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155. Contributors

Author

Abeles, Aryeh M., primary, Aglietti, Paolo, additional, Ali, Azhar A., additional, Amendola, Annunziato, additional, Anderson, Allen F., additional, Anderson, Christian Noel, additional, Archibald, Jason D., additional, Arendt, Elizabeth, additional, Argenson, Jean-Noël, additional, Austin, Amy F., additional, Bach, Bernard R., additional, Backstein, David, additional, Baer, Geoffrey S., additional, Bajaj, Sarvottam, additional, Baldini, Andrea, additional, Baldwin, Mark A., additional, Barber-Westin, Sue, additional, Barker, Joseph, additional, Beauchamp, Christopher P., additional, Bédard, Martin, additional, Berend, Keith R., additional, Berger, Richard A., additional, Bernasek, Thomas, additional, Berry, Daniel J., additional, Bert, Jack M., additional, Bonner, Kevin F., additional, Brekke, Adam C., additional, Briggs, Karen K., additional, Brockett, Claire L., additional, Brooks, Michael K., additional, Browne, James A., additional, Bryant, Brandon J., additional, Burak, Jarett S., additional, Burge, Alissa, additional, Bush-Joseph, Charles, additional, Buvanendran, Asokumar, additional, Callaghan, John, additional, Carter, Tom R., additional, Chen, Eli, additional, Chhabra, Anikar, additional, Chu, Constance R., additional, Clark, Randy, additional, Clarke, Henry D., additional, Cohen, David E., additional, Cole, Brian J., additional, Coon, Thomas M., additional, Currier, John H., additional, Cushner, Fred D., additional, Dahm, Diane L., additional, Damron, Timothy A., additional, DeAngelis, Joseph P., additional, Deasy, Bridget M., additional, DeJour, David, additional, Della Valle, Craig J., additional, Dellon, A. Lee, additional, Demey, Guillaume, additional, Dennis, Douglas A., additional, Deutsch, Ezra, additional, Dickey, Ian D., additional, Diduch, David R., additional, Easley, Mark E., additional, Economopoulos, Kostas, additional, Engh, Gerard A., additional, Fanelli, Gregory C., additional, Farr, Jack, additional, Farrell, Christopher M., additional, Fehring, Thomas K., additional, Feller, Julian, additional, Finnoff, Jonathan T., additional, Fisher, John, additional, Fitz, Wolfgang, additional, Fitzpatrick, Clare K., additional, Fletcher, John P., additional, Flynn, John M., additional, Franks, Andrew G., additional, Friedman, Richard J., additional, Friel, Nicole A., additional, Fu, Freddie H., additional, Fulkerson, John P., additional, Fullick, Robert Kyle, additional, Ganley, Theodore J., additional, Garbuz, Donald S., additional, Gharaibeh, Burhan, additional, Gill, Thomas J., additional, Goddard, Maria S., additional, Gomoll, Andreas, additional, Gonzalez, Carlos, additional, Gooding, Christopher R., additional, Grumet, Robert C., additional, Gwathmey, F. Winston, additional, Haas, Steve, additional, Hafez, Mahmoud, additional, Haidukewych, George J., additional, Hajnik, Christopher A., additional, Hanssen, Arlen D., additional, Harner, Christopher D., additional, Hart, Joseph M., additional, Healy, William L., additional, Heeckt, Peter F., additional, Henry, Sarah E., additional, Heyworth, Benton E., additional, Hinton, Richard Y., additional, Hofmann, Aaron A., additional, Hofmann, Siegfried, additional, Holt, Ginger E., additional, Horlocker, Terese T., additional, Howell, Stephen M., additional, Huard, Johnny, additional, Hui, Catherine, additional, Hulet, Christophe, additional, Hull, Maury L., additional, Hungerford, Marc W., additional, Infante, Anthony F., additional, Insall, John N., additional, Jacofsky, David J., additional, Jarvis, James G., additional, Jennings, Louise, additional, Johnston, Charles E., additional, Jonna, V. Karthik, additional, Keller, Thomas, additional, Kesselman, Donna R., additional, Kessler, Craig, additional, Khakharia, Saurabh, additional, Khanuja, Harpal S., additional, Kim, Raymond H., additional, Kim, Sung Jae, additional, Kissin, Yair D., additional, Klingele, Kevin, additional, Kocher, Mininder S., additional, Komistek, Richard D., additional, Konin, Gabrielle P., additional, Kopp, Sandra L., additional, Kopydlowski, Nathan, additional, Kramer, Dennis, additional, Kuenze, Christopher M., additional, Lachiewicz, Paul F., additional, Lang, Jason E., additional, Langford, Joshua R., additional, LaPrade, Robert F., additional, Laz, Peter J., additional, Leidl, Matthew, additional, Leone, James M., additional, Leszko, Filip, additional, Levi, David, additional, Levi, Gabriel, additional, Lewis, Randall J., additional, Lind, Martin, additional, Lindvall, Eric M., additional, Lionberger, David R., additional, Liporace, Frank A., additional, Logan, Martin, additional, Lombardi, Adolph V., additional, Long, William J., additional, Lonner, Jess H., additional, Lustig, Sébastien, additional, Lyons, Steven, additional, Maak, Travis G., additional, Macalena, Jeffrey A., additional, Madoff, Samuel D., additional, Maeno, Shinichi, additional, Magnussen, Robert A., additional, Maher, Suzanne A., additional, Mahfouz, Mohamed R., additional, Mai, Sabine, additional, Marinello, Patrick G., additional, Mason, J. Bohannon, additional, Masri, Bassam A., additional, Masur, Henry, additional, Math, Kevin R., additional, Mather, Richard C., additional, Mathis, Kenneth B., additional, Matsuda, Shuichi, additional, McCandless, Jeremy, additional, McClure, Kristen E., additional, Meneghini, R. Michael, additional, Miller, Mark, additional, Mintz, Douglas, additional, Mont, Michael A., additional, Moorman, Claude T., additional, Morris, Michael J., additional, Morrison, William B., additional, Morse, Kenneth R., additional, Mueller, John Kyle P., additional, Muellner, Thomas, additional, Murray, David, additional, Musahl, Volker, additional, Neel, Michael D., additional, Nelson, Joshua, additional, Nett, Michael P., additional, Neyret, Philippe, additional, Noble, Philip C., additional, Noyes, Frank R., additional, O’Connor, Mary I., additional, Oetgen, Matthew E., additional, Pagnano, Mark W., additional, Palestro, Christopher J., additional, Parratte, Sebastien, additional, Parsley, Brian S., additional, Patil, Nilesh, additional, Pedersen, Henrik B., additional, Peterson, Lars, additional, Pillinger, Michael H., additional, Pinczewski, Leo, additional, Post, William R., additional, Rachala, Sridhar R., additional, Radnay, Craig S., additional, Rana, Adam J., additional, Randall, R. Lor, additional, Reiffel, Robert S., additional, Ries, Michael D., additional, Robinson, Samuel P., additional, Rodeo, Scott A., additional, Rodkey, William G., additional, Rodriquez, Jose, additional, Roehrig, Gregory J., additional, Rosenberg, Aaron G., additional, Rosenthal, Pamela B., additional, Rullkoetter, Paul J., additional, Saggin, Paulo R.F., additional, Salmon, Lucy, additional, Sanders, Roy, additional, Schenck, Robert C., additional, Schindler, Oliver S., additional, Schreiber, Verena M., additional, Scott, Richard D., additional, Scott, Susan Craig, additional, Scott, W. Norman, additional, Scuderi, Giles R., additional, Seidenstein, Ari D., additional, Sekiya, Jon K., additional, Servien, Elvire, additional, Severson, Erik P., additional, Sgaglione, Nicholas A., additional, Sharma, Adrija, additional, Sherman, Seth L., additional, Shin, Michael S., additional, Siebert, Werner E., additional, Sierra, Rafael J., additional, Sikes, C. Van, additional, Skaggs, David L., additional, Smith, Gideon P., additional, Solomon, Gary E., additional, Spindler, Kurt P., additional, Spitzer, Andrew I., additional, Springer, Bryan D., additional, Steadman, J. Richard, additional, Stets, Kelly, additional, Stevens, Anna L., additional, Stiehl, James B., additional, Strauss, Eric J., additional, Stuart, Michael, additional, Stulberg, S. David, additional, Tannenbaum, Eric, additional, Taylor, Dean C., additional, Templeton, Kimberly, additional, Thompson, Stephen R., additional, Thornhill, Thomas, additional, Treme, Gehron, additional, Tria, Alfred J., additional, Turman, Kimberly A., additional, Uhthoff, Hans K., additional, Unger, Anthony S., additional, Vail, Thomas Parker, additional, Van Citters, Douglas W., additional, Van Thiel, Geoffrey S., additional, Vasiliadis, Haris S., additional, Vigorita, Vincent J., additional, Vince, Kelly G., additional, Violante, Bruno, additional, Voos, James E., additional, Vyas, Shail, additional, Walz, Daniel M., additional, Warwick, David, additional, Webber, Nicholas P., additional, Weiss, Jennifer, additional, Weiss, Kurt R., additional, Weissman, Barbara N., additional, Whiteside, Leo A., additional, Wickiewicz, Thomas L., additional, Williams, Bryan S., additional, Williams, Riley J., additional, Yen, Yi-Meng, additional, Zhang, Hong, additional, Zingde, Sumesh M., additional, and Zoga, Adam C., additional

