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1. Designing to Support Equity-as-Transformation Perspectives for Multilingual Science Learners

Author

Ashlyn Pierson, D. Teo Keifert, Bethany Daniel, Sarah Lee, Tessaly Jen, Adam Bell, Heather Johnson, Rachel Askew, and Andrea Henrie

Abstract

In this paper, we examine how researchers and teachers in a multi-year professional development program shifted their conceptualizations of equity. Following (Grapin et al (2023) Sci Educ 107:999-1032), we ground our analysis in two conceptualizations of equity that exist across fields: equity-as-access (learners should have access to disciplinary knowledge, practices, and career paths) and equity-as-transformation (learners should transform what it means to learn and participate in disciplines). In this study, we describe a professional development (PD) design initially intended to support equitable science teaching and learning by focusing on representations. This initial framing did not distinguish between conceptions of equity-as-access versus equity-as-transformation. As a result, the PD did not provide facilitators or teachers with resources for ideological sensemaking towards equity-as-transformation. Catalyzed by teachers' request for PD focused on multilingual learners (MLs), we noticed aspects of our design that offered only images of equity-as-access. In response, we designed activities for teachers that offered space and resources for considering equity-as-transformation. As a case study (Yin (2014) Case study research: design and methods, SAGE) using interaction analysis (Jordan and Henderson (1995) J Learn Sci 4:39-103) of PD videos, we describe how we PD activities and facilitation strategies to integrate transformative conceptualizations of equity. These findings have implications for both research and practice. In terms of research, they demonstrate the importance of using multiple lenses to consider equity in science classrooms. In terms of practice, they underscore the importance of providing teachers with opportunities to explicitly connect new perspectives of equity with day-to-day experiences of classroom teaching.

Published
2024
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3. Multiple Representations in Elementary Science: Building Shared Understanding While Leveraging Students' Diverse Ideas and Practices

Author

Pierson, Ashlyn E., Keifert, D. Teo, Lee, Sarah J., Henrie, Andrea, Johnson, Heather J., and Enyedy, Noel

Abstract

Research has explored how science teachers can create equitable learning environments. In addition, research demonstrates that representations can be powerful tools for supporting disciplinary learning and inviting and leveraging students' diverse ideas and practices. Yet, professional development (PD) about representations has primarily focused on teachers' knowledge of disciplinary practices rather than on how teachers can value and build upon students' representations as resources for equitable sensemaking. In this paper, we present cases from a year-long professional development program with in-service elementary teachers designed to support science teaching with representations. Through our work with these teachers, we have illustrated an approach to using representations that supports equitable sensemaking by: (1) making space for students to create personally meaningful representations, (2) amplifying students' representations, and (3) helping students iteratively refine their representations and ideas. These findings extend literature about inclusive science teaching by illustrating how focusing on students' representations can support equitable sensemaking and by addressing tensions that emerge between equitable teaching, science standards that prioritize canonical knowledge and practices, and monoglossic language ideologies.

Published
2023
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4. Ideological Sensemaking in an Elementary Science Professional Development Community

Author

Bethany Daniel, Ashlyn E. Pierson, and D. Teo Keifert

Abstract

Background: Ideologies are socially constructed frameworks for sensemaking that influence teaching and learning. Drawing on Learning Sciences research on ideologies, we explore how an elementary science professional development (PD) community used substrate (shared interactional resources) in sensemaking interactions to reify or rearticulate dominant ideologies. Method: We analyzed PD interactions to understand how PD community members used substrate across multiple timescales as part of ideological sensemaking. Findings: We first show how participants drew on substrate to rearticulate ideologies about young learners' capabilities in science. We then show how limited resources available in substrate impeded interactional engagement with deficit narratives of multilingual learners. Contribution: Practically, we demonstrate how ideological rearticulation requires establishing intentionally designed substrate as a resource for later PD and facilitation that surfaces and challenges dominant ideologies. Methodologically, we show how substrate--often analyzed at microgenetic scales--can be traced back over longer timescales to understand longitudinal learning.

Published
2023
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10. Caring Relations Across Interaction Analysis Labs

Author

Love, Candice, primary, Jen, Tessaly, additional, Metts, Elizabeth, additional, Keifert, D. Teo, additional, Gentry, Andria, additional, Goeke, Megan, additional, Carpenter, Zack, additional, DeLiema, David, additional, Hufnagle, Ashley, additional, Vogelstein, Lauren, additional, Steinberg, Rebecca, additional, Thomas, Curtis, additional, Champion, Dionne, additional, Appleby, Lara, additional, Wagh, Aditi, additional, Blake, Ali R., additional, Velamur, Arundhati, additional, Y., Jasmine, additional, and Marin, Ananda, additional

Published
2024
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13. Designing to support equity-as-transformation perspectives for multilingual science learners.

Author

Pierson, Ashlyn, Keifert, D. Teo, Daniel, Bethany, Lee, Sarah, Jen, Tessaly, Bell, Adam, Johnson, Heather, Askew, Rachel, and Henrie, Andrea

Subjects
TEACHER development, CAREER development, SCIENCE education, SCIENCE teachers, SCIENCE classrooms
Abstract

In this paper, we examine how researchers and teachers in a multi-year professional development program shifted their conceptualizations of equity. Following (Grapin et al (2023) Sci Educ 107:999–1032), we ground our analysis in two conceptualizations of equity that exist across fields: equity-as-access (learners should have access to disciplinary knowledge, practices, and career paths) and equity-as-transformation (learners should transform what it means to learn and participate in disciplines). In this study, we describe a professional development (PD) design initially intended to support equitable science teaching and learning by focusing on representations. This initial framing did not distinguish between conceptions of equity-as-access versus equity-as-transformation. As a result, the PD did not provide facilitators or teachers with resources for ideological sensemaking towards equity-as-transformation. Catalyzed by teachers' request for PD focused on multilingual learners (MLs), we noticed aspects of our design that offered only images of equity-as-access. In response, we designed activities for teachers that offered space and resources for considering equity-as-transformation. As a case study (Yin (2014) Case study research: design and methods, SAGE) using interaction analysis (Jordan and Henderson (1995) J Learn Sci 4:39–103) of PD videos, we describe how we PD activities and facilitation strategies to integrate transformative conceptualizations of equity. These findings have implications for both research and practice. In terms of research, they demonstrate the importance of using multiple lenses to consider equity in science classrooms. In terms of practice, they underscore the importance of providing teachers with opportunities to explicitly connect new perspectives of equity with day-to-day experiences of classroom teaching. [ABSTRACT FROM AUTHOR]

Published
2024
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20. Cofactor Dynamics Couples the Protein Surface to the Heme in Cytochrome c, Facilitating Electron Transfer

Author

William Shen, Ruijie D. Teo, David N. Beratan, and Jeffrey J. Warren

Subjects
Electron Transport, Materials Chemistry, Cytochromes c, Electrons, Heme, Physical and Theoretical Chemistry, Article, Ruthenium, Surfaces, Coatings and Films
Abstract

Electron transport through biomolecules and in biological transport networks is of great importance to bioenergetics and biocatalysis. More generally, it is of crucial importance to understand how the pathways that connect buried metallocofactors to other cofactors, and to protein surfaces, affect the biological chemistry of metalloproteins. In terms of electron transfer (ET), the strongest coupling pathways usually comprise covalent and hydrogen bonded networks, with a limited number of through-space contacts. Herein, we set out to determine the relative roles of hydrogen bonds involved in ET via an established heme-to-surface tunneling pathway in cytochrome (cyt) c (i.e., heme-W59-D60-E61-N62). A series of cyt c variants were produced where a ruthenium tris(diimine) photooxidant was placed at position 62 via covalent modification of the N62C residue. Surprisingly, variants where the H-bonding residues W59 and D60 were replaced (i.e., W59F and D60A), showed no change in ET rate from the ferrous heme to Ru(III). In contrast, changing the composition of an alternate tunneling pathway (i.e., heme-M64-N63-C62) with the M64L substitution shows a factor of two decrease in the rate of heme-to-Ru ET. This pathway involves a through-space tunneling step between the heme and M64 residue, and such steps are usually disfavored. To rationalize why the heme-M64-N63-C62 is preferred, molecular dynamics (MD) simulations and Pathways analysis were employed. These simulations show that the change in heme-Ru ET rates is attributed to different conformations with compressed donor-acceptor distances, by ca. 2 Å in pathway distance, in the M64-containing protein as compared to the M64L protein. The change in distance is correlated with changes in the electronic coupling that are in accord with the experimentally observed heme-Ru ET rates. Remarkably, the M64L variation at the core of the protein translates to changes in cofactor dynamics at the protein surface. The surface changes identified by MD simulations include dynamic anion-π and dipole-dipole interactions. These interactions influence the strength of tunneling pathways and ET rates by facilitating decreases in through-space tunneling distances in key coupling pathways.

Published
2022
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21. Disrupted myelin lipid metabolism differentiates frontotemporal dementia caused by GRN and C9orf72 gene mutations

Author

Oana C. Marian, Jonathan D. Teo, Jun Yup Lee, Huitong Song, John B. Kwok, Ramon Landin-Romero, Glenda Halliday, and Anthony S. Don

Subjects
Cellular and Molecular Neuroscience, Neurology (clinical), Pathology and Forensic Medicine
Abstract

Heterozygous mutations in the GRN gene and hexanucleotide repeat expansions in C9orf72 are the two most common genetic causes of Frontotemporal Dementia (FTD) with TDP-43 protein inclusions. The triggers for neurodegeneration in FTD with GRN (FTD-GRN) or C9orf72 (FTD-C9orf72) gene abnormalities are unknown, although evidence from mouse and cell culture models suggests that GRN mutations disrupt lysosomal lipid catabolism. To determine how brain lipid metabolism is affected in familial FTD with TDP-43 inclusions, and how this is related to myelin and lysosomal markers, we undertook comprehensive lipidomic analysis, enzyme activity assays, and western blotting on grey and white matter samples from the heavily-affected frontal lobe and less-affected parietal lobe of FTD-GRN cases, FTD-C9orf72 cases, and age-matched neurologically-normal controls. Substantial loss of myelin-enriched sphingolipids (sulfatide, galactosylceramide, sphingomyelin) and myelin proteins was observed in frontal white matter of FTD-GRN cases. A less-pronounced, yet statistically significant, loss of sphingolipids was also observed in FTD-C9orf72. FTD-GRN was distinguished from FTD-C9orf72 and control cases by increased acylcarnitines in frontal grey matter and marked accumulation of cholesterol esters in both frontal and parietal white matter, indicative of myelin break-down. Both FTD-GRN and FTD-C9orf72 cases showed significantly increased lysosomal and phagocytic protein markers, however galactocerebrosidase activity, required for lysosomal catabolism of galactosylceramide and sulfatide, was selectively increased in FTD-GRN. We conclude that both C9orf72 and GRN mutations are associated with disrupted lysosomal homeostasis and white matter lipid loss, but GRN mutations cause a more pronounced disruption to myelin lipid metabolism. Our findings support the hypothesis that hyperactive myelin lipid catabolism is a driver of gliosis and neurodegeneration in FTD-GRN. Since FTD-GRN is associated with white matter hyperintensities by MRI, our data provides important biochemical evidence supporting the use of MRI measures of white matter integrity in the diagnosis and management of FTD.

Published
2023
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22. Evaluation of all-atom force fields in viral capsid simulations and properties

Author

Ruijie D. Teo and D. Peter Tieleman

Subjects
0303 health sciences, 03 medical and health sciences, 010304 chemical physics, General Chemical Engineering, 0103 physical sciences, General Chemistry, 01 natural sciences, 030304 developmental biology, 3. Good health
Abstract

As the past century has been characterized by waves of viral pandemics, there is an ever-growing role for molecular simulation-based research. In this study, we utilize all-atom molecular dynamics to simulate an enterovirus-D68 capsid and examine the dependency of viral capsid dynamics and properties on AMBER and CHARMM force fields. Out of the six force fields studied, we note that CHARMM36m and CHARMM36 generate secondary structures that are most consistent with protein structural data and sample the largest conformational space. The ion distribution and radius of gyration of the capsid are similar across all force fields investigated.

Published
2022
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23. Early microglial response, myelin deterioration and lethality in mice deficient for very long chain ceramide synthesis in oligodendrocytes

Author

Jonathan D. Teo, Oana C. Marian, Alanna G. Spiteri, Madeline Nicholson, Huitong Song, Jasmine X. Y. Khor, Holly P. McEwen, Anjie Ge, Monokesh K. Sen, Laura Piccio, Jessica L. Fletcher, Nicholas J. C. King, Simon S. Murray, Jens C. Brüning, and Anthony S. Don

Subjects
Cellular and Molecular Neuroscience, Neurology
Abstract

The sphingolipids galactosylceramide (GalCer), sulfatide (ST) and sphingomyelin (SM) are essential for myelin stability and function. GalCer and ST are synthesized mostly from C22-C24 ceramides, generated by Ceramide Synthase 2 (CerS2). To clarify the requirement for C22-C24 sphingolipid synthesis in myelin biosynthesis and stability, we generated mice lacking CerS2 specifically in myelinating cells (CerS2

Published
2022

24. Ablation of sphingosine kinase 2 suppresses fatty liver-associated hepatocellular carcinoma via downregulation of ceramide transfer protein

Author

Xin Tracy Liu, Long Hoa Chung, Da Liu, Jinbiao Chen, Yu Huang, Jonathan D. Teo, Xingxing Daisy Han, Yinan Zhao, Fiona H. X. Guan, Collin Tran, Jun Yup Lee, Timothy A. Couttas, Ken Liu, Geoffery W. McCaughan, Mark D. Gorrell, Anthony S. Don, Shubiao Zhang, and Yanfei Qi

Subjects
Cancer Research, Molecular Biology
Abstract

Hepatocellular carcinoma (HCC) accounts for 90% of primary liver cancer, the third leading cause of cancer-associated death worldwide. With the increasing prevalence of metabolic conditions, non-alcoholic fatty liver disease (NAFLD) is emerging as the fastest-growing HCC risk factor, and it imposes an additional layer of difficulty in HCC management. Dysregulated hepatic lipids are generally believed to constitute a deleterious environment cultivating the development of NAFLD-associated HCC. However, exactly which lipids or lipid regulators drive this process remains elusive. We report herein that sphingosine kinase 2 (SphK2), a key sphingolipid metabolic enzyme, plays a critical role in NAFLD-associated HCC. Ablation of Sphk2 suppressed HCC development in NAFLD livers via inhibition of hepatocyte proliferation both in vivo and in vitro. Mechanistically, SphK2 deficiency led to downregulation of ceramide transfer protein (CERT) that, in turn, decreased the ratio of pro-cancer sphingomyelin (SM) to anti-cancer ceramide. Overexpression of CERT restored hepatocyte proliferation, colony growth and cell cycle progression. In conclusion, the current study demonstrates that SphK2 is an essential lipid regulator in NAFLD-associated HCC, providing experimental evidence to support clinical trials of SphK2 inhibitors as systemic therapies against HCC.

