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1. Demonstrating dynamic surface codes

Author

Eickbusch, Alec, McEwen, Matt, Sivak, Volodymyr, Bourassa, Alexandre, Atalaya, Juan, Claes, Jahan, Kafri, Dvir, Gidney, Craig, Warren, Christopher W., Gross, Jonathan, Opremcak, Alex, Miao, Nicholas Zobrist Kevin C., Roberts, Gabrielle, Satzinger, Kevin J., Bengtsson, Andreas, Neeley, Matthew, Livingston, William P., Greene, Alex, Rajeev, Acharya, Beni, Laleh Aghababaie, Aigeldinger, Georg, Alcaraz, Ross, Andersen, Trond I., Ansmann, Markus, Frank, Arute, Arya, Kunal, Asfaw, Abraham, Babbush, Ryan, Ballard, Brian, Bardin, Joseph C., Bilmes, Alexander, Jenna, Bovaird, Bowers, Dylan, Brill, Leon, Broughton, Michael, Browne, David A., Buchea, Brett, Buckley, Bob B., Tim, Burger, Burkett, Brian, Bushnell, Nicholas, Cabrera, Anthony, Campero, Juan, Chang, Hung-Shen, Chiaro, Ben, Chih, Liang-Ying, Cleland, Agnetta Y., Cogan, Josh, Collins, Roberto, Conner, Paul, Courtney, William, Alexander, Crook, L., Curtin, Ben, Das, Sayan, Barba, Alexander Del Toro, Demura, Sean, De Lorenzo, Laura, Di Paolo, Agustin, Donohoe, Paul, Drozdov, Ilya K., Dunsworth, Andrew, Elbag, Aviv Moshe, Elzouka, Mahmoud, Erickson, Catherine, Ferreira, Vinicius S., Burgos, Leslie Flores, Forati, Ebrahim, Fowler, Austin G., Foxen, Brooks, Ganjam, Suhas, Gonzalo, Garcia, Gasca, Robert, Genois, Élie, Giang, William, Gilboa, Dar, Gosula, Raja, Dau, Alejandro Grajales, Dietrich, Graumann, Ha, Tan, Habegger, Steve, Hansen, Monica, Harrigan, Matthew P., Harrington, Sean D., Heslin, Stephen, Heu, Paula, Higgott, Oscar, Hiltermann, Reno, Hilton, Jeremy, Huang, Hsin-Yuan, Huff, Ashley, Huggins, William J., Jeffrey, Evan, Jiang, Zhang, Jin, Xiaoxuan, Jones, Cody, Joshi, Chaitali, Juhas, Pavol, Kabel, Andreas, Kang, Hui, Amir, Karamlou, H., Kechedzhi, Kostyantyn, Khaire, Trupti, Khattar, Tanuj, Khezri, Mostafa, Kim, Seon, Kobrin, Bryce, Korotkov, Alexander N., Kostritsa, Fedor, Kreikebaum, John Mark, Kurilovich, Vladislav D., Landhuis, David, Tiano, Lange-Dei, Langley, Brandon W., Lau, Kim-Ming, Ledford, Justin, Lee, Kenny, Lester, Brian J., Guevel, Loïck Le, Wing, Li, Yan, Lill, Alexander T., Locharla, Aditya, Lucero, Erik, Lundahl, Daniel, Lunt, Aaron, Madhuk, Sid, Maloney, Ashley, Mandrà, Salvatore, Martin, Leigh S., Martin, Orion, Maxfield, Cameron, McClean, Jarrod R., Meeks, Seneca, Anthony, Megrant, Molavi, Reza, Molina, Sebastian, Montazeri, Shirin, Movassagh, Ramis, Newman, Michael, Nguyen, Anthony, Nguyen, Murray, Ni, Chia-Hung, Oas, Logan, Orosco, Raymond, Ottosson, Kristoffer, Pizzuto, Alex, Potter, Rebecca, Pritchard, Orion, Quintana, Chris, Ramachandran, Ganesh, Reagor, Matthew J., Rhodes, David M., Rosenberg, Eliott, Rossi, Elizabeth, Sankaragomathi, Kannan, Schurkus, Henry F., Shearn, Michael J., Shorter, Aaron, Shutty, Noah, Shvarts, Vladimir, Small, Spencer, Smith, W. Clarke, Springer, Sofia, Sterling, George, Suchard, Jordan, Szasz, Aaron, Sztein, Alex, Thor, Douglas, Tomita, Eifu, Torres, Alfredo, Torunbalci, M. Mert, Vaishnav, Abeer, Vargas, Justin, Sergey, Vdovichev, Vidal, Guifre, Heidweiller, Catherine Vollgraff, Waltman, Steven, Waltz, Jonathan, Wang, Shannon X., Ware, Brayden, Weidel, Travis, White, Theodore, Wong, Kristi, Woo, Bryan W. K., Woodson, Maddy, Xing, Cheng, Yao, Z. Jamie, Yeh, Ping, Ying, Bicheng, Yoo, Juhwan, Yosri, Noureldin, Young, Grayson, Zalcman, Adam, Yaxing, Zhang, Zhu, Ningfeng, Boixo, Sergio, Kelly, Julian, Smelyanskiy, Vadim, Neven, Hartmut, Bacon, Dave, Chen, Zijun, Klimov, Paul V., Roushan, Pedram, Neill, Charles, Chen, Yu, and Morvan, Alexis

Subjects
Quantum Physics
Abstract

A remarkable characteristic of quantum computing is the potential for reliable computation despite faulty qubits. This can be achieved through quantum error correction, which is typically implemented by repeatedly applying static syndrome checks, permitting correction of logical information. Recently, the development of time-dynamic approaches to error correction has uncovered new codes and new code implementations. In this work, we experimentally demonstrate three time-dynamic implementations of the surface code, each offering a unique solution to hardware design challenges and introducing flexibility in surface code realization. First, we embed the surface code on a hexagonal lattice, reducing the necessary couplings per qubit from four to three. Second, we walk a surface code, swapping the role of data and measure qubits each round, achieving error correction with built-in removal of accumulated non-computational errors. Finally, we realize the surface code using iSWAP gates instead of the traditional CNOT, extending the set of viable gates for error correction without additional overhead. We measure the error suppression factor when scaling from distance-3 to distance-5 codes of $\Lambda_{35,\text{hex}} = 2.15(2)$, $\Lambda_{35,\text{walk}} = 1.69(6)$, and $\Lambda_{35,\text{iSWAP}} = 1.56(2)$, achieving state-of-the-art error suppression for each. With detailed error budgeting, we explore their performance trade-offs and implications for hardware design. This work demonstrates that dynamic circuit approaches satisfy the demands for fault-tolerance and opens new alternative avenues for scalable hardware design., Comment: 11 pages, 5 figures, Supplementary Information