Published
2012
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157. Contributors

Author

Abdollahi, Karim, primary, Ahmed, Shafeeq, additional, Ali, Mir Haroon, additional, Allen, David B., additional, Almekinders, Louis C., additional, Amendola, Annunziato, additional, Andrews, James R., additional, Arciero, Robert A., additional, Armstrong, April, additional, Atkinson, Robert E., additional, Baer, Geoffrey S., additional, Bahr, Roald, additional, Barber-Westin, Sue D., additional, Bederka, Bryce, additional, Bennett, J. Michael, additional, Best, Thomas M., additional, Beynnon, Bruce D., additional, Billante, Mark J., additional, Bonci, Leslie, additional, Borom, Andrew H., additional, Bradley, James P., additional, Branam, Barton R., additional, Brinker, Mark R., additional, Brockmeier, Stephen F., additional, Brodsky, James W., additional, Brown, David E., additional, Brown, Lauren, additional, Brown, Thomas E., additional, Brubaker, Shawn M., additional, Bruck, Nathan, additional, Buckwalter, Joseph A., additional, Burkhead, Wayne Z., additional, Busconi, Brian, additional, Butters, Kenneth P., additional, Canale, S. Terry, additional, Cantu, Robert C., additional, Cantu, Robert V., additional, Choi, Chang-Hyuk, additional, Choi, Luke, additional, Clanton, Thomas O., additional, Clement, Jack, additional, Cole, Brian J., additional, Corley, Fred G., additional, Craft, Jason A., additional, Curtis, Ralph J., additional, Cuomo, Frances, additional, DeBerardino, Thomas M., additional, Debski, Richard E., additional, DeHart, Marc M., additional, DeMaio, Marlene, additional, Deutsch, Allen, additional, Dexter, William W., additional, Diduch, David R., additional, Dillin, William, additional, Dugas, Jeffrey R., additional, Edson, Craig J., additional, Edwards, T. Bradley, additional, Eifert-Mangine, Marsha, additional, Eismont, Frank J., additional, Elkousy, Hussein, additional, Fanelli, Gregory C., additional, Ferretti, Mario, additional, Fetzer, Gary B., additional, Field, Larry D., additional, Fitzpatrick, Daniel C., additional, Ford, Kevin R., additional, Fowler, Donald E., additional, Frisella, W. Anthony, additional, Fu, Freddie H., additional, Gamez, Lorenzo, additional, Gamradt, Seth C., additional, Garrett, William E., additional, Gartsman, Gary M., additional, Gerber, Christian, additional, Giza, Eric, additional, Golish, S. Raymond, additional, Gómez, Jorge E., additional, Gomoll, Andreas H., additional, Griffin, Letha Y., additional, Grondin, Philippe P., additional, Grove, Andrew J., additional, Guttman, Dan, additional, Guyton, Gregory P., additional, Harner, Christopher D., additional, Harris, Justin D., additional, Hart, Jennifer A., additional, Hart, Joseph M., additional, Haskell, Andrew, additional, Herman, Martin J., additional, Hewett, Timothy E., additional, Hirose, Christopher B., additional, Honkamp, Nicholas J., additional, Huber, Florian G., additional, Ingari, Jack V., additional, Johnson, Darren L., additional, Johnson, Rob, additional, Johnson, Robert J., additional, Johnson, Ron M., additional, Keene, James S., additional, Khan, Sami O., additional, Kim, Richard Y., additional, Kirkendall, Donald T., additional, Kitchel, Scott H., additional, Klein, Sandra E., additional, Knopp, William, additional, Kocher, Mininder, additional, Koenig, Melissa D., additional, Krishnan, Sumant G., additional, Kron, Irving L., additional, Kuhn, John E., additional, LaPrade, Robert F., additional, Lauerman, William C., additional, Lawless, Christine, additional, Lebolt, James, additional, Cezar da Silva Leitao, Igor, additional, Lin, Kenneth C., additional, Lindenfeld, Thomas N., additional, Lisle, Turner C., additional, Lowe, Walter R., additional, Lunardini, David J., additional, Maffet, Mark W., additional, Mair, Jeffrey J., additional, Mangine, Robert, additional, Mann, Roger A., additional, Mastronarde, John G., additional, Mattacola, Carl G., additional, Mazzocca, Augustus D., additional, McBride, Wendy, additional, McCamey, Kendra, additional, McClincy, Michael P., additional, McDevitt, Edward R., additional, McMahon, Patrick J., additional, McVean, Jennifer J.F., additional, Middendorf, W. Andrew, additional, Miller, Chealon D., additional, Miller, Mark D., additional, Morrey, Bernard F., additional, Moutzouros, Vasilios, additional, Mow, Van C., additional, Myer, Gregory D., additional, Noyes, Frank R., additional, O'Brien, Eugene T., additional, Ocloo, Agbecko, additional, O'Connor, Daniel P., additional, Okeke, Nnamdi, additional, Owens, Brett D., additional, Paine, Russ, additional, Parekh, Selene G., additional, Parham, William D., additional, Parker, Richard D., additional, Parsons, Johnathan P., additional, Patel, Jayesh K., additional, Paterno, Mark V., additional, Petrie, Russell S., additional, Pizzutillo, Peter D., additional, Pleacher, Michael D., additional, Postolache, Teodor T., additional, Provencher, Matthew T., additional, Ranawat, Anil S., additional, Rauh, Michael A., additional, Regan, William D., additional, Reynolds, Scott B., additional, Richardson, David R., additional, Riehl, John T., additional, Ring, David, additional, Rinheimer, Kristin N., additional, Robinson, Samuel P., additional, Rockwood, Charles A., additional, Rodeo, Scott A., additional, Romeo, Anthony A., additional, Rosenwasser, Melvin P., additional, Rosipal, Charles E., additional, Sanders, Timothy G., additional, Savoie, Felix H., additional, Saxton, David L., additional, Schorfhaar, Andrew J., additional, Sekiya, Jon K., additional, Shah, Agam, additional, Shen, Wei, additional, Shepler, Thomas, additional, Silvers, Holly J., additional, Singhal, Manuj, additional, Steiner, Timothy, additional, Steinmann, Scott P., additional, Sullivan, J. Andy, additional, Taylor, Dean C., additional, Tejwani, Samir G., additional, Thomas, Richard J., additional, Thompson, Paul D., additional, Tomaszewski, Daniel J., additional, Topper, Steven M., additional, Torg, Joseph S., additional, Vangsness, C. Thomas, additional, von Knoch, Marius, additional, Wapner, Keith L., additional, Warren, Russell F., additional, Waterman, Scott, additional, Watkins, Robert G., additional, Whatley, Adam Nelson, additional, Wickwire, Alexis C., additional, Wilkins, Kaye E., additional, Williams, Gerald R., additional, Williams, Matthew D., additional, Wirth, Michael A., additional, Wolfe, Valerie M., additional, Wolters, Brett W., additional, Woo, Savio L.-Y., additional, Wood, Robert M., additional, Wood, Virchel E., additional, Yanke, Adam, additional, Zavala, John A., additional, and Zupanc, Mary L., additional