Published
2022
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25. Erratum: Search for fractionally charged particles in pp collisions at √s = 7 TeV [Phys. Rev. D 87, 092008 (2013)]

Author

S. Chatrchyan, V. Khachatryan, A. M. Sirunyan, A. Tumasyan, W. Adam, E. Aguilo, T. Bergauer, M. Dragicevic, J. Erö, C. Fabjan, M. Friedl, R. Frühwirth, V. M. Ghete, J. Hammer, N. Hörmann, J. Hrubec, M. Jeitler, W. Kiesenhofer, V. Knünz, M. Krammer, I. Krätschmer, D. Liko, I. Mikulec, M. Pernicka, B. Rahbaran, C. Rohringer, H. Rohringer, R. Schöfbeck, J. Strauss, A. Taurok, W. Waltenberger, G. Walzel, E. Widl, C. -E. Wulz, V. Mossolov, N. Shumeiko, J. Suarez Gonzalez, M. Bansal, S. Bansal, T. Cornelis, E. A. De Wolf, X. Janssen, S. Luyckx, L. Mucibello, S. Ochesanu, B. Roland, R. Rougny, M. Selvaggi, Z. Staykova, H. Van Haevermaet, P. Van Mechelen, N. Van Remortel, A. Van Spilbeeck, F. Blekman, S. Blyweert, J. D’Hondt, R. Gonzalez Suarez, A. Kalogeropoulos, M. Maes, A. Olbrechts, W. Van Doninck, P. Van Mulders, G. P. Van Onsem, I. Villella, B. Clerbaux, G. De Lentdecker, V. Dero, A. P. R. Gay, T. Hreus, A. Léonard, P. E. Marage, A. Mohammadi, T. Reis, L. Thomas, G. Vander Marcken, C. Vander Velde, P. Vanlaer, J. Wang, V. Adler, K. Beernaert, A. Cimmino, S. Costantini, G. Garcia, M. Grunewald, B. Klein, J. Lellouch, A. Marinov, J. Mccartin, A. A. Ocampo Rios, D. Ryckbosch, N. Strobbe, F. Thyssen, M. Tytgat, P. Verwilligen, S. Walsh, E. Yazgan, N. Zaganidis, S. Basegmez, G. Bruno, R. Castello, L. Ceard, C. Delaere, T. du Pree, D. Favart, L. Forthomme, A. Giammanco, J. Hollar, V. Lemaitre, J. Liao, O. Militaru, C. Nuttens, D. Pagano, A. Pin, K. Piotrzkowski, N. Schul, J. M. Vizan Garcia, N. Beliy, T. Caebergs, E. Daubie, G. H. Hammad, G. A. Alves, M. Correa Martins Junior, D. De Jesus Damiao, T. Martins, M. E. Pol, M. H. G. Souza, W. L. Aldá Júnior, W. Carvalho, A. Custódio, E. M. Da Costa, C. De Oliveira Martins, S. Fonseca De Souza, D. Matos Figueiredo, L. Mundim, H. Nogima, V. Oguri, W. L. Prado Da Silva, A. Santoro, L. Soares Jorge, A. Sznajder, T. S. Anjos, C. A. Bernardes, F. A. Dias, T. R. Fernandez Perez Tomei, E. M. Gregores, C. Lagana, F. Marinho, P. G. Mercadante, S. F. Novaes, Sandra S. Padula, V. Genchev, P. Iaydjiev, S. Piperov, M. Rodozov, S. Stoykova, G. Sultanov, V. Tcholakov, R. Trayanov, M. Vutova, A. Dimitrov, R. Hadjiiska, V. Kozhuharov, L. Litov, B. Pavlov, P. Petkov, J. G. Bian, G. M. Chen, H. S. Chen, C. H. Jiang, D. Liang, S. Liang, X. Meng, J. Tao, X. Wang, Z. Wang, H. Xiao, M. Xu, J. Zang, Z. Zhang, C. Asawatangtrakuldee, Y. Ban, Y. Guo, W. Li, S. Liu, Y. Mao, S. J. Qian, H. Teng, D. Wang, L. Zhang, W. Zou, C. Avila, J. P. Gomez, B. Gomez Moreno, A. F. Osorio Oliveros, J. C. Sanabria, N. Godinovic, D. Lelas, R. Plestina, D. Polic, I. Puljak, Z. Antunovic, M. Kovac, V. Brigljevic, S. Duric, K. Kadija, J. Luetic, S. Morovic, A. Attikis, M. Galanti, G. Mavromanolakis, J. Mousa, C. Nicolaou, F. Ptochos, P. A. Razis, M. Finger, Y. Assran, S. Elgammal, A. Ellithi Kamel, S. Khalil, M. A. Mahmoud, A. Radi, M. Kadastik, M. Müntel, M. Raidal, L. Rebane, A. Tiko, P. Eerola, G. Fedi, M. Voutilainen, J. Härkönen, A. Heikkinen, V. Karimäki, R. Kinnunen, M. J. Kortelainen, T. Lampén, K. Lassila-Perini, S. Lehti, T. Lindén, P. Luukka, T. Mäenpää, T. Peltola, E. Tuominen, J. Tuominiemi, E. Tuovinen, D. Ungaro, L. Wendland, K. Banzuzi, A. Karjalainen, A. Korpela, T. Tuuva, M. Besancon, S. Choudhury, M. Dejardin, D. Denegri, B. Fabbro, J. L. Faure, F. Ferri, S. Ganjour, A. Givernaud, P. Gras, G. Hamel de Monchenault, P. Jarry, E. Locci, J. Malcles, L. Millischer, A. Nayak, J. Rander, A. Rosowsky, I. Shreyber, M. Titov, S. Baffioni, F. Beaudette, L. Benhabib, L. Bianchini, M. Bluj, C. Broutin, P. Busson, C. Charlot, N. Daci, T. Dahms, L. Dobrzynski, R. Granier de Cassagnac, M. Haguenauer, P. Miné, C. Mironov, I. N. Naranjo, M. Nguyen, C. Ochando, P. Paganini, D. Sabes, R. Salerno, Y. Sirois, C. Veelken, A. Zabi, J. -L. Agram, J. Andrea, D. Bloch, D. Bodin, J. -M. Brom, M. Cardaci, E. C. Chabert, C. Collard, E. Conte, F. Drouhin, C. Ferro, J. -C. Fontaine, D. Gelé, U. Goerlach, P. Juillot, A. -C. Le Bihan, P. Van Hove, F. Fassi, D. Mercier, S. Beauceron, N. Beaupere, O. Bondu, G. Boudoul, J. Chasserat, R. Chierici, D. Contardo, P. Depasse, H. El Mamouni, J. Fay, S. Gascon, M. Gouzevitch, B. Ille, T. Kurca, M. Lethuillier, L. Mirabito, S. Perries, L. Sgandurra, V. Sordini, Y. Tschudi, P. Verdier, S. Viret, Z. Tsamalaidze, G. Anagnostou, C. Autermann, S. Beranek, M. Edelhoff, L. Feld, N. Heracleous, O. Hindrichs, R. Jussen, K. Klein, J. Merz, A. Ostapchuk, A. Perieanu, F. Raupach, J. Sammet, S. Schael, D. Sprenger, H. Weber, B. Wittmer, V. Zhukov, M. Ata, J. Caudron, E. Dietz-Laursonn, D. Duchardt, M. Erdmann, R. Fischer, A. Güth, T. Hebbeker, C. Heidemann, K. Hoepfner, D. Klingebiel, P. Kreuzer, M. Merschmeyer, A. Meyer, M. Olschewski, P. Papacz, H. Pieta, H. Reithler, S. A. Schmitz, L. Sonnenschein, J. Steggemann, D. Teyssier, M. Weber, M. Bontenackels, V. Cherepanov, Y. Erdogan, G. Flügge, H. Geenen, M. Geisler, W. Haj Ahmad, F. Hoehle, B. Kargoll, T. Kress, Y. Kuessel, J. Lingemann, A. Nowack, L. Perchalla, O. Pooth, P. Sauerland, A. Stahl, M. Aldaya Martin, J. Behr, W. Behrenhoff, U. Behrens, M. Bergholz, A. Bethani, K. Borras, A. Burgmeier, A. Cakir, L. Calligaris, A. Campbell, E. Castro, F. Costanza, D. Dammann, C. Diez Pardos, G. Eckerlin, D. Eckstein, G. Flucke, A. Geiser, I. Glushkov, P. Gunnellini, S. Habib, J. Hauk, G. Hellwig, H. Jung, M. Kasemann, P. Katsas, C. Kleinwort, H. Kluge, A. Knutsson, M. Krämer, D. Krücker, E. Kuznetsova, W. Lange, W. Lohmann, B. Lutz, R. Mankel, I. Marfin, M. Marienfeld, I. -A. Melzer-Pellmann, A. B. Meyer, J. Mnich, A. Mussgiller, S. Naumann-Emme, O. Novgorodova, J. Olzem, H. Perrey, A. Petrukhin, D. Pitzl, A. Raspereza, P. M. Ribeiro Cipriano, C. Riedl, E. Ron, M. Rosin, J. Salfeld-Nebgen, R. Schmidt, T. Schoerner-Sadenius, N. Sen, A. Spiridonov, M. Stein, R. Walsh, C. Wissing, V. Blobel, J. Draeger, H. Enderle, J. Erfle, U. Gebbert, M. Görner, T. Hermanns, R. S. Höing, K. Kaschube, G. Kaussen, H. Kirschenmann, R. Klanner, J. Lange, B. Mura, F. Nowak, T. Peiffer, N. Pietsch, D. Rathjens, C. Sander, H. Schettler, P. Schleper, E. Schlieckau, A. Schmidt, M. Schröder, T. Schum, M. Seidel, V. Sola, H. Stadie, G. Steinbrück, J. Thomsen, L. Vanelderen, C. Barth, J. Berger, C. Böser, T. Chwalek, W. De Boer, A. Descroix, A. Dierlamm, M. Feindt, M. Guthoff, C. Hackstein, F. Hartmann, T. Hauth, M. Heinrich, H. Held, K. H. Hoffmann, U. Husemann, I. Katkov, J. R. Komaragiri, P. Lobelle Pardo, D. Martschei, S. Mueller, Th. Müller, M. Niegel, A. Nürnberg, O. Oberst, A. Oehler, J. Ott, G. Quast, K. Rabbertz, F. Ratnikov, N. Ratnikova, S. Röcker, F. -P. Schilling, G. Schott, H. J. Simonis, F. M. Stober, D. Troendle, R. Ulrich, J. Wagner-Kuhr, S. Wayand, T. Weiler, M. Zeise, G. Daskalakis, T. Geralis, S. Kesisoglou, A. Kyriakis, D. Loukas, I. Manolakos, A. Markou, C. Markou, C. Mavrommatis, E. Ntomari, L. Gouskos, T. J. Mertzimekis, A. Panagiotou, N. Saoulidou, I. Evangelou, C. Foudas, P. Kokkas, N. Manthos, I. Papadopoulos, V. Patras, G. Bencze, C. Hajdu, P. Hidas, D. Horvath, F. Sikler, V. Veszpremi, G. Vesztergombi, N. Beni, S. Czellar, J. Molnar, J. Palinkas, Z. Szillasi, J. Karancsi, P. Raics, Z. L. Trocsanyi, B. Ujvari, S. B. Beri, V. Bhatnagar, N. Dhingra, R. Gupta, M. Kaur, M. Z. Mehta, N. Nishu, L. K. Saini, A. Sharma, J. B. Singh, Ashok Kumar, Arun Kumar, S. Ahuja, A. Bhardwaj, B. C. Choudhary, S. Malhotra, M. Naimuddin, K. Ranjan, V. Sharma, R. K. Shivpuri, S. Banerjee, S. Bhattacharya, S. Dutta, B. Gomber, Sa. Jain, Sh. Jain, R. Khurana, S. Sarkar, M. Sharan, A. Abdulsalam, R. K. Choudhury, D. Dutta, S. Kailas, V. Kumar, P. Mehta, A. K. Mohanty, L. M. Pant, P. Shukla, T. Aziz, S. Ganguly, M. Guchait, M. Maity, G. Majumder, K. Mazumdar, G. B. Mohanty, B. Parida, K. Sudhakar, N. Wickramage, S. Dugad, H. Arfaei, H. Bakhshiansohi, S. M. Etesami, A. Fahim, M. Hashemi, H. Hesari, A. Jafari, M. Khakzad, M. Mohammadi Najafabadi, S. Paktinat Mehdiabadi, B. Safarzadeh, M. Zeinali, M. 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Marionneau, A. C. Mignerey, K. Pedro, A. Peterman, A. Skuja, J. Temple, M. B. Tonje, S. C. Tonwar, E. Twedt, A. Apyan, G. Bauer, J. Bendavid, W. Busza, E. Butz, I. A. Cali, M. Chan, V. Dutta, G. Gomez Ceballo, M. Goncharov, K. A. Hahn, Y. Kim, M. Klute, K. Krajczar, P. D. Luckey, T. Ma, S. Nahn, C. Pau, D. Ralph, C. Roland, G. Roland, M. Rudolph, G. S. F. Stephan, F. Stöckli, K. Sumorok, K. Sung, D. Velicanu, E. A. Wenger, R. Wolf, B. Wyslouch, M. Yang, Y. Yilmaz, A. S. Yoon, M. Zanetti, S. I. Cooper, B. Dahme, A. De Benedetti, G. Franzoni, A. Gude, S. C. Kao, K. Klapoetke, Y. Kubota, J. Man, N. Pastika, R. Rusack, M. Sasseville, A. Singovsky, N. Tambe, J. Turkewitz, L. M. Cremaldi, R. Kroeger, L. Perera, R. Rahmat, D. A. Sander, E. Avdeeva, K. Bloom, S. Bose, J. Butt, D. R. Clae, A. Dominguez, M. Ead, J. Keller, I. Kravchenko, J. Lazo-Flore, H. Malbouisson, S. Malik, G. R. Snow, A. Godshalk, I. Iashvili, S. Jain, A. Kharchilava, A. Kumar, G. Alverson, E. Barberi, D. Baumgartel, M. Chasco, J. Haley, D. Nash, D. Trocino, D. Wood, J. Zhang, A. Anastassov, A. Kubik, N. Mucia, N. Odell, R. A. Ofierzynski, B. Pollack, A. Pozdnyakov, M. Schmitt, S. Stoynev, M. Velasco, S. Won, L. Antonelli, D. Berry, A. Brinkerhoff, K. M. Chan, M. Hildreth, C. Jessop, D. J. Karmgard, J. Kolb, K. Lannon, W. Luo, S. Lynch, N. Marinelli, D. M. Morse, T. Pearson, M. Planer, R. Ruchti, J. Slaunwhite, N. Vall, M. Wayne, M. Wolf, B. Bylsma, L. S. Durkin, C. Hill, R. Hughe, K. Kotov, T. Y. Ling, D. Puigh, M. Rodenburg, C. Vuosalo, G. William, B. L. Winer, N. Adam, E. Berry, P. Elmer, D. Gerbaudo, V. Halyo, P. Hebda, J. Hegeman, A. Hunt, P. Jindal, D. Lopes Pegna, P. Lujan, D. Marlow, T. Medvedeva, M. Mooney, J. Olsen, P. Piroué, X. Quan, A. Raval, B. Safdi, H. Saka, D. Stickland, C. Tully, J. S. Werner, A. Zuranski, E. Brownson, A. Lopez, H. Mendez, J. E. Ramirez Varga, E. Alagoz, V. E. Barne, D. Benedetti, G. Bolla, D. Bortoletto, M. De Mattia, A. Everett, Z. Hu, M. Jone, O. Koybasi, M. Kre, A. T. Laasanen, N. Leonardo, V. Maroussov, P. Merkel, D. H. Miller, N. Neumeister, I. Shipsey, D. Silver, A. Svyatkovskiy, M. Vidal Marono, H. D. Yoo, J. Zablocki, Y. Zheng, S. Guragain, N. Parashar, A. Adair, C. Boulahouache, K. M. Ecklund, F. J. M. Geurt, B. P. Padley, R. Redjimi, J. Robert, J. Zabel, B. Betchart, A. Bodek, Y. S. Chung, R. Covarelli, P. de Barbaro, R. Demina, Y. Eshaq, T. Ferbel, A. Garcia-Bellido, P. Goldenzweig, J. Han, A. Harel, D. C. Miner, D. Vishnevskiy, M. Zielinski, A. Bhatti, R. Ciesielski, L. Demortier, K. Gouliano, G. Lungu, C. Mesropian, S. Arora, A. Barker, J. P. Chou, C. Contreras-Campana, E. Contreras-Campana, D. Duggan, D. Ferencek, Y. Gershtein, R. Gray, E. Halkiadaki, D. Hida, A. Lath, S. Panwalkar, R. Patel, V. Rekovic, J. Roble, K. Rose, S. Salur, S. Schnetzer, C. Seitz, S. Somalwar, R. Stone, S. Thoma, G. Cerizza, M. Hollingsworth, S. Spanier, Z. C. Yang, A. York, R. Eusebi, W. Flanagan, J. Gilmore, T. Kamon, V. Khotilovich, R. Montalvo, I. Osipenkov, Y. Pakhotin, A. Perloff, J. Roe, A. Safonov, T. Sakuma, S. Sengupta, I. Suarez, A. Tatarinov, D. Toback, N. Akchurin, J. Damgov, C. Dragoiu, P. R. Dudero, C. Jeong, K. Kovitanggoon, S. W. Lee, T. Libeiro, Y. Roh, I. Volobouev, E. Appelt, A. G. Delannoy, C. Florez, S. Greene, A. Gurrola, W. John, P. Kurt, C. Maguire, A. Melo, M. Sharma, P. Sheldon, B. Snook, S. Tuo, J. Velkovska, M. W. Arenton, M. Balaz, S. Boutle, B. Cox, B. Franci, J. Goodell, R. Hirosky, A. Ledovskoy, C. Lin, C. Neu, J. Wood, S. Gollapinni, R. Harr, P. E. Karchin, C. Kottachchi Kankanamge Don, P. Lamichhane, A. Sakharov, M. Anderson, D. Belknap, L. Borrello, D. Carlsmith, M. Cepeda, S. Dasu, E. Frii, L. Gray, K. S. Grogg, M. Grothe, R. Hall-Wilton, M. Herndon, A. Hervé, P. Klabber, J. Kluka, A. Lanaro, C. Lazaridi, J. Leonard, R. Lovele, A. Mohapatra, I. Ojalvo, F. Palmonari, G. A. Pierro, I. Ro, A. Savin, W. H. Smith, and J. Swanson