Published
2024

2. Scaling and logic in the color code on a superconducting quantum processor

Author

Lacroix, Nathan, Bourassa, Alexandre, Heras, Francisco J. H., Zhang, Lei M., Bausch, Johannes, Senior, Andrew W., Edlich, Thomas, Shutty, Noah, Sivak, Volodymyr, Bengtsson, Andreas, McEwen, Matt, Higgott, Oscar, Kafri, Dvir, Claes, Jahan, Morvan, Alexis, Chen, Zijun, Zalcman, Adam, Madhuk, Sid, Acharya, Rajeev, Beni, Laleh Aghababaie, Aigeldinger, Georg, Alcaraz, Ross, Andersen, Trond I., Ansmann, Markus, Arute, Frank, Arya, Kunal, Asfaw, Abraham, Atalaya, Juan, Babbush, Ryan, Ballard, Brian, Bardin, Joseph C., Bilmes, Alexander, Blackwell, Sam, Bovaird, Jenna, Bowers, Dylan, Brill, Leon, Broughton, Michael, Browne, David A., Buchea, Brett, Buckley, Bob B., Burger, Tim, Burkett, Brian, Bushnell, Nicholas, Cabrera, Anthony, Campero, Juan, Chang, Hung-Shen, Chiaro, Ben, Chih, Liang-Ying, Cleland, Agnetta Y., Cogan, Josh, Collins, Roberto, Conner, Paul, Courtney, William, Crook, Alexander L., Curtin, Ben, Das, Sayan, Demura, Sean, De Lorenzo, Laura, Di Paolo, Agustin, Donohoe, Paul, Drozdov, Ilya, Dunsworth, Andrew, Eickbusch, Alec, Elbag, Aviv Moshe, Elzouka, Mahmoud, Erickson, Catherine, Ferreira, Vinicius S., Burgos, Leslie Flores, Forati, Ebrahim, Fowler, Austin G., Foxen, Brooks, Ganjam, Suhas, Garcia, Gonzalo, Gasca, Robert, Genois, Élie, Giang, William, Gilboa, Dar, Gosula, Raja, Dau, Alejandro Grajales, Graumann, Dietrich, Greene, Alex, Gross, Jonathan A., Ha, Tan, Habegger, Steve, Hansen, Monica, Harrigan, Matthew P., Harrington, Sean D., Heslin, Stephen, Heu, Paula, Hiltermann, Reno, Hilton, Jeremy, Hong, Sabrina, Huang, Hsin-Yuan, Huff, Ashley, Huggins, William J., Jeffrey, Evan, Jiang, Zhang, Jin, Xiaoxuan, Joshi, Chaitali, Juhas, Pavol, Kabel, Andreas, Kang, Hui, Karamlou, Amir H., Kechedzhi, Kostyantyn, Khaire, Trupti, Khattar, Tanuj, Khezri, Mostafa, Kim, Seon, Klimov, Paul V., Kobrin, Bryce, Korotkov, Alexander N., Kostritsa, Fedor, Kreikebaum, John Mark, Kurilovich, Vladislav D., Landhuis, David, Lange-Dei, Tiano, Langley, Brandon W., Laptev, Pavel, Lau, Kim-Ming, Ledford, Justin, Lee, Kenny, Lester, Brian J., Guevel, Loïck Le, Li, Wing Yan, Li, Yin, Lill, Alexander T., Livingston, William P., Locharla, Aditya, Lucero, Erik, Lundahl, Daniel, Lunt, Aaron, Maloney, Ashley, Mandrà, Salvatore, Martin, Leigh S., Martin, Orion, Maxfield, Cameron, McClean, Jarrod R., Meeks, Seneca, Megrant, Anthony, Miao, Kevin C., Molavi, Reza, Molina, Sebastian, Montazeri, Shirin, Movassagh, Ramis, Neill, Charles, Newman, Michael, Nguyen, Anthony, Nguyen, Murray, Ni, Chia-Hung, Niu, Murphy Y., Oas, Logan, Oliver, William D., Orosco, Raymond, Ottosson, Kristoffer, Pizzuto, Alex, Potter, Rebecca, Pritchard, Orion, Quintana, Chris, Ramachandran, Ganesh, Reagor, Matthew J., Resnick, Rachel, Rhodes, David M., Roberts, Gabrielle, Rosenberg, Eliott, Rosenfeld, Emma, Rossi, Elizabeth, Roushan, Pedram, Sankaragomathi, Kannan, Schurkus, Henry F., Shearn, Michael J., Shorter, Aaron, Shvarts, Vladimir, Small, Spencer, Smith, W. Clarke, Springer, Sofia, Sterling, George, Suchard, Jordan, Szasz, Aaron, Sztein, Alex, Thor, Douglas, Tomita, Eifu, Torres, Alfredo, Torunbalci, M. Mert, Vaishnav, Abeer, Vargas, Justin, Vdovichev, Sergey, Vidal, Guifre, Heidweiller, Catherine Vollgraff, Waltman, Steven, Waltz, Jonathan, Wang, Shannon X., Ware, Brayden, Weidel, Travis, White, Theodore, Wong, Kristi, Woo, Bryan W. K., Woodson, Maddy, Xing, Cheng, Yao, Z. Jamie, Yeh, Ping, Ying, Bicheng, Yoo, Juhwan, Yosri, Noureldin, Young, Grayson, Zhang, Yaxing, Zhu, Ningfeng, Zobrist, Nicholas, Neven, Hartmut, Kohli, Pushmeet, Davies, Alex, Boixo, Sergio, Kelly, Julian, Jones, Cody, Gidney, Craig, and Satzinger, Kevin J.

Subjects
Quantum Physics
Abstract

Quantum error correction is essential for bridging the gap between the error rates of physical devices and the extremely low logical error rates required for quantum algorithms. Recent error-correction demonstrations on superconducting processors have focused primarily on the surface code, which offers a high error threshold but poses limitations for logical operations. In contrast, the color code enables much more efficient logic, although it requires more complex stabilizer measurements and decoding techniques. Measuring these stabilizers in planar architectures such as superconducting qubits is challenging, and so far, realizations of color codes have not addressed performance scaling with code size on any platform. Here, we present a comprehensive demonstration of the color code on a superconducting processor, achieving logical error suppression and performing logical operations. Scaling the code distance from three to five suppresses logical errors by a factor of $\Lambda_{3/5}$ = 1.56(4). Simulations indicate this performance is below the threshold of the color code, and furthermore that the color code may be more efficient than the surface code with modest device improvements. Using logical randomized benchmarking, we find that transversal Clifford gates add an error of only 0.0027(3), which is substantially less than the error of an idling error correction cycle. We inject magic states, a key resource for universal computation, achieving fidelities exceeding 99% with post-selection (retaining about 75% of the data). Finally, we successfully teleport logical states between distance-three color codes using lattice surgery, with teleported state fidelities between 86.5(1)% and 90.7(1)%. This work establishes the color code as a compelling research direction to realize fault-tolerant quantum computation on superconducting processors in the near future.