Published
2010
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158. Um sistema computacional para auxiliar no planejamento de cortes em bobinas de aço

Author

Robinson Samuel Hoto, Fernando Spolador, and Nelson Maculan

Subjects
Problema de corte, Duas fases, Padrões compartimentados., Technology (General), T1-995, Science (General), Q1-390
Abstract

O planejamento de cortes em bobinas de aço é um problema de otimização combinatória. Algumas empresas do setor de metalurgia efetuam a laminação a frio do aço destas bobinas para que ele adquira propriedades físicas desejáveis. Nesse caso, os padrões de corte devem ser compostos por compartimentos de itens compatíveis para o processo de laminação, dificultando a tarefa do planejamento dos cortes. Um compartimento representa uma bobina intermediária a ser laminada, de modo que é possível combinar bobinas intermediárias com diferentes necessidades de laminação em uma mesma bobina do estoque. Neste trabalho, é apresentado o sistema RollCut, que auxilia o planejamento dos cortes de bobinas.

Published
2007
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159. Problemas de corte em duas fases: uma revisão parcial

Author

Robinson Samuel Hoto, Fernando Spolador, Marcos Arenales, and Nelson Maculan

Subjects
Corte e empacotamento, Duas fases, Padrões compartimentados., Technology (General), T1-995, Science (General), Q1-390
Abstract

Problemas de Corte e Empacotamento são amplamente estudados e diversos trabalhos a respeito do tema podem ser encontrados na literatura, seja no aspecto puramente teórico, seja nas aplicações práticas. Dentre estes inúmeros problemas, alguns autores relataram ao longo dos anos, casos em que o processo de corte necessita ser efetuado em duas fases. Este trabalho, que é parcial, pretende iniciar uma revisão de problemas de corte em duas fases.

Published
2007
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162. Tissue engineered autologous cartilage-bone grafts for temporomandibular joint regeneration

Author

Chen, David, primary, Wu, Josephine Y., additional, Kennedy, Kelsey M., additional, Yeager, Keith, additional, Bernhard, Jonathan C., additional, Ng, Johnathan J., additional, Zimmerman, Brandon K., additional, Robinson, Samuel, additional, Durney, Krista M., additional, Shaeffer, Courtney, additional, Vila, Olaia F., additional, Takawira, Catherine, additional, Gimble, Jeffrey M., additional, Guo, X. Edward, additional, Ateshian, Gerard A., additional, Lopez, Mandi J., additional, Eisig, Sidney B., additional, and Vunjak-Novakovic, Gordana, additional

Published
2020
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163. Neurotoxic peptides from the venom of the giant Australian stinging tree

Author

Gilding, Edward K., primary, Jami, Sina, additional, Deuis, Jennifer R., additional, Israel, Mathilde R., additional, Harvey, Peta J., additional, Poth, Aaron G., additional, Rehm, Fabian B. H., additional, Stow, Jennifer L., additional, Robinson, Samuel D., additional, Yap, Kuok, additional, Brown, Darren L., additional, Hamilton, Brett R., additional, Andersson, David, additional, Craik, David J., additional, Vetter, Irina, additional, and Durek, Thomas, additional

Published
2020
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172. The Tarantula Venom Peptide Eo1a Binds to the Domain II S3-S4 Extracellular Loop of Voltage-Gated Sodium Channel NaV1.8 to Enhance Activation.