Subjects
LHC, CMS
Abstract

Erratum: Search for fractionally charged particles in pp collisions at sqrt(s) = 7 TeV [Phys. Rev. D 87, 092008 (2013)]

Published
2022

26. Somatic mutations of GNA11 and GNAQ in CTNNB1-mutant aldosterone-producing adenomas presenting in puberty, pregnancy or menopause

Author

Sam O’Toole, Peyman Björklund, Samuel Backman, Per Hellman, Eva Wozniak, Sumedha Garg, Morris J. Brown, Emily Goodchild, Junhua Zhou, Alison Marker, Antoinette Tuthill, Giulia Argentesi, Caroline Joyce, Xilin Wu, Sheerazed Boulkroun, Celso E Gomez Sanchez, Russell Senanayake, Satyamaanasa Polubothu, Kate E Lines, Lou Metherell, Suzanne Jordan, Jyn Ling Kuan, Zenia Tiang, Laila Parvanta, Fiona E. Karet Frankl, Veronica A Kinsler, Rajesh V. Thakker, Elena A.B. Azizan, Fabio L. Fernandes-Rosa, Maria-Christina Zennaro, David Klinzing, Laurence Amar, Emily Cottrell, William Drake, Helen L Storr, Ada E. D. Teo, Juan Pablo Kaski, Roger Foo, Charles A. Mein, Tobias Åkerström, Daniel M. Berney, Claudia P. Cabrera, Anna K Gluck, Mark Gurnell, Queen Mary University of London (QMUL), National University of Malaysia [Bandar Baru Bangi] (UKM), Paris-Centre de Recherche Cardiovasculaire (PARCC (UMR_S 970/ U970)), Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Addenbrooke's Hospital, Cambridge University NHS Trust, Metabolic Research Laboratories [Cambridge, UK] (University of Cambridge), Wellcome Trust - MRC Cambridge-Addenbrooke’s Hospital [Cambridge, UK], Uppsala University, Royal Free Hospital [London, UK], University College of London [London] (UCL), University of Oxford, Cork University Hospital [Cork, Ireland] (CUH), University of Cambridge [UK] (CAM), National University of Singapore (NUS), St Bartholomew's Hospital (London), Agency for science, technology and research [Singapore] (A*STAR), University of Mississippi Medical Center (UMMC), and Fernandes Rosa, Fabio

Subjects
Adult, Male, endocrine system, medicine.medical_specialty, Adolescent, education, [SDV.GEN] Life Sciences [q-bio]/Genetics, Biology, medicine.disease_cause, Article, Human chorionic gonadotropin, chemistry.chemical_compound, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Pregnancy, Internal medicine, Hyperaldosteronism, Genetics, medicine, Humans, Aldosterone, beta Catenin, [SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, [SDV.GEN]Life Sciences [q-bio]/Genetics, Mutation, GNA11, Adrenal gland, Adrenal cortex, Puberty, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, Middle Aged, Adrenal Cortex Neoplasms, GTP-Binding Protein alpha Subunits, [SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, medicine.anatomical_structure, Endocrinology, chemistry, Zona glomerulosa, Adrenocortical Adenoma, GTP-Binding Protein alpha Subunits, Gq-G11, Female, Menopause, GNAQ
Abstract

Most aldosterone-producing adenomas (APAs) have gain-of-function somatic mutations of ion channels or transporters. However, their frequency in aldosterone-producing cell clusters of normal adrenal gland suggests a requirement for codriver mutations in APAs. Here we identified gain-of-function mutations in both CTNNB1 and GNA11 by whole-exome sequencing of 3/41 APAs. Further sequencing of known CTNNB1-mutant APAs led to a total of 16 of 27 (59%) with a somatic p.Gln209His, p.Gln209Pro or p.Gln209Leu mutation of GNA11 or GNAQ. Solitary GNA11 mutations were found in hyperplastic zona glomerulosa adjacent to double-mutant APAs. Nine of ten patients in our UK/Irish cohort presented in puberty, pregnancy or menopause. Among multiple transcripts upregulated more than tenfold in double-mutant APAs was LHCGR, the receptor for luteinizing or pregnancy hormone (human chorionic gonadotropin). Transfections of adrenocortical cells demonstrated additive effects of GNA11 and CTNNB1 mutations on aldosterone secretion and expression of genes upregulated in double-mutant APAs. In adrenal cortex, GNA11/Q mutations appear clinically silent without a codriver mutation of CTNNB1. Sequence analysis identifies gain-of-function somatic mutations in GNA11 or GNAQ in CTNNB1-mutant aldosterone-producing adenomas. Most patients with these mutations presented during puberty, pregnancy or menopause, with elevated LHCGR expression.

Published
2021
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27. Modulation of Phospholipid Bilayer Properties by Simvastatin

Author

Ruijie D. Teo and D. Peter Tieleman

Subjects
Simvastatin, Lipid Bilayers, Molecular Dynamics Simulation, 01 natural sciences, 03 medical and health sciences, chemistry.chemical_compound, Molecular dynamics, 0103 physical sciences, Materials Chemistry, Membrane fluidity, medicine, Physical and Theoretical Chemistry, Lipid bilayer, POPC, Phospholipids, 030304 developmental biology, 0303 health sciences, 010304 chemical physics, Chemistry, Cholesterol, Bilayer, 3. Good health, Surfaces, Coatings and Films, Membrane, Phosphatidylcholines, Biophysics, lipids (amino acids, peptides, and proteins), medicine.drug
Abstract

Simvastatin (Zocor) is one of the most prescribed drugs for reducing high cholesterol. Although simvastatin is ingested in its inactive lactone form, it is converted to its active dihydroxyheptanoate form by carboxylesterases in the liver. The dihydroxyheptanoate form can also be converted back to its original lactone form. Unfortunately, some of the side effects associated with the intake of simvastatin and other lipophilic statins at higher doses include statin-associated myopathy (SAM) and, in more severe cases, kidney failure. While the cause of SAM is unknown, it is hypothesized that these side effects are dependent on the localization of statins in lipid bilayers and their impact on bilayer properties. In this work, we carry out all-atom molecular dynamics simulations on both the lactone and dihydroxyheptanoate forms of simvastatin (termed "SN" and "SA", respectively) with a pure 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) lipid bilayer and a POPC/cholesterol (30 mol %) binary mixture as membrane models. Additional simulations were carried out with multiple simvastatin molecules to mimic in vitro conditions that produced pleiotropic effects. Both SN and SA spontaneously diffused into the lipid bilayer, and a longer simulation time of 4 μs was needed for the complete incorporation of multiple SAs into the bilayer. By constructing potential mean force and electron density profiles, we find that SN localizes deeper within the hydrophobic interior of the bilayer and that SA has a greater tendency to form hydrogen-bonding interactions with neighboring water molecules and lipid headgroups. For the pure POPC bilayer, both SN and SA increase membrane order, while membrane fluidity increases for the POPC/cholesterol bilayer.