Published
2024

3. Observation of disorder-free localization and efficient disorder averaging on a quantum processor

Author

Gyawali, Gaurav, Cochran, Tyler, Lensky, Yuri, Rosenberg, Eliott, Karamlou, Amir H., Kechedzhi, Kostyantyn, Berndtsson, Julia, Westerhout, Tom, Asfaw, Abraham, Abanin, Dmitry, Acharya, Rajeev, Beni, Laleh Aghababaie, Andersen, Trond I., Ansmann, Markus, Arute, Frank, Arya, Kunal, Astrakhantsev, Nikita, Atalaya, Juan, Babbush, Ryan, Ballard, Brian, Bardin, Joseph C., Bengtsson, Andreas, Bilmes, Alexander, Bortoli, Gina, Bourassa, Alexandre, Bovaird, Jenna, Brill, Leon, Broughton, Michael, Browne, David A., Buchea, Brett, Buckley, Bob B., Buell, David A., Burger, Tim, Burkett, Brian, Bushnell, Nicholas, Cabrera, Anthony, Campero, Juan, Chang, Hung-Shen, Chen, Zijun, Chiaro, Ben, Claes, Jahan, Cleland, Agnetta Y., Cogan, Josh, Collins, Roberto, Conner, Paul, Courtney, William, Crook, Alexander L., Das, Sayan, Debroy, Dripto M., De Lorenzo, Laura, Barba, Alexander Del Toro, Demura, Sean, Di Paolo, Agustin, Donohoe, Paul, Drozdov, Ilya, Dunsworth, Andrew, Earle, Clint, Eickbusch, Alec, Elbag, Aviv Moshe, Elzouka, Mahmoud, Erickson, Catherine, Faoro, Lara, Fatemi, Reza, Ferreira, Vinicius S., Burgos, Leslie Flores, Forati, Ebrahim, Fowler, Austin G., Foxen, Brooks, Ganjam, Suhas, Gasca, Robert, Giang, William, Gidney, Craig, Gilboa, Dar, Gosula, Raja, Dau, Alejandro Grajales, Graumann, Dietrich, Greene, Alex, Gross, Jonathan A., Habegger, Steve, Hamilton, Michael C., Hansen, Monica, Harrigan, Matthew P., Harrington, Sean D., Heslin, Stephen, Heu, Paula, Hill, Gordon, Hilton, Jeremy, Hoffmann, Markus R., Huang, Hsin-Yuan, Huff, Ashley, Huggins, William J., Ioffe, Lev B., Isakov, Sergei V., Jeffrey, Evan, Jiang, Zhang, Jones, Cody, Jordan, Stephen, Joshi, Chaitali, Juhas, Pavol, Kafri, Dvir, Kang, Hui, Khaire, Trupti, Khattar, Tanuj, Khezri, Mostafa, Kieferová, Mária, Kim, Seon, Klimov, Paul V., Klots, Andrey R., Kobrin, Bryce, Korotkov, Alexander N., Kostritsa, Fedor, Kreikebaum, John Mark, Kurilovich, Vladislav D., Landhuis, David, Lange-Dei, Tiano, Langley, Brandon W., Laptev, Pavel, Lau, Kim-Ming, Guevel, Loïck Le, Ledford, Justin, Lee, Joonho, Lee, Kenny, Lester, Brian J., Li, Wing Yan, Lill, Alexander T., Liu, Wayne, Livingston, William P., Locharla, Aditya, Lundahl, Daniel, Lunt, Aaron, Madhuk, Sid, Maloney, Ashley, Mandrà, Salvatore, Martin, Leigh S., Martin, Steven, Martin, Orion, Maxfield, Cameron, McClean, Jarrod R., McEwen, Matt, Meeks, Seneca, Megrant, Anthony, Mi, Xiao, Miao, Kevin C., Mieszala, Amanda, Molina, Sebastian, Montazeri, Shirin, Morvan, Alexis, Movassagh, Ramis, Neill, Charles, Nersisyan, Ani, Newman, Michael, Nguyen, Anthony, Nguyen, Murray, Ni, Chia-Hung, Niu, Murphy Yuezhen, Oliver, William D., Ottosson, Kristoffer, Pizzuto, Alex, Potter, Rebecca, Pritchard, Orion, Pryadko, Leonid P., Quintana, Chris, Reagor, Matthew J., Rhodes, David M., Roberts, Gabrielle, Rocque, Charles, Rubin, Nicholas C., Saei, Negar, Sankaragomathi, Kannan, Satzinger, Kevin J., Schurkus, Henry F., Schuster, Christopher, Shearn, Michael J., Shorter, Aaron, Shutty, Noah, Shvarts, Vladimir, Sivak, Volodymyr, Skruzny, Jindra, Small, Spencer, Smith, W. Clarke, Springer, Sofia, Sterling, George, Suchard, Jordan, Szalay, Marco, Szasz, Aaron, Sztein, Alex, Thor, Douglas, Torunbalci, M. Mert, Vaishnav, Abeer, Vdovichev, Sergey, Vidal, Guifré, Heidweiller, Catherine Vollgraff, Waltman, Steven, Wang, Shannon X., White, Theodore, Wong, Kristi, Woo, Bryan W. K., Xing, Cheng, Yao, Z. Jamie, Yeh, Ping, Ying, Bicheng, Yoo, Juhwan, Yosri, Noureldin, Young, Grayson, Zalcman, Adam, Zhang, Yaxing, Zhu, Ningfeng, Zobrist, Nicholas, Boixo, Sergio, Kelly, Julian, Lucero, Erik, Chen, Yu, Smelyanskiy, Vadim, Neven, Hartmut, Kovrizhin, Dmitry, Knolle, Johannes, Halimeh, Jad C., Aleiner, Igor, Moessner, Roderich, and Roushan, Pedram

Subjects
Quantum Physics, Condensed Matter - Disordered Systems and Neural Networks, Condensed Matter - Strongly Correlated Electrons, High Energy Physics - Lattice
Abstract

One of the most challenging problems in the computational study of localization in quantum manybody systems is to capture the effects of rare events, which requires sampling over exponentially many disorder realizations. We implement an efficient procedure on a quantum processor, leveraging quantum parallelism, to efficiently sample over all disorder realizations. We observe localization without disorder in quantum many-body dynamics in one and two dimensions: perturbations do not diffuse even though both the generator of evolution and the initial states are fully translationally invariant. The disorder strength as well as its density can be readily tuned using the initial state. Furthermore, we demonstrate the versatility of our platform by measuring Renyi entropies. Our method could also be extended to higher moments of the physical observables and disorder learning.

