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858 results on '"Linton, MacRae F."'

151. Bioinformatic analysis of endogenous and exogenous small RNAs on lipoproteins

Author

Allen, Ryan M., primary, Zhao, Shilin, additional, Ramirez Solano, Marisol A., additional, Zhu, Wanying, additional, Michell, Danielle L., additional, Wang, Yuhuan, additional, Shyr, Yu, additional, Sethupathy, Praveen, additional, Linton, MacRae F., additional, Graf, Gregory A., additional, Sheng, Quanhu, additional, and Vickers, Kasey C., additional

Published
2018
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153. Abstract 553: Scavenging Reactive Aldehydes With 5'-o-pentyl-pyridoxamine (PPM) Improves HDL Function and Reduces Atherosclerosis in Ldlr Deficient Mice

Author

Huang, Jiansheng, primary, Zhang, Linda, additional, Yancey, Patricia, additional, Tao, Huan, additional, Ding, Lei, additional, Zhang, Youmin, additional, Oates, John, additional, Amarnath, Venkataraman, additional, Roberts, Jackson, additional, Davies, Sean, additional, and Linton, MacRae F, additional

Published
2018
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159. Effect of drug therapy on net cholesterol efflux capacity of HDL-enriched serum in rheumatoid arthritis

Author

Ormseth, Michelle J., Yancey, Patricia G., Solus, Joseph F., Bridges, S. Louis, Curtis, Jeffrey R., Linton, MacRae F., Fazio, Sergio, Davies, Sean S., Roberts, L. Jackson, Vickers, Kasey C., Kon, Valentina, and Stein, C. Michael

Subjects
Male, Serum, Adalimumab, Biological Transport, Blood Sedimentation, Middle Aged, Antibodies, Monoclonal, Humanized, Article, Arthritis, Rheumatoid, Cholesterol, Methotrexate, Antirheumatic Agents, Humans, Female, Longitudinal Studies, Lipoproteins, HDL
Abstract

Patients with rheumatoid arthritis (RA) have an increased risk of coronary heart disease (CHD). Some RA therapies may modify this risk, but the underlying mechanisms are unclear. The cholesterol efflux capacity of high-density lipoprotein (HDL) is associated with a reduced CHD risk in non-RA populations; however, inflammation may impair the function of HDL. The aim of this study was to evaluate whether reduced inflammation resulting from treatment with methotrexate (MTX), adalimumab (ADA), or tocilizumab (TCZ) would increase the net cholesterol efflux capacity of HDL in patients with RA.A longitudinal multicenter study repository (Treatment Efficacy and Toxicity in Rheumatoid Arthritis Database and Repository) provided clinical information for and serum samples from 70 patients with RA before and 6 months after starting treatment with a new drug (MTX [n = 23], ADA [n = 22], or TCZ [n = 25]). Disease activity was measured using the Disease Activity Score in 28 joints using the erythrocyte sedimentation rate (DAS28-ESR). The net cholesterol efflux capacity was measured in paired serum samples using THP-1 macrophages, and total cellular cholesterol was measured by fluorometric assay.The DAS28-ESR decreased with all treatments (P 0.001). Net cholesterol efflux capacity was not significantly changed after 6 months of new RA therapy (mean ± SD 36.9 ± 17.3% units at baseline versus 38.0% ± 16.9% units at 6 months [P = 0.58]). However, change in net cholesterol efflux capacity was associated with change in the DAS28-ESR (ρ = -0.25, P = 0.04). In a post hoc analysis of patients with impaired net cholesterol efflux capacity at baseline, treatment with TCZ resulted in significant improvement in net cholesterol efflux capacity (21.9 ± 14.7% units at baseline versus 31.3% ± 12.8% units at 6 months [P 0.02]), but this was not observed with MTX or ADA.Net cholesterol efflux capacity of HDL cholesterol did not change significantly after 6 months of new RA therapy, except in patients with impaired baseline cholesterol efflux capacity who were receiving TCZ. Change in disease activity was associated with change in the net cholesterol efflux capacity.

Published
2016

160. Loss of Macrophage LDL Receptor Related Protein 1 (LRP1) Confers Resistance to the Anti-atherogenic Effects of TNFα Inhibition

Author

Zhu, Lin, Giunzioni, Ilaria, Tavori, Hagai, Covarrubias, Roman, Ding, Lei, Zhang, Youmin, Ormseth, Michelle, Major, Amy S., Stafford, John M., Linton, MacRae F., and Fazio, Sergio

Subjects
Anti-Inflammatory Agents, Aortic Diseases, Drug Resistance, Apoptosis, Diet, High-Fat, Article, Monocytes, Necrosis, Apolipoproteins E, Cell Movement, Animals, Antigens, Ly, Genetic Predisposition to Disease, Aorta, Bone Marrow Transplantation, Mice, Knockout, Tumor Necrosis Factor-alpha, Macrophages, Tumor Suppressor Proteins, Adalimumab, Atherosclerosis, Plaque, Atherosclerotic, Disease Models, Animal, Phenotype, Receptors, LDL, Female, Low Density Lipoprotein Receptor-Related Protein-1, Whole-Body Irradiation, Signal Transduction
Abstract

Antiatherosclerotic effects of tumor necrosis factor-α (TNF-α) blockade in patients with systemic inflammatory states are not conclusively demonstrated, which suggests that effects depend on the cause of inflammation. Macrophage LRP1 (low-density lipoprotein receptor-related protein 1) and apoE contribute to inflammation through different pathways. We studied the antiatherosclerosis effects of TNF-α blockade in hyperlipidemic mice lacking either LRP1 (MΦLRP1(-/-)) or apoE from macrophages.Lethally irradiated low-density lipoprotein receptor (LDLR)(-/-) mice were reconstituted with bone marrow from either wild-type, MΦLRP1(-/-), apoE(-/-) or apoE(-/-)/MΦLRP1(-/-)(DKO) mice, and then treated with the TNF-α inhibitor adalimumab while fed a Western-type diet. Adalimumab reduced plasma TNF-α concentration, suppressed blood ly6C(hi) monocyte levels and their migration into the lesion, and reduced lesion cellularity and inflammation in both wild-type→LDLR(-/-) and apoE(-/-)→LDLR(-/-) mice. Overall, adalimumab reduced lesion burden by 52% to 57% in these mice. Adalimumab reduced TNF-α and blood ly6C(hi) monocyte levels in MΦLRP1(-/-)→LDLR(-/-) and DKO→LDLR(-/-) mice, but it did not suppress ly6C(hi) monocyte migration into the lesion or atherosclerosis progression.Our results show that TNF-α blockade exerts antiatherosclerotic effects that are dependent on the presence of macrophage LRP1.

Published
2016

161. Local Effects of Human PCSK9 on the Atherosclerotic Lesion

Author

Giunzioni, Ilaria, Tavori, Hagai, Covarrubias, Roman, Major, Amy S., Ding, Lei, Zhang, Youmin, DeVay, Rachel M., Hong, Liang, Fan, Daping, Predazzi, Irene M., Rashid, Shirya, Linton, MacRae F., and Fazio, Sergio

Subjects
Mice, Knockout, Transplantation Chimera, Serine Endopeptidases, Fluorescent Antibody Technique, Mice, Transgenic, Atherosclerosis, Flow Cytometry, Immunohistochemistry, Article, Mice, Inbred C57BL, Disease Models, Animal, Mice, Receptors, LDL, Macrophages, Peritoneal, Animals, Humans, Immunoprecipitation, lipids (amino acids, peptides, and proteins), Proprotein Convertases, Proprotein Convertase 9
Abstract

Proprotein convertase subtilisin/kexin type 9 (PCSK9) promotes atherosclerosis by increasing low-density lipoprotein (LDL) cholesterol levels through degradation of hepatic LDL receptor (LDLR). Studies have described the systemic effects of PCSK9 on atherosclerosis, but whether PCSK9 has local and direct effects on the plaque is unknown. To study the local effect of human PCSK9 (hPCSK9) on atherosclerotic lesion composition, independently of changes in serum cholesterol levels, we generated chimeric mice expressing hPCSK9 exclusively from macrophages, using marrow from hPCSK9 transgenic (hPCSK9tg) mice transplanted into apoE(-/-) and LDLR(-/-) mice, which were then placed on a high-fat diet (HFD) for 8 weeks. We further characterized the effect of hPCSK9 expression on the inflammatory responses in the spleen and by mouse peritoneal macrophages (MPM) in vitro. We found that MPMs from transgenic mice express both murine (m) Pcsk9 and hPCSK9 and that the latter reduces macrophage LDLR and LRP1 surface levels. We detected hPCSK9 in the serum of mice transplanted with hPCSK9tg marrow, but did not influence lipid levels or atherosclerotic lesion size. However, marrow-derived PCSK9 progressively accumulated in lesions of apoE(-/-) recipient mice, while increasing the infiltration of Ly6C(hi) inflammatory monocytes by 32% compared with controls. Expression of hPCSK9 also increased CD11b- and Ly6C(hi) -positive cell numbers in spleens of apoE(-/-) mice. In vitro, expression of hPCSK9 in LPS-stimulated macrophages increased mRNA levels of the pro-inflammatory markers Tnf and Il1b (40% and 45%, respectively) and suppressed those of the anti-inflammatory markers Il10 and Arg1 (30% and 44%, respectively). All PCSK9 effects were LDLR-dependent, as PCSK9 protein was not detected in lesions of LDLR(-/-) recipient mice and did not affect macrophage or splenocyte inflammation. In conclusion, PCSK9 directly increases atherosclerotic lesion inflammation in an LDLR-dependent but cholesterol-independent mechanism, suggesting that therapeutic PCSK9 inhibition may have vascular benefits secondary to LDL reduction.

Published
2015

163. Self-association of human PCSK9 correlates with its LDLR-degrading activity

Author

Daping Fan, Yancey, Patricia G., Shenfeng Qiu, Lei Ding, Weeber, Edwin J., Linton, MacRae F., and Fazio, Sergio

Subjects
Blood cholesterol -- Genetic aspects, Low density lipoprotein receptors -- Research, Monomers -- Comparative analysis, Polymers -- Comparative analysis, Biological sciences, Chemistry
Abstract

The correlation between the human proprotein convertase subtilisin/kexin type 9 (PCSK9) and LDLR degradation is discussed. The analysis reveals that a mixture of PCSK9 monomers, dimers and trimers exhibit better LDLR-degrading activity than a single monomer.

Published
2008

167. Abstract 208: Isolevuglandin, a Highly Reactive γ-ketoaldehyde Formed from the Isoprostane Pathway, Induces Deleterious Structural and Functional Consequences to High-density Lipoprotein

Author

Zhang, Linda S, primary, Tao, Huan, additional, Pleasent, Tiffany, additional, Borja, Mark S, additional, Oda, Michael N, additional, Jerome, W. Gray, additional, Yancey, Patricia G, additional, Roberts, L. Jackson, additional, Linton, MacRae F, additional, and Davies, Sean S, additional

Published
2017
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168. Net cholesterol efflux capacity of HDL enriched serum and coronary atherosclerosis in rheumatoid arthritis

Author

Ormseth, Michelle J., primary, Yancey, Patricia G., additional, Yamamoto, Suguru, additional, Oeser, Annette M., additional, Gebretsadik, Tebeb, additional, Shintani, Ayumi, additional, Linton, MacRae F., additional, Fazio, Sergio, additional, Davies, Sean S., additional, Roberts, L. Jackson, additional, Vickers, Kasey C., additional, Raggi, Paolo, additional, Kon, Valentina, additional, and Stein, C. Michael, additional

Published
2016
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169. Identification of SPRR3 as a novel atheroprotective factor that promotes adaptive Akt signaling in VSMCs

Author

Segedy, Amanda K., Pyle, Amy L., Li, Bin, Zhang, Youmin, Babaev, Vladimir R., Jat, Parmjit, Fazio, Sergio, Atkinson, James B., Linton, MacRae F., and Young, Pampee P.

Subjects
Male, Mice, Knockout, Cell Survival, Macrophages, Myocytes, Smooth Muscle, Endothelial Cells, Apoptosis, Atherosclerosis, Adaptation, Physiological, Article, Plaque, Atherosclerotic, Mice, Inbred C57BL, Mice, Apolipoproteins E, Cornified Envelope Proline-Rich Proteins, Disease Progression, Animals, Female, Phosphorylation, Proto-Oncogene Proteins c-akt, Cell Proliferation, Signal Transduction
Abstract

Atherosclerosis is the primary driver of cardiovascular disease, the leading cause of death worldwide. Identification of naturally occurring atheroprotective genes has become a major goal for the development of interventions that will limit atheroma progression and associated adverse events. To this end, we have identified small proline-rich repeat protein (SPRR3) as selectively upregulated in vascular smooth muscle cells (VSMCs) of atheroma-bearing arterial tissue versus healthy arterial tissue. In this study, we sought to determine the role of SPRR3 in atheroma pathophysiology.We found that atheroprone apolipoprotein E-null mice lacking SPRR3 developed significantly greater atheroma burden. To determine the cellular driver(s) of this increase, we evaluated SPRR3-dependent changes in bone marrow-derived cells, endothelial cells, and VSMCs. Bone marrow transplant of SPRR3-expressing cells into SPRR3(-/-)apolipoprotein E-deficient recipients failed to rescue atheroma burden. Similarly, endothelial cells did not exhibit a response to SPRR3 loss. However, atheromas from SPRR3-deficient mice exhibited increased TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling)-positive VSMCs compared with control. Cell death in SPRR3-deficient VSMCs was significantly increased in vitro. Conversely, SPRR3-overexpressing VSMCs exhibited reduced apoptosis compared with control. We also observed a PI3K (phosphatidylinositol 3-kinase)/Akt-dependent positive association between SPRR3 expression and levels of active Akt in VSMCs. The survival advantage seen in SPRR3-overexpressing VSMCs was abrogated after the addition of a PI3K/Akt pathway inhibitor.These results indicate that SPRR3 protects the lesion from VSMC loss by promoting survival signaling in plaque VSMCs, thereby significantly decreasing atherosclerosis progression. As the first identified atheroma-specific VSMC prosurvival factor, SPRR3 represents a potential target for lesion-specific modulation of VSMC survival.

Published
2014

170. Loss of Macrophage Low-Density Lipoprotein Receptor–Related Protein 1 Confers Resistance to the Antiatherogenic Effects of Tumor Necrosis Factor-α Inhibition

Author

Zhu, Lin, primary, Giunzioni, Ilaria, additional, Tavori, Hagai, additional, Covarrubias, Roman, additional, Ding, Lei, additional, Zhang, Youmin, additional, Ormseth, Michelle, additional, Major, Amy S., additional, Stafford, John M., additional, Linton, MacRae F., additional, and Fazio, Sergio, additional

Published
2016
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172. Treatment Gaps in Adults With Heterozygous Familial Hypercholesterolemia in the United States

Author

deGoma, Emil M., primary, Ahmad, Zahid S., additional, O’Brien, Emily C., additional, Kindt, Iris, additional, Shrader, Peter, additional, Newman, Connie B., additional, Pokharel, Yashashwi, additional, Baum, Seth J., additional, Hemphill, Linda C., additional, Hudgins, Lisa C., additional, Ahmed, Catherine D., additional, Gidding, Samuel S., additional, Duffy, Danielle, additional, Neal, William, additional, Wilemon, Katherine, additional, Roe, Matthew T., additional, Rader, Daniel J., additional, Ballantyne, Christie M., additional, Linton, MacRae F., additional, Duell, P. Barton, additional, Shapiro, Michael D., additional, Moriarty, Patrick M., additional, and Knowles, Joshua W., additional

Published
2016
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177. Abstract 632: Modification of HDL by γ-Ketoaldehydes Causes impaired HDL Function in Familial Hypercholesterolemia

Author

Tao, Huan, primary, Yancey, Patricia G, additional, Huang, Jiansheng, additional, Blakemore, John L, additional, Zhang, Youmin, additional, Ding, Lei, additional, Fazio, Sergio, additional, Vickers, Kasey C, additional, Oates, John A, additional, Roberts, L. Jackson, additional, Davies, Sean S, additional, and Linton, MacRae F, additional

Published
2016
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183. HDL

Author

Kon, Valentina, primary and Linton, MacRae F., additional

Published
2016
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185. Local effects of human PCSK9 on the atherosclerotic lesion

Author

Giunzioni, Ilaria, primary, Tavori, Hagai, additional, Covarrubias, Roman, additional, Major, Amy S, additional, Ding, Lei, additional, Zhang, Youmin, additional, DeVay, Rachel M, additional, Hong, Liang, additional, Fan, Daping, additional, Predazzi, Irene M, additional, Rashid, Shirya, additional, Linton, MacRae F, additional, and Fazio, Sergio, additional

Published
2015
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186. Abstract 12169: LDL-C Levels and Treatment Patterns Among Adults With Heterozygous Familial Hypercholesterolemia in the United States: Data From the CASCADE-FH Registry

Author

deGoma, Emil M, primary, Ahmad, Zahid S, additional, O'Brien, Emily, additional, Kindt, Iris, additional, Shrader, Peter, additional, Newman, Connie B, additional, Pokharel, Yashashwi, additional, Rader, Daniel J, additional, Moriarty, Patrick M, additional, Gidding, Samuel S, additional, Duell, P. Barton, additional, Shapiro, Michael D, additional, Linton, MacRae F, additional, Ballantyne, Christie M, additional, Duffy, Danielle, additional, Baum, Seth J, additional, Hemphill, Linda C, additional, Neal, William A, additional, Hudgins, Lisa C, additional, Ahmed, Catherine D, additional, Wilemon, Katherine A, additional, Row, Matthew T, additional, and Knowles, Joshua W, additional

Published
2015
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188. Free Fatty Acids are Associated with Metabolic Syndrome and Insulin Resistance, but not Inflammation in SLE Patients

Author

Ormseth, Michelle J, Swift, Larry L, Fazio, Sergio, Linton, MacRae F, Raggi, Paolo, Solus, Joseph F, Oeser, Annette, Bian, Aihua, Gebretsadik, Tebeb, Shintani, Ayumi, and Stein, C Michael

Subjects
Adult, Male, Coronary Artery Disease, Fatty Acids, Nonesterified, Coronary Angiography, Article, Risk Factors, Odds Ratio, Prevalence, Humans, Lupus Erythematosus, Systemic, Triglycerides, Inflammation, Metabolic Syndrome, Endothelial Cells, Middle Aged, Prognosis, Coronary Vessels, Tennessee, Up-Regulation, Cholesterol, Cross-Sectional Studies, Logistic Models, Case-Control Studies, Multivariate Analysis, Cytokines, lipids (amino acids, peptides, and proteins), Calcium, Female, Inflammation Mediators, Insulin Resistance, Tomography, X-Ray Computed, Biomarkers, Immunosuppressive Agents
Abstract

Free fatty acids (FFAs) are implicated in the pathogenesis of insulin resistance and atherosclerosis. Inflammatory cytokines promote lipolysis and increase FFAs, a cause of endothelial dysfunction and increased atherosclerosis risk. We hypothesized that increased inflammation is associated with increased FFAs, resulting in insulin resistance and atherosclerosis in patients with systemic lupus erythematosus (SLE). We measured clinical variables, serum FFAs, homeostasis model assessment for insulin resistance (HOMA), inflammatory cytokines, markers of endothelial activation, cholesterol concentrations and coronary artery calcium in 156 patients with SLE and 90 controls. We compared FFAs in patients with SLE and controls using Wilcoxon rank sum tests and further tested for the independent association between FFAs and disease status with adjustment for age, race and sex using multivariable regression models. We assessed the relationship between FFAs and continuous variables of interest using Spearman correlation and multivariable regression analysis. Levels of FFAs were higher in patients with SLE than controls (0.55 mmol/l (0.37-0.71) vs 0.44 mmol/l (0.32-0.60), P = 0.02). Levels of FFAs remained significantly higher among patients with SLE after adjustment for age, race and sex (P = 0.03) but not after further adjustment for body mass index (P = 0.13). FFA levels did not differ according to the usage of current immunosuppressive medications in univariate and adjusted analysis (all P 0.05). Among patients with SLE, concentrations of FFAs were higher among those with metabolic syndrome compared to those without (0.66 mmol/l (0.46-0.81) vs 0.52 mmol/l (0.35-0.66), P 0.001). FFAs were positively correlated with insulin resistance (HOMA) (rho = 0.23, P = 0.004, P adjusted = 0.006) and triglyceride levels (rho = 0.22, P = 0.01, P adjusted = 0.004). FFAs were not associated with inflammatory cytokines (IL-6, TNF-α) (all P 0.05) but were positively associated with levels of E-selectin (rho = 0.33, P = 0.001, P adjusted = 0.001) and ICAM-1 (rho = 0.35, P 0.001, P adjusted = 0.001). FFAs were correlated with coronary artery calcium score (rho = 0.20, P = 0.01) but this was attenuated after adjustment for age, race and sex (P = 0.33). From our study we concluded that FFAs are elevated in patients with SLE, particularly those with metabolic syndrome. FFAs in patients with SLE are not associated with markers of generalized inflammation but are associated with insulin resistance and markers of endothelial activation.

Published
2012

190. Sex‐Specific Parental Effects on Offspring Lipid Levels

Author

Predazzi, Irene M., primary, Sobota, Rafal S., additional, Sanna, Serena, additional, Bush, William S., additional, Bartlett, Jacquelaine, additional, Lilley, Jessica S., additional, Linton, MacRae F., additional, Schlessinger, David, additional, Cucca, Francesco, additional, Fazio, Sergio, additional, and Williams, Scott M., additional

Published
2015
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191. Isolevuglandin-Type Lipid Aldehydes Induce the Inflammatory Response of Macrophages by Modifying Phosphatidylethanolamines and Activating the Receptor for Advanced Glycation Endproducts

Author

Guo, Lilu, primary, Chen, Zhongyi, additional, Amarnath, Venkataraman, additional, Yancey, Patricia G., additional, Van Lenten, Brian J., additional, Savage, Justin R., additional, Fazio, Sergio, additional, Linton, MacRae F., additional, and Davies, Sean S., additional

Published
2015
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192. Uric acid correlates to oxidation and inflammation in opposite directions in women

Author

Wu, Sheng Hui, primary, Shu, Xiao Ou, additional, Milne, Ginger, additional, Xiang, Yong-Bing, additional, Zhang, Xianglan, additional, Cai, Qiuyin, additional, Fazio, Sergio, additional, Linton, MacRae F., additional, Chen, Honglei, additional, Purdue, Mark, additional, Rothman, Nathaniel, additional, Gao, Yu-Tang, additional, Zheng, Wei, additional, and Yang, Gong, additional

Published
2015
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193. Response to Letter Regarding Article, “Proprotein Convertase Subtilisin Kexin Type 9 Promotes Intestinal Overproduction of Triglyceride-Rich Apolipoprotein B Lipoproteins Through Both Low-Density Lipoprotein Receptor–Dependent and –Independent Mechanisms”

Author

Rashid, Shirya, primary, Tavori, Hagai, additional, Brown, Patrick E., additional, Linton, MacRae F., additional, He, Jane, additional, Giunzioni, Ilaria, additional, and Fazio, Sergio, additional

Published
2015
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196. Diagnosing Familial Hypercholesterolemia (FH) in the United States: Results from the CASCADE FH Patient Registry*†

Author

Ahmad, Zahid, primary, Newman, Connie B., additional, O'Brien, Emily C., additional, Shrader, Peter, additional, deGoma, Emil M., additional, Ahmed, Catherine, additional, Moriarty, Patrick M., additional, Linton, MacRae F., additional, Shapiro, Michael D., additional, Duell, Barton, additional, Ballantyne, Christie M., additional, Neal, William, additional, Duffy, Danielle, additional, Hudgins, Lisa C., additional, Hemphill, Linda C., additional, Underberg, James A., additional, Watson, Karol E., additional, Gidding, Samuel S., additional, Baum, Seth J., additional, Wilemon, Katherine, additional, Pickhardt, Dave, additional, Kindt, Iris, additional, Rader, Daniel J., additional, Roe, Matthew T., additional, and Knowles, Joshua W., additional

Published
2015
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197. INITIAL RESULTS FROM THE CASCADE-FH REGISTRY: CASCADE SCREENING FOR AWARENESS AND DETECTION OF FAMILIAL HYPERCHOLESTEROLEMIA

Author

O’Brien, Emily Claire, primary, DeGoma, Emil, additional, Moriarty, Patrick, additional, Linton, MacRae F., additional, Shapiro, Michael, additional, Duell, Bart, additional, Ballantyne, Christie, additional, Neal, William, additional, Ahmad, Zahid, additional, Duffy, Danielle, additional, Hudgins, Lisa, additional, Hemphill, Linda, additional, Underberg, James, additional, Watson, Karol, additional, Gidding, Samuel, additional, Baum, Seth, additional, Dilzell, Kristen, additional, Ross, Joyce, additional, Pickhardt, David, additional, Kindt, Iris, additional, Rader, Daniel, additional, Wilemon, Katherine, additional, Roe, Matthew, additional, and Knowles, Joshua, additional

Published
2015
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