Published
2021
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29. Early microglial response, myelin deterioration and lethality in mice deficient for very long chain ceramide synthesis in oligodendrocytes

Author

Jonathan D Teo, Oana C Marian, Alanna G Spiteri, Madeline Nicholson, Huitong Song, Jasmine XY Khor, Holly P McEwen, Laura Piccio, Jessica L Fletcher, Nicholas JC King, Simon S Murray, Jens C Brüning, and Anthony S Don

Abstract

The sphingolipids galactosylceramide (GalCer), sulfatide (ST) and sphingomyelin (SM) are essential for myelin stability and function. GalCer and ST are synthesized mostly from C22-C24 ceramides, generated by Ceramide Synthase 2 (CerS2). To clarify the requirement for C22-C24 sphingolipid synthesis in myelin lipid biosynthesis and stability, we generated mice lacking CerS2 specifically in myelinating cells (CerS2ΔO/ΔO). At 6 weeks of age, normal-appearing myelin had formed in CerS2ΔO/ΔO mice, however there was a reduction in myelin thickness and the percentage of myelinated axons. Pronounced loss of C22-C24 sphingolipids in myelin of CerS2ΔO/ΔO mice was compensated by greatly increased levels of C18 sphingolipids. A distinct microglial population expressing high levels of activation and phagocytic markers such as CD64, CD11c, MHC class II, and CD68 was apparent at 6 weeks of age in CerS2ΔO/ΔO mice, and had increased by 10 weeks. Increased staining for denatured myelin basic protein was also apparent in 6-week-old CerS2ΔO/ΔO mice. By 16 weeks, CerS2ΔO/ΔO mice showed pronounced myelin atrophy, motor deficits, and axon beading, a hallmark of axon stress. 90% of CerS2ΔO/ΔO mice died between 16 and 26 weeks of age. This study highlights the importance of sphingolipid acyl chain length for the structural integrity of myelin, demonstrating how a modest reduction in lipid chain length causes exposure of a denatured myelin protein epitope and expansion of phagocytic microglia, followed by axon pathology, myelin degeneration, and motor deficits. Understanding the molecular trigger for microglial activation should aid the development of therapeutics for demyelinating and neurodegenerative diseases.Main PointsOligodendrocytes lacking CerS2 produce myelin using sphingolipids with C16/C18 instead of C22/C24 N-acyl chainsC22/C24 myelin sphingolipids are essential for myelin stability, microglial quiescence, and survival beyond young adulthoodTable of Contents Image

Published
2022
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30. Somatic mutations of GNA11 and GNAQ in CTNNB1-mutant aldosterone-producing adenomas presenting in puberty, pregnancy or menopause

Author

Giulia Argentesi, Chaz Mein, Laila Parvanta, Anna K Gluck, Mark Gurnell, Caroline Joyce, Antoinette Tuthill, Xilin Wu, Lou Metherell, Elena A.B. Azizan, Emily Goodchild, Sam O’Toole, Suzanne Jordan, Veronika Kinsler, Alison Marker, William Drake, Helen L Storr, Rajesh V. Thakker, Sumedha Garg, Morris J. Brown, Daniel M. Berney, Frankl Fiona Karet, Claudia P. Cabrera, Emily Cottrell, Russell Senanayake, Eva Wozniak, Ada E. D. Teo, Kate E Lines, and Junhua Zhou

Subjects
medicine.medical_specialty, Pregnancy, Aldosterone, GNA11, Somatic cell, business.industry, Mutant, medicine.disease, Menopause, chemistry.chemical_compound, Endocrinology, chemistry, Internal medicine, medicine, business, GNAQ
Published
2021
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31. Mutation effects on charge transport through the p58c iron–sulfur protein

Author

Ruijie D. Teo, David N. Beratan, and Agostino Migliore

Subjects
010304 chemical physics, DNA repair, DNA replication, Solvation, General Chemistry, 010402 general chemistry, 01 natural sciences, Molecular mechanics, 0104 chemical sciences, Chemistry, chemistry.chemical_compound, Molecular dynamics, chemistry, 0103 physical sciences, Cluster (physics), Biophysics, Primase, DNA
Abstract

Functional electron transfer between the [Fe4S4] cluster and the nucleic acid is impacted by a Y345C mutation in the p58c subunit of human primase., Growing experimental evidence indicates that iron–sulfur proteins play key roles in DNA repair and replication. In particular, charge transport between [Fe4S4] clusters, mediated by proteins and DNA, may convey signals to coordinate enzyme action. Human primase is a well studied [Fe4S4] protein, and its p58c domain (which contains an [Fe4S4] cluster) plays a role in the initiation of DNA replication. The Y345C mutation in p58c is linked to gastric tumors and may influence the protein-mediated charge transport. The complexity of protein–DNA systems, and the intricate electronic structure of [Fe4S4] clusters, have impeded progress into understanding functional charge transport in these systems. In this study, we built force fields to describe the high potential [Fe4S4] cluster in both oxidation states. The parameterization is compatible with AMBER force fields and enabled well-balanced molecular dynamics simulations of the p58c–RNA/DNA complex relevant to the initiation of DNA replication. Using the molecular mechanics Poisson–Boltzmann and surface area solvation method on the molecular dynamics trajectories, we find that the p58c mutation induces a modest change in the p58c–duplex binding free energy in agreement with recent experiments. Through kinetic modeling and analysis, we identify key features of the main charge transport pathways in p58c. In particular, we find that the Y345C mutation partially changes the composition and frequency of the most efficient (and potentially relevant to the biological function) charge transport pathways between the [Fe4S4] cluster and the duplex. Moreover, our approach sets the stage for a deeper understanding of functional charge transfer in [Fe4S4] protein–DNA complexes.

Published
2020
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32. Force of Infection and True Infection Rate of Dengue in Singapore: Implications for Dengue Control and Management

Author

Li Wei Ang, Li Kiang Tan, Sally Lam, Alex R. Cook, Lilac Liu, D. Teo, Yuan Shi, Rachel Chua, Haoyang Sun, Swee Ling Low, Lee Ching Ng, Hwee Huang Tan, and Wing Yan Wong

Subjects
Adult, Male, Adolescent, Epidemiology, Practice of Epidemiology, infectious disease, 030231 tropical medicine, Population, vector control, Force of infection, Dengue fever, 03 medical and health sciences, 0302 clinical medicine, basic reproduction number, Seroepidemiologic Studies, Medicine, Seroprevalence, Humans, education, 030304 developmental biology, Aged, 0303 health sciences, education.field_of_study, Singapore, seroprevalence, business.industry, Outbreak, Bayes Theorem, Middle Aged, medicine.disease, dengue, Confidence interval, Infectious disease (medical specialty), Bayesian model, Immunoglobulin G, Communicable Disease Control, Female, business, Basic reproduction number, Demography, force of infection
Abstract

National data on dengue notifications do not capture all dengue infections and do not reflect the true intensity of disease transmission. To assess the true dengue infection rate and disease control efforts in Singapore, we conducted age-stratified serosurveys among residents after a 2013 outbreak that was the largest dengue outbreak on record. The age-weighted prevalence of dengue immunoglobulin G among residents was 49.8% (95% confidence interval: 48.4, 51.1) in 2013 and 48.6% (95% confidence interval: 47.0, 50.0) in 2017; prevalence increased with age. Combining these data with those from previous serosurveys, the year-on-year estimates of the dengue force of infection from 1930 to 2017 revealed a significant decrease from the late 1960s to the mid-1990s, after which the force of infection remained stable at approximately 10 per 1,000 persons per year. The reproduction number (R0) had also declined since the 1960s. The reduction in dengue transmission may be attributed to the sustained national vector program and partly to a change in the age structure of the population. The improved estimated ratio of notified cases to true infections, from 1:14 in 2005–2009 to 1:6 in 2014–2017, signifies that the national notification system, which relies on diagnosed cases, has improved over time. The data also suggest that the magnitudes of dengue epidemics cannot be fairly compared across calendar years and that the current disease control program remains applicable.

Published
2019

33. Sphingosine kinase 2 is essential for remyelination following cuprizone intoxication

Author

Jun Yup Lee, Jonathan D. Teo, Anthony S. Don, Holly P. McEwen, Huitong Song, and Thomas Duncan

Subjects
Ceramide, medicine.medical_specialty, Sphingosine kinase, Biology, Corpus Callosum, Cellular and Molecular Neuroscience, chemistry.chemical_compound, Myelin, Cuprizone, Mice, Internal medicine, medicine, Animals, Sphingosine-1-phosphate, Remyelination, Myelin Sheath, Sphingosine, Sphingosine Kinase 2, Oligodendrocyte, Mice, Inbred C57BL, SPHK2, Disease Models, Animal, Oligodendroglia, Phosphotransferases (Alcohol Group Acceptor), medicine.anatomical_structure, Endocrinology, Neurology, chemistry, Myelin maintenance, Demyelinating Diseases
Abstract

Therapeutics that promote oligodendrocyte survival and remyelination are needed to restore neurological function in demyelinating diseases. Sphingosine 1-phosphate (S1P) is an essential lipid metabolite that signals through five G-protein coupled receptors. S1P receptor agonists such as Fingolimod are valuable immunosuppressants used to treat multiple sclerosis, and promote oligodendrocyte survival. However, the role for endogenous S1P, synthesized by the enzyme sphingosine kinase 2 (SphK2), in oligodendrocyte survival and myelination has not been established. This study investigated the requirement for SphK2 in oligodendrocyte survival and remyelination using the cuprizone mouse model of acute demyelination, followed by spontaneous remyelination. Oligodendrocyte density did not differ between untreated wild- type (WT) and SphK2 knockout (SphK2-/-) mice. However, cuprizone treatment caused significantly greater loss of mature oligodendrocytes in SphK2-/- compared to WT mice. Following cuprizone withdrawal, spontaneous remyelination occurred in WT but not SphK2-/- mice, even though progenitor and mature oligodendrocyte density increased in both genotypes. Levels of cytotoxic sphingosine and ceramide were higher in the corpus callosum of SphK2-/- mice, and in contrast to WT mice, did not decline following cuprizone withdrawal in SphK2-/- mice. We also observed a significant reduction in myelin thickness with ageing in SphK2-/- compared to WT mice. These results provide the first evidence that SphK2, the dominant enzyme catalysing S1P synthesis in the adult brain, is essential for remyelination following a demyelinating insult and myelin maintenance with ageing. We propose that persistently high levels of sphingosine and ceramide, a direct consequence of SphK2 deficiency, may block remyelination.Table of Contents ImageMain PointsThe lipid kinase sphingosine kinase 2 (SphK2) is essential for remyelination following a demyelinating insult (cuprizone).SphK2 protects against cuprizone-mediated oligodendrocyte loss.SphK2 deficiency leads to thinner myelin with ageing.

Published
2021

34. Temperature Dependence of Charge and Spin Transfer in Azurin

Author

David N. Beratan, Agostino Migliore, Raanan Carmieli, Ruijie D. Teo, Yutao Sang, Suryakant Mishra, Israel Pecht, David H. Waldeck, Harry B. Gray, Jonas Fransson, Francesco Tassinari, Senthil Kumar Karuppannan, and Ron Naaman

Subjects
Fysikalisk kemi, Materials science, Spins, Quantitative Biology::Molecular Networks, 02 engineering and technology, Electron, 010402 general chemistry, 021001 nanoscience & nanotechnology, Spin-exchange interaction, 01 natural sciences, Redox, Electric charge, Physical Chemistry, Article, 0104 chemical sciences, Surfaces, Coatings and Films, Electronic, Optical and Magnetic Materials, Quantitative Biology::Subcellular Processes, Electron transfer, General Energy, Chemical physics, Physical and Theoretical Chemistry, Azurin, 0210 nano-technology, Spin (physics)
Abstract

The steady-state charge and spin transfer yields were measured for three different Ru-modified azurin derivatives in protein films on silver electrodes. While the charge-transfer yields exhibit weak temperature dependences, consistent with operation of a near activation-less mechanism, the spin selectivity of the electron transfer improves as temperature increases. This enhancement of spin selectivity with temperature is explained by a vibrationally induced spin exchange interaction between the Cu(II) and its chiral ligands. These results indicate that distinct mechanisms control charge and spin transfer within proteins. As with electron charge transfer, proteins deliver polarized electron spins with a yield that depends on the protein’s structure. This finding suggests a new role for protein structure in biochemical redox processes.

Published
2021

35. Oxalate decarboxylase uses electron hole hopping for catalysis

Author

Ruijie D. Teo, Matthew J. Burg, Steven D. Bruner, David N. Beratan, Alexander Angerhofer, Alvaro Montoya, Umar T. Twahir, and Anthony J. Pastore

Subjects
0301 basic medicine, Decarboxylation, Stereochemistry, Carboxy-Lyases, Protein subunit, Protein Data Bank (RCSB PDB), LRET, long-range electron transfer, Electrons, Crystallography, X-Ray, Biochemistry, Oxalate, Catalysis, Oxalate decarboxylase, 03 medical and health sciences, chemistry.chemical_compound, PDB, Protein Data Bank, Catalytic Domain, VIE, vertical ionization energy, long-range electron transfer, Molecular Biology, X-ray crystallography, Manganese, Binding Sites, 030102 biochemistry & molecular biology, Chemistry, Tryptophan, oxalate decarboxylase, Substrate (chemistry), Cell Biology, Protein tertiary structure, tryptophan pair, Oxygen, Kinetics, 030104 developmental biology, OxDC, oxalate decarboxylase, Bacillus subtilis, Research Article
Abstract

The hexameric low-pH stress response enzyme oxalate decarboxylase catalyzes the decarboxylation of the oxalate mono-anion in the soil bacterium Bacillus subtilis. A single protein subunit contains two Mn-binding cupin domains, and catalysis depends on Mn(III) at the N-terminal site. The present study suggests a mechanistic function for the C-terminal Mn as an electron hole donor for the N-terminal Mn. The resulting spatial separation of the radical intermediates directs the chemistry toward decarboxylation of the substrate. A π-stacked tryptophan pair (W96/W274) links two neighboring protein subunits together, thus reducing the Mn-to-Mn distance from 25.9 A (intrasubunit) to 21.5 A (intersubunit). Here, we used theoretical analysis of electron hole-hopping paths through redox-active sites in the enzyme combined with site-directed mutagenesis and X-ray crystallography to demonstrate that this tryptophan pair supports effective electron hole hopping between the C-terminal Mn of one subunit and the N-terminal Mn of the other subunit through two short hops of ∼8.5 A. Replacement of W96, W274, or both with phenylalanine led to a large reduction in catalytic efficiency, whereas replacement with tyrosine led to recovery of most of this activity. W96F and W96Y mutants share the wildtype tertiary structure. Two additional hole-hopping networks were identified leading from the Mn ions to the protein surface, potentially protecting the enzyme from high Mn oxidation states during turnover. Our findings strongly suggest that multistep hole-hopping transport between the two Mn ions is required for enzymatic function, adding to the growing examples of proteins that employ aromatic residues as hopping stations.