Published
2024

4. Visualizing Dynamics of Charges and Strings in (2+1)D Lattice Gauge Theories

Author

Cochran, Tyler A., Jobst, Bernhard, Rosenberg, Eliott, Lensky, Yuri D., Gyawali, Gaurav, Eassa, Norhan, Will, Melissa, Abanin, Dmitry, Acharya, Rajeev, Beni, Laleh Aghababaie, Andersen, Trond I., Ansmann, Markus, Arute, Frank, Arya, Kunal, Asfaw, Abraham, Atalaya, Juan, Babbush, Ryan, Ballard, Brian, Bardin, Joseph C., Bengtsson, Andreas, Bilmes, Alexander, Bourassa, Alexandre, Bovaird, Jenna, Broughton, Michael, Browne, David A., Buchea, Brett, Buckley, Bob B., Burger, Tim, Burkett, Brian, Bushnell, Nicholas, Cabrera, Anthony, Campero, Juan, Chang, Hung-Shen, Chen, Zijun, Chiaro, Ben, Claes, Jahan, Cleland, Agnetta Y., Cogan, Josh, Collins, Roberto, Conner, Paul, Courtney, William, Crook, Alexander L., Curtin, Ben, Das, Sayan, Demura, Sean, De Lorenzo, Laura, Di Paolo, Agustin, Donohoe, Paul, Drozdov, Ilya, Dunsworth, Andrew, Eickbusch, Alec, Elbag, Aviv Moshe, Elzouka, Mahmoud, Erickson, Catherine, Ferreira, Vinicius S., Burgos, Leslie Flores, Forati, Ebrahim, Fowler, Austin G., Foxen, Brooks, Ganjam, Suhas, Gasca, Robert, Genois, Élie, Giang, William, Gilboa, Dar, Gosula, Raja, Dau, Alejandro Grajales, Graumann, Dietrich, Greene, Alex, Gross, Jonathan A., Habegger, Steve, Hansen, Monica, Harrigan, Matthew P., Harrington, Sean D., Heu, Paula, Higgott, Oscar, Hilton, Jeremy, Huang, Hsin-Yuan, Huff, Ashley, Huggins, William J., Jeffrey, Evan, Jiang, Zhang, Jones, Cody, Joshi, Chaitali, Juhas, Pavol, Kafri, Dvir, Kang, Hui, Karamlou, Amir H., Kechedzhi, Kostyantyn, Khaire, Trupti, Khattar, Tanuj, Khezri, Mostafa, Kim, Seon, Klimov, Paul V., Kobrin, Bryce, Korotkov, Alexander N., Kostritsa, Fedor, Kreikebaum, John Mark, Kurilovich, Vladislav D., Landhuis, David, Lange-Dei, Tiano, Langley, Brandon W., Lau, Kim-Ming, Ledford, Justin, Lee, Kenny, Lester, Brian J., Guevel, Loïck Le, Li, Wing Yan, Lill, Alexander T., Livingston, William P., Locharla, Aditya, Lundahl, Daniel, Lunt, Aaron, Madhuk, Sid, Maloney, Ashley, Mandrà, Salvatore, Martin, Leigh S., Martin, Orion, Maxfield, Cameron, McClean, Jarrod R., McEwen, Matt, Meeks, Seneca, Megrant, Anthony, Miao, Kevin C., Molavi, Reza, Molina, Sebastian, Montazeri, Shirin, Movassagh, Ramis, Neill, Charles, Newman, Michael, Nguyen, Anthony, Nguyen, Murray, Ni, Chia-Hung, Niu, Murphy Yuezhen, Oliver, William D., Ottosson, Kristoffer, Pizzuto, Alex, Potter, Rebecca, Pritchard, Orion, Quintana, Chris, Ramachandran, Ganesh, Reagor, Matthew J., Rhodes, David M., Roberts, Gabrielle, Sankaragomathi, Kannan, Satzinger, Kevin J., Schurkus, Henry F., Shearn, Michael J., Shorter, Aaron, Shutty, Noah, Shvarts, Vladimir, Sivak, Volodymyr, Small, Spencer, Smith, W. Clarke, Springer, Sofia, Sterling, George, Suchard, Jordan, Szasz, Aaron, Sztein, Alex, Thor, Douglas, Torunbalci, M. Mert, Vaishnav, Abeer, Vargas, Justin, Vdovichev, Sergey, Vidal, Guifre, Heidweiller, Catherine Vollgraff, Waltman, Steven, Wang, Shannon X., Ware, Brayden, White, Theodore, Wong, Kristi, Woo, Bryan W. K., Xing, Cheng, Yao, Z. Jamie, Yeh, Ping, Ying, Bicheng, Yoo, Juhwan, Yosri, Noureldin, Young, Grayson, Zalcman, Adam, Zhang, Yaxing, Zhu, Ningfeng, Zobris, Nicholas, Boixo, Sergio, Kelly, Julian, Lucero, Erik, Chen, Yu, Smelyanskiy, Vadim, Neven, Hartmut, Gammon-Smith, Adam, Pollmann, Frank, Knap, Michael, and Roushan, Pedram

Subjects
Quantum Physics, Condensed Matter - Strongly Correlated Electrons, High Energy Physics - Lattice
Abstract

Lattice gauge theories (LGTs) can be employed to understand a wide range of phenomena, from elementary particle scattering in high-energy physics to effective descriptions of many-body interactions in materials. Studying dynamical properties of emergent phases can be challenging as it requires solving many-body problems that are generally beyond perturbative limits. We investigate the dynamics of local excitations in a $\mathbb{Z}_2$ LGT using a two-dimensional lattice of superconducting qubits. We first construct a simple variational circuit which prepares low-energy states that have a large overlap with the ground state; then we create particles with local gates and simulate their quantum dynamics via a discretized time evolution. As the effective magnetic field is increased, our measurements show signatures of transitioning from deconfined to confined dynamics. For confined excitations, the magnetic field induces a tension in the string connecting them. Our method allows us to experimentally image string dynamics in a (2+1)D LGT from which we uncover two distinct regimes inside the confining phase: for weak confinement the string fluctuates strongly in the transverse direction, while for strong confinement transverse fluctuations are effectively frozen. In addition, we demonstrate a resonance condition at which dynamical string breaking is facilitated. Our LGT implementation on a quantum processor presents a novel set of techniques for investigating emergent particle and string dynamics.