Author

Deuis, Jennifer R., Ragnarsson, Lotten, Robinson, Samuel D., Dekan, Zoltan, Chan, Lerena, Jin, Ai-Hua, Tran, Poanna, McMahon, Kirsten L., Li, Shengnan, Wood, John N., Cox, James J., King, Glenn F., Herzig, Volker, and Vetter, Irina

Subjects
SODIUM channels, PEPTIDES, VENOM, TARANTULAS, CONUS, BINDING sites
Abstract

Venoms from cone snails and arachnids are a rich source of peptide modulators of voltage-gated sodium (NaV) channels, however relatively few venom-derived peptides with activity at the mammalian NaV1.8 subtype have been isolated. Here, we describe the discovery and functional characterisation of β-theraphotoxin-Eo1a, a peptide from the venom of the Tanzanian black and olive baboon tarantula Encyocratella olivacea that modulates NaV1.8. Eo1a is a 37-residue peptide that increases NaV1.8 peak current (EC50 894 ± 146 nM) and causes a large hyperpolarising shift in both the voltage-dependence of activation (ΔV50–20.5 ± 1.2 mV) and steady-state fast inactivation (ΔV50–15.5 ± 1.8 mV). At a concentration of 10 μM, Eo1a has varying effects on the peak current and channel gating of NaV1.1–NaV1.7, although its activity is most pronounced at NaV1.8. Investigations into the binding site of Eo1a using NaV1.7/NaV1.8 chimeras revealed a critical contribution of the DII S3-S4 extracellular loop of NaV1.8 to toxin activity. Results from this work may form the basis for future studies that lead to the rational design of spider venom-derived peptides with improved potency and selectivity at NaV1.8. [ABSTRACT FROM AUTHOR]

Published
2022
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173. The three-dimensional structure of an H-superfamily conotoxin reveals a granulin fold arising from a common ICK cysteine framework

Author

Nielsen, Lau D, Foged, Mads M., Albert, Anastasia, Bertelsen, Andreas B., Søltoft, Cecilie L, Robinson, Samuel D., Petersen, Steen Vang, Purcell, Anthony W., Olivera, Baldomero M., Norton, Raymond S., Vasskog, Terje, Safavi-Hemami, Helena, Teilum, Kaare, Ellgaard, Lars, Nielsen, Lau D, Foged, Mads M., Albert, Anastasia, Bertelsen, Andreas B., Søltoft, Cecilie L, Robinson, Samuel D., Petersen, Steen Vang, Purcell, Anthony W., Olivera, Baldomero M., Norton, Raymond S., Vasskog, Terje, Safavi-Hemami, Helena, Teilum, Kaare, and Ellgaard, Lars

Abstract

Venomous marine cone snails produce peptide toxins (conotoxins) that bind ion channels and receptors with high specificity and therefore are important pharmacological tools. Conotoxins contain conserved cysteine residues that form disulfide bonds that stabilize their structures. To gain structural insight into the large, yet poorly characterized conotoxin H-superfamily, we used NMR and CD spectroscopy along with MS-based analyses to investigate H-Vc7.2 from Conus victoriae, a peptide with a VI/VII cysteine framework. This framework has CysI-CysIV/CysII-CysV/CysIII-CysVI connectivities, which have invariably been associated with the inhibitor cystine knot (ICK) fold. However, the solution structure of recombinantly expressed and purified H-Vc7.2 revealed that although it displays the expected cysteine connectivities, H-Vc7.2 adopts a different fold consisting of two stacked β-hairpins with opposing β-strands connected by two parallel disulfide bonds, a structure homologous to the N-terminal region of the human granulin protein. Using structural comparisons, we subsequently identified several toxins and nontoxin proteins with this "mini-granulin" fold. These findings raise fundamental questions concerning sequence-structure relationships within peptides and proteins and the key determinants that specify a given fold.

Published
2019

174. Expression of the oxygen-sensitive transcription factor subunit HIF-1 alpha in patients suffering from secondary Raynaud syndrome

Author

Heger, Lukas Andreas, Kerber, Mark, Hortmann, Marcus, Robinson, Samuel, Mauler, Maximilian, Stallmann, Daniela, Duerschmied, Daniel, Bode, Christoph, Hehrlein, Christoph, Ahrens, Ingo, Heger, Lukas Andreas, Kerber, Mark, Hortmann, Marcus, Robinson, Samuel, Mauler, Maximilian, Stallmann, Daniela, Duerschmied, Daniel, Bode, Christoph, Hehrlein, Christoph, and Ahrens, Ingo

Abstract

Anti-ischemic therapy remains a challenge due to the complexity of hypoxia response pathways. Hypoxia-inducible factor (HIF)-1 is a heterodimer transcription factor consisting of 2 subunits, HIF-1 alpha and HIF-1 beta. Hypoxia-dependent activation of HIF-1 alpha regulates cellular O-2 homeostasis. Raynaud syndrome (RS), as a comorbidity of the autoimmune disease systemic sclerosis (SS), is characterized by vasospasms that limit blood flow to the limbs, resulting in hypoxia. A single-center randomized study was conducted to compare prostaglandin E1 (PgE1) therapy with a treatment combining PgE1 and an endothelin-1 blocker, bosentan. A total of 30 patients suffering from SS with RS were enrolled. We examined the regulation of HIF-1 alpha, its target heme oxygenase-1 (HMOX-1), and the serum levels of the HIF-1 alpha protein in a subset of patients as well as in ten healthy individuals. The expression of HIF-1 alpha and HMOX-1 in monocytes was measured using absolute plasmid-based quantitative real-time PCR, whereas serum HIF-1 alpha levels were measured with ELISA. Samples were taken at the time of randomization and after 24 weeks. We found that HIF-1 alpha and HMOX-1 mRNA expression in monocytes and serum HIF-1 alpha protein levels were significantly higher in the SS/RS patients compared to the healthy control group. Single-drug therapy significantly increased HIF-1 alpha and HMOX-1 mRNA expression in monocytes and serum HIF-1 alpha protein levels in the SS/RS patients compared to those at the time of randomization, whereas combining PgE1 with an endothelin-1 blocker prevented the further increases in HIF-1 alpha and HMOX-1 expression. We propose HIF-1 alpha and HMOX-1 as novel markers for anti-ischemic therapy in RS.

Published
2019

175. The mitochondria-targeting peptide elamipretide diminishes circulating HtrA2 in ST-segment elevation myocardial infarction

Author

Hortmann, Marcus, Robinson, Samuel, Mohr, Moritz, Mauler, Maximillian, Stallmann, Daniela, Reinoehl, Jochen, Duerschmied, Daniel, Peter, Karlheinz, Carr, James, Gibson, C. Michael, Bode, Christoph, Ahrens, Ingo, Hortmann, Marcus, Robinson, Samuel, Mohr, Moritz, Mauler, Maximillian, Stallmann, Daniela, Reinoehl, Jochen, Duerschmied, Daniel, Peter, Karlheinz, Carr, James, Gibson, C. Michael, Bode, Christoph, and Ahrens, Ingo