Published
2021

36. Correlation between Charge Transport and Base Excision Repair in the MutY-DNA Glycosylase

Author

Ruijie D. Teo, David N. Beratan, Agostino Migliore, Xiaochen Du, and Héctor Luis Torres Vera

Subjects
Mutation, Guanine, DNA Repair, Chemistry, Base pair, DNA replication, Base excision repair, Pathway analysis, medicine.disease_cause, Article, Surfaces, Coatings and Films, Nucleobase, DNA Glycosylases, DNA glycosylase, Materials Chemistry, Nucleic acid, medicine, Biophysics, Physical and Theoretical Chemistry, N-Glycosyl Hydrolases, DNA Damage
Abstract

Experimental evidence suggests that DNA-mediated redox signaling between high-potential [Fe(4)S(4)] proteins is relevant to DNA replication and repair processes, and protein-mediated charge transfer (CT) between [Fe(4)S(4)] clusters and nucleic acids is a fundamental component of the signaling and repair mechanisms. We analyzed the dominant CT pathways in the base excision repair glycosylase MutY using molecular dynamics (MD) simulations and hole hopping pathway analysis. We find that the adenine nucleobase of the mismatched A·oxoG DNA base pair facilitates [Fe(4)S(4)]-DNA CT prior to adenine excision by MutY. We also find that the R153L mutation in MutY (linked to colorectal adenomatous polyposis) influences the dominant [Fe4S4]-DNA CT pathways and appreciably decreases their effective CT rates.

Published
2020

37. A Novel Function of Sphingosine Kinase 2 in the Metabolism of Sphinga-4,14-Diene Lipids

Author

Jonathan D. Teo, Yepy H Rustam, Jinbiao Chen, Yanfei Qi, Anthony S. Don, Gavin E. Reid, Huitong Song, and Timothy A. Couttas

Subjects
0301 basic medicine, Ceramide, sphingosine kinase 2, Endocrinology, Diabetes and Metabolism, Sphingosine kinase, lcsh:QR1-502, Biochemistry, Article, lcsh:Microbiology, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, brain lipids, ceramide, Sphingosine-1-phosphate, SphK2, Molecular Biology, 030304 developmental biology, mass spectrometry, 0303 health sciences, sphingolipids, biology, Sphingosine, sphingosine, Kinase, Catabolism, Chemistry, sphingadiene, Sphingosine Kinase 2, Metabolism, Sphingolipid, 3. Good health, SPHK2, 030104 developmental biology, Sphingosine kinase 1, sphingosine kinase, 030220 oncology & carcinogenesis, biology.protein, lipids (amino acids, peptides, and proteins), 030217 neurology & neurosurgery
Abstract

The number, position, and configuration of double bonds in lipids affect membrane fluidity and the recruitment of signaling proteins. Studies on mammalian sphingolipids have focused on those with a saturated sphinganine or mono-unsaturated sphingosine long chain base. Using high-resolution liquid chromatography-tandem mass spectrometry (LC-MS/MS), we observed a marked accumulation of lipids containing a di-unsaturated sphingadiene base in the hippocampus of mice lacking the metabolic enzyme sphingosine kinase 2 (SphK2). The double bonds were localized to positions C4&ndash, C5 and C14&ndash, C15 of sphingadiene using ultraviolet photodissociation-tandem mass spectrometry (UVPD-MS/MS). Phosphorylation of sphingoid bases by sphingosine kinase 1 (SphK1) or SphK2 forms the penultimate step in the lysosomal catabolism of all sphingolipids. Both SphK1 and SphK2 phosphorylated sphinga-4,14-diene as efficiently as sphingosine, however deuterated tracer experiments in an oligodendrocyte cell line demonstrated that ceramides with a sphingosine base are more rapidly metabolized than those with a sphingadiene base. Since SphK2 is the dominant sphingosine kinase in brain, we propose that the accumulation of sphingadiene-based lipids in SphK2-deficient brains results from the slower catabolism of these lipids, combined with a bottleneck in the catabolic pathway created by the absence of SphK2. We have therefore uncovered a previously unappreciated role for SphK2 in lipid quality control.

Published
2020

38. 2′-Deoxy-2′-fluoro-arabinonucleic acid: a valid alternative to DNA for biotechnological applications using charge transport

Author

Elizabeth R. Smithwick, Agostino Migliore, and Ruijie D. Teo

Subjects
Materials science, General Physics and Astronomy, 02 engineering and technology, Molecular Dynamics Simulation, Conductivity, 010402 general chemistry, 01 natural sciences, Article, Nucleobase, Molecular dynamics, chemistry.chemical_compound, Physical and Theoretical Chemistry, Arabinonucleotides, Charge (physics), DNA, 021001 nanoscience & nanotechnology, Thermal conduction, 0104 chemical sciences, chemistry, Chemical physics, Biotechnology, Electronics, Chemical stability, 0210 nano-technology, Biosensor
Abstract

The non-biological 2’-deoxy-2’-fluoro-arabinonucleic acid (2’F-ANA) may be used as a valid alternative to DNA in biomedical and electronic applications because of its higher resistance to hydrolysis and nuclease degradation. However, the advantage of using 2’F-ANA in such applications also depends on its charge-transfer properties compared to DNA. In this study, we compare the charge conduction properties of model 2’F-ANA and DNA double-strands, using structural snapshots from MD simulations to calculate the electronic couplings and reorganization energies associated with the hole transfer steps between adjacent nucleobase pairs. Inserting these charge-transfer parameters into a kinetic model for charge conduction, we find similar conductive properties for DNA and 2’F-ANA. Moreover, we find that 2’F-ANA’s enhanced chemical stability does not correspond to a reduction in the nucleobase π-stack structural flexibility relevant to both electronic couplings and reorganization free energies. Our results promote the use of 2’F-ANA in applications that can be based on charge transport, such as biosensing and chip technology, where its chemical stability and conductivity can advantageously combine.

Published
2019
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39. A selective inhibitor of ceramide synthase 1 reveals a novel role in fat metabolism

Author

Kyle L. Hoehn, Corrine E. Fiveash, Greg M. Kowalski, Jonathan D. Teo, Carsten Schmitz-Peiffer, Timothy A. Couttas, Hemna Govindaraju, Magdalene K. Montgomery, Gregory J. Cooney, Amanda E. Brandon, Anthony S. Don, Brenna Osborne, Jonathan C. Morris, Nigel Turner, Abhirup Das, Holly P. McEwen, Thomas Fath, Hamish D. Toop, Elysha N. Taylor, Xin Ying Lim, Clinton R. Bruce, and Stephen M. Butler

Subjects
Male, 0301 basic medicine, Ceramide, Science, Cell Respiration, General Physics and Astronomy, Adipose tissue, Diet, High-Fat, Article, General Biochemistry, Genetics and Molecular Biology, Inhibitory Concentration 50, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Insulin resistance, medicine, Animals, Humans, Enzyme Inhibitors, Muscle, Skeletal, lcsh:Science, Ceramide synthase, Beta oxidation, Sphingolipids, Multidisciplinary, Chemistry, Fatty Acids, Skeletal muscle, Ceramide synthase 1, General Chemistry, Lipid Metabolism, medicine.disease, Sphingolipid, Mitochondria, 3. Good health, Mice, Inbred C57BL, HEK293 Cells, 030104 developmental biology, medicine.anatomical_structure, Liver, Biochemistry, lcsh:Q, Insulin Resistance, Oxidoreductases, Oxidation-Reduction, 030217 neurology & neurosurgery
Abstract

Specific forms of the lipid ceramide, synthesized by the ceramide synthase enzyme family, are believed to regulate metabolic physiology. Genetic mouse models have established C16 ceramide as a driver of insulin resistance in liver and adipose tissue. C18 ceramide, synthesized by ceramide synthase 1 (CerS1), is abundant in skeletal muscle and suggested to promote insulin resistance in humans. We herein describe the first isoform-specific ceramide synthase inhibitor, P053, which inhibits CerS1 with nanomolar potency. Lipidomic profiling shows that P053 is highly selective for CerS1. Daily P053 administration to mice fed a high-fat diet (HFD) increases fatty acid oxidation in skeletal muscle and impedes increases in muscle triglycerides and adiposity, but does not protect against HFD-induced insulin resistance. Our inhibitor therefore allowed us to define a role for CerS1 as an endogenous inhibitor of mitochondrial fatty acid oxidation in muscle and regulator of whole-body adiposity., Ceramides are signalling molecules that regulate several physiological functions including insulin sensitivity. Here the authors report a selective ceramide synthase 1 inhibitor that counteracts lipid accumulation within the muscle and adiposity by increasing fatty acid oxidation but without affecting insulin sensitivity in mice fed with an obesogenic diet.

Published
2018
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40. Machine Learning Approaches for Metalloproteins

Author

Yue Yu, Ruobing Wang, and Ruijie D. Teo

Subjects
Models, Molecular, Binding Sites, Protein Stability, Organic Chemistry, Pharmaceutical Science, Analytical Chemistry, Machine Learning, Structure-Activity Relationship, Chemistry (miscellaneous), Drug Design, Metalloproteins, Proteolysis, Drug Discovery, Molecular Medicine, Amino Acid Sequence, Physical and Theoretical Chemistry, Protein Binding
Abstract

Metalloproteins are a family of proteins characterized by metal ion binding, whereby the presence of these ions confers key catalytic and ligand-binding properties. Due to their ubiquity among biological systems, researchers have made immense efforts to predict the structural and functional roles of metalloproteins. Ultimately, having a comprehensive understanding of metalloproteins will lead to tangible applications, such as designing potent inhibitors in drug discovery. Recently, there has been an acceleration in the number of studies applying machine learning to predict metalloprotein properties, primarily driven by the advent of more sophisticated machine learning algorithms. This review covers how machine learning tools have consolidated and expanded our comprehension of various aspects of metalloproteins (structure, function, stability, ligand-binding interactions, and inhibitors). Future avenues of exploration are also discussed.

Published
2022
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41. The effect of insulin receptor deletion in neuropeptide Y neurons on hippocampal dependent cognitive function in aging mice

Author

Elisabeth K. Goodman, Caitlin S. Mitchell, Jonathan D. Teo, Joanne M. Gladding, Kirsten N. Abbott, Neda Rafiei, Lei Zhang, Herbert Herzog, and Denovan P. Begg

Subjects
Mice, Knockout, Neurons, Aging, Behavior, Animal, General Neuroscience, Neurosciences. Biological psychiatry. Neuropsychiatry, General Medicine, npy, Hippocampus, Receptor, Insulin, Mice, Inbred C57BL, Disease Models, Animal, Mice, insulin receptors, Animals, morris water maze, Cognitive Dysfunction, Neuropeptide Y, Maze Learning, RC321-571, Spatial Memory
Abstract

Insulin is known to act in the central nervous system to regulate several physiological and behavioural outcomes, including energy balance, glucose homeostasis and cognitive functioning. However, the neuronal populations through which insulin enhances cognitive performance remain unidentified. Insulin receptors are found in neuropeptide-Y (NPY) expressing neurons, which are abundant in the hypothalamus and hippocampus; regions involved in feeding behaviour and spatial memory, respectively. Here we show that mice with a tissue specific knockout of insulin receptors in NPY expressing neurons (IRlox/lox; NPYCre/+) display an impaired performance in the probe trial of the Morris Water Maze compared with control mice at both the 6 and the 12, but not at the 24 months time point, consistent with a crucial role of insulin and NPY in cognitive functioning. By 24 months of age all groups demonstrated similar reductions in spatial memory performance. Together, these data suggest that the mechanisms through which insulin influences cognitive functioning are, at least in part, via insulin receptor signaling in NPY expressing neurons. These results also highlight that cognitive impairments observed in aging may be due to impaired insulin signaling.

Published
2022
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42. CTNNB1-Mutant Aldosterone-Producing Adenomas With Somatic Mutations of GNA11/GNAQ Have Distinct Phenotype and Genotype

Author

William Drake, Helen L Storr, Sam O’Toole, Giulia Argentesi, Alison Marker, Xilin Wu, Morris J. Brown, Eva Wozniak, Daniel M. Berney, Claudia P. Cabrera, Junhua Zhou, Suzanne Jordan, Emily Cottrell, Ada E. D. Teo, Rajesh V. Thakker, Maria-Christina Zennaro, Fabio L. Fernandes-Rosa, Kate E Lines, Charles A. Mein, Sheerazed Boulkroun, Louise A. Metherell, and Elena A.B. Azizan

Subjects
Genetics, Aldosterone, GNA11, Somatic cell, Endocrinology, Diabetes and Metabolism, Mutant, education, Adrenal - Basic and Translational Aspects, Biology, Phenotype, chemistry.chemical_compound, chemistry, Genotype, mental disorders, Adrenal, GNAQ, psychological phenomena and processes, AcademicSubjects/MED00250
Abstract

Background: We report (this meeting) somatic mutation of GNA11/Q in CTNNB1-mutant APAs. The recurrent co-driver mutation causes reversible hypertension in puberty, pregnancy, or menopause. We have investigated the molecular mechanism of this association. Methods: Gene expression profiles in 3 double mutant APAs were studied by unsupervised hierarchical clustering analysis and enrichment analysis of 362 differentially expressed genes and validated by qPCR, IFC and IHC in 10 double mutant APAs or transfected primary adrenal cells. Multiple region biopsies were performed in 7 adrenals adjacent to double-mutant APAs and 4 APAs with KCNJ5 or CACNA1D mutations. The findings of APA mutations in adjacent adrenals were replicated in each case by ddPCR ± NGS. Results: Unsupervised hierarchical clustering analysis showed clustering of the double-mutant APAs, and a high proportion of genes were many-fold upregulated compared to other APAs. LHCGR, TMEM132E, DKK1, C9orf84, FAP, GNRHR and MPP3 are among the genes with high expression. A small number of genes are down-regulated in the double-mutant APAs, including CYP11B1. qPCR confirmed an average of ~10 to 1000-fold higher expression of the hallmark genes in double-mutants. Enrichment analysis showed significant enrichment of features or terms concerned with cell junction and cell adhesion (P

Published
2021

43. Measurements of the associated production of a Z boson and b jets in pp collisions at $${\sqrt{s}} = 8\,\text {TeV} $$ s = 8 TeV

Author

V. Khachatryan, A. M. Sirunyan, A. Tumasyan, W. Adam, E. Asilar, T. Bergauer, J. Brandstetter, E. Brondolin, M. Dragicevic, J. Erö, M. Flechl, M. Friedl, R. Frühwirth, V. M. Ghete, C. Hartl, N. Hörmann, J. Hrubec, M. Jeitler, A. König, M. Krammer, I. Krätschmer, D. Liko, T. Matsushita, I. Mikulec, D. Rabady, N. Rad, B. Rahbaran, H. Rohringer, J. Schieck, J. Strauss, W. Treberer-Treberspurg, W. Waltenberger, C.-E. Wulz, V. Mossolov, N. Shumeiko, J. Suarez Gonzalez, S. Alderweireldt, T. Cornelis, E. A. De Wolf, X. Janssen, A. Knutsson, J. Lauwers, S. Luyckx, M. Van De Klundert, H. Van Haevermaet, P. Van Mechelen, N. Van Remortel, A. Van Spilbeeck, S. Abu Zeid, F. Blekman, J. D’Hondt, N. Daci, I. De Bruyn, K. Deroover, N. Heracleous, J. Keaveney, S. Lowette, S. Moortgat, L. Moreels, A. Olbrechts, Q. Python, D. Strom, S. Tavernier, W. Van Doninck, P. Van Mulders, I. Van Parijs, H. Brun, C. Caillol, B. Clerbaux, G. De Lentdecker, G. Fasanella, L. Favart, R. Goldouzian, A. Grebenyuk, G. Karapostoli, T. Lenzi, A. Léonard, T. Maerschalk, A. Marinov, A. Randle-conde, T. Seva, C. Vander Velde, P. Vanlaer, R. Yonamine, F. Zenoni, F. Zhang, L. Benucci, A. Cimmino, S. Crucy, D. Dobur, A. Fagot, G. Garcia, M. Gul, J. Mccartin, A. A. Ocampo Rios, D. Poyraz, D. Ryckbosch, S. Salva, R. Schöfbeck, M. Sigamani, M. Tytgat, W. Van Driessche, E. Yazgan, N. Zaganidis, C. Beluffi, O. Bondu, S. Brochet, G. Bruno, A. Caudron, L. Ceard, S. De Visscher, C. Delaere, M. Delcourt, L. Forthomme, B. Francois, A. Giammanco, A. Jafari, P. Jez, M. Komm, V. Lemaitre, A. Magitteri, A. Mertens, M. Musich, C. Nuttens, K. Piotrzkowski, L. Quertenmont, M. Selvaggi, M. Vidal Marono, S. Wertz, N. Beliy, G. H. Hammad, W. L. Aldá Júnior, F. L. Alves, G. A. Alves, L. Brito, M. Correa Martins Junior, M. Hamer, C. Hensel, A. Moraes, M. E. Pol, P. Rebello Teles, E. Belchior Batista Das Chagas, W. Carvalho, J. Chinellato, A. Custódio, E. M. Da Costa, D. De Jesus Damiao, C. De Oliveira Martins, S. Fonseca De Souza, L. M. Huertas Guativa, H. Malbouisson, D. Matos Figueiredo, C. Mora Herrera, L. Mundim, H. Nogima, W. L. Prado Da Silva, A. Santoro, A. Sznajder, E. J. Tonelli Manganote, A. Vilela Pereira, S. Ahuja, C. A. Bernardes, A. De Souza Santos, S. Dogra, T. R. Fernandez Perez Tomei, E. M. Gregores, P. G. Mercadante, C. S. Moon, S. F. Novaes, Sandra S. Padula, D. Romero Abad, J. C. Ruiz Vargas, A. Aleksandrov, R. Hadjiiska, P. Iaydjiev, M. Rodozov, S. Stoykova, G. Sultanov, M. Vutova, A. Dimitrov, I. Glushkov, L. Litov, B. Pavlov, P. Petkov, W. Fang, M. Ahmad, J. G. Bian, G. M. Chen, H. S. Chen, M. Chen, T. Cheng, R. Du, C. H. Jiang, D. Leggat, R. Plestina, F. Romeo, S. M. Shaheen, A. Spiezia, J. Tao, C. Wang, Z. Wang, H. Zhang, C. Asawatangtrakuldee, Y. Ban, Q. Li, S. Liu, Y. Mao, S. J. Qian, D. Wang, Z. Xu, C. Avila, A. Cabrera, L. F. Chaparro Sierra, C. Florez, J. P. Gomez, B. Gomez Moreno, J. C. Sanabria, N. Godinovic, D. Lelas, I. Puljak, P. M. Ribeiro Cipriano, Z. Antunovic, M. Kovac, V. Brigljevic, D. Ferencek, K. Kadija, J. Luetic, S. Micanovic, L. Sudic, A. Attikis, G. Mavromanolakis, J. Mousa, C. Nicolaou, F. Ptochos, P. A. Razis, H. Rykaczewski, M. Finger, M. Finger Jr., E. Carrera Jarrin, A. A. Abdelalim, E. El-khateeb, T. Elkafrawy, M. A. Mahmoud, B. Calpas, M. Kadastik, M. Murumaa, L. Perrini, M. Raidal, A. Tiko, C. Veelken, P. Eerola, J. Pekkanen, M. Voutilainen, J. Härkönen, V. Karimäki, R. Kinnunen, T. Lampén, K. Lassila-Perini, S. Lehti, T. Lindén, P. Luukka, T. Peltola, J. Tuominiemi, E. Tuovinen, L. Wendland, J. Talvitie, T. Tuuva, M. Besancon, F. Couderc, M. Dejardin, D. Denegri, B. Fabbro, J. L. Faure, C. Favaro, F. Ferri, S. Ganjour, A. Givernaud, P. Gras, G. Hamel de Monchenault, P. Jarry, E. Locci, M. Machet, J. Malcles, J. Rander, A. Rosowsky, M. Titov, A. Zghiche, A. Abdulsalam, I. Antropov, S. Baffioni, F. Beaudette, P. Busson, L. Cadamuro, E. Chapon, C. Charlot, O. Davignon, L. Dobrzynski, R. Granier de Cassagnac, M. Jo, S. Lisniak, P. Miné, I. N. Naranjo, M. Nguyen, C. Ochando, G. Ortona, P. Paganini, P. Pigard, S. Regnard, R. Salerno, Y. Sirois, T. Strebler, Y. Yilmaz, A. Zabi, J.-L. Agram, J. Andrea, A. Aubin, D. Bloch, J.-M. Brom, M. Buttignol, E. C. Chabert, N. Chanon, C. Collard, E. Conte, X. Coubez, J.-C. Fontaine, D. Gelé, U. Goerlach, C. Goetzmann, A.-C. Le Bihan, J. A. Merlin, K. Skovpen, P. Van Hove, S. Gadrat, S. Beauceron, C. Bernet, G. Boudoul, E. Bouvier, C. A. Carrillo Montoya, R. Chierici, D. Contardo, B. Courbon, P. Depasse, H. El Mamouni, J. Fan, J. Fay, S. Gascon, M. Gouzevitch, B. Ille, F. Lagarde, I. B. Laktineh, M. Lethuillier, L. Mirabito, A. L. Pequegnot, S. Perries, A. Popov, J. D. Ruiz Alvarez, D. Sabes, V. Sordini, M. Vander Donckt, P. Verdier, S. Viret, T. Toriashvili, I. Bagaturia, C. Autermann, S. Beranek, L. Feld, A. Heister, M. K. Kiesel, K. Klein, M. Lipinski, A. Ostapchuk, M. Preuten, F. Raupach, S. Schael, C. Schomakers, J. F. Schulte, J. Schulz, T. Verlage, H. Weber, V. Zhukov, M. Ata, M. Brodski, E. Dietz-Laursonn, D. Duchardt, M. Endres, M. Erdmann, S. Erdweg, T. Esch, R. Fischer, A. Güth, T. Hebbeker, C. Heidemann, K. Hoepfner, S. Knutzen, M. Merschmeyer, A. Meyer, P. Millet, S. Mukherjee, M. Olschewski, K. Padeken, P. Papacz, T. Pook, M. Radziej, H. Reithler, M. Rieger, F. Scheuch, L. Sonnenschein, D. Teyssier, S. Thüer, V. Cherepanov, Y. Erdogan, G. Flügge, H. Geenen, M. Geisler, F. Hoehle, B. Kargoll, T. Kress, A. Künsken, J. Lingemann, A. Nehrkorn, A. Nowack, I. M. Nugent, C. Pistone, O. Pooth, A. Stahl, M. Aldaya Martin, I. Asin, K. Beernaert, O. Behnke, U. Behrens, K. Borras, A. Campbell, P. Connor, C. Contreras-Campana, F. Costanza, C. Diez Pardos, G. Dolinska, S. Dooling, G. Eckerlin, D. Eckstein, T. Eichhorn, E. Gallo, J. Garay Garcia, A. Geiser, A. Gizhko, J. M. Grados Luyando, P. Gunnellini, A. Harb, J. Hauk, M. Hempel, H. Jung, A. Kalogeropoulos, O. Karacheban, M. Kasemann, J. Kieseler, C. Kleinwort, I. Korol, W. Lange, A. Lelek, J. Leonard, K. Lipka, A. Lobanov, W. Lohmann, R. Mankel, I.-A. Melzer-Pellmann, A. B. Meyer, G. Mittag, J. Mnich, A. Mussgiller, E. Ntomari, D. Pitzl, R. Placakyte, A. Raspereza, B. Roland, M. Ö. Sahin, P. Saxena, T. Schoerner-Sadenius, C. Seitz, S. Spannagel, N. Stefaniuk, K. D. Trippkewitz, G. P. Van Onsem, R. Walsh, C. Wissing, V. Blobel, M. Centis Vignali, A. R. Draeger, T. Dreyer, J. Erfle, E. Garutti, K. Goebel, D. Gonzalez, M. Görner, J. Haller, M. Hoffmann, R. S. Höing, A. Junkes, R. Klanner, R. Kogler, N. Kovalchuk, T. Lapsien, T. Lenz, I. Marchesini, D. Marconi, M. Meyer, M. Niedziela, D. Nowatschin, J. Ott, F. Pantaleo, T. Peiffer, A. Perieanu, N. Pietsch, J. Poehlsen, C. Sander, C. Scharf, P. Schleper, E. Schlieckau, A. Schmidt, S. Schumann, J. Schwandt, H. Stadie, G. Steinbrück, F. M. Stober, H. Tholen, D. Troendle, E. Usai, L. Vanelderen, A. Vanhoefer, B. Vormwald, C. Barth, C. Baus, J. Berger, C. Böser, E. Butz, T. Chwalek, F. Colombo, W. De Boer, A. Descroix, A. Dierlamm, S. Fink, F. Frensch, R. Friese, M. Giffels, A. Gilbert, D. Haitz, F. Hartmann, S. M. Heindl, U. Husemann, I. Katkov, A. Kornmayer, P. Lobelle Pardo, B. Maier, H. Mildner, M. U. Mozer, T. Müller, Th. Müller, M. Plagge, G. Quast, K. Rabbertz, S. Röcker, F. Roscher, M. Schröder, G. Sieber, H. J. Simonis, R. Ulrich, J. Wagner-Kuhr, S. Wayand, M. Weber, T. Weiler, S. Williamson, C. Wöhrmann, R. Wolf, G. Anagnostou, G. Daskalakis, T. Geralis, V. A. Giakoumopoulou, A. Kyriakis, D. Loukas, A. Psallidas, I. Topsis-Giotis, A. Agapitos, S. Kesisoglou, A. Panagiotou, N. Saoulidou, E. Tziaferi, I. Evangelou, G. Flouris, C. Foudas, P. Kokkas, N. Loukas, N. Manthos, I. Papadopoulos, E. Paradas, J. Strologas, N. Filipovic, G. Bencze, C. Hajdu, P. Hidas, D. Horvath, F. Sikler, V. Veszpremi, G. Vesztergombi, A. J. Zsigmond, N. Beni, S. Czellar, J. Karancsi, J. Molnar, Z. Szillasi, M. Bartók, A. Makovec, P. Raics, Z. L. Trocsanyi, B. Ujvari, S. Choudhury, P. Mal, K. Mandal, A. Nayak, D. K. Sahoo, N. Sahoo, S. K. Swain, S. Bansal, S. B. Beri, V. Bhatnagar, R. Chawla, R. Gupta, U. Bhawandeep, A. K. Kalsi, A. Kaur, M. Kaur, R. Kumar, A. Mehta, M. Mittal, J. B. Singh, G. Walia, Ashok Kumar, A. Bhardwaj, B. C. Choudhary, R. B. Garg, S. Keshri, A. Kumar, S. Malhotra, M. Naimuddin, N. Nishu, K. Ranjan, R. Sharma, V. Sharma, R. Bhattacharya, S. Bhattacharya, K. Chatterjee, S. Dey, S. Dutta, S. Ghosh, N. Majumdar, A. Modak, K. Mondal, S. Mukhopadhyay, S. Nandan, A. Purohit, A. Roy, D. Roy, S. Roy Chowdhury, S. Sarkar, M. Sharan, R. Chudasama, D. Dutta, V. Jha, V. Kumar, A. K. Mohanty, L. M. Pant, P. Shukla, A. Topkar, S. Chauhan, S. Dube, A. Kapoor, K. Kothekar, A. Rane, S. Sharma, H. Bakhshiansohi, H. Behnamian, S. M. Etesami, A. Fahim, M. Khakzad, M. Mohammadi Najafabadi, M. Naseri, S. Paktinat Mehdiabadi, F. Rezaei Hosseinabadi, B. Safarzadeh, M. Zeinali, M. Felcini, M. Grunewald, M. Abbrescia, C. Calabria, C. Caputo, A. Colaleo, D. Creanza, L. Cristella, N. De Filippis, M. De Palma, L. Fiore, G. Iaselli, G. Maggi, M. Maggi, G. Miniello, S. My, S. Nuzzo, A. Pompili, G. Pugliese, R. Radogna, A. Ranieri, G. Selvaggi, L. Silvestris, R. Venditti, G. Abbiendi, C. Battilana, D. Bonacorsi, S. Braibant-Giacomelli, L. Brigliadori, R. Campanini, P. Capiluppi, A. Castro, F. R. Cavallo, S. S. Chhibra, G. Codispoti, M. Cuffiani, G. M. Dallavalle, F. Fabbri, A. Fanfani, D. Fasanella, P. Giacomelli, C. Grandi, L. Guiducci, S. Marcellini, G. Masetti, A. Montanari, F. L. Navarria, A. Perrotta, A. M. Rossi, T. Rovelli, G. P. Siroli, N. Tosi, G. Cappello, M. Chiorboli, S. Costa, A. Di Mattia, F. Giordano, R. Potenza, A. Tricomi, C. Tuve, G. Barbagli, V. Ciulli, C. Civinini, R. D’Alessandro, E. Focardi, V. Gori, P. Lenzi, M. Meschini, S. Paoletti, G. Sguazzoni, L. Viliani, L. Benussi, S. Bianco, D. Piccolo, F. Primavera, V. Calvelli, F. Ferro, M. Lo Vetere, M. R. Monge, E. Robutti, S. Tosi, L. Brianza, M. E. Dinardo, S. Fiorendi, S. Gennai, A. Ghezzi, P. Govoni, S. 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Linn, P. Markowitz, G. Martinez, J. L. Rodriguez, A. Ackert, J. R. Adams, T. Adams, A. Askew, S. Bein, J. Bochenek, B. Diamond, J. Haas, S. Hagopian, V. Hagopian, K. F. Johnson, A. Khatiwada, H. Prosper, A. Santra, M. Weinberg, M. M. Baarmand, V. Bhopatkar, S. Colafranceschi, M. Hohlmann, H. Kalakhety, D. Noonan, T. Roy, F. Yumiceva, M. R. Adams, L. Apanasevich, D. Berry, R. R. Betts, I. Bucinskaite, R. Cavanaugh, O. Evdokimov, L. Gauthier, C. E. Gerber, D. J. Hofman, P. Kurt, C. O’Brien, I. D. Sandoval Gonzalez, P. Turner, N. Varelas, Z. Wu, M. Zakaria, J. Zhang, B. Bilki, W. Clarida, K. Dilsiz, S. Durgut, R. P. Gandrajula, M. Haytmyradov, V. Khristenko, J.-P. Merlo, H. Mermerkaya, A. Mestvirishvili, A. Moeller, J. Nachtman, H. Ogul, Y. Onel, F. Ozok, A. Penzo, C. Snyder, E. Tiras, J. Wetzel, K. Yi, I. Anderson, B. Blumenfeld, A. Cocoros, N. Eminizer, D. Fehling, L. Feng, A. V. Gritsan, P. Maksimovic, M. Osherson, J. Roskes, U. Sarica, M. Swartz, M. Xiao, Y. Xin, C. You, P. Baringer, A. Bean, C. Bruner, J. Castle, R. P. Kenny III, A. Kropivnitskaya, D. Majumder, M. Malek, W. Mcbrayer, M. Murray, S. Sanders, R. Stringer, Q. Wang, A. Ivanov, K. Kaadze, S. Khalil, M. Makouski, Y. Maravin, A. Mohammadi, L. K. Saini, N. Skhirtladze, S. Toda, D. Lange, F. Rebassoo, D. Wright, C. Anelli, A. Baden, O. Baron, A. Belloni, B. Calvert, S. C. Eno, C. Ferraioli, J. A. Gomez, N. J. Hadley, S. Jabeen, R. G. Kellogg, T. Kolberg, J. Kunkle, Y. Lu, A. C. Mignerey, Y. H. Shin, A. Skuja, M. B. Tonjes, S. C. Tonwar, A. Apyan, R. Barbieri, A. Baty, R. Bi, K. Bierwagen, S. Brandt, W. Busza, I. A. Cali, Z. Demiragli, L. Di Matteo, G. Gomez Ceballos, M. Goncharov, D. Gulhan, D. Hsu, Y. Iiyama, G. M. Innocenti, M. Klute, D. Kovalskyi, K. Krajczar, Y. S. Lai, Y.-J. Lee, A. Levin, P. D. Luckey, A. C. Marini, C. Mcginn, C. Mironov, S. Narayanan, X. Niu, C. Paus, C. Roland, G. Roland, J. Salfeld-Nebgen, G. S. F. Stephans, K. Sumorok, K. Tatar, M. Varma, D. Velicanu, J. Veverka, T. W. Wang, B. Wyslouch, M. Yang, V. Zhukova, A. C. Benvenuti, B. Dahmes, A. Evans, A. Finkel, A. Gude, P. Hansen, S. Kalafut, S. C. Kao, K. Klapoetke, Y. Kubota, Z. Lesko, J. Mans, S. Nourbakhsh, N. Ruckstuhl, R. Rusack, N. Tambe, J. Turkewitz, J. G. Acosta, S. Oliveros, E. Avdeeva, R. Bartek, K. Bloom, S. Bose, D. R. Claes, A. Dominguez, C. Fangmeier, R. Gonzalez Suarez, R. Kamalieddin, D. Knowlton, I. Kravchenko, F. Meier, J. Monroy, F. Ratnikov, J. E. Siado, G. R. Snow, B. Stieger, M. Alyari, J. Dolen, J. George, A. Godshalk, C. Harrington, I. Iashvili, J. Kaisen, A. Kharchilava, A. Parker, S. Rappoccio, B. Roozbahani, G. Alverson, E. Barberis, D. Baumgartel, M. Chasco, A. Hortiangtham, A. Massironi, D. M. Morse, D. Nash, T. Orimoto, R. Teixeira De Lima, D. Trocino, R.-J. Wang, D. Wood, K. A. Hahn, A. Kubik, J. F. Low, N. Mucia, N. Odell, B. Pollack, M. H. Schmitt, K. Sung, M. Trovato, M. Velasco, N. Dev, M. Hildreth, C. Jessop, D. J. Karmgard, N. Kellams, K. Lannon, N. Marinelli, F. Meng, C. Mueller, Y. Musienko, M. Planer, A. Reinsvold, R. Ruchti, N. Rupprecht, G. Smith, S. Taroni, N. Valls, M. Wayne, M. Wolf, A. Woodard, L. Antonelli, J. Brinson, B. Bylsma, L. S. Durkin, S. Flowers, A. Hart, C. Hill, R. Hughes, W. Ji, B. Liu, W. Luo, D. Puigh, M. Rodenburg, B. L. Winer, H. W. Wulsin, O. Driga, P. Elmer, J. Hardenbrook, P. Hebda, S. A. Koay, P. Lujan, D. Marlow, T. Medvedeva, M. Mooney, J. Olsen, C. Palmer, P. Piroué, D. Stickland, C. Tully, A. Zuranski, A. Barker, V. E. Barnes, D. Benedetti, L. Gutay, M. K. Jha, M. Jones, A. W. Jung, K. Jung, D. H. Miller, N. Neumeister, B. C. Radburn-Smith, X. Shi, J. Sun, A. Svyatkovskiy, F. Wang, W. Xie, L. Xu, N. Parashar, J. Stupak, A. Adair, B. Akgun, Z. Chen, K. M. Ecklund, F. J. M. Geurts, M. Guilbaud, W. Li, B. Michlin, M. Northup, B. P. Padley, R. Redjimi, J. Roberts, J. Rorie, Z. Tu, J. Zabel, B. Betchart, A. Bodek, P. de Barbaro, R. Demina, Y. t. Duh, Y. Eshaq, T. Ferbel, M. Galanti, A. Garcia-Bellido, J. Han, O. Hindrichs, A. Khukhunaishvili, K. H. Lo, P. Tan, M. Verzetti, J. P. Chou, E. Contreras-Campana, Y. Gershtein, T. A. Gómez Espinosa, E. Halkiadakis, M. Heindl, D. Hidas, E. Hughes, S. Kaplan, R. Kunnawalkam Elayavalli, S. Kyriacou, A. Lath, K. Nash, H. Saka, S. Salur, S. Schnetzer, D. Sheffield, S. Somalwar, R. Stone, S. Thomas, P. Thomassen, M. Walker, M. Foerster, J. Heideman, G. Riley, K. Rose, S. Spanier, K. Thapa, O. Bouhali, A. Castaneda Hernandez, A. Celik, M. Dalchenko, M. De Mattia, A. Delgado, S. Dildick, R. Eusebi, J. Gilmore, T. Huang, T. Kamon, V. Krutelyov, R. Mueller, I. Osipenkov, Y. Pakhotin, R. Patel, A. Perloff, L. Perniè, D. Rathjens, A. Safonov, A. Tatarinov, K. A. Ulmer, N. Akchurin, C. Cowden, J. Damgov, C. Dragoiu, P. R. Dudero, J. Faulkner, S. Kunori, K. Lamichhane, T. Libeiro, S. Undleeb, I. Volobouev, E. Appelt, A. G. Delannoy, S. Greene, A. Gurrola, R. Janjam, W. Johns, C. Maguire, A. Melo, H. Ni, P. Sheldon, S. Tuo, J. Velkovska, Q. Xu, M. W. Arenton, P. Barria, B. Cox, B. Francis, J. Goodell, R. Hirosky, A. Ledovskoy, H. Li, C. Neu, T. Sinthuprasith, X. Sun, Y. Wang, E. Wolfe, F. Xia, C. Clarke, R. Harr, P. E. Karchin, C. Kottachchi Kankanamge Don, P. Lamichhane, J. Sturdy, D. A. Belknap, D. Carlsmith, S. Dasu, L. Dodd, S. Duric, B. Gomber, M. Grothe, M. Herndon, A. Hervé, P. Klabbers, A. Lanaro, A. Levine, K. Long, R. Loveless, A. Mohapatra, I. Ojalvo, T. Perry, G. A. Pierro, G. Polese, T. Ruggles, T. Sarangi, A. Savin, N. Smith, W. H. Smith, D. Taylor, P. Verwilligen, N. Woods, T. Aziz, S. Bhowmik, R. M. Chatterjee, R. K. Dewanjee, S. Dugad, S. Ganguly, M. Guchait, A. Gurtu, Sa. Jain, G. Kole, S. Kumar, B. Mahakud, M. Maity, G. Majumder, K. Mazumdar, S. Mitra, G. B. Mohanty, B. Parida, T. Sarkar, N. Sur, B. Sutar, N. Wickramage, and CMS Collaboration

Subjects
Astrophysics::High Energy Astrophysical Phenomena, High Energy Physics::Phenomenology, lcsh:QB460-466, lcsh:QC770-798, High Energy Physics::Experiment, lcsh:Astrophysics, lcsh:Nuclear and particle physics. Atomic energy. Radioactivity
Abstract

Measurements of the associated production of a $$\mathrm{Z}$$ Z boson with at least one jet originating from a b quark in proton–proton collisions at $$\sqrt{s} = 8\,\text {TeV} $$ s = 8 TeV are presented. Differential cross sections are measured with data collected by the CMS experiment corresponding to an integrated luminosity of 19.8 $$\,\text {fb}^{-1}$$ fb - 1 . $$\mathrm{Z}$$ Z bosons are reconstructed through their decays to electrons and muons. Cross sections are measured as a function of observables characterizing the kinematics of the $$\mathrm{b}$$ b jet and the $$\mathrm{Z}$$ Z boson. Ratios of differential cross sections for the associated production with at least one $$\mathrm{b}$$ b jet to the associated production with any jet are also presented. The production of a $$\mathrm{Z}$$ Z boson with at least two $$\mathrm{b}$$ b jets is investigated, and differential cross sections are measured for the dijet system. Results are compared to theoretical predictions, testing two different flavour schemes for the choice of initial-state partons.

Published
2017
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44. Hypoxic postconditioning improves behavioural deficits at 6 weeks following hypoxic-ischemic brain injury in neonatal rats

Author

Nicole M. Jones, Jonathan D. Teo, and Margaret J. Morris

Subjects
Hypoxic ischemic brain injury, Neuroprotection, Rats, Sprague-Dawley, Reflex, Righting, 03 medical and health sciences, Behavioral Neuroscience, Grip strength, High morbidity, 0302 clinical medicine, 030225 pediatrics, medicine, Animals, Ischemic Postconditioning, Hand Strength, Mental Disorders, Age Factors, Brain, Recognition, Psychology, Hypoxia (medical), Rats, Disease Models, Animal, Treatment Outcome, medicine.anatomical_structure, Animals, Newborn, Anesthesia, Hypoxia-Ischemia, Brain, Exploratory Behavior, Analysis of variance, Righting reflex, medicine.symptom, Forelimb, Psychology, Neuroscience, Locomotion, 030217 neurology & neurosurgery
Abstract

Hypoxic-ischemic (HI) brain injury in newborns is associated with high morbidity and mortality, with many babies suffering neurological deficits. Recently, we showed that hypoxic postconditioning (PostC) immediately post injury can protect against HI up to one week in neonatal rats. Here, we aimed to examine whether long term functional deficits were also improved by PostC. Sprague-Dawley rats were assigned to control (C) or HI group on postnatal day 7 (P7). The HI group underwent unilateral carotid artery occlusion followed by hypoxia (7% oxygen, 3 h). Half of each group were randomly assigned to the PostC group (8% oxygen, 1 h/day for 5 days post-injury), or normoxic group, where animals were kept under ambient conditions. Righting reflex and negative geotaxis tests were performed on P8 and P14. On P42, rats underwent further behavioural tests of motor function and memory (forelimb grip strength, grid walking and novel object recognition tasks). Brain injury was assessed using histological scoring of brain sections. At P14, PostC reduced the righting reflex deficit compared to HI alone. Long-term (6 weeks) behavioural deficits were observed in grid walking and novel object recognition tests after HI alone, with both functions improved following PostC. Following HI, there was an increase in brain injury assessed by histological scoring compared to control, and this damage was reduced by PostC. This novel finding of long-term histological neuroprotection accompanied by functional improvements by PostC further demonstrates the clinical potential of mild hypoxia for the treatment of HI brain injury.

Published
2017
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45. Insulin controls food intake and energy balance via NPY neurons

Author

Lei Zhang, Herbert Herzog, Amanda E. Brandon, Qiao-Ping Wang, Denovan P. Begg, Jonathan D. Teo, Jens C. Brüning, Gregory J. Cooney, Kim Loh, Melissa Fu, Rishikesh N. Kulkarni, G. Gregory Neely, Yue Qi, and Paul A. Baldock

Subjects
0301 basic medicine, lcsh:Internal medicine, medicine.medical_specialty, medicine.medical_treatment, Hypothalamus, NPY, Brief Communication, Energy homeostasis, 03 medical and health sciences, Internal medicine, mental disorders, medicine, Biological neural network, Glucose homeostasis, Insulin, Obesity, lcsh:RC31-1245, Molecular Biology, biology, Cell Biology, Neuropeptide Y receptor, Phenotype, humanities, Insulin receptor, 030104 developmental biology, Endocrinology, nervous system, biology.protein
Abstract

Objectives Insulin signaling in the brain has been implicated in the control of satiety, glucose homeostasis and energy balance. However, insulin signaling is dispensable in energy homeostasis controlling AgRP or POMC neurons and it is unclear which other neurons regulate these effects. Here we describe an ancient insulin/NPY neuronal network that governs energy homeostasis across phyla. Methods To address the role of insulin action specifically in NPY neurons, we generated a variety of models by selectively removing insulin signaling in NPY neurons in flies and mice and testing the consequences on energy homeostasis. Results By specifically targeting the insulin receptor in both fly and mouse NPY expressing neurons, we found NPY-specific insulin signaling controls food intake and energy expenditure, and lack of insulin signaling in NPY neurons leads to increased energy stores and an obese phenotype. Additionally, the lack of insulin signaling in NPY neurons leads to a dysregulation of GH/IGF-1 axis and to altered insulin sensitivity. Conclusions Taken together, these results suggest that insulin actions in NPY neurons is critical for maintaining energy balance and an impairment of this pathway may be causally linked to the development of metabolic diseases., Graphical abstract Image 1, Highlights • Insulin controls feeding via non-AgRP expressing NPY-neurons in flies and mice. • Energy expenditure is regulated by insulin responsive NPY neurons. • Insulin signaling in NPY neurons is required for maintaining whole body glucose homeostasis and insulin sensitivity. • Central insulin-NPY pathways regulate bone mass and growth development.

Published
2017

46. Sphingosine 1-phosphate but not Fingolimod protects neurons against excitotoxic cell death by inducing neurotrophic gene expression in astrocytes

Author

Merryn Brettle, Timothy A. Couttas, Anthony S. Don, Yanfei Qi, Holly Stefen, Sean J. Humphrey, Thomas Fath, Collin Tran, Benjamin Heng, Gilles J. Guillemin, and Jonathan D. Teo

Subjects
0301 basic medicine, Sphingosine 1 Phosphate Receptor Modulators, Biochemistry, Neuroprotection, Hippocampus, 03 medical and health sciences, Cellular and Molecular Neuroscience, chemistry.chemical_compound, Mice, 0302 clinical medicine, Neurotrophic factors, Sphingosine, hemic and lymphatic diseases, Animals, Humans, Sphingosine-1-phosphate, Nerve Growth Factors, S1PR1, S1PR2, Neurons, biology, Cell Death, Chemistry, Fingolimod Hydrochloride, Cell biology, 030104 developmental biology, Neuroprotective Agents, Gene Expression Regulation, Astrocytes, biology.protein, lipids (amino acids, peptides, and proteins), Lysophospholipids, Leukemia inhibitory factor, 030217 neurology & neurosurgery, Neurotrophin
Abstract

Sphingosine 1-phosphate (S1P) is an essential lipid metabolite that signals through a family of five G protein-coupled receptors, S1PR1-S1PR5, to regulate cell physiology. The multiple sclerosis drug Fingolimod (FTY720) is a potent S1P receptor agonist that causes peripheral lymphopenia. Recent research has demonstrated direct neuroprotective properties of FTY720 in several neurodegenerative paradigms; however, neuroprotective properties of the native ligand S1P have not been established. We aimed to establish the significance of neurotrophic factor up-regulation by S1P for neuroprotection, comparing S1P with FTY720. S1P induced brain-derived neurotrophic factor (BDNF), leukemia inhibitory factor (LIF), platelet-derived growth factor B (PDGFB), and heparin-binding EGF-like growth factor (HBEGF) gene expression in primary human and murine astrocytes, but not in neurons, and to a much greater extent than FTY720. Accordingly, S1P but not FTY720 protected cultured neurons against excitotoxic cell death in a primary murine neuron-glia coculture model, and a neutralizing antibody to LIF blocked this S1P-mediated neuroprotection. Antagonists of S1PR1 and S1PR2 both inhibited S1P-mediated neurotrophic gene induction in human astrocytes, indicating that simultaneous activation of both receptors is required. S1PR2 signaling was transduced through Gα13 and the small GTPase Rho, and was necessary for the up-regulation and activation of the transcription factors FOS and JUN, which regulate LIF, BDNF, and HBEGF transcription. In summary, we show that S1P protects hippocampal neurons against excitotoxic cell death through up-regulation of neurotrophic gene expression, particularly LIF, in astrocytes. This up-regulation requires both S1PR1 and S1PR2 signaling. FTY720 does not activate S1PR2, explaining its relative inefficacy compared to S1P.

Published
2019

48. International Forum regarding practices related to donor haemoglobin and iron

Author

Manish J. Gandhi, André Lebrun, Jed B. Gorlin, Hany Kamel, Harvey G. Klein, J. Faed, J. Chay, Anne F. Eder, Giovani Vandewalle, Johanna Castrén, Whitney R. Steele, Vered Yahalom, D. Teo, Andreas Holbro, Gilles Delage, Rachid Djoudi, Joanne Pink, Veronica Gendelman, Michael J. Germain, J. N. S. Leung, Laura Infanti, Anthony J. Keller, Anne-Marie Fillet, Miquel Lozano, C. C. Y. Chu, Andreas Buser, Gail Miflin, Karin Magnussen, Eilat Shinar, Ralph R. Vassallo, Geneviève Woimant, E. M. O'Neill, Cheuk-Kwong Lee, Kamille A. West, Veerle Compernolle, Hwee Huang Tan, K. van den Hurk, Mindy Goldman, Joanna Speedy, Pierre Robillard, J. M. Cardenas, and Public and occupational health

Subjects
education.field_of_study, medicine.medical_specialty, Anemia, business.industry, Population, MEDLINE, Hematology, General Medicine, 030204 cardiovascular system & hematology, medicine.disease, Surgery, 03 medical and health sciences, 0302 clinical medicine, Donation, Family medicine, medicine, education, business, 030215 immunology
Published
2016
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49. Cell-Penetrating Protein/Corrole Nanoparticles

Author

Harry B. Gray, Angel J. Di Bilio, Qiu-Cheng Chen, John Termini, Irena Saltsman, Ruijie D. Teo, Mona Shahgholi, Matan Soll, Sarah Cohen, Tridib K. Goswami, Punnajit Lim, and Zeev Gross

Subjects
Male, 0301 basic medicine, Very low-density lipoprotein, Chromatography, Gas, Magnetic Resonance Spectroscopy, Porphyrins, lcsh:Medicine, Sulfides, Endoplasmic Reticulum, Microscopy, Atomic Force, Article, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Cell Line, Tumor, Humans, Corrole, lcsh:Science, Chromatography, High Pressure Liquid, chemistry.chemical_classification, Multidisciplinary, Chemistry, Endoplasmic reticulum, lcsh:R, Cryoelectron Microscopy, Hydrogen Peroxide, Flow Cytometry, Bioavailability, 030104 developmental biology, Transferrin, Lipophilicity, Biophysics, Nanoparticles, lcsh:Q, Microscopy, Electrochemical, Scanning, Lysosomes, Oxidation-Reduction, 030217 neurology & neurosurgery, Drug metabolism, Conjugate
Abstract

Recent work has highlighted the potential of metallocorroles as versatile platforms for the development of drugs and imaging agents, since the bioavailability, physicochemical properties and therapeutic activity can be dramatically altered by metal ion substitution and/or functional group replacement. Significant advances in cancer treatment and imaging have been reported based on work with a water-soluble bis-sulfonated gallium corrole in both cellular and rodent-based models. We now show that cytotoxicities increase in the order Ga

Published
2019

50. Prevalence of hepatitis C virus infection and the IL28B genotype polymorphism among blood donors and high-risk populations

Author

D. Teo, Rajneesh Kumar, Hwee Huang Tan, Kwai Peng Chan, Sobhana Thangaraju, Benjy Yi-Min Soh, Lina Hui Lin Choong, Wan Cheng Chow, Clement Yi-Hao Lin, and Victoria Ekstrom

Subjects
Halfway Houses, medicine.medical_specialty, education.field_of_study, High risk populations, business.industry, Hepatitis C virus, Population, virus diseases, Il28b genotype, General Medicine, Hepatitis C, 030204 cardiovascular system & hematology, medicine.disease, medicine.disease_cause, 03 medical and health sciences, 0302 clinical medicine, Polymorphism (computer science), Internal medicine, Genotype, medicine, Original Article, 030212 general & internal medicine, education, business
Abstract

INTRODUCTION To study the prevalence of hepatitis C virus (HCV) infection in blood donor (BD), haemodialysis (HD) and intravenous drug user (IVDU) populations in Singapore and assess the IL28B polymorphism if HCV positive. METHODS The BD population were healthy volunteers, the HD population were patients who were on haemodialysis for at least six months of follow-up between January 2009 and December 2014. IVDU population was from inmates at halfway houses who consented. RESULTS Between 2011 and 2014, of 161,658 individuals who underwent screening prior to blood donation, 95 (0.059%) were positive for HCV. Of the 42 sera available, common genotypes (GTs) were GT-3 (47.6%) and GT-1 (31.0%). Of 1,575 HD patients, 2.2% were anti-HCV positive. The HCV GT distribution was HCV GT-1 (32.4%), HCV GT-3 (20.5%) and GT-6 (8.8%). 83 halfway house inmates were screened. Of the 47 IVDUs, 36.2% were anti-HCV positive with predominant GT-3 (%). IL28B polymorphism was noted to be CC predominantly 85.3%. CONCLUSION Prevalence of HCV infection has decreased in both the BD and HD populations. However, it remains high in the IVDU population. GT-1 remains the most common in the HD population; however, GT-3 infection is now more common among the BD population in Singapore. IL28B - CC is the predominant variant among the HCV-infected individuals in Singapore.

Published
2019

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