Published
2024

5. Quantum error correction below the surface code threshold

Author

Acharya, Rajeev, Aghababaie-Beni, Laleh, Aleiner, Igor, Andersen, Trond I., Ansmann, Markus, Arute, Frank, Arya, Kunal, Asfaw, Abraham, Astrakhantsev, Nikita, Atalaya, Juan, Babbush, Ryan, Bacon, Dave, Ballard, Brian, Bardin, Joseph C., Bausch, Johannes, Bengtsson, Andreas, Bilmes, Alexander, Blackwell, Sam, Boixo, Sergio, Bortoli, Gina, Bourassa, Alexandre, Bovaird, Jenna, Brill, Leon, Broughton, Michael, Browne, David A., Buchea, Brett, Buckley, Bob B., Buell, David A., Burger, Tim, Burkett, Brian, Bushnell, Nicholas, Cabrera, Anthony, Campero, Juan, Chang, Hung-Shen, Chen, Yu, Chen, Zijun, Chiaro, Ben, Chik, Desmond, Chou, Charina, Claes, Jahan, Cleland, Agnetta Y., Cogan, Josh, Collins, Roberto, Conner, Paul, Courtney, William, Crook, Alexander L., Curtin, Ben, Das, Sayan, Davies, Alex, De Lorenzo, Laura, Debroy, Dripto M., Demura, Sean, Devoret, Michel, Di Paolo, Agustin, Donohoe, Paul, Drozdov, Ilya, Dunsworth, Andrew, Earle, Clint, Edlich, Thomas, Eickbusch, Alec, Elbag, Aviv Moshe, Elzouka, Mahmoud, Erickson, Catherine, Faoro, Lara, Farhi, Edward, Ferreira, Vinicius S., Burgos, Leslie Flores, Forati, Ebrahim, Fowler, Austin G., Foxen, Brooks, Ganjam, Suhas, Garcia, Gonzalo, Gasca, Robert, Genois, Élie, Giang, William, Gidney, Craig, Gilboa, Dar, Gosula, Raja, Dau, Alejandro Grajales, Graumann, Dietrich, Greene, Alex, Gross, Jonathan A., Habegger, Steve, Hall, John, Hamilton, Michael C., Hansen, Monica, Harrigan, Matthew P., Harrington, Sean D., Heras, Francisco J. H., Heslin, Stephen, Heu, Paula, Higgott, Oscar, Hill, Gordon, Hilton, Jeremy, Holland, George, Hong, Sabrina, Huang, Hsin-Yuan, Huff, Ashley, Huggins, William J., Ioffe, Lev B., Isakov, Sergei V., Iveland, Justin, Jeffrey, Evan, Jiang, Zhang, Jones, Cody, Jordan, Stephen, Joshi, Chaitali, Juhas, Pavol, Kafri, Dvir, Kang, Hui, Karamlou, Amir H., Kechedzhi, Kostyantyn, Kelly, Julian, Khaire, Trupti, Khattar, Tanuj, Khezri, Mostafa, Kim, Seon, Klimov, Paul V., Klots, Andrey R., Kobrin, Bryce, Kohli, Pushmeet, Korotkov, Alexander N., Kostritsa, Fedor, Kothari, Robin, Kozlovskii, Borislav, Kreikebaum, John Mark, Kurilovich, Vladislav D., Lacroix, Nathan, Landhuis, David, Lange-Dei, Tiano, Langley, Brandon W., Laptev, Pavel, Lau, Kim-Ming, Guevel, Loïck Le, Ledford, Justin, Lee, Kenny, Lensky, Yuri D., Leon, Shannon, Lester, Brian J., Li, Wing Yan, Li, Yin, Lill, Alexander T., Liu, Wayne, Livingston, William P., Locharla, Aditya, Lucero, Erik, Lundahl, Daniel, Lunt, Aaron, Madhuk, Sid, Malone, Fionn D., Maloney, Ashley, Mandrá, Salvatore, Martin, Leigh S., Martin, Steven, Martin, Orion, Maxfield, Cameron, McClean, Jarrod R., McEwen, Matt, Meeks, Seneca, Megrant, Anthony, Mi, Xiao, Miao, Kevin C., Mieszala, Amanda, Molavi, Reza, Molina, Sebastian, Montazeri, Shirin, Morvan, Alexis, Movassagh, Ramis, Mruczkiewicz, Wojciech, Naaman, Ofer, Neeley, Matthew, Neill, Charles, Nersisyan, Ani, Neven, Hartmut, Newman, Michael, Ng, Jiun How, Nguyen, Anthony, Nguyen, Murray, Ni, Chia-Hung, O'Brien, Thomas E., Oliver, William D., Opremcak, Alex, Ottosson, Kristoffer, Petukhov, Andre, Pizzuto, Alex, Platt, John, Potter, Rebecca, Pritchard, Orion, Pryadko, Leonid P., Quintana, Chris, Ramachandran, Ganesh, Reagor, Matthew J., Rhodes, David M., Roberts, Gabrielle, Rosenberg, Eliott, Rosenfeld, Emma, Roushan, Pedram, Rubin, Nicholas C., Saei, Negar, Sank, Daniel, Sankaragomathi, Kannan, Satzinger, Kevin J., Schurkus, Henry F., Schuster, Christopher, Senior, Andrew W., Shearn, Michael J., Shorter, Aaron, Shutty, Noah, Shvarts, Vladimir, Singh, Shraddha, Sivak, Volodymyr, Skruzny, Jindra, Small, Spencer, Smelyanskiy, Vadim, Smith, W. Clarke, Somma, Rolando D., Springer, Sofia, Sterling, George, Strain, Doug, Suchard, Jordan, Szasz, Aaron, Sztein, Alex, Thor, Douglas, Torres, Alfredo, Torunbalci, M. Mert, Vaishnav, Abeer, Vargas, Justin, Vdovichev, Sergey, Vidal, Guifre, Villalonga, Benjamin, Heidweiller, Catherine Vollgraff, Waltman, Steven, Wang, Shannon X., Ware, Brayden, Weber, Kate, White, Theodore, Wong, Kristi, Woo, Bryan W. K., Xing, Cheng, Yao, Z. Jamie, Yeh, Ping, Ying, Bicheng, Yoo, Juhwan, Yosri, Noureldin, Young, Grayson, Zalcman, Adam, Zhang, Yaxing, Zhu, Ningfeng, and Zobrist, Nicholas

Subjects
Quantum Physics
Abstract

Quantum error correction provides a path to reach practical quantum computing by combining multiple physical qubits into a logical qubit, where the logical error rate is suppressed exponentially as more qubits are added. However, this exponential suppression only occurs if the physical error rate is below a critical threshold. In this work, we present two surface code memories operating below this threshold: a distance-7 code and a distance-5 code integrated with a real-time decoder. The logical error rate of our larger quantum memory is suppressed by a factor of $\Lambda$ = 2.14 $\pm$ 0.02 when increasing the code distance by two, culminating in a 101-qubit distance-7 code with 0.143% $\pm$ 0.003% error per cycle of error correction. This logical memory is also beyond break-even, exceeding its best physical qubit's lifetime by a factor of 2.4 $\pm$ 0.3. We maintain below-threshold performance when decoding in real time, achieving an average decoder latency of 63 $\mu$s at distance-5 up to a million cycles, with a cycle time of 1.1 $\mu$s. To probe the limits of our error-correction performance, we run repetition codes up to distance-29 and find that logical performance is limited by rare correlated error events occurring approximately once every hour, or 3 $\times$ 10$^9$ cycles. Our results present device performance that, if scaled, could realize the operational requirements of large scale fault-tolerant quantum algorithms., Comment: 10 pages, 4 figures, Supplementary Information

Published
2024

6. STATE OF ARTS OF MONUMENTAL STONES DIAGNOSIS AND MONITORING

Author

P. Tiano and C. Riminesi

Subjects
Technology, Engineering (General). Civil engineering (General), TA1-2040, Applied optics. Photonics, TA1501-1820
Abstract

The conservation and maintenance of a monumental stone building is a complex aim where different disciplines are involved. First step is concerning the determination of the state of conservation of stone material present, than determine its modification on time, as such and after conservation treatments applied on: cleaning, protecting, strengthening. In order to fulfill such objectives suitable parameters must be selected and the most appropriate diagnostic techniques for their quantitative evaluation operated. In this context, the determination of the surface water absorption, moisture content, colour variation and mechanical properties are important parameters for the control, and the monitoring over time, of the state of conservation of the monumental stone surfaces. These parameters are strongly related not only to the stone characteristics but also to the evaluation of products’s performance: efficiency and durability. Their rate of variation, determined in monitoring campaigns, is fundamental for elaborate by properly predictive model a schedule maintenance protocol.