Abstract

Background: The extent of myocardial damage in patients with ST-segment elevation myocardial infarction (STEMI) depends on both the time to reperfusion as well as injury induced by ischaemia-reperfusion resulting in a cascade of cellular and humoral reactions. As a consequence of ischaemia-reperfusion in the heart, the high-temperature requirement serine peptidase 2 (HtrA2) is translocated from the mitochondria to the cytosol, whereupon it induces protease activity-dependent apoptosis mediated via caspases. Myocardial damage induced by reperfusion cannot be monitored due to a current lack in specific biomarkers. We examined the serum level of HtrA2 as a potentially novel biomarker for mitochondrial-induced cardiomyocyte apoptosis. Methods: After informed consent, peripheral blood was obtained from patients (n=19) with first-time acute anterior STEMI after percutaneous coronary intervention. Within this group, 10 of the patients received the mitochondria-targeting peptide elamipretide (phase 2a clinical study EMBRACE (NCT01572909)). Blood was also obtained from a control group of healthy donors (n=16). The serum level of HtrA2 was measured by an enzyme-linked immunosorbent assay (ELISA). In a murine model of myocardial ischaemia-reperfusion injury, HtrA2 was determined in plasma by ELISA after left anterior descending artery occlusion. Results: HtrA2 median was significantly increased in patients with STEMI compared to healthy controls 392.4 (240.7-502.8) pg/mL vs. 1805.5 (981.3-2220.1) pg/mL (P <= 0.05). Elamipretide significantly reduced the HtrA2 median serum level after myocardial infarction 1805.5 (981.3-2220.1) pg/mL vs. 496.5 (379.4-703.8) pg/mL (P <= 0.05). Left anterior descending artery occlusion in mice significantly increased HtrA2 mean in plasma (117.4 fg/ml +/- SEM 28.1 vs. 525.2 fg/ml +/- SEM 96; P <= 0.05). Conclusion: Compared to healthy controls, we found significantly increased serum levels of HtrA2 in patients with STEMI. The result was validated

Published
2019

177. GEM detector conductor manufacturing experience

Author

Martovetsky, Nicolai N., Pace, James R., Reardon, Paul J., Richied, Donald E., Camille, Richard J., Marston, Peter G., Smith, Bradford Smith, Deis, Gary A., Bohanan, Jeff S., Gertsen, John H., Heck, Jack L., Howell, L. Neville, Robinson, Samuel C., and Marti, Hanspeter

Subjects
Superconductors -- Design and construction, Electric conductors -- Design and construction, Business, Electronics, Electronics and electrical industries
Abstract

Feasibility studies concerning the manufacture of cable-in-conduit conductors for the GEM detector magnet are presented. Specifically, the fabrication of the niobium titanium strands, twisted cables and conduits are discussed along with methods of cable pulling, aluminum sheath assembly and aluminum sheath welding. These experiments revealed that CICC cables of niobium titanium require post-cabling annealing when the required residual resistivity ratio is higher than 130.

Published
1995

179. Fusobacterium nucleatum secretes amyloid-like FadA to enhance pathogenicity.

Author

Qing Meng, Qiuqiang Gao, Mehrazarin, Shebli, Tangwanichgapong, Kamonchanok, Yu Wang, Yiming Huang, Yutong Pan, Robinson, Samuel, Ziwen Liu, Zangiabadi, Amirali, Lux, Renate, Papapanou, Panos N., Guo, X. Edward, Wang, Harris, Berchowitz, Luke E., and Han, Yiping W.

Abstract

Fusobacterium nucleatum (Fn) is a Gram-negative oral commensal, prevalent in various human diseases. It is unknown how this common commensal converts to a rampant pathogen. We report that Fn secretes an adhesin (FadA) with amyloid properties via a Fap2-like autotransporter to enhance its virulence. The extracellular FadA binds Congo Red, Thioflavin-T, and antibodies raised against human amyloid b42. Fn produces amyloid-like FadA under stress and disease conditions, but not in healthy sites or tissues. It functions as a scaffold for biofilm formation, confers acid tolerance, and mediates Fn binding to host cells. Furthermore, amyloidlike FadA induces periodontal bone loss and promotes CRC progression in mice, with virulence attenuated by amyloid-binding compounds. The uncleaved signal peptide of FadA is required for the formation and stability of mature amyloid FadA fibrils. We propose a model in which hydrophobic signal peptides serve as "hooks" to crosslink neighboring FadA filaments to form a stable amyloid-like structure. Our study provides a potential mechanistic link between periodontal disease and CRC and suggests antiamyloid therapies as possible interventions for Fn-mediated disease processes. [ABSTRACT FROM AUTHOR]

Published
2021
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180. SARS-CoV-2 Viral Load in the Nasopharynx at Time of First Infection Among Unvaccinated Individuals: A Secondary Cross-Protocol Analysis of 4 Randomized Trials.

Author

Fisher, Leigh H., Kee, Jia Jin, Liu, Albert, Espinosa, Claudia M., Randhawa, April K., Ludwig, James, Magaret, Craig A., Robinson, Samuel T., Gilbert, Peter B., Hyrien, Ollivier, Kublin, James G., Rouphael, Nadine, Falsey, Ann R., Sobieszczyk, Magdalena E., El Sahly, Hana M., Grinsztejn, Beatriz, Gray, Glenda E., Kotloff, Karen L., Gay, Cynthia L., and Leav, Brett

Published
2024
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181. Hiding in Plain Sight: An Exploration of the Classification of LGBT Materials in Libraries and Bookstores

Author

Robinson, Samuel

Subjects
Library of Congress classification, LGBT literature, Dewey decimal classification, LGBT library materials, LGBT literary prizes, Classification of books
Abstract

The goal of this study has been to analyze the classification of prominent, award winning books on LGBT topics, to see how these topics are being treated in libraries and bookstores today. These materials have, in the past, been placed in a variety of locations throughout the library, sometimes with unsavory connotations. This study, however, does more to show the limited reach of even the most acclaimed fiction and nonfiction LGBT titles in today’s libraries and bookstores, with eleven books from the sample appearing in three or fewer institutions. Those books that were frequently held across all institutions visited were frequently organized alphabetically by author or topic, and very few of them were discoverable or browsable based upon their LGBT content.

Published
2018
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184. Characterization of the First Conotoxin from Conus ateralbus, a Vermivorous Cone Snail from the Cabo Verde Archipelago

Author

Neves, Jorge L. B., primary, Imperial, Julita S., additional, Morgenstern, David, additional, Ueberheide, Beatrix, additional, Gajewiak, Joanna, additional, Antunes, Agostinho, additional, Robinson, Samuel D., additional, Espino, Samuel, additional, Watkins, Maren, additional, Vasconcelos, Vitor, additional, and Olivera, Baldomero M., additional

Published
2019
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185. Na V 1.6 regulates excitability of mechanosensitive sensory neurons

Author

Israel, Mathilde R., primary, Tanaka, Brian S., additional, Castro, Joel, additional, Thongyoo, Panumart, additional, Robinson, Samuel D., additional, Zhao, Peng, additional, Deuis, Jennifer R., additional, Craik, David J., additional, Durek, Thomas, additional, Brierley, Stuart M., additional, Waxman, Stephen G, additional, Dib‐Hajj, Sulayman D., additional, and Vetter, Irina, additional

Published
2019
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186. The three-dimensional structure of an H-superfamily conotoxin reveals a granulin fold arising from a common ICK cysteine framework

