. Assessment of circulating CRIP1 (cystein-rich protein 1) levels as biomarkers showed a strong association with increased risk for incident stroke (hazard ratio, 1.06; 95% confidence interval, 1.03-1.09; <i>P</i>=5.0×10<sup>-5</sup>). Our comprehensive analysis of global gene expression highlights 8 novel transcripts significantly associated with BP, providing a link between gene expression and BP. Translational approaches further established evidence for the potential use of CRIP1 as emerging disease-related biomarker.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/8bf9j0jr"><img src="/cms-assets/5362e6cb578041809a6f4d2be931aea523702ad7f7ea7adf3eef600ff1008a4c" alt="Cover page: Transcriptome-Wide Analysis Identifies Novel Associations With Blood Pressure"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/21t098hn"><div class="c-clientmarkup">Association analysis between an epigenetic alcohol risk score and blood pressure</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ABui%2C%20Helena">Bui, Helena</a>; </li><li><a href="/search/?q=author%3AKeshawarz%2C%20Amena">Keshawarz, Amena</a>; </li><li><a href="/search/?q=author%3AWang%2C%20Mengyao">Wang, Mengyao</a>; </li><li><a href="/search/?q=author%3ALee%2C%20Mikyeong">Lee, Mikyeong</a>; </li><li><a href="/search/?q=author%3ARatliff%2C%20Scott%20M">Ratliff, Scott M</a>; </li><li><a href="/search/?q=author%3ALin%2C%20Lisha">Lin, Lisha</a>; </li><li><a href="/search/?q=author%3ABirditt%2C%20Kira%20S">Birditt, Kira S</a>; </li><li><a href="/search/?q=author%3AFaul%2C%20Jessica%20D">Faul, Jessica D</a>; </li><li><a href="/search/?q=author%3APeters%2C%20Annette">Peters, Annette</a>; </li><li><a href="/search/?q=author%3AGieger%2C%20Christian">Gieger, Christian</a>; </li><li><a href="/search/?q=author%3ADelerue%2C%20Thomas">Delerue, Thomas</a>; </li><li><a href="/search/?q=author%3AKardia%2C%20Sharon%20LR">Kardia, Sharon LR</a>; </li><li><a href="/search/?q=author%3AZhao%2C%20Wei">Zhao, Wei</a>; </li><li><a href="/search/?q=author%3AGuo%2C%20Xiuqing">Guo, Xiuqing</a>; </li><li><a href="/search/?q=author%3AYao%2C%20Jie">Yao, Jie</a>; </li><li><a href="/search/?q=author%3ARotter%2C%20Jerome%20I">Rotter, Jerome I</a>; </li><li><a href="/search/?q=author%3ALi%2C%20Yi">Li, Yi</a>; </li><li><a href="/search/?q=author%3ALiu%2C%20Xue">Liu, Xue</a>; </li><li><a href="/search/?q=author%3ALiu%2C%20Dan">Liu, Dan</a>; </li><li><a href="/search/?q=author%3ATavares%2C%20Juliana%20F">Tavares, Juliana F</a>; </li><li><a href="/search/?q=author%3APehlivan%2C%20G%C3%B6khan">Pehlivan, Gökhan</a>; </li><li><a href="/search/?q=author%3ABreteler%2C%20Monique%20MB">Breteler, Monique MB</a>; </li><li><a href="/search/?q=author%3AKarabegovic%2C%20Irma">Karabegovic, Irma</a>; </li><li><a href="/search/?q=author%3AOchoa-Rosales%2C%20Carolina">Ochoa-Rosales, Carolina</a>; </li><li><a href="/search/?q=author%3AVoortman%2C%20Trudy">Voortman, Trudy</a>; </li><li><a href="/search/?q=author%3AGhanbari%2C%20Mohsen">Ghanbari, Mohsen</a>; </li><li><a href="/search/?q=author%3Avan%20Meurs%2C%20Joyce%20BJ">van Meurs, Joyce BJ</a>; </li><li><a href="/search/?q=author%3ANasr%2C%20Mohamed%20Kamal">Nasr, Mohamed Kamal</a>; </li><li><a href="/search/?q=author%3AD%C3%B6rr%2C%20Marcus">Dörr, Marcus</a>; </li><li><a href="/search/?q=author%3AGrabe%2C%20Hans%20J">Grabe, Hans J</a>; </li><li><a href="/search/?q=author%3ALondon%2C%20Stephanie%20J">London, Stephanie J</a>; </li><li><a href="/search/?q=author%3ATeumer%2C%20Alexander">Teumer, Alexander</a>; </li><li><a href="/search/?q=author%3AWaldenberger%2C%20Melanie">Waldenberger, Melanie</a>; </li><li><a href="/search/?q=author%3AWeir%2C%20David%20R">Weir, David R</a>; </li><li><a href="/search/?q=author%3ASmith%2C%20Jennifer%20A">Smith, Jennifer A</a>; </li><li><a href="/search/?q=author%3ALevy%2C%20Daniel">Levy, Daniel</a>; </li><li><a href="/search/?q=author%3AMa%2C%20Jiantao">Ma, Jiantao</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ALiu%2C%20Chunyu">Liu, Chunyu</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucla_postprints">UCLA Previously Published Works</a> (<!-- -->2024<!-- -->)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Background</h3>Epigenome-wide association studies have identified multiple DNA methylation sites (CpGs) associated with alcohol consumption, an important lifestyle risk factor for cardiovascular diseases. This study aimed to test the hypothesis that an alcohol consumption epigenetic risk score (ERS) is associated with blood pressure (BP) traits.<h3>Results</h3>We implemented an ERS based on a previously reported epigenetic signature of 144 alcohol-associated CpGs in meta-analysis of participants of European ancestry. We found a one-unit increment of ERS was associated with eleven drinks of alcohol consumed per day, on average, across several cohorts (p < 0.0001). We examined the association of the ERS with systolic blood pressure (SBP), diastolic blood pressure (DBP), and hypertension (HTN) in 3,898 Framingham Heart Study (FHS) participants. Cross-sectional analyses in FHS revealed that a one-unit increment of the ERS was associated with 1.93 mm Hg higher SBP (p = 4.64E-07), 0.68 mm Hg higher DBP (p = 0.006), and an odds ratio of 1.78 for HTN (p < 2E-16). Meta-analysis of the cross-sectional association of the ERS with BP traits in eight independent external cohorts (n = 11,544) showed similar relationships with BP levels, i.e., a one-unit increase in ERS was associated with 0.74 mm Hg (p = 0.002) higher SBP and 0.50 mm Hg (p = 0.0006) higher DBP, but not with HTN. Longitudinal analyses in FHS (n = 3260) and five independent external cohorts (n = 4021) showed that the baseline ERS was not associated with a change in BP over time or with incident HTN.<h3>Conclusions</h3>Our findings demonstrate that the ERS has potential clinical utility in assessing lifestyle factors related to cardiovascular risk, especially when self-reported behavioral data (e.g., alcohol consumption) are unreliable or unavailable.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/21t098hn"><img src="/cms-assets/2b978c8026e54b2e6f48a41d8042810fd8cca5bfa398fb3b63c9a83ec2a5688a" alt="Cover page: Association analysis between an epigenetic alcohol risk score and blood pressure"/></a></div></section><nav class="c-pagination--next"><ul><li><a href="" aria-label="you are on result set 1" class="c-pagination__item--current">1</a></li><li><a href="" aria-label="go 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Diego"},{"id":"ucsf","name":"UCSF"},{"id":"ucsb","name":"UC Santa Barbara"},{"id":"ucsc","name":"UC Santa Cruz"},{"id":"ucop","name":"UC Office of the President"},{"id":"lbnl","name":"Lawrence Berkeley National Laboratory"},{"id":"anrcs","name":"UC Agriculture & Natural Resources"}],"logo":null,"bgColor":null,"elColor":null,"directSubmit":null,"directSubmitURL":null,"directManageURLauthor":null,"directManageURLeditor":null,"nav_bar":[{"id":1,"name":"About eScholarship","type":"folder","sub_nav":[{"id":5,"name":"About eScholarship","slug":"aboutEschol","type":"page","url":"/aboutEschol"},{"id":11,"name":"eScholarship Repository","slug":"repository","type":"page","url":"/repository"},{"id":28,"url":"/publishing","name":"eScholarship Publishing","type":"link"},{"id":29,"name":"Site policies","slug":"policies","type":"page","url":"/policies"},{"id":13,"name":"Terms of Use and Copyright Information","slug":"terms","type":"page","url":"/terms"},{"id":26,"name":"Coming 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Resources"}],"query":{"q":"author:Teumer, Alexander","sort":"rel","rows":"10","info_start":"0","start":"0","filters":{}},"count":103,"info_count":0,"infoResults":[],"searchResults":[{"id":"qt30t3n9z8","title":"Insulin-Like Growth Factor, Inflammation, and MRI Markers of Alzheimer\u2019s Disease in Predominantly Middle-Aged Adults","abstract":"<h4>Background</h4>Insulin-like growth factor 1 (IGF-1) signaling has been implicated in Alzheimer's disease pathogenesis, and further evidence suggests inflammation can be a moderator of this association. However, most research to date has been conducted on older adults.<h4>Objective</h4>To investigate the association of serum IGF-1 and IGF binding protein 3 (IGFBP-3) concentrations with MRI markers of Alzheimer's disease in predominantly middle-aged adults, and further assess moderation by chronic inflammation.<h4>Methods</h4>We included participants from the Framingham Heart Study (n\u200A=\u200A1,852, mean age 46\u00B18, 46% men) and the Study of Health in Pomerania (n\u200A=\u200A674, mean age 50\u00B113, 42% men) with available serum IGF-1, IFGBP-3, as well as brain MRI. IGF-1 and IFGBP-3 were related to MRI outcomes (i.e., total brain, cortical gray matter, white matter, white matter hyperintensities (WMH), and hippocampal volumes) using multivariable regression models adjusting for potential confounders. Subgroup analyses by C-reactive protein (CRP) concentrations were also performed. Cohort-specific summary statistics were meta-analyzed using random-effects models and corrected for multiple comparisons.<h4>Results</h4>Meta-analysis results revealed that higher IGF-1 concentrations were associated with lower WMH (estimate [\u03B2] [95% CI], -0.05 [-0.09, -0.02], p\u200A=\u200A0.006) and larger hippocampal volumes (0.07 [0.02, 0.12], p\u200A=\u200A0.01), independent of vascular risk factors. These associations occurred predominantly in individuals with CRP concentrations <\u200A75th percentile. We did not observe associations between IGFBP-3 and MRI outcomes.<h4>Conclusion</h4>Our findings suggest that IGF-1-related signaling may be implicated in brain health as early as midlife.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Wittfeld, Katharina","fname":"Katharina","lname":"Wittfeld"},{"name":"Raman, Mekala R","fname":"Mekala R","lname":"Raman"},{"name":"Conner, Sarah C","fname":"Sarah C","lname":"Conner"},{"name":"Aslam, Asra","fname":"Asra","lname":"Aslam"},{"name":"Teumer, Alexander","fname":"Alexander","lname":"Teumer"},{"name":"Nauck, Matthias","fname":"Matthias","lname":"Nauck"},{"name":"Hosten, Norbert","fname":"Norbert","lname":"Hosten"},{"name":"Habes, Mohamad","fname":"Mohamad","lname":"Habes"},{"name":"DeCarli, Charles","email":"cdecarli@ucdavis.edu","fname":"Charles","lname":"DeCarli","ORCID_id":"0000-0003-1914-2693"},{"name":"Vasan, Ramachandran S","fname":"Ramachandran S","lname":"Vasan"},{"name":"Beiser, Alexa S","fname":"Alexa S","lname":"Beiser"},{"name":"Himali, Jayandra J","fname":"Jayandra J","lname":"Himali"},{"name":"Seshadri, Sudha","fname":"Sudha","lname":"Seshadri"},{"name":"Grabe, Hans J","fname":"Hans J","lname":"Grabe"},{"name":"Satizabal, Claudia L","fname":"Claudia L","lname":"Satizabal"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":149,"asset_id":"eb157c1711c8831e564c8b5e30e04871f5782b645a05bf8164259f2d0c5f700a","timestamp":1688172629,"image_type":"png"},"pub_year":2022,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC Davis Previously Published Works","link_path":"ucd_postprints"}},{"id":"qt2sz5n70h","title":"Neandertal Introgression Sheds Light on Modern Human Endocranial Globularity.","abstract":"One of the features that distinguishes modern humans from our extinct relatives and ancestors is a globular shape of the braincase [1-4]. As the endocranium closely mirrors the outer shape of the brain, these differences might reflect altered neural architecture [4, 5]. However, in the absence of fossil brain tissue, the underlying neuroanatomical changes as well as their genetic bases remain elusive. To better understand the biological foundations of modern human endocranial shape, we turn to our closest extinct relatives: the Neandertals. Interbreeding between modern humans and Neandertals has resulted in introgressed fragments of Neandertal DNA in the genomes of present-day non-Africans [6, 7]. Based on shape analyses of fossil skull endocasts, we derive a measure of endocranial globularity from structural MRI scans of thousands of modern humans and study the effects of introgressed fragments of Neandertal DNA on this phenotype. We find that Neandertal alleles on chromosomes 1 and 18 are associated with reduced endocranial globularity. These alleles influence expression of two nearby genes, UBR4 and PHLPP1, which are involved in neurogenesis and myelination, respectively. Our findings show how integration of fossil skull data with archaic genomics and neuroimaging can suggest developmental mechanisms that may contribute to the unique modern human endocranial shape.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Gunz, Philipp","fname":"Philipp","lname":"Gunz"},{"name":"Tilot, Amanda","fname":"Amanda","lname":"Tilot"},{"name":"Wittfeld, Katharina","fname":"Katharina","lname":"Wittfeld"},{"name":"Teumer, Alexander","fname":"Alexander","lname":"Teumer"},{"name":"Shapland, Chin","fname":"Chin","lname":"Shapland"},{"name":"Dannemann, Michael","fname":"Michael","lname":"Dannemann"},{"name":"Vernot, Benjamin","fname":"Benjamin","lname":"Vernot"},{"name":"Neubauer, Simon","fname":"Simon","lname":"Neubauer"},{"name":"Guadalupe, Tulio","fname":"Tulio","lname":"Guadalupe"},{"name":"Fern\u00E1ndez, Guill\u00E9n","fname":"Guill\u00E9n","lname":"Fern\u00E1ndez"},{"name":"Brunner, Han","fname":"Han","lname":"Brunner"},{"name":"Enard, Wolfgang","fname":"Wolfgang","lname":"Enard"},{"name":"Fallon, James","fname":"James","lname":"Fallon"},{"name":"Hosten, Norbert","fname":"Norbert","lname":"Hosten"},{"name":"V\u00F6lker, Uwe","fname":"Uwe","lname":"V\u00F6lker"},{"name":"Profico, Antonio","fname":"Antonio","lname":"Profico"},{"name":"Di Vincenzo, Fabio","fname":"Fabio","lname":"Di Vincenzo"},{"name":"Manzi, Giorgio","fname":"Giorgio","lname":"Manzi"},{"name":"Kelso, Janet","fname":"Janet","lname":"Kelso"},{"name":"St Pourcain, Beate","fname":"Beate","lname":"St Pourcain"},{"name":"Hublin, Jean-Jacques","fname":"Jean-Jacques","lname":"Hublin"},{"name":"Franke, Barbara","fname":"Barbara","lname":"Franke"},{"name":"P\u00E4\u00E4bo, Svante","fname":"Svante","lname":"P\u00E4\u00E4bo"},{"name":"Grabe, Hans","fname":"Hans","lname":"Grabe"},{"name":"Fisher, Simon","fname":"Simon","lname":"Fisher"},{"name":"Van Erp, Theodorus","email":"tvanerp@uci.edu","fname":"Theodorus","lname":"Van Erp"},{"name":"Macciardi, Fabio","email":"fmacciar@uci.edu","fname":"Fabio","lname":"Macciardi"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":149,"asset_id":"e54c273ceba17455d4a6f58bb68146eb436f0c9acec3f6b92daba4dea81e590b","timestamp":1695221549,"image_type":"png"},"pub_year":2019,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC Irvine Previously Published Works","link_path":"uci_postprints"}},{"id":"qt6jv896t8","title":"Investigation of the Interplay between Circulating Lipids and IGF-I and Relevance to Breast Cancer Risk: An Observational and Mendelian Randomization Study","abstract":"<h4>Background</h4>Circulating lipids and insulin-like growth factor 1 (IGF-I) have been reliably associated with breast cancer. Observational studies suggest an interplay between lipids and IGF-I, however, whether these relationships are causal and if pathways from these phenotypes to breast cancer overlap is unclear.<h4>Methods</h4>Mendelian randomization (MR) was conducted to estimate the relationship between lipids or IGF-I and breast cancer risk using genetic summary statistics for lipids (low-density lipoprotein cholesterol, LDL-C; high-density lipoprotein cholesterol, HDL-C; triglycerides, TGs), IGF-I and breast cancer from GLGC/UKBB (<i>N</i> = 239,119), CHARGE/UKBB (<i>N</i> = 252,547), and Breast Cancer Association Consortium (<i>N</i> = 247,173), respectively. Cross-sectional observational and MR analyses were conducted to assess the bi-directional relationship between lipids and IGF-I in SHIP (<i>N</i> = 3,812) and UKBB (<i>N</i> = 422,389), and using genetic summary statistics from GLGC (<i>N</i> = 188,577) and CHARGE/UKBB (<i>N</i> = 469,872).<h4>Results</h4>In multivariable MR (MVMR) analyses, the OR for breast cancer per 1-SD increase in HDL-C and TG was 1.08 [95% confidence interval (CI), 1.04-1.13] and 0.94 (95% CI, 0.89-0.98), respectively. The OR for breast cancer per 1-SD increase in IGF-I was 1.09 (95% CI, 1.04-1.15). MR analyses suggested a bi-directional TG-IGF-I relationship (TG-IGF-I <i>\u03B2</i> per 1-SD: -0.13; 95% CI, -0.23 to -0.04; and IGF-I-TG <i>\u03B2</i> per 1-SD: -0.11; 95% CI, -0.18 to -0.05). There was little evidence for a causal relationship between HDL-C and LDL-C with IGF-I. In MVMR analyses, associations of TG or IGF-I with breast cancer were robust to adjustment for IGF-I or TG, respectively.<h4>Conclusions</h4>Our findings suggest a causal role of HDL-C, TG, and IGF-I in breast cancer. Observational and MR analyses support an interplay between IGF-I and TG; however, MVMR estimates suggest that TG and IGF-I may act independently to influence breast cancer.<h4>Impact</h4>Our findings should be considered in the development of prevention strategies for breast cancer, where interventions are known to modify circulating lipids and IGF-I.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Tan, Vanessa Y","fname":"Vanessa Y","lname":"Tan"},{"name":"Bull, Caroline J","fname":"Caroline J","lname":"Bull"},{"name":"Biernacka, Kalina M","fname":"Kalina M","lname":"Biernacka"},{"name":"Teumer, Alexander","fname":"Alexander","lname":"Teumer"},{"name":"Richardson, Tom G","fname":"Tom G","lname":"Richardson"},{"name":"Sanderson, Eleanor","fname":"Eleanor","lname":"Sanderson"},{"name":"Corbin, Laura J","fname":"Laura J","lname":"Corbin"},{"name":"Dudding, Tom","fname":"Tom","lname":"Dudding"},{"name":"Qi, Qibin","fname":"Qibin","lname":"Qi"},{"name":"Kaplan, Robert C","fname":"Robert C","lname":"Kaplan"},{"name":"Rotter, Jerome I","email":"jrotter@labiomed.org","fname":"Jerome I","lname":"Rotter","ORCID_id":"0000-0001-7191-1723"},{"name":"Friedrich, Nele","fname":"Nele","lname":"Friedrich"},{"name":"V\u00F6lker, Uwe","fname":"Uwe","lname":"V\u00F6lker"},{"name":"Mayerle, Julia","fname":"Julia","lname":"Mayerle"},{"name":"Perks, Claire M","fname":"Claire M","lname":"Perks"},{"name":"Holly, Jeff MP","fname":"Jeff MP","lname":"Holly"},{"name":"Timpson, Nicholas J","fname":"Nicholas J","lname":"Timpson"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":149,"asset_id":"4909efe3874be8739b695323e9e21ad738d1920672a0c152dda28b1f5c7a8afa","timestamp":1658457160,"image_type":"png"},"pub_year":2021,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UCLA Previously Published Works","link_path":"ucla_postprints"}},{"id":"qt2xz868qv","title":"Full exploitation of high dimensionality in brain imaging: The JPND working group statement and findings","abstract":"Advances in technology enable increasing amounts of data collection from individuals for biomedical research. Such technologies, for example, in genetics and medical imaging, have also led to important scientific discoveries about health and disease. The combination of multiple types of high-throughput data for complex analyses, however, has been limited by analytical and logistic resources to handle high-dimensional data sets. In our previous EU Joint Programme-Neurodegenerative Disease Research (JPND) Working Group, called HD-READY, we developed methods that allowed successful combination of omics data with neuroimaging. Still, several issues remained to fully leverage high-dimensional multimodality data. For instance, high-dimensional features, such as voxels and vertices, which are common in neuroimaging, remain difficult to harmonize. In this Full-HD Working Group, we focused on such harmonization of high-dimensional neuroimaging phenotypes in combination with other omics data and how to make the resulting ultra-high-dimensional data easily accessible in neurodegeneration research.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Adams, Hieab HH","fname":"Hieab HH","lname":"Adams"},{"name":"Roshchupkin, Gennady V","fname":"Gennady V","lname":"Roshchupkin"},{"name":"DeCarli, Charles","email":"cdecarli@ucdavis.edu","fname":"Charles","lname":"DeCarli","ORCID_id":"0000-0003-1914-2693"},{"name":"Franke, Barbara","fname":"Barbara","lname":"Franke"},{"name":"Grabe, Hans J","fname":"Hans J","lname":"Grabe"},{"name":"Habes, Mohamad","fname":"Mohamad","lname":"Habes"},{"name":"Jahanshad, Neda","fname":"Neda","lname":"Jahanshad"},{"name":"Medland, Sarah E","fname":"Sarah E","lname":"Medland"},{"name":"Niessen, Wiro","fname":"Wiro","lname":"Niessen"},{"name":"Satizabal, Claudia L","fname":"Claudia L","lname":"Satizabal"},{"name":"Schmidt, Reinhold","fname":"Reinhold","lname":"Schmidt"},{"name":"Seshadri, Sudha","fname":"Sudha","lname":"Seshadri"},{"name":"Teumer, Alexander","fname":"Alexander","lname":"Teumer"},{"name":"Thompson, Paul M","fname":"Paul M","lname":"Thompson"},{"name":"Vernooij, Meike W","fname":"Meike W","lname":"Vernooij"},{"name":"Wittfeld, Katharina","fname":"Katharina","lname":"Wittfeld"},{"name":"Ikram, M Arfan","fname":"M Arfan","lname":"Ikram"}],"editors":[{"name":"Jovicich, Jorge","fname":"Jorge","lname":"Jovicich"},{"name":"Frisoni, Giovanni B","fname":"Giovanni B","lname":"Frisoni"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":167,"asset_id":"be8c8909d5c60fe7091a9f9ea91bcc82055595544906ec19d6181dab0511b34c","timestamp":1658458880,"image_type":"png"},"pub_year":2019,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC Davis Previously Published Works","link_path":"ucd_postprints"}},{"id":"qt0mx5k9z3","title":"Neandertal Introgression Sheds Light on Modern Human Endocranial Globularity","abstract":"One of the features that distinguishes modern humans from our extinct relatives and ancestors is a globular shape of the braincase [1-4]. As the endocranium closely mirrors the outer shape of the brain, these differences might reflect altered neural architecture [4, 5]. However, in the absence of fossil brain tissue, the underlying neuroanatomical changes as well as their genetic bases remain elusive. To better understand the biological foundations of modern human endocranial shape, we turn to our closest extinct relatives: the Neandertals. Interbreeding between modern humans and Neandertals has resulted in introgressed fragments of Neandertal DNA in the genomes of present-day non-Africans [6, 7]. Based on shape analyses of fossil skull endocasts, we derive a measure of endocranial globularity from structural MRI scans of thousands of modern humans and study the effects of introgressed fragments of Neandertal DNA on this phenotype. We find that Neandertal alleles on chromosomes 1 and 18 are associated with reduced endocranial globularity. These alleles influence expression of two nearby genes, UBR4 and PHLPP1, which are involved in neurogenesis and myelination, respectively. Our findings show how integration of fossil skull data with archaic genomics and neuroimaging can suggest developmental mechanisms that may contribute to the unique modern human endocranial shape.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Gunz, Philipp","fname":"Philipp","lname":"Gunz"},{"name":"Tilot, Amanda K","fname":"Amanda K","lname":"Tilot"},{"name":"Wittfeld, Katharina","fname":"Katharina","lname":"Wittfeld"},{"name":"Teumer, Alexander","fname":"Alexander","lname":"Teumer"},{"name":"Shapland, Chin Yang","fname":"Chin Yang","lname":"Shapland"},{"name":"van Erp, Theo GM","email":"tvanerp@uci.edu","fname":"Theo GM","lname":"van Erp","ORCID_id":"0000-0002-2465-2797"},{"name":"Dannemann, Michael","fname":"Michael","lname":"Dannemann"},{"name":"Vernot, Benjamin","fname":"Benjamin","lname":"Vernot"},{"name":"Neubauer, Simon","fname":"Simon","lname":"Neubauer"},{"name":"Guadalupe, Tulio","fname":"Tulio","lname":"Guadalupe"},{"name":"Fern\u00E1ndez, Guill\u00E9n","fname":"Guill\u00E9n","lname":"Fern\u00E1ndez"},{"name":"Brunner, Han G","fname":"Han G","lname":"Brunner"},{"name":"Enard, Wolfgang","fname":"Wolfgang","lname":"Enard"},{"name":"Fallon, James","fname":"James","lname":"Fallon"},{"name":"Hosten, Norbert","fname":"Norbert","lname":"Hosten"},{"name":"V\u00F6lker, Uwe","fname":"Uwe","lname":"V\u00F6lker"},{"name":"Profico, Antonio","fname":"Antonio","lname":"Profico"},{"name":"Di Vincenzo, Fabio","fname":"Fabio","lname":"Di Vincenzo"},{"name":"Manzi, Giorgio","fname":"Giorgio","lname":"Manzi"},{"name":"Kelso, Janet","fname":"Janet","lname":"Kelso"},{"name":"St. Pourcain, Beate","fname":"Beate","lname":"St. Pourcain"},{"name":"Hublin, Jean-Jacques","fname":"Jean-Jacques","lname":"Hublin"},{"name":"Franke, Barbara","fname":"Barbara","lname":"Franke"},{"name":"P\u00E4\u00E4bo, Svante","fname":"Svante","lname":"P\u00E4\u00E4bo"},{"name":"Macciardi, Fabio","email":"fmacciar@uci.edu","fname":"Fabio","lname":"Macciardi","ORCID_id":"0000-0003-0537-4266"},{"name":"Grabe, Hans J","fname":"Hans J","lname":"Grabe"},{"name":"Fisher, Simon E","fname":"Simon E","lname":"Fisher"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":149,"asset_id":"e54c273ceba17455d4a6f58bb68146eb436f0c9acec3f6b92daba4dea81e590b","timestamp":1581372786,"image_type":"png"},"pub_year":2019,"genre":"article","rights":"https://creativecommons.org/licenses/by/4.0/","peerReviewed":true,"unitInfo":{"displayName":"UC Irvine Previously Published Works","link_path":"uci_postprints"}},{"id":"qt8sm5d1xw","title":"Distinct genetic liability profiles define clinically relevant patient strata across common diseases.","abstract":"Stratified medicine holds great promise to tailor treatment to the needs of individual patients. While genetics holds great potential to aid patient stratification, it remains a major challenge to operationalize complex genetic risk factor profiles to deconstruct clinical heterogeneity. Contemporary approaches to this problem rely on polygenic risk scores (PRS), which provide only limited clinical utility and lack a clear biological foundation. To overcome these limitations, we develop the CASTom-iGEx approach to stratify individuals based on the aggregated impact of their genetic risk factor profiles on tissue specific gene expression levels. The paradigmatic application of this approach to coronary artery disease or schizophrenia patient cohorts identified diverse strata or biotypes. These biotypes are characterized by distinct endophenotype profiles as well as clinical parameters and are fundamentally distinct from PRS based groupings. In stark contrast to the latter, the CASTom-iGEx strategy discovers biologically meaningful and clinically actionable patient subgroups, where complex genetic liabilities are not randomly distributed across individuals but rather converge onto distinct disease relevant biological processes. These results support the notion of different patient biotypes characterized by partially distinct pathomechanisms. Thus, the universally applicable approach presented here has the potential to constitute an important component of future personalized medicine paradigms.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Trastulla, Lucia","fname":"Lucia","lname":"Trastulla"},{"name":"Dolgalev, Georgii","fname":"Georgii","lname":"Dolgalev"},{"name":"Moser, Sylvain","fname":"Sylvain","lname":"Moser"},{"name":"Jim\u00E9nez-Barr\u00F3n, Laura","fname":"Laura","lname":"Jim\u00E9nez-Barr\u00F3n"},{"name":"Andlauer, Till","fname":"Till","lname":"Andlauer"},{"name":"von Scheidt, Moritz","fname":"Moritz","lname":"von Scheidt"},{"name":"Budde, Monika","fname":"Monika","lname":"Budde"},{"name":"Heilbronner, Urs","fname":"Urs","lname":"Heilbronner"},{"name":"Papiol, Sergi","fname":"Sergi","lname":"Papiol"},{"name":"Teumer, Alexander","fname":"Alexander","lname":"Teumer"},{"name":"Homuth, Georg","fname":"Georg","lname":"Homuth"},{"name":"V\u00F6lzke, Henry","fname":"Henry","lname":"V\u00F6lzke"},{"name":"D\u00F6rr, Marcus","fname":"Marcus","lname":"D\u00F6rr"},{"name":"Falkai, Peter","fname":"Peter","lname":"Falkai"},{"name":"Schulze, Thomas","fname":"Thomas","lname":"Schulze"},{"name":"Gagneur, Julien","fname":"Julien","lname":"Gagneur"},{"name":"Iorio, Francesco","fname":"Francesco","lname":"Iorio"},{"name":"M\u00FCller-Myhsok, Bertram","fname":"Bertram","lname":"M\u00FCller-Myhsok"},{"name":"Schunkert, Heribert","fname":"Heribert","lname":"Schunkert"},{"name":"Ziller, Michael","fname":"Michael","lname":"Ziller"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":172,"asset_id":"2dc260d3b4c7e970982a365bd838259e0c53519a0c16b354654e60ff8b60da8d","timestamp":1733934136,"image_type":"png"},"pub_year":2024,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UCLA Previously Published Works","link_path":"ucla_postprints"}},{"id":"qt7597c7wp","title":"Genome-wide association and functional studies identify a role for IGFBP3 in hip osteoarthritis","abstract":"<h4>Objectives</h4>To identify genetic associations with hip osteoarthritis (HOA), we performed a meta-analysis of genome-wide association studies (GWAS) of HOA.<h4>Methods</h4>The GWAS meta-analysis included approximately 2.5 million imputed HapMap single nucleotide polymorphisms (SNPs). HOA cases and controls defined radiographically and by total hip replacement were selected from the Osteoporotic Fractures in Men (MrOS) Study and the Study of Osteoporotic Fractures (SOF) (654 cases and 4697 controls, combined). Replication of genome-wide significant SNP associations (p \u22645\u00D710(-8)) was examined in five studies (3243 cases and 6891 controls, combined). Functional studies were performed using in vitro models of chondrogenesis and osteogenesis.<h4>Results</h4>The A allele of rs788748, located 65 kb upstream of the IGFBP3 gene, was associated with lower HOA odds at the genome-wide significance level in the discovery stage (OR 0.71, p=2\u00D710(-8)). The association replicated in five studies (OR 0.92, p=0.020), but the joint analysis of discovery and replication results was not genome-wide significant (p=1\u00D710(-6)). In separate study populations, the rs788748 A allele was also associated with lower circulating IGFBP3 protein levels (p=4\u00D710(-13)), suggesting that this SNP or a variant in linkage disequilibrium could be an IGFBP3 regulatory variant. Results from functional studies were consistent with association results. Chondrocyte hypertrophy, a deleterious event in OA pathogenesis, was largely prevented upon IGFBP3 knockdown in chondrocytes. Furthermore, IGFBP3 overexpression induced cartilage catabolism and osteogenic differentiation.<h4>Conclusions</h4>Results from GWAS and functional studies provided suggestive links between IGFBP3 and HOA.","content_type":null,"author_hide":null,"authors":[{"name":"Evans, Daniel S","fname":"Daniel S","lname":"Evans"},{"name":"Cailotto, Frederic","fname":"Frederic","lname":"Cailotto"},{"name":"Parimi, Neeta","fname":"Neeta","lname":"Parimi"},{"name":"Valdes, Ana M","fname":"Ana M","lname":"Valdes"},{"name":"Casta\u00F1o-Betancourt, Martha C","fname":"Martha C","lname":"Casta\u00F1o-Betancourt"},{"name":"Liu, Youfang","fname":"Youfang","lname":"Liu"},{"name":"Kaplan, Robert C","fname":"Robert C","lname":"Kaplan"},{"name":"Bidlingmaier, Martin","fname":"Martin","lname":"Bidlingmaier"},{"name":"Vasan, Ramachandran S","fname":"Ramachandran S","lname":"Vasan"},{"name":"Teumer, Alexander","fname":"Alexander","lname":"Teumer"},{"name":"Tranah, Gregory J","fname":"Gregory J","lname":"Tranah"},{"name":"Nevitt, Michael C","email":"michael.nevitt@ucsf.edu","fname":"Michael C","lname":"Nevitt"},{"name":"Cummings, Steven R","email":"steven.cummings@ucsf.edu","fname":"Steven R","lname":"Cummings"},{"name":"Orwoll, Eric S","fname":"Eric S","lname":"Orwoll"},{"name":"Barrett-Connor, Elizabeth","fname":"Elizabeth","lname":"Barrett-Connor"},{"name":"Renner, Jordan B","fname":"Jordan B","lname":"Renner"},{"name":"Jordan, Joanne M","fname":"Joanne M","lname":"Jordan"},{"name":"Doherty, Michael","fname":"Michael","lname":"Doherty"},{"name":"Doherty, Sally A","fname":"Sally A","lname":"Doherty"},{"name":"Uitterlinden, Andre G","fname":"Andre G","lname":"Uitterlinden"},{"name":"van Meurs, Joyce BJ","fname":"Joyce BJ","lname":"van Meurs"},{"name":"Spector, Tim D","fname":"Tim D","lname":"Spector"},{"name":"Lories, Rik J","fname":"Rik J","lname":"Lories"},{"name":"Lane, Nancy E","email":"nelane@ucdavis.edu","fname":"Nancy E","lname":"Lane"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":null,"pub_year":2015,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC Davis Previously Published Works","link_path":"ucd_postprints"}},{"id":"qt2gp960sb","title":"Association of eGFR-Related Loci Identified by GWAS with Incident CKD and ESRD","abstract":"Family studies suggest a genetic component to the etiology of chronic kidney disease (CKD) and end stage renal disease (ESRD). Previously, we identified 16 loci for eGFR in genome-wide association studies, but the associations of these single nucleotide polymorphisms (SNPs) for incident CKD or ESRD are unknown. We thus investigated the association of these loci with incident CKD in 26,308 individuals of European ancestry free of CKD at baseline drawn from eight population-based cohorts followed for a median of 7.2 years (including 2,122 incident CKD cases defined as eGFR <60ml/min/1.73m(2) at follow-up) and with ESRD in four case-control studies in subjects of European ancestry (3,775 cases, 4,577 controls). SNPs at 11 of the 16 loci (UMOD, PRKAG2, ANXA9, DAB2, SHROOM3, DACH1, STC1, SLC34A1, ALMS1/NAT8, UBE2Q2, and GCKR) were associated with incident CKD; p-values ranged from p\u200A=\u200A4.1e-9 in UMOD to p\u200A=\u200A0.03 in GCKR. After adjusting for baseline eGFR, six of these loci remained significantly associated with incident CKD (UMOD, PRKAG2, ANXA9, DAB2, DACH1, and STC1). SNPs in UMOD (OR\u200A=\u200A0.92, p\u200A=\u200A0.04) and GCKR (OR\u200A=\u200A0.93, p\u200A=\u200A0.03) were nominally associated with ESRD. In summary, the majority of eGFR-related loci are either associated or show a strong trend towards association with incident CKD, but have modest associations with ESRD in individuals of European descent. Additional work is required to characterize the association of genetic determinants of CKD and ESRD at different stages of disease progression.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"B\u00F6ger, Carsten A","fname":"Carsten A","lname":"B\u00F6ger"},{"name":"Gorski, Mathias","fname":"Mathias","lname":"Gorski"},{"name":"Li, Man","fname":"Man","lname":"Li"},{"name":"Hoffmann, Michael M","fname":"Michael M","lname":"Hoffmann"},{"name":"Huang, Chunmei","fname":"Chunmei","lname":"Huang"},{"name":"Yang, Qiong","fname":"Qiong","lname":"Yang"},{"name":"Teumer, Alexander","fname":"Alexander","lname":"Teumer"},{"name":"Krane, Vera","fname":"Vera","lname":"Krane"},{"name":"O'Seaghdha, Conall M","fname":"Conall M","lname":"O'Seaghdha"},{"name":"Kutalik, Zolt\u00E1n","fname":"Zolt\u00E1n","lname":"Kutalik"},{"name":"Wichmann, H-Erich","fname":"H-Erich","lname":"Wichmann"},{"name":"Haak, Thomas","fname":"Thomas","lname":"Haak"},{"name":"Boes, Eva","fname":"Eva","lname":"Boes"},{"name":"Coassin, Stefan","fname":"Stefan","lname":"Coassin"},{"name":"Coresh, Josef","fname":"Josef","lname":"Coresh"},{"name":"Kollerits, Barbara","fname":"Barbara","lname":"Kollerits"},{"name":"Haun, Margot","fname":"Margot","lname":"Haun"},{"name":"Paulweber, Bernhard","fname":"Bernhard","lname":"Paulweber"},{"name":"K\u00F6ttgen, Anna","fname":"Anna","lname":"K\u00F6ttgen"},{"name":"Li, Guo","fname":"Guo","lname":"Li"},{"name":"Shlipak, Michael G","email":"michael.shlipak@ucsf.edu","fname":"Michael G","lname":"Shlipak"},{"name":"Powe, Neil","email":"neil.powe@ucsf.edu","fname":"Neil","lname":"Powe","ORCID_id":"0000-0003-2347-3620"},{"name":"Hwang, Shih-Jen","fname":"Shih-Jen","lname":"Hwang"},{"name":"Dehghan, Abbas","fname":"Abbas","lname":"Dehghan"},{"name":"Rivadeneira, Fernando","fname":"Fernando","lname":"Rivadeneira"},{"name":"Uitterlinden, Andr\u00E9","fname":"Andr\u00E9","lname":"Uitterlinden"},{"name":"Hofman, Albert","fname":"Albert","lname":"Hofman"},{"name":"Beckmann, Jacques S","fname":"Jacques S","lname":"Beckmann"},{"name":"Kr\u00E4mer, Bernhard K","fname":"Bernhard K","lname":"Kr\u00E4mer"},{"name":"Witteman, Jacqueline","fname":"Jacqueline","lname":"Witteman"},{"name":"Bochud, Murielle","fname":"Murielle","lname":"Bochud"},{"name":"Siscovick, David","fname":"David","lname":"Siscovick"},{"name":"Rettig, Rainer","fname":"Rainer","lname":"Rettig"},{"name":"Kronenberg, Florian","fname":"Florian","lname":"Kronenberg"},{"name":"Wanner, Christoph","fname":"Christoph","lname":"Wanner"},{"name":"Thadhani, Ravi I","fname":"Ravi I","lname":"Thadhani"},{"name":"Heid, Iris M","fname":"Iris M","lname":"Heid"},{"name":"Fox, Caroline S","fname":"Caroline S","lname":"Fox"},{"name":"Kao, WH","fname":"WH","lname":"Kao"}],"editors":[{"name":"Kim, Stuart K","fname":"Stuart K","lname":"Kim"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":179,"asset_id":"51ff3997f26a78365d0be918eb6a2979bf552bd01682fd951cbdc4ed6a902658","timestamp":1589676224,"image_type":"png"},"pub_year":2011,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UC San Francisco Previously Published Works","link_path":"ucsf_postprints"}},{"id":"qt8bf9j0jr","title":"Transcriptome-Wide Analysis Identifies Novel Associations With Blood Pressure","abstract":"Hypertension represents a major cardiovascular risk factor. The pathophysiology of increased blood pressure (BP) is not yet completely understood. Transcriptome profiling offers possibilities to uncover genetics effects on BP. Based on 2 populations including 2549 individuals, a meta-analyses of monocytic transcriptome-wide profiles were performed to identify transcripts associated with BP. Replication was performed in 2 independent studies of whole-blood transcriptome data including 1990 individuals. For identified candidate genes, a direct link between long-term changes in BP and gene expression over time and by treatment with BP-lowering therapy was assessed. The predictive value of protein levels encoded by candidate genes for subsequent cardiovascular disease was investigated. Eight transcripts (<i>CRIP1</i>, <i>MYADM</i>, <i>TIPARP</i>, <i>TSC22D3</i>, <i>CEBPA</i>, <i>F12, LMNA</i>, and <i>TPPP3</i>) were identified jointly accounting for up to 13% (95% confidence interval, 8.7-16.2) of BP variability. Changes in <i>CRIP1</i>, <i>MYADM</i>, <i>TIPARP</i>, <i>LMNA</i>, <i>TSC22D3</i>, <i>CEBPA</i>, and <i>TPPP3</i> expression associated with BP changes-among these, <i>CRIP1</i> gene expression was additionally correlated to measures of cardiac hypertrophy. Assessment of circulating CRIP1 (cystein-rich protein 1) levels as biomarkers showed a strong association with increased risk for incident stroke (hazard ratio, 1.06; 95% confidence interval, 1.03-1.09; <i>P</i>=5.0\u00D710<sup>-5</sup>). Our comprehensive analysis of global gene expression highlights 8 novel transcripts significantly associated with BP, providing a link between gene expression and BP. Translational approaches further established evidence for the potential use of CRIP1 as emerging disease-related biomarker.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Zeller, Tanja","fname":"Tanja","lname":"Zeller"},{"name":"Schurmann, Claudia","fname":"Claudia","lname":"Schurmann"},{"name":"Schramm, Katharina","fname":"Katharina","lname":"Schramm"},{"name":"M\u00FCller, Christian","fname":"Christian","lname":"M\u00FCller"},{"name":"Kwon, Soonil","fname":"Soonil","lname":"Kwon"},{"name":"Wild, Philipp S","fname":"Philipp S","lname":"Wild"},{"name":"Teumer, Alexander","fname":"Alexander","lname":"Teumer"},{"name":"Herrington, David","fname":"David","lname":"Herrington"},{"name":"Schillert, Arne","fname":"Arne","lname":"Schillert"},{"name":"Iacoviello, Licia","fname":"Licia","lname":"Iacoviello"},{"name":"Kratzer, Adelheid","fname":"Adelheid","lname":"Kratzer"},{"name":"Jagodzinski, Annika","fname":"Annika","lname":"Jagodzinski"},{"name":"Karakas, Mahir","fname":"Mahir","lname":"Karakas"},{"name":"Ding, Jingzhong","fname":"Jingzhong","lname":"Ding"},{"name":"Neumann, Johannes T","fname":"Johannes T","lname":"Neumann"},{"name":"Kuulasmaa, Kari","fname":"Kari","lname":"Kuulasmaa"},{"name":"Gieger, Christian","fname":"Christian","lname":"Gieger"},{"name":"Kacprowski, Tim","fname":"Tim","lname":"Kacprowski"},{"name":"Schnabel, Renate B","fname":"Renate B","lname":"Schnabel"},{"name":"Roden, Michael","fname":"Michael","lname":"Roden"},{"name":"Wahl, Simone","fname":"Simone","lname":"Wahl"},{"name":"Rotter, Jerome I","email":"jrotter@labiomed.org","fname":"Jerome I","lname":"Rotter","ORCID_id":"0000-0001-7191-1723"},{"name":"Ojeda, Francisco","fname":"Francisco","lname":"Ojeda"},{"name":"Carstensen-Kirberg, Maren","fname":"Maren","lname":"Carstensen-Kirberg"},{"name":"Tregouet, David-Alexandre","fname":"David-Alexandre","lname":"Tregouet"},{"name":"D\u00F6rr, Marcus","fname":"Marcus","lname":"D\u00F6rr"},{"name":"Meitinger, Thomas","fname":"Thomas","lname":"Meitinger"},{"name":"Lackner, Karl J","fname":"Karl J","lname":"Lackner"},{"name":"Wolf, Petra","fname":"Petra","lname":"Wolf"},{"name":"Felix, Stephan B","fname":"Stephan B","lname":"Felix"},{"name":"Landmesser, Ulf","fname":"Ulf","lname":"Landmesser"},{"name":"Costanzo, Simona","fname":"Simona","lname":"Costanzo"},{"name":"Ziegler, Andreas","fname":"Andreas","lname":"Ziegler"},{"name":"Liu, Yongmei","fname":"Yongmei","lname":"Liu"},{"name":"V\u00F6lker, Uwe","fname":"Uwe","lname":"V\u00F6lker"},{"name":"Palmas, Walter","fname":"Walter","lname":"Palmas"},{"name":"Prokisch, Holger","fname":"Holger","lname":"Prokisch"},{"name":"Guo, Xiuqing","fname":"Xiuqing","lname":"Guo"},{"name":"Herder, Christian","fname":"Christian","lname":"Herder"},{"name":"Blankenberg, Stefan","fname":"Stefan","lname":"Blankenberg"},{"name":"Homuth, Georg","fname":"Georg","lname":"Homuth"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":162,"asset_id":"5362e6cb578041809a6f4d2be931aea523702ad7f7ea7adf3eef600ff1008a4c","timestamp":1684040242,"image_type":"png"},"pub_year":2017,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UCLA Previously Published Works","link_path":"ucla_postprints"}},{"id":"qt21t098hn","title":"Association analysis between an epigenetic alcohol risk score and blood pressure","abstract":"<h4>Background</h4>Epigenome-wide association studies have identified multiple DNA methylation sites (CpGs) associated with alcohol consumption, an important lifestyle risk factor for cardiovascular diseases. This study aimed to test the hypothesis that an alcohol consumption epigenetic risk score (ERS) is associated with blood pressure (BP) traits.<h4>Results</h4>We implemented an ERS based on a previously reported epigenetic signature of 144 alcohol-associated CpGs in meta-analysis of participants of European ancestry. We found a one-unit increment of ERS was associated with eleven drinks of alcohol consumed per day, on average, across several cohorts (p\u2009<\u20090.0001). We examined the association of the ERS with systolic blood pressure (SBP), diastolic blood pressure (DBP), and hypertension (HTN) in 3,898 Framingham Heart Study (FHS) participants. Cross-sectional analyses in FHS revealed that a one-unit increment of the ERS was associated with 1.93 mm Hg higher SBP (p\u2009=\u20094.64E-07), 0.68 mm Hg higher DBP (p\u2009=\u20090.006), and an odds ratio of 1.78 for HTN (p\u2009<\u20092E-16). Meta-analysis of the cross-sectional association of the ERS with BP traits in eight independent external cohorts (n\u2009=\u200911,544) showed similar relationships with BP levels, i.e., a one-unit increase in ERS was associated with 0.74 mm Hg (p\u2009=\u20090.002) higher SBP and 0.50 mm Hg (p\u2009=\u20090.0006) higher DBP, but not with HTN. Longitudinal analyses in FHS (n\u2009=\u20093260) and five independent external cohorts (n\u2009=\u20094021) showed that the baseline ERS was not associated with a change in BP over time or with incident HTN.<h4>Conclusions</h4>Our findings demonstrate that the ERS has potential clinical utility in assessing lifestyle factors related to cardiovascular risk, especially when self-reported behavioral data (e.g., alcohol consumption) are unreliable or unavailable.","content_type":"application/pdf","author_hide":null,"authors":[{"name":"Bui, Helena","fname":"Helena","lname":"Bui"},{"name":"Keshawarz, Amena","fname":"Amena","lname":"Keshawarz"},{"name":"Wang, Mengyao","fname":"Mengyao","lname":"Wang"},{"name":"Lee, Mikyeong","fname":"Mikyeong","lname":"Lee"},{"name":"Ratliff, Scott M","fname":"Scott M","lname":"Ratliff"},{"name":"Lin, Lisha","fname":"Lisha","lname":"Lin"},{"name":"Birditt, Kira S","fname":"Kira S","lname":"Birditt"},{"name":"Faul, Jessica D","fname":"Jessica D","lname":"Faul"},{"name":"Peters, Annette","fname":"Annette","lname":"Peters"},{"name":"Gieger, Christian","fname":"Christian","lname":"Gieger"},{"name":"Delerue, Thomas","fname":"Thomas","lname":"Delerue"},{"name":"Kardia, Sharon LR","fname":"Sharon LR","lname":"Kardia"},{"name":"Zhao, Wei","fname":"Wei","lname":"Zhao"},{"name":"Guo, Xiuqing","fname":"Xiuqing","lname":"Guo"},{"name":"Yao, Jie","fname":"Jie","lname":"Yao"},{"name":"Rotter, Jerome I","email":"jrotter@labiomed.org","fname":"Jerome I","lname":"Rotter","ORCID_id":"0000-0001-7191-1723"},{"name":"Li, Yi","fname":"Yi","lname":"Li"},{"name":"Liu, Xue","fname":"Xue","lname":"Liu"},{"name":"Liu, Dan","fname":"Dan","lname":"Liu"},{"name":"Tavares, Juliana F","fname":"Juliana F","lname":"Tavares"},{"name":"Pehlivan, G\u00F6khan","fname":"G\u00F6khan","lname":"Pehlivan"},{"name":"Breteler, Monique MB","fname":"Monique MB","lname":"Breteler"},{"name":"Karabegovic, Irma","fname":"Irma","lname":"Karabegovic"},{"name":"Ochoa-Rosales, Carolina","fname":"Carolina","lname":"Ochoa-Rosales"},{"name":"Voortman, Trudy","fname":"Trudy","lname":"Voortman"},{"name":"Ghanbari, Mohsen","fname":"Mohsen","lname":"Ghanbari"},{"name":"van Meurs, Joyce BJ","fname":"Joyce BJ","lname":"van Meurs"},{"name":"Nasr, Mohamed Kamal","fname":"Mohamed Kamal","lname":"Nasr"},{"name":"D\u00F6rr, Marcus","fname":"Marcus","lname":"D\u00F6rr"},{"name":"Grabe, Hans J","fname":"Hans J","lname":"Grabe"},{"name":"London, Stephanie J","fname":"Stephanie J","lname":"London"},{"name":"Teumer, Alexander","fname":"Alexander","lname":"Teumer"},{"name":"Waldenberger, Melanie","fname":"Melanie","lname":"Waldenberger"},{"name":"Weir, David R","fname":"David R","lname":"Weir"},{"name":"Smith, Jennifer A","fname":"Jennifer A","lname":"Smith"},{"name":"Levy, Daniel","fname":"Daniel","lname":"Levy"},{"name":"Ma, Jiantao","fname":"Jiantao","lname":"Ma"},{"name":"Liu, Chunyu","fname":"Chunyu","lname":"Liu"}],"supp_files":[{"type":"pdf","count":0},{"type":"image","count":0},{"type":"video","count":0},{"type":"audio","count":0},{"type":"zip","count":0},{"type":"other","count":0}],"thumbnail":{"width":121,"height":175,"asset_id":"2b978c8026e54b2e6f48a41d8042810fd8cca5bfa398fb3b63c9a83ec2a5688a","timestamp":1731526538,"image_type":"png"},"pub_year":2024,"genre":"article","rights":null,"peerReviewed":true,"unitInfo":{"displayName":"UCLA Previously Published Works","link_path":"ucla_postprints"}}],"facets":[{"display":"Type of Work","fieldName":"type_of_work","facets":[{"value":"article","count":103,"displayName":"Article"},{"value":"monograph","count":0,"displayName":"Book"},{"value":"dissertation","count":0,"displayName":"Theses"},{"value":"multimedia","count":0,"displayName":"Multimedia"}]},{"display":"Peer Review","fieldName":"peer_reviewed","facets":[{"value":"1","count":103,"displayName":"Peer-reviewed only"}]},{"display":"Supplemental 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