Published
2017
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9. Investigating the effects of mobile bottom fishing on benthic carbon processing and storage: a systematic review protocol

Author

Felgate, Stacey L., Aldridge, John, Bolam, Stefan G., Breimann, Sarah, de Borger, Emil, Claes, Jolien, Depestele, Jochen, Epstein, Graham, Garcia, Clement, Hicks, Natalie, Kaiser, Michel, Laverick, Jack H., Lessin, Gennadi, O’Neill, Finbarr G., Paradis, Sarah, Parker, Ruth, Pereira, Ryan, Poulton, Alex J., Powell, Claire, Smeaton, Craig, Snelgrove, Paul, Tiano, Justin, van der Molen, Johan, van de Velde, Sebastiaan, and Sciberras, Marija

Published
2024
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15. Estrogen receptor α protects pancreatic β-cells from apoptosis by preserving mitochondrial function and suppressing endoplasmic reticulum stress

Author

Zhou, Zhenqi, Ribas, Vicent, Rajbhandari, Prashant, Drew, Brian G, Moore, Timothy M, Fluitt, Amy H, Reddish, Britany R, Whitney, Kate A, Georgia, Senta, Vergnes, Laurent, Reue, Karen, Liesa, Marc, Shirihai, Orian, van der Bliek, Alexander M, Chi, Nai-Wen, Mahata, Sushil K, Tiano, Joseph P, Hewitt, Sylvia C, Tontonoz, Peter, Korach, Kenneth S, Mauvais-Jarvis, Franck, and Hevener, Andrea L

Subjects
Biochemistry and Cell Biology, Biological Sciences, Diabetes, Autoimmune Disease, Estrogen, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Metabolic and endocrine, Animals, Apoptosis, Cell Survival, Endoplasmic Reticulum Stress, Estrogen Receptor alpha, Female, Insulin, Insulin-Secreting Cells, Metalloproteases, Mice, Mice, Knockout, Mitochondria, Mitochondrial Proteins, Mitophagy, Reactive Oxygen Species, Transcription Factor CHOP, apoptosis, endoplasmic reticulum stress, estrogen action, estrogen receptor, insulin secretion, mitochondrial dynamics, mitochondrial metabolism, Chemical Sciences, Medical and Health Sciences, Biochemistry & Molecular Biology, Biological sciences, Biomedical and clinical sciences, Chemical sciences
Abstract

Estrogen receptor α (ERα) action plays an important role in pancreatic β-cell function and survival; thus, it is considered a potential therapeutic target for the treatment of type 2 diabetes in women. However, the mechanisms underlying the protective effects of ERα remain unclear. Because ERα regulates mitochondrial metabolism in other cell types, we hypothesized that ERα may act to preserve insulin secretion and promote β-cell survival by regulating mitochondrial-endoplasmic reticulum (EndoRetic) function. We tested this hypothesis using pancreatic islet-specific ERα knockout (PERαKO) mice and Min6 β-cells in culture with Esr1 knockdown (KD). We found that Esr1-KD promoted reactive oxygen species production that associated with reduced fission/fusion dynamics and impaired mitophagy. Electron microscopy showed mitochondrial enlargement and a pro-fusion phenotype. Mitochondrial cristae and endoplasmic reticulum were dilated in Esr1-KD compared with ERα replete Min6 β-cells. Increased expression of Oma1 and Chop was paralleled by increased oxygen consumption and apoptosis susceptibility in ERα-KD cells. In contrast, ERα overexpression and ligand activation reduced both Chop and Oma1 expression, likely by ERα binding to consensus estrogen-response element sites in the Oma1 and Chop promoters. Together, our findings suggest that ERα promotes β-cell survival and insulin secretion through maintenance of mitochondrial fission/fusion-mitophagy dynamics and EndoRetic function, in part by Oma1 and Chop repression.

Published
2018

18. A First-Principles Study of CdSe Nanoclusters Capped by Thiol Ligands

Author

Wu, Shanshan, McGuigan, Michael, Tiano, Amanda L., Wong, Stanislaus S., and Glimm, James G.

Subjects
Condensed Matter - Materials Science
Abstract

A first-principles study of small CdnSen quantum dots (QDs) (n = 6, 13, and 33) has been performed for the study of QD-sensitized solar cells. We assessed the effects of the passivating thiol-radical ligands on the optimized structure, the energy gap, and on the absorption spectrum. The simplest thiol, methanethiol, and four other thiol type ligands, namely - cysteine (Cys), mercaptopropionic acid (MPA), and their reduced-chain analogues, were investigated. We have come to the following conclusions. (a) Thiol-radical ligands possessed greater effects on the structure and electronic properties of the CdSe QDs than thiol ligands alone. (b) The sulfur 3p orbitals were localized as the midgap states for the thiol-radical-ligated complex, which altered the absorption spectrum of bare Cd6Se6 by inducing a new lower energy absorption peak at 2.37 eV. (c) The thiol-radical-ligated complex was also found to be sensitive to the position and number of ligands. (d) Both the amine group on Cys and the carboxyl group on Cys and MPA showed a strong tendency to bond with the neighboring Cd atom, especially when the length of the ligand was reduced. This formation of Cd-N and Cd-O bonds resulted in smaller HOMO-LUMO gaps and a stronger binding between the ligands and the surface atoms of CdSe nanoclusters.

Published
2013

20. A First-Principles Study of Thiol Ligated CdSe Nanoclusters

Author

Wu, Shanshan, McGuigan, Michael, Tiano, Amanda L., Wong, Stanislaus S., and Glimm, James G.