Author

Nielsen, Lau D., primary, Foged, Mads M., additional, Albert, Anastasia, additional, Bertelsen, Andreas B., additional, Søltoft, Cecilie L., additional, Robinson, Samuel D., additional, Petersen, Steen V., additional, Purcell, Anthony W., additional, Olivera, Baldomero M., additional, Norton, Raymond S., additional, Vasskog, Terje, additional, Safavi-Hemami, Helena, additional, Teilum, Kaare, additional, and Ellgaard, Lars, additional

Published
2019
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188. Fish-hunting cone snail venoms are a rich source of minimized ligands of the vertebrate insulin receptor

Author

Ahorukomeye, Peter, primary, Disotuar, Maria M, primary, Gajewiak, Joanna, additional, Karanth, Santhosh, additional, Watkins, Maren, additional, Robinson, Samuel D, additional, Flórez Salcedo, Paula, additional, Smith, Nicholas A, additional, Smith, Brian J, additional, Schlegel, Amnon, additional, Forbes, Briony E, additional, Olivera, Baldomero, additional, Hung-Chieh Chou, Danny, additional, and Safavi-Hemami, Helena, additional

Published
2019
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189. Author response: Fish-hunting cone snail venoms are a rich source of minimized ligands of the vertebrate insulin receptor

Author

Ahorukomeye, Peter, primary, Disotuar, Maria M, primary, Gajewiak, Joanna, additional, Karanth, Santhosh, additional, Watkins, Maren, additional, Robinson, Samuel D, additional, Flórez Salcedo, Paula, additional, Smith, Nicholas A, additional, Smith, Brian J, additional, Schlegel, Amnon, additional, Forbes, Briony E, additional, Olivera, Baldomero, additional, Hung-Chieh Chou, Danny, additional, and Safavi-Hemami, Helena, additional

Published
2018
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192. Production, composition, and mode of action of the painful defensive venom produced by a limacodid caterpillar, Doratifera vulnerans.

Author

Walker, Andrew A., Robinson, Samuel D., Paluzzi, Jean-Paul V., Merritt, David J., Nixon, Samantha A., Schroeder, Christina I., Jin, Jiayi, Goudarzi, Mohaddeseh Hedayati, Kotze, Andrew C., Dekan, Zoltan, Sombke, Andy, Alewood, Paul F., Fry, Bryan G., Epstein, Marc E., Vetter, Irina, and King, Glenn F.

Subjects
*VENOM, *SPIDER venom, *PEPTIDOMIMETICS, *MOLECULAR evolution, *CONVERGENT evolution
Abstract

Venoms have evolved independently several times in Lepidoptera. Limacodidae is a family with worldwide distribution, many of which are venomous in the larval stage, but the composition and mode of action of their venom is unknown. Here, we use imaging technologies, transcriptomics, proteomics, and functional assays to provide a holistic picture of the venom system of a limacodid caterpillar, Doratifera vulnerans. Contrary to dogma that defensive venoms are simple in composition, D. vulnerans produces a complex venom containing 151 proteinaceous toxins spanning 59 families, most of which are peptides <10 kDa. Three of the most abundant families of venom peptides (vulnericins) are 1) analogs of the adipokinetic hormone/corazonin-related neuropeptide, some of which are picomolar agonists of the endogenous insect receptor; 2) linear cationic peptides derived from cecropin, an insect innate immune peptide that kills bacteria and parasites by disrupting cell membranes; and 3) disulfide-rich knottins similar to those that dominate spider venoms. Using venom fractionation and a suite of synthetic venom peptides, we demonstrate that the cecropin-like peptides are responsible for the dominant pain effect observed in mammalian in vitro and in vivo nociception assays and therefore are likely to cause pain after natural envenomations by D. vulnerans. Our data reveal convergent molecular evolution between limacodids, hymenopterans, and arachnids and demonstrate that lepidopteran venoms are an untapped source of novel bioactive peptides. [ABSTRACT FROM AUTHOR]

Published
2021
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193. Knowledge and attitudes of Australian dermatologists towards sentinel lymph node biopsy for melanoma: a mixed methods study.

Author

Smith, Andrea L, Watts, Caroline G, Robinson, Samuel, Schmid, Helen, Goumas, Chris, Mar, Victoria J, Thompson, John F, Rapport, Frances, Cust, Anne E, Braithwaite, J, Gyorki, DE, Henderson, M, Hong, AM, Kelly, JW, Long, GV, Menzies, AM, Morton, RL, Saw, RPM, Scolyer, RA, and Spillane, AJ

Subjects
SENTINEL lymph node biopsy, MELANOMA, CANCER patients, DERMATOLOGISTS, ATTITUDE (Psychology)
Abstract

Background/Objectives: In melanoma management, sentinel lymph node biopsy (SLNB) is used to stage patients and to indicate prognosis. More recently, it has been used to select patients for adjuvant therapy. This study aimed to report knowledge of and attitudes towards SLNB for patients with melanoma among Australian dermatologists. Methods: Mixed methods study using cross‐sectional questionnaires (n = 88) and semi‐structured interviews (n = 13), May–September 2019. Results: Of the dermatologists surveyed, 56% thought SLNB had an important role in melanoma management, 26% were unsure and 18% thought SLNB unimportant. Of the 92% who would discuss SLNB with their patients, the main stated value of SLNB was for assessing eligibility for adjuvant therapies (79%); only 60% indicated SLNB was of value for providing prognostic information, and just over half (53%) thought it could improve staging. Interview data indicated that attitudes towards SLNB are shifting among dermatologists, driven by data from landmark clinical trials and the influence of professional networks. Accordingly, interviewees adopted one of three positions in relation to SLNB: (a) believed in utility of SLNB and adhered to the guidelines; (b) were unconvinced about utility of SLNB but adhered to the guidelines; and (c) were unconvinced about utility of SLNB and did not adhere to the guidelines. Conclusion: Although most of the dermatologists surveyed were familiar with and follow the SLNB recommendations, some disagreement with and distrust of the recommendations was evident. Greater acceptance of the SLNB recommendations appeared to be driven by the improved outcomes demonstrated in stage III patients receiving adjuvant systemic therapy. [ABSTRACT FROM AUTHOR]

Published
2021
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194. The zebrafish grime mutant uncovers an evolutionarily conserved role for Tmem161b in the control of cardiac rhythm.

Author

Koopman, Charlotte D., De Angelis, Jessica, Iyer, Swati P., Verkerk, Arie O., Da Silva, Jason, Berecki, Geza, Jeanes, Angela, Baillie, Gregory J., Paterson, Scott, Uribe, Veronica, Ehrlich, Ophelia V., Robinson, Samuel D., Garric, Laurence, Petrou, Steven, Simons, Cas, Vetter, Irina, Hogan, Benjamin M., de Boer, Teun P., Bakkers, Jeroen, and Smith, Kelly A.

Subjects
ARRHYTHMIA, BRACHYDANIO, CELL imaging, RHYTHM, BLOOD flow, COMMERCIAL products
Abstract

The establishment of cardiac function in the developing embryo is essential to ensure blood flow and, therefore, growth and survival of the animal. The molecular mechanisms controlling normal cardiac rhythm remain to be fully elucidated. From a forward genetic screen, we identified a unique mutant, grime, that displayed a specific cardiac arrhythmia phenotype. We show that loss-of-function mutations in tmem161b are responsible for the phenotype, identifying Tmem161b as a regulator of cardiac rhythm in zebrafish. To examine the evolutionary conservation of this function, we generated knockout mice for Tmem161b. Tmem161b knockout mice are neonatal lethal and cardiomyocytes exhibit arrhythmic calcium oscillations. Mechanistically, we find that Tmem161b is expressed at the cell membrane of excitable cells and live imaging shows it is required for action potential repolarization in the developing heart. Electrophysiology on isolated cardiomyocytes demonstrates that Tmem161b is essential to inhibit Ca2+ and K+ currents in cardiomyocytes. Importantly, Tmem161b haploinsufficiency leads to cardiac rhythm phenotypes, implicating it as a candidate gene in heritable cardiac arrhythmia. Overall, these data describe Tmem161b as a highly conserved regulator of cardiac rhythm that functions to modulate ion channel activity in zebrafish and mice. [ABSTRACT FROM AUTHOR]

Published
2021
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195. Chip-based digital PCR as a novel detection method for quantifying microRNAs in acute myocardial infarction patients

Author

Robinson, Samuel, Follo, Marie, Haenel, David, Mauler, Maximilian, Stallmann, Daniela, Andreas, Lukas Heger, Helbing, Thomas, Duerschmied, Daniel, Peter, Karlheinz, Bode, Christoph, Ahrens, Ingo, Hortmann, Marcus, Robinson, Samuel, Follo, Marie, Haenel, David, Mauler, Maximilian, Stallmann, Daniela, Andreas, Lukas Heger, Helbing, Thomas, Duerschmied, Daniel, Peter, Karlheinz, Bode, Christoph, Ahrens, Ingo, and Hortmann, Marcus

Abstract

miRNAs have shown promise as potential biomarkers for acute myocardial infarction (AMI). However, the current used quantitative real-time PCR (qRT-PCR) allows solely for relative expression of nucleic acids and it is susceptible to day-to-day variability, which has limited the validity of using the miRNAs as biomarkers. In this study we explored the technical qualities and diagnostic potential of a new technique, chip-based digital PCR, in quantifying the miRNAs in patients with AMI and ischaemia-reperfusion injury (I/R). In a dilution series of synthetic C elegans-miR-39, chip-based digital PCR displayed a lower coefficient of variation (8.9% vs 46.3%) and a lower limit of detection (0.2 copies/mu L vs 1.1 copies/mu L) compared with qRT-PCR. In the serum collected from 24 patients with ST-elevation myocardial infarction (STEMI) and 20 patients with stable coronary artery disease (CAD) patients after percutaneous coronary intervention (PCI), we used qRT-PCR and multiplexed chip-based digital PCR to quantify the serum levels of miRNA-21 and miRNA-499 as they have been validated in AMI in prior studies. In STEMI, I/R injury was assessed via measurement of ST-segment resolution (ST-R). Chip-based digital PCR revealed a statistical significance in the difference of miR-21 levels between stable CAD and STEMI groups (118.8 copies/mu L vs 59 copies/mu L; P=0.0300), whereas qRT-PCR was unable to reach significance (136.4 copies/mu L vs 122.8 copies/mu L; P=0.2273). For miR-499 levels, both chip-based digital PCR and qRT-PCR revealed statistically significant differences between stable CAD and STEMI groups (2 copies/mu L vs 8.5 copies/mu L, P=0.0011; 0 copies/mu L vs 19.4 copies/mu L; P<0.0001). There was no association between miR-21/499 levels and ST-R post-PCI. Our results show that the chip-based digital PCR exhibits superior technical qualities and promises to be a superior method for quantifying miRNA levels in the circulation, which may become a more accurate and repr

Published
2018

196. Digital PCR for Quantifying Circulating MicroRNAs in Acute Myocardial Infarction and Cardiovascular Disease

Author

Benning, Louise, Robinson, Samuel, Follo, Marie, Heger, Lukas Andreas, Stallmann, Daniela, Duerschmied, Daniel, Bode, Christoph, Ahrens, Ingo, Hortmann, Marcus, Benning, Louise, Robinson, Samuel, Follo, Marie, Heger, Lukas Andreas, Stallmann, Daniela, Duerschmied, Daniel, Bode, Christoph, Ahrens, Ingo, and Hortmann, Marcus

Abstract

Circulating serum microRNAs (miRNAs) have shown promise as biomarkers for the cardiovascular disease and acute myocardial infarction (AMI), being released from the cardiovascular cells into the circulation. Circulating miRNAs are highly stable and can be quantified. The quantitative expression of specific miRNAs can be linked to the pathology, and some miRNAs show high tissue and disease specificity. Finding novel biomarkers for cardiovascular diseases is of importance for medical research. Quite recently, digital polymerase chain reaction (dPCR) has been invented. dPCR, combined with fluorescent hydrolysis probes, enables specific direct absolute quantification. dPCR exhibits superior technical qualities, including a low variability, high linearity, and high sensitivity compared to the quantitative polymerase chain reaction (qPCR). Thus, dPCR is a more accurate and reproducible method for directly quantifying miRNAs, particularly for the use in large multi-center cardiovascular clinical trials. In this publication, we describe how to effectively perform digital PCR in order to assess the absolute copy number in serum samples.

Published
2018

197. Peptides from the venomous marine snail Conus victoriae: identification, characterisation and potential applications

Author

Robinson, Samuel David

Subjects
complex mixtures, Uncategorized
Abstract

Animal venoms represent a vast library of bioactive peptides and proteins with proven potential not only as research tools but also as drug leads and therapeutics. Several drugs based on venom peptides have been approved for the treatment of medical conditions including diabetes, hypertension and chronic pain. An additional ten in clinical trials, as well as several others in preclinical stages of development, have the potential to treat a wider range of conditions, including cancer, HIV, myocardial infarction, stroke, heart failure and multiple sclerosis. Components from the venoms of cone snails (genus Conus) show particular promise, with each Conus venom consisting of a mixture of hundreds of peptides (conotoxins) with a diverse array of molecular targets. Several conotoxins have found applications as important research tools, while some are being used or developed as therapeutics. Chapter 1 is structured as a review of conotoxins in the context of gene superfamily. The overall objective of the research described in this thesis has been the discovery, functional and structural characterisation, and optimisation (for a therapeutic endpoint) of conotoxins from an Australian species of cone snail, Conus victoriae. The initial discovery phase involved the generation of a C. victoriae venom gland transcriptome. To this end, a combination of state-of-the-art techniques in molecular biology and bioinformatics was utilized, including cDNA library normalization, high-throughput 454 sequencing, de novo transcriptome assembly and annotation with BLAST and profile hidden Markov models (pHMMs). Over 100 unique conotoxin sequences from 20 gene superfamilies were discovered (the largest and most diverse Conus venom gland library published to date), as described in Chapter 2. Subsequent matching of the transcriptome to a mass spectrometry profile of the crude venom was used to interrogate venom peptide composition and confirm post-translational modifications present in the mature venom peptides. Promising peptides were chosen for further functional and structural characterisation and produced synthetically. Chapter 3 describes the structural characterisation of one such peptide, contryphan_Vc1 and the subsequent discovery of a new elementary peptide fold and its potential application. Chapter 4 describes the unique method of discovery and interesting activity profile of another novel peptide, CNF-Vc1. One potential drawback of conotoxins as potential therapeutics is that they suffer from the generic problems of peptides in vivo. Significant efforts are being made in modifying peptides to improve their therapeutic potential. In the final chapter of this thesis, this step in venom peptide drug development is illustrated with the modification of α-conotoxin-Vc1.1, an analgesic peptide from the venom of C. victoriae. The approach used was the selective replacement of the native disulfides in the peptide with non-reducible dicarba bridges in an effort to improve its in vivo stability profile. Importantly, this modification resulted in a more favourable selectivity profile for the peptide, which may further improve its therapeutic utility. Awards: Winner of the Mollie Holman Doctoral Medal for Excellence, Faculty of Pharmacy and Pharmaceutical Sciences, 2015.

Published
2017
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198. Optimized channel allocation in emerging mobile cellular networks.

Author

Asuquo, Daniel, Ekpenyong, Moses, Udoh, Samuel, Robinson, Samuel, and Attai, Kingsley

Subjects
STANDARD deviations, QUALITY of service, BACK propagation, ALGORITHMS, SOFT computing
Abstract

The task of optimizing service quality in wireless networks is a continuous research that requires the design of efficient channel allocation schemes. The problem is how limited channel resources can be maximally utilized, to guarantee seamless communication while maintaining excellent service quality. Whereas, fixed channel allocation (FCA) schemes treat new and handoff calls equally without preference to normally prioritized handoff calls; dynamic channel allocation (DCA) schemes accommodate users mobility in randomly changing network conditions. However, classical Erlang-B models are deficient and do not consider users mobility and dynamically changing traffic of the mobile network environment. A modified Erlang-B dynamic channel allocation (MEB-DCA) scheme is therefore introduced in this paper, for improved network performance. The MEB-DCA algorithm introduces a conditional threshold for handoff request assignment to ensure that communication systems do not unnecessarily prioritize handoff calls at the detriment of new calls. Deriving knowledge from imprecise network data is difficult when developing functional relationships between parameters, requiring advanced modeling techniques with cognitive experience. Soft computing techniques have been shown to handle this challenge given its ability to represent precisely, both data and expert knowledge. An adaptive neuro-fuzzy inference system-based dynamic channel allocation (ANFIS-DCA) framework was proposed to automate the learning of communication parameters for optimized channel allocation decisions. Network parameters considered were received signal strength indication impacted by user mobility, number of guard and general channels, carried traffic, and handoff blocking threshold. The performance of the proposed ANFIS-DCA model was found to outsmart the static FCA and back propagation neural network-based DCA (NN-DCA) schemes using mean square error and root mean square error as performance measures. Our approach can be effectively deployed to improve channel allocation, resource utilization, network capacity, and satisfy users experience. [ABSTRACT FROM AUTHOR]

Published
2020
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199. THE PROBLEM OF THE COMPARTMENTALIZED KNAPSACK: A PROPOSAL OF THREE NEW HEURISTICS.

Author

HENRIQUE PIMENTA-ZANON, MATHEUS, SAKURAY, FABIO, and Vieira Hoto, Robinson Samuel

Subjects
HEURISTIC, PROBABILITY theory, MATHEMATICAL optimization, MATHEMATICAL analysis, SYSTEM analysis
Abstract

The problem of the compartmentalized knapsack is classified as NP-Hard and has several models, both for linear and non-linear cases. The development of new heuristics for a resolution in a runtime useful for applications becomes necessary. In this work, three new heuristics are proposed, using the particularity of the linear model pro- posed by Inarejos (2017), which are considered only pk compartments available for each class, being pkX, pkGREEDY and pkMTComp, the latter is based on the algorithm of Martello and Totti (1991). The heuristic pkMTComp presents solutions close to opti- mum value, being a promising method in solving the problem of the compartmentalized knapsack, when compared with other heuristics recognized in the literature. [ABSTRACT FROM AUTHOR]

Published
2020

200. Mechanosensitive Ca2+ signaling and coordination is diminished in osteocytes of aged mice during ex vivo tibial loading.

Author

Morrell, Andrea E., Robinson, Samuel T., Silva, Matthew J., and Guo, X. Edward

Subjects
*OSTEOPOROSIS, *BONE growth, *BONE resorption, *INTRACELLULAR calcium, *BONES, *EGG incubation, *BONE lengthening (Orthopedics), *OSTEOCLASTOGENESIS
Abstract

Purpose: The osteocyte is considered the major mechanosensor in bone, capable of detecting forces at a cellular level to coordinate bone formation and resorption. The pathology of age-related bone loss, a hallmark of osteoporosis, is attributed in part to impaired osteocyte mechanosensing. However, real-time evidence of the effect of aging on osteocyte responses to mechanical load is lacking. Intracellular calcium (Ca2+) oscillations have been characterized as an early mechanosensitive response in osteocytes in systems of multiple scales and thus can serve as a real-time measure of osteocyte mechanosensitivity. Our objective was to utilize an ex vivo model to investigate potentially altered mechanosensing in the osteocyte network with aging. Methods: Tibiae were explanted from young-adult (5 mo) and aged (22 mo) female mice and incubated with Fluo-8 AM to visualize osteocyte intracellular Ca2+. Whole tibiae were cyclically loaded while in situ osteocyte Ca2+ dynamics were simultaneously imaged with confocal microscopy. Responsive osteocyte percentage and Ca2+ peak characteristics were quantified, as well as signaling synchrony between paired cells in the field of view. Results: Fewer osteocytes responded to mechanical loading in aged mice compared to young-adult and did so in a delayed manner. Osteocytes from aged mice also lacked the well-correlated relationship between Ca2+ signaling synchrony and cell-cell distance exhibited by young-adult osteocytes. Conclusions: We have demonstrated, for the first time, real-time evidence of the diminished mechanosensing and lack of signaling coordination in aged osteocyte networks in tibial explants, which may contribute to pathology of age-induced bone loss. [ABSTRACT FROM AUTHOR]

Published
2020
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