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4. Forecasting Parking Search Times Using Big Data

Author

Milia, Kleio, Hedengran, Magnus Duus, Jansson, Thomas, Rodrigues, Filipe, Azevedo, Carlos Lima, Meyer, Gereon, Series Editor, Beiker, Sven, Editorial Board Member, Bekiaris, Evangelos, Editorial Board Member, Cornet, Henriette, Editorial Board Member, D'Agosto, Marcio de Almeida, Editorial Board Member, Di Giusto, Nevio, Editorial Board Member, di Paola-Galloni, Jean-Luc, Editorial Board Member, Hofmann, Karsten, Editorial Board Member, Kováčiková, Tatiana, Editorial Board Member, Langheim, Jochen, Editorial Board Member, Van Mierlo, Joeri, Editorial Board Member, Voege, Tom, Editorial Board Member, Antoniou, Constantinos, editor, Busch, Fritz, editor, Rau, Andreas, editor, and Hariharan, Mahesh, editor

Published
2023
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6. Do Robots Increase Wealth Dispersion?

Author

Gomes, Francisco, Jansson, Thomas, and Karabulut, Yigitcan

Subjects
INDUSTRIAL robots, WEALTH distribution, HOUSEHOLDS, INVESTMENT policy, AUTOMATION, AUTOMATION & economics, WEALTH, HUMAN capital
Abstract

We document significant negative effects of exposure to increased automation at work on household wealth accumulation. Beyond the income and savings channels, we uncover a novel mechanism contributing to the negative wealth effects of automation that arises through the endogenous optimal portfolio decisions of households. We show that households rebalance their financial wealth away from the stock market in response to increased human capital risk induced by pervasive automation, thereby attaining lower wealth levels and relative positions in the wealth distribution. Our evidence suggests that the portfolio channel amplifies the inequality-enhancing effects of increased automation. Authors have furnished an Internet Appendix , which is available on the Oxford University Press Web site next to the link to the final published paper online. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Maternal Docosahexaenoic Acid Supplementation Alters Maternal and Fetal Docosahexaenoic Acid Status and Placenta Phospholipids in Pregnancies Complicated by High Body Mass Index.

Author

Bidne, Katie L., Zemski Berry, Karin, Dillon, Mairead, Jansson, Thomas, and Powell, Theresa L.

Abstract

Introduction: An optimal fetal supply of docosahexaenoic acid (DHA) is critical for normal brain development. The relationship between maternal DHA intake and DHA delivery to the fetus is complex and is dependent on placental handling of DHA. Little data exist on placental DHA levels in pregnancies supplemented with the recommended dose of 200 mg/d. Our objective was to determine how prenatal DHA at the recommended 200 mg/d impacts maternal, placental, and fetal DHA status in both normal-weight and high-BMI women compared to women taking no supplements. Methods: Maternal blood, placenta, and cord blood were collected from 30 healthy pregnant women (BMI 18.9–43.26 kg/m2) giving birth at term. Red blood cells (RBCs) and villous tissue were isolated, and lipids were extracted to determine DHA content by LC-MS/MS. Data were analyzed by supplement group (0 vs. 200 mg/d) and maternal BMI (normal weight or high BMI) using two-way ANOVA. We measured maternal choline levels in maternal and cord plasma samples. Results: Supplementation with 200 mg/d DHA significantly increased (p < 0.05) maternal and cord RBC DHA content only in pregnancies complicated by high BMI. We did not find any impact of choline levels on maternal or cord RBC phospholipids. There were no significant differences in total placental DHA content by supplementation or maternal BMI (p > 0.05). Placental levels of phosphatidylinositol (PI) and phosphatidic acid containing DHA species were higher (p < 0.05) in high-BMI women without DHA supplementation compared to both normal-BMI and high-BMI women taking DHA supplements. Conclusion: Maternal DHA supplementation at recommended doses cord increased RBC DHA content only in pregnancies complicated by higher BMI. Surprisingly, we found that obesity was related to an increase in placental PI and phosphatidic acid species, which was ameliorated by DHA supplementation. Phosphatidic acid activates placental mTOR, which regulates amino acid transport and may explain previous findings of the impact of DHA on placental function. Current recommendations for DHA supplementation may not be achieving the goal of improving fetal DHA levels in normal-weight women. [ABSTRACT FROM AUTHOR]

Published
2024
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13. Maternal Serum Metabolomics in Mid-Pregnancy Identifies Lipid Pathways as a Key Link to Offspring Obesity in Early Childhood.

Author

Francis, Ellen C., Kechris, Katerina, Johnson, Randi K., Rawal, Shristi, Pathmasiri, Wimal, Rushing, Blake R., Du, Xiuxia, Jansson, Thomas, Dabelea, Dana, Sumner, Susan J., and Perng, Wei

Subjects
CHILDHOOD obesity, METABOLOMICS, GESTATIONAL diabetes, FREE fatty acids, PREGNANCY, PREGNANT women, METABOLIC disorders, POLYMER networks
Abstract

Maternal metabolism during pregnancy shapes offspring health via in utero programming. In the Healthy Start study, we identified five subgroups of pregnant women based on conventional metabolic biomarkers: Reference (n = 360); High HDL-C (n = 289); Dyslipidemic–High TG (n = 149); Dyslipidemic–High FFA (n = 180); Insulin Resistant (IR)–Hyperglycemic (n = 87). These subgroups not only captured metabolic heterogeneity among pregnant participants but were also associated with offspring obesity in early childhood, even among women without obesity or diabetes. Here, we utilize metabolomics data to enrich characterization of the metabolic subgroups and identify key compounds driving between-group differences. We analyzed fasting blood samples from 1065 pregnant women at 18 gestational weeks using untargeted metabolomics. We used weighted gene correlation network analysis (WGCNA) to derive a global network based on the Reference subgroup and characterized distinct metabolite modules representative of the different metabolomic profiles. We used the mummichog algorithm for pathway enrichment and identified key compounds that differed across the subgroups. Eight metabolite modules representing pathways such as the carnitine–acylcarnitine translocase system, fatty acid biosynthesis and activation, and glycerophospholipid metabolism were identified. A module that included 189 compounds related to DHA peroxidation, oxidative stress, and sex hormone biosynthesis was elevated in the Insulin Resistant–Hyperglycemic vs. the Reference subgroup. This module was positively correlated with total cholesterol (R:0.10; p-value < 0.0001) and free fatty acids (R:0.07; p-value < 0.05). Oxidative stress and inflammatory pathways may underlie insulin resistance during pregnancy, even below clinical diabetes thresholds. These findings highlight potential therapeutic targets and strategies for pregnancy risk stratification and reveal mechanisms underlying the developmental origins of metabolic disease risk. [ABSTRACT FROM AUTHOR]

Published
2024
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14. Regulation of placental amino acid transport in health and disease.

Author

Shimada, Hiroshi, Powell, Theresa L., and Jansson, Thomas

Subjects
AMINO acid transport, FETAL growth disorders, FETAL growth retardation, ESSENTIAL amino acids, PLACENTA, CARDIOVASCULAR diseases, PLACENTA diseases
Abstract

Abnormal fetal growth, i.e., intrauterine growth restriction (IUGR) or fetal growth restriction (FGR) and fetal overgrowth, is associated with increased perinatal morbidity and mortality and is strongly linked to the development of metabolic and cardiovascular disease in childhood and later in life. Emerging evidence suggests that changes in placental amino acid transport may contribute to abnormal fetal growth. This review is focused on amino acid transport in the human placenta, however, relevant animal models will be discussed to add mechanistic insights. At least 25 distinct amino acid transporters with different characteristics and substrate preferences have been identified in the human placenta. Of these, System A, transporting neutral nonessential amino acids, and System L, mediating the transport of essential amino acids, have been studied in some detail. Importantly, decreased placental Systems A and L transporter activity is strongly associated with IUGR and increased placental activity of these two amino acid transporters has been linked to fetal overgrowth in human pregnancy. An array of factors in the maternal circulation, including insulin, IGF‐1, and adiponectin, and placental signaling pathways such as mTOR, have been identified as key regulators of placental Systems A and L. Studies using trophoblast‐specific gene targeting in mice have provided compelling evidence that changes in placental Systems A and L are mechanistically linked to altered fetal growth. It is possible that targeting specific placental amino acid transporters or their upstream regulators represents a novel intervention to alleviate the short‐ and long‐term consequences of abnormal fetal growth in the future. [ABSTRACT FROM AUTHOR]

Published
2024
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24. Polygons on a Rotating Fluid Surface

Author

Jansson, Thomas R. N., Haspang, Martin P., Jensen, Kaare H., Hersen, Pascal, and Bohr, Tomas

Subjects
Physics - Fluid Dynamics, Physics - General Physics
Abstract

We report a novel and spectacular instability of a fluid surface in a rotating system. In a flow driven by rotating the bottom plate of a partially filled, stationary cylindrical container, the shape of the free surface can spontaneously break the axial symmetry and assume the form of a polygon rotating rigidly with a speed different from that of the plate. With water we have observed polygons with up to 6 corners. It has been known for many years that such flows are prone to symmetry breaking, but apparently the polygonal surface shapes have never been observed. The creation of rotating internal waves in a similar setup was observed for much lower rotation rates, where the free surface remains essentially flat. We speculate that the instability is caused by the strong azimuthal shear due to the stationary walls and that it is triggered by minute wobbling of the rotating plate. The slight asymmetry induces a tendency for mode-locking between the plate and the polygon, where the polygon rotates by one corner for each complete rotation of the plate.

Published
2005
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30. Oleic acid stimulation of amino acid uptake in primary human trophoblast cells is mediated by phosphatidic acid and mTOR signaling.

Author

Silva, Elena, Ferchaud‐Roucher, Véronique, Kramer, Anita, Madi, Lana, Pantham, Priyadarshini, Chassen, Stephanie, Jansson, Thomas, and Powell, Theresa L.

Subjects
PHOSPHATIDIC acids, OLEIC acid, FETUS, AMINO acids, AMINO acid transport, TROPHOBLAST
Abstract

Normal fetal development is critically dependent on optimal nutrient supply by the placenta, and placental amino acid transport has been demonstrated to be positively associated with fetal growth. Mechanistic target of rapamycin (mTOR) is a positive regulator of placental amino acid transporters, such as System A. Oleic acid (OA) has been previously shown to have a stimulatory role on placental mTOR signaling and System A amino acid uptake in primary human trophoblast (PHT) cells. We investigated the mechanistic link between OA and System A activity in PHT. We found that inhibition of mTOR complex 1 or 2, using small interfering RNA to knock down raptor or rictor, prevented OA‐stimulated System A amino acid transport indicating the interaction of OA with mTOR. Phosphatidic acid (PA) is a key intermediary for phospholipid biosynthesis and a known regulator of the mTOR pathway; however, phospholipid biosynthetic pathways have not been extensively studied in placenta. We identified placental isoforms of acyl transferase enzymes involved in de novo phospholipid synthesis. Silencing of 1‐acylglycerol‐3‐phosphate‐O‐acyltransferase‐4, an enzyme in this pathway, prevented OA mediated stimulation of mTOR and System A amino acid transport. These data indicate that OA stimulates mTOR and amino acid transport in PHT cells mediated through de novo synthesis of PA. We speculate that fatty acids in the maternal circulation, such as OA, regulate placental functions critical for fetal growth by interaction with mTOR and that late pregnancy hyperlipidemia may be critical for increasing nutrient transfer to the fetus. [ABSTRACT FROM AUTHOR]

Published
2024
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31. Cord blood DNA methylation of immune and lipid metabolism genes is associated with maternal triglycerides and child adiposity.

Author

Waldrop, Stephanie W., Niemiec, Sierra, Wood, Cheyret, Gyllenhammer, Lauren E., Jansson, Thomas, Friedman, Jacob E., Tryggestad, Jeanie B., Borengasser, Sarah J., Davidson, Elizabeth J., Yang, Ivana V., Kechris, Katerina, Dabelea, Dana, and Boyle, Kristen E.

Subjects
CORD blood, DNA methylation, LIPID metabolism, OBESITY, HDL cholesterol, CHOLESTERYL ester transfer protein
Abstract

Objective: Fetal exposures may impact offspring epigenetic signatures and adiposity. The authors hypothesized that maternal metabolic traits associate with cord blood DNA methylation, which, in turn, associates with child adiposity. Methods: Fasting serum was obtained in 588 pregnant women (27–34 weeks' gestation), and insulin, glucose, high‐density lipoprotein cholesterol, triglycerides, and free fatty acids were measured. Cord blood DNA methylation and child adiposity were measured at birth, 4–6 months, and 4–6 years. The association of maternal metabolic traits with DNA methylation (429,246 CpGs) for differentially methylated probes (DMPs) and regions (DMRs) was tested. The association of the first principal component of each DMR with child adiposity was tested, and mediation analysis was performed. Results: Maternal triglycerides were associated with the most DMPs and DMRs of all traits tested (261 and 198, respectively, false discovery rate < 0.05). DMRs were near genes involved in immune function and lipid metabolism. Triglyceride‐associated CpGs were associated with child adiposity at 4–6 months (32 CpGs) and 4–6 years (2 CpGs). One, near CD226, was observed at both timepoints, mediating 10% and 22% of the relationship between maternal triglycerides and child adiposity at 4–6 months and 4–6 years, respectively. Conclusions: DNA methylation may play a role in the association of maternal triglycerides and child adiposity. [ABSTRACT FROM AUTHOR]

Published
2024
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43. A novel technique using chronic infusion of small extracellular vesicles from gestational diabetes mellitus causes glucose intolerance in pregnant mice

Author

James-Allan, Laura B, primary, Rosario, Frederick J, additional, Madi, Lana, additional, Barner, Kelsey, additional, Nair, Soumyalekshmi, additional, Lai, Andrew, additional, Carrion, Flavio, additional, Powell, Theresa L, additional, Salomon, Carlos, additional, and Jansson, Thomas, additional

Published
2022
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47. Contributors

Author

Abbasi, Soraya, primary, Abbey, James, additional, Adzick, N. Scott, additional, Ahn, Sun-Young, additional, Albertine, Kurt H., additional, Allegaert, Karel, additional, Alper, Seth L., additional, Altit, Gabriel, additional, Altschuler, Steven M., additional, Alvaro, Ruben E., additional, Amorosa, Jennifer M.H., additional, Anbuhl, Kelsey L., additional, Andersen, Claus Yding, additional, Anderson, Richard A., additional, Askenazi, David J., additional, Auten, Richard Lambert, additional, Autmizguine, Julie, additional, Azhibekov, Timur, additional, Back, Stephen A., additional, Badaut, Jérôme, additional, Baker, Peter Russell, additional, Ballard, Philip L., additional, Bancalari, Eduardo H., additional, Barichello, Tatiana, additional, Battaglia, Frederick, additional, Baum, Michel, additional, Beggs, Simon, additional, Bell, Edward F., additional, Benchimol, Corinne, additional, Benders, Manon J.N.L., additional, Bennet, Laura, additional, Bennett, Phillip R., additional, Berger, Melvin, additional, Bernhard, Wolfgang, additional, Bertram, John F., additional, Bhosle, Vikrant K., additional, Bhutani, Vinod K., additional, Black, M. Jane, additional, Bliss, Joseph M., additional, Bolender, David L., additional, Brandenburg, Joline E., additional, Broussard, Delma L., additional, Brown, Laura Davidson, additional, Burrin, Douglas G., additional, Cannon, Barbara, additional, Caplan, Michael, additional, Carlson, Susan E., additional, Carlton, David P., additional, Caruana, Georgina, additional, Cashore, William J., additional, Chaemsaithong, Piya, additional, Chaiyasit, Noppadol, additional, Charlton, Jennifer R., additional, Cheatham, Carol L., additional, Chemtob, Sylvain, additional, Chen, Yi-Yung, additional, Chevalier, Robert L., additional, Chheda, Sadhana, additional, Childs, Andrew J., additional, Christensen, Robert D., additional, Chu, Alison, additional, Chu, David H., additional, Cilio, Maria Roberta, additional, Clark, David A., additional, Cleary-Goldman, Jane, additional, Clemente, Ethel G., additional, Clements, John A., additional, Clyman, Ronald I., additional, Cohen, Susan S., additional, Colombo, John, additional, Cowett, Richard M., additional, Crawford, Peter A., additional, Crowe, James E., additional, Cullen-McEwen, Luise A., additional, Cutfield, Wayne S., additional, D'Alton, Mary E., additional, Danzer, Enrico, additional, Delacourt, Christophe, additional, Devaskar, Sherin U., additional, Diacovo, Thomas G., additional, Docheva, Nikolina, additional, Dormans, John P., additional, Dysart, Kevin, additional, El-Khuffash, Afif, additional, Ellis, Peter James, additional, Empey, Kerry McGarr, additional, Ercal, Baris, additional, Erdős, Melinda, additional, Erickson, Robert P., additional, Fahim, Mohamed A., additional, Faksh, Arij, additional, Frank, Hans-Georg, additional, Friedlich, Philippe S., additional, Friedman, Jed, additional, Gao, Yuansheng, additional, Garland, Marianne, additional, Geddes, Donna, additional, Georgieff, Michael K., additional, Gien, Jason, additional, Giussani, Dino A., additional, Goldman, Armond S., additional, González, Efrén, additional, Good, Misty, additional, Grant, Denis M., additional, Green, Lucy R., additional, Grigoriou, Emmanouil, additional, Grimberg, Adda, additional, Gross, Ian, additional, Grunau, Ruth E., additional, Guignard, Jean-Pierre, additional, Gunn, Alistair Jan, additional, Gurtunca, Nursen, additional, Hadchouel, Alice, additional, Haddad, Gabriel G., additional, Hagberg, Henrik, additional, Hale, Thomas, additional, Hambidge, K. Michael, additional, Hammerman, Cathy, additional, Hansen, Thor Willy Ruud, additional, Hanson, Mark A., additional, Harding, Richard, additional, Harris, Mary Catherine, additional, Hartmann, Peter, additional, Hassiotou, Foteini, additional, Haugen, Guttorm, additional, Hawkes, Colin P., additional, Hay, William W., additional, Hayward, Christina E., additional, Heine, Vivi M., additional, Hellström, Ann, additional, Helmrath, Michael A., additional, Hendricks-Muñoz, Karen D., additional, Herrera, Emilio, additional, Hiatt, Michael J., additional, Hoath, Steven B., additional, Hooper, Stuart B., additional, Huang, Stephen A., additional, Iacobellli, Silvia, additional, Inder, Terrie E., additional, Iruela-Arispe, M. Luisa, additional, Jadcherla, Sudarshan R., additional, Jain, Deepak, additional, Jansson, Thomas, additional, Jefferies, John Lynn, additional, Jetton, Jennifer G., additional, Jobe, Alan H., additional, Johnson, Lois H., additional, Johnston, Richard B., additional, Jones, Rebecca Lee, additional, Jose, Pedro A., additional, Kalhan, Satish C., additional, Kallapur, Suhas G., additional, Kaplan, Michael, additional, Kaplan, Stanley, additional, Karpen, Heidi Eigenrauch, additional, Karpen, Saul J., additional, Karumanchi, S. Ananth, additional, Kaskel, Frederick J., additional, Katheria, Anup C., additional, Katz, Lorraine E. Levitt, additional, Keeney, Susan E., additional, Kern, Steven E., additional, Khanjani, Shirin, additional, Kilpatrick, Laurie E., additional, Kim, Chang-Ryul, additional, Kinsella, John P., additional, Kiserud, Torvid, additional, Koenig, Joyce M., additional, Kollmann, Tobias R., additional, Kolls, Jay K., additional, Krebs, Nancy F., additional, Kulik, Thomas J., additional, Kutikov, Jessica Katz, additional, Lakshminrusimha, Satyan, additional, Lamola, Angelo A., additional, Lasunción, Miguel Angel, additional, Lavoie, Pascal M., additional, LeBien, Tucker W., additional, Lee, Mary M., additional, Lee, Matthew K., additional, Lee, Yvonne K., additional, Leibel, Sandra, additional, Levine, Fred, additional, Levy, Ofer, additional, Liu, Yang, additional, Lobritto, Steven, additional, Loomis, Cynthia A., additional, Lopez, Colleen A., additional, MacIntyre, David A., additional, Mahe, Maxime M., additional, Maheshwari, Akhil, additional, Mankouski, Anastasiya, additional, Mantilla, Carlos B., additional, Marchant, Arnaud, additional, Margolis, Kara Gross, additional, Mariscalco, M. Michele, additional, Maródi, László, additional, Maršál, Karel, additional, Martin, Richard J., additional, Matsell, Douglas G., additional, Matthews, Dwight E., additional, McArdle, Harry J., additional, McManaman, James L., additional, McNamara, Patrick J., additional, McQuillen, Patrick S., additional, McQuinn, Tim C., additional, Mercer, Judith S., additional, Meschia, Giacomo, additional, Miller, Steven P., additional, Minoo, Parviz, additional, Monagle, Paul, additional, Mortola, Jacopo P., additional, Muglia, Louis J., additional, Munshi, Upender K., additional, Namgung, Ran, additional, Narasimhan, Sumana, additional, Nedergaard, Jan, additional, Neu, Josef, additional, Nigam, Sanjay K., additional, Nogee, Lawrence M., additional, Noori, Shahab, additional, O'Brien, Barbara M., additional, Ohls, Robin K., additional, Ortega-Senovilla, Henar, additional, O'Sullivan, Justin M., additional, Owusu, Sarah A., additional, Pal, Abhijeet, additional, Panitch, Howard B., additional, Penn, Anna A., additional, Penn, Raymond B., additional, Pernia, Cameron, additional, Philipps, Anthony F., additional, Picoraro, Joseph A., additional, Pisani, Francesco, additional, Pleasure, David, additional, Pleasure, Jeanette R., additional, Pleasure, Samuel J., additional, Pomeroy, Scott L., additional, Post, Martin, additional, Prakash, Y.S., additional, Prozialeck, Joshua D., additional, Pysher, Theodore J., additional, Quigley, Raymond, additional, Rabinovitch, Marlene, additional, Raffay, Thomas M., additional, Raj, J. Usha, additional, Ramsey, Haley, additional, Rana, Sarosh, additional, Randis, Tara Marie, additional, Ranger, Manon, additional, Ratner, Adam J., additional, Regnault, Timothy R.H., additional, Rigatto, Henrique, additional, Rintoul, Natalie E., additional, Romero, Roberto, additional, Rose, James C., additional, Rosenfeld, Charles R., additional, Ross, A. Catharine, additional, Rozycki, Henry J., additional, Ryan, Thomas D., additional, Sahni, Rakesh, additional, Sajti, Eniko, additional, Sarnat, Harvey B., additional, Satlin, Lisa M., additional, Saugstad, Ola Didrik, additional, Schierding, William, additional, Schmalstieg, Frank C., additional, Schwartz, George J., additional, Schwartz, Jeffrey, additional, Segar, Jeffrey L., additional, Selewski, David T., additional, Seri, Istvan, additional, Shaffer, Thomas H., additional, Shah, Kara N., additional, Shearer, Martin J., additional, Shojaie, Sharareh, additional, Shroyer, Noah F., additional, Sibley, Colin P., additional, Sieck, Gary C., additional, Simmons, Rebecca A., additional, Sivieri, Emidio M., additional, Smith, Francine G., additional, Smith, Lois E.H., additional, Smyth, Ian M., additional, Snarr, Brian S., additional, Snyder, Evan Y., additional, Sola-Visner, Martha, additional, Solhaug, Michael J., additional, Sperling, Mark A., additional, Srinivasan, Lakshmi, additional, Stahl, Andreas, additional, Stanley, Charles A., additional, Steinhorn, Robin H., additional, Stonestreet, Barbara S., additional, Strasburger, Janette F., additional, Styne, Dennis M., additional, Sussel, Lori, additional, Tam, Emily W.Y., additional, Tan, Libo, additional, Thornton, Claire, additional, Tollin, Daniel J., additional, Tóth, Beáta, additional, Towbin, Jeffrey A., additional, Trocle, Ashley, additional, Truog, William E., additional, Tsang, Reginald C., additional, Uhler, Kristin M., additional, Van Den Anker, John N., additional, van Goudoever, Johannes (Hans) B., additional, Vannucci, Susan J., additional, Vickers, Mark H., additional, Virgintino, Daniela, additional, Volpe, Joseph J., additional, Vora, Neeta L., additional, Vyas, Neha V., additional, Wacker-Gussmann, Annette, additional, Wallace, Megan J., additional, Walsh, Brian H., additional, Wang, Alice M., additional, Warburton, David, additional, Ward, Robert M., additional, Watterberg, Kristi L., additional, Werner, Lynne A., additional, Wershil, Barry K., additional, Wert, Susan E., additional, Wessels, Andy, additional, Whitsett, Jeffrey A., additional, Wise, Michael, additional, Wolf, Matthias T., additional, Wolfson, Marla R., additional, Wong, Hector R., additional, Wynn, James L., additional, Yeo, Lami, additional, Yip, Stephen, additional, Yoder, Bradley A, additional, Yoder, Mervin C., additional, Yoshimoto, Momoko, additional, Yuskaitis, Christopher J., additional, Zhou, Dan, additional, and Zovein, Ann, additional

Published
2017
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