Subjects
Condensed Matter - Mesoscale and Nanoscale Physics, Condensed Matter - Materials Science
Abstract

A first-principles study of small CdnSen Quantum Dots (QD) ('n' =6, 12, 13, and 33) has been performed for application to QD solar cell development. We separately assess the effects of the particle size and the passivating ligands upon the optimized structure and the energy gap (from a density functional theory (DFT) calculation) and the corresponding absorption spectrum (from a time-dependent density functional theory (TDDFT) calculation). The structures of four thiol ligands, namely - cysteine (Cys), mercaptopropionic acid (MPA), and their reduced-chain analogues, are investigated. We have documented significant passivation effects of the surfactants upon the structure and the optical absorption properties of the CdSe quantum dots: The surface Cd-Se bonds are weakened, whereas the core bonds are strengthened. A blue shift of the absorption spectrum by ~0.2 eV is observed. Also, the optical absorption intensity is enhanced by the passivation. By contrast, we have observed that varying the length of ligands yields only a minor effect upon the absorption properties: a shorter alkane chain might induce a slightly stronger interaction between the -NH2 group and the nearest surface Se atom, which is observed as a stronger ligand binding energy. For Cd12Se12, which is regarded as the 'non-magic' size QD, neither the self-relaxation nor the ligand passivation could fully stabilize the structure or improve the poor electronic properties. We also observe that the category of thiol ligands possesses a better ability to open the band gap of CdSe QD than either phosphine oxide or amine ligands. Our estimation of the absorption peak of the Cys-capped QDs ranges from 413 nm to 460 nm, which is consistent to the experimental peak as 422 nm., Comment: This paper has been withdrawn by conflicting of interests

Published
2012

21. Training Head Start Teachers in Behavior Management Using Parent-Child Interaction Therapy: A Preliminary Investigation

Author

Tiano, Jennifer D. and McNeil, Cheryl B.

Abstract

The current project evaluated the use of behavior management techniques utilized in Parent- Child Interaction Therapy (PCIT) in head start classrooms. The sample included seven Head Start classrooms; four classrooms receiving treatment and three classrooms receiving no treatment. Evaluation of the progress included observation of teacher and student behavior and teacher report of class manageability and number of time-outs. Results indicated that child behavior improved throughout the study for both groups. Both groups of teachers also gave fewer timeouts, criticized the children less often, and rated their classes as more manageable from pre- to post-treatment. Teachers receiving training gave more labeled praise following treatment. These findings provide initial support for improving teacher behavior modification skills through the use of PCIT skills modified for Head Start classrooms. (Contains 1 table.)

Published
2006

22. Managing Classroom Behavior of Head Start Children Using Response Cost and Token Economy Procedures

Author

Tiano, Jennifer D., Fortson, Beverly L., McNeil, Cheryl B., and Humphreys, Lisa A.

Abstract

The efficacy of three behavior management techniques used in a Head Start classroom was examined. The three techniques included: (a) techniques currently used by the teacher, (b) response cost, and (c) the Level System (token economy). The current study used an ABACA single subject withdrawal design with follow-up where all conditions were implemented until stability was reached. Classroom behavior was evaluated by both behavioral observation and teacher report. Children's and teacher's behavior were examined. No conclusions could be made concerning the efficacy (i.e., inappropriate behavior) of the techniques. Teachers used more labeled praise statements and fewer critical statements during the Level System condition than all other conditions. (Contains 4 figures.)

Published
2005

24. Impact of phosphate binder type on coronary artery calcification in hemodialysis patients.

Author

Shantouf, R, Ahmadi, N, Flores, F, Tiano, J, Gopal, A, Kalantar-Zadeh, K, and Budoff, MJ

Subjects
Reproductive Medicine, Biomedical and Clinical Sciences, Kidney Disease, Assistive Technology, Clinical Research, Bioengineering, Heart Disease, Heart Disease - Coronary Heart Disease, Cardiovascular, Biomarkers, Calcinosis, Chelating Agents, Coronary Disease, Cross-Sectional Studies, Female, Humans, Hyperphosphatemia, Kidney Failure, Chronic, Logistic Models, Male, Middle Aged, Polyamines, Renal Dialysis, Sevelamer, Treatment Outcome, chronic kidney disease, maintenance hemodialysis (MHD) patient, electron beam computerized tomography, coronary artery calcium score, phosphate binders, diabetes mellitus, Clinical Sciences, Urology & Nephrology, Clinical sciences
Abstract

AimsIn individuals with chronic kidney disease (CKD), including those undergoing maintenance hemodialysis (MHD), coronary artery calcification (CAC) is common. We hypothesized that, in MHD patients, intake of the calcium-free phosphate binder sevelamer is associated with lower CAC compared to calcium-based phosphate binders (CBPB).Material and methodsThis is a cross-sectional study of MHD patients, who underwent computerized tomography to assess coronary artery calcium scores (CACS). Patients were stratified into two mutually exclusive groups based on taking only a CBPB vs. sevelamer. Logistic regression was used to calculate adjusted odds ratio (OR) of CACS > or = 400, CACS 100 < or =; CACS < 400, 10 < or =; CACS < 100 vs. CACS < 10.Results117 MHD patients were either on a CBPB alone (n = 60) or sevelamer alone (n = 57). Despite increased prevalence of DM in the sevelamer group (58%) as compared to the CBPB group (35%), CACS was significantly lower with sevelamer use (283 + or - 83 vs. 494 + or - 94, p = 0.02). The OR of significant CACS > or =; 400 vs. CAC < 10 was 4.35 (95% confidence interval: 1.5 - 9.9, p = 0.008) for CBPB compared with sevelamer, after controlling for case-mix, cholesterol-lowering medication, DM, and inflammatory markers.ConclusionIn our cohort, significant CAC was significantly more prevalent among MHD patients taking CBPB as compared to sevelamer monotherapy.

Published
2010

26. Effects of Sevelamer and Calcium-Based Phosphate Binders on Lipid and Inflammatory Markers in Hemodialysis Patients

Author

Shantouf, Ronney, Budoff, Matthew J, Ahmadi, Naser, Tiano, Jima, Flores, Ferdinand, and Kalantar-Zadeh, Kamyar

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Bioengineering, Assistive Technology, Cardiovascular, Kidney Disease, 6.1 Pharmaceuticals, Good Health and Well Being, Age Factors, Aged, C-Reactive Protein, Calcium, Chelating Agents, Cohort Studies, Female, Humans, Inflammation, Lipids, Male, Middle Aged, Polyamines, Prospective Studies, Renal Dialysis, Renal Insufficiency, Sevelamer, Treatment Outcome, end-stage renal disease, cardiac computed tomography, coronary calcium, phosphate binders, Urology & Nephrology, Clinical sciences
Abstract

IntroductionCardiovascular disease accounts for almost half of all deaths in individuals with chronic kidney disease stage 5 despite advances in both dialysis treatment and cardiology. A combination of lipid-lowering and anti-inflammatory effects along with avoidance of hypercalcemia should be taken into account when choosing phosphorus binders for maintenance hemodialysis (MHD) patients.MethodsWe examined the association of sevelamer versus calcium-based phosphorus binders with lipid profile, inflammatory markers including C-reactive protein (CRP), and mineral metabolism in MHD patients who participated in the Nutritional and Inflammatory Evaluation of Dialysis Patients (NIED) study from October 2001 to July 2005.ResultsOf the 787 MHD patients in the NIED study, 697 were on either sevelamer, a calcium-based binder, or both and eligible for this study. We compared the groups based on taking sevelamer monotherapy (n = 283) or calcium binder monotherapy (n = 266) for serum phosphate control. There were no differences between the groups on dialysis vintage. There were significant differences in age, serum calcium and phosphorus levels, as well as intact parathyroid hormone levels. Using a logistic regression models, the sevelamer group had a higher odds of serum CRP

Published
2008

29. Efficacy of glucagon-like peptide-1 and estrogen dual agonist in pancreatic islets protection and pre-clinical models of insulin-deficient diabetes

Author

Taylor Fuselier, Paula Mota de Sa, M.M. Fahd Qadir, Beibei Xu, Camille Allard, Mathew M. Meyers, Joseph P. Tiano, Bin S. Yang, Vasily Gelfanov, Sarah H. Lindsey, Richard D. Dimarchi, and Franck Mauvais-Jarvis

Subjects
Proteomics, Islets of Langerhans, Mice, Glucagon-Like Peptide 1, Insulin, Regular, Human, Diabetes Mellitus, Estrogen Receptor alpha, Animals, Insulin, Estrogens, General Biochemistry, Genetics and Molecular Biology, Streptozocin
Abstract

We study the efficacy of a glucagon-like peptide-1 (GLP-1) and estrogen dual agonist (GLP1-E2) in pancreatic islet protection. GLP1-E2 provides superior protection from insulin-deficient diabetes induced by multiple low-dose streptozotocin (MLD-STZ-diabetes) and by the Akita mutation in mice than a GLP-1 monoagonist. GLP1-E2 does not protect from MLD-STZ-diabetes in estrogen receptor-α (ERα)-deficient mice and fails to prevent diabetes in Akita mice following GLP-1 receptor (GLP-1R) antagonism, demonstrating the requirement of GLP-1R and ERα for GLP1-E2 antidiabetic actions. In the MIN6 β cell model, GLP1-E2 activates estrogen action following clathrin-dependent, GLP-1R-mediated internalization and lysosomal acidification. In cultured human islet, proteomic bioinformatic analysis reveals that GLP1-E2 amplifies the antiapoptotic pathways activated by monoagonists. However, in cultured mouse islets, GLP1-E2 provides antiapoptotic protection similar to monoagonists. Thus, GLP1-E2 promotes GLP-1 and E2 antiapoptotic signals in cultured islets, but

Published
2022

32. Aspalathin Alleviates Skeletal Muscle Insulin Resistance and Mitochondrial Dysfunction.

Author

MAZIBUKO-MBEJE, Sithandiwe E., MTHEMBU, Sinenhlanhla X. H., MULLER, Christo J. F., ZIQUBU, Khanyisani, MUVHULAWA, Ndivhuwo, MODIBEDI, Reneilwe V., TIANO, Luca, and DLUDLA, Phiwayinkosi V.

Subjects
INSULIN resistance, MITOCHONDRIAL pathology, TYPE 2 diabetes, PROTEIN kinase B, TRANSCRIPTION factors
Abstract

Natural compounds may bear promising therapeutic benefits against metabolic diseases such as type 2 diabetes mellitus (T2DM), which are characterized by a state of insulin resistance and mitochondrial dysfunction. Here, we examined the cellular mechanisms by which aspalathin, a dihydrochalcone C-glucoside unique to rooibos, may ameliorate palmitate-induced insulin resistance and mitochondrial dysfunction in cultured C2C12 myotubules. This current study demonstrated that aspalathin remains effective in improving glucose uptake in insulin-resistant skeletal muscle cells, supported by the upregulation of insulin-dependent signaling that involves the activation of insulin receptor (IR) and direct phosphorylation of protein kinase B (AKT). Interestingly, aspalathin also improved mitochondrial respiration and function, which was evident by an increased expression of carnitine palmitoyltransferase 1 (Cpt1), fatty acid transport protein 1 (Fatp1), sirtuin 1 (Sirt1), nuclear respiratory factor 1 (Nrf1), and transcription factor A, mitochondrial (Tfam). Importantly, our results showed that aspalathin treatment was effective in ameliorating the devastating outcomes of insulin resistance and mitochondrial dysfunction that are linked with an undesired pro-inflammatory response, by reducing the levels of well-known pro-inflammatory markers such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and protein kinase C-theta (PKC-θ). Thus, beyond improving glucose uptake and insulin signaling, the current study brings a new perspective in the therapeutic benefits of aspalathin in improving mitochondrial respiration and blocking inflammation to attenuate the detrimental effect of palmitate in skeletal muscle cells. [ABSTRACT FROM AUTHOR]

Published
2022
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33. Designing lattices for impact protection using transfer learning

Author

Gongora, Aldair E., Snapp, Kelsey L., Pang, Richard, Tiano, Thomas M., Reyes, Kristofer G., Whiting, Emily, Lawton, Timothy J., Morgan, Elise F., and Brown, Keith A.

Abstract

Like many specialty applications, the pace of designing structures for impact protection is limited by its reliance on specialized testing. Here, we develop a transfer learning approach to determine how more widely available quasi-static testing can be used to predict impact protection. We first extensively test a parametric family of lattices in both impact and quasi-static domains and train a model that predicts impact performance to within 8% using only quasi-static measurements. Next, we test the transferability of this model using a distinct family of lattices and find that performance rank was well predicted even for structures whose behavior extrapolated beyond the training set. Finally, we combine 812 quasi-static and 141 impact tests to train a model that predicts absolute impact performance of novel lattices with 18% error. These results highlight a path for accelerating design for specialty applications and that transferrable mechanical insight can be obtained in a data-driven manner.

Published
2022
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34. Trends in Academic Dentistry and Oral Health Research Funding by Gender

Author

C F Hildebolt, J P Tiano, O Contreras, M N Garcia, J Horsford, and D Stewart

Subjects
Male, Medical education, Biomedical Research, Dental research, education, Oral Health, Oral health, Dental education, Research Personnel, United States, National Institutes of Health (U.S.), Dentistry, Workforce, Original Reports, Humans, Female, Psychology, General Dentistry, health care economics and organizations
Abstract

Introduction: Dental and oral health researchers compose a small share of the research workforce, and within this group female researchers form a much smaller share than male researchers. Additionally, a majority of full-time faculty appointments at dental schools are held by men, with women making up only 39% of full-time appointments. These factors suggest that there could be disparities between men and women in obtaining research funding. Objective: The focus of our study was to determine whether there are gender differences in award funding obtained from the National Institute of Dental and Craniofacial Research or the National Institutes of Health (NIH). Methods: NIH administrative data were analyzed by focusing on Research Project Grants (RPGs), the primary and most commonly used mechanism to support investigator-initiated research projects. Analyses involved 1 or 2 of the following variables: number of unique applicants or awardees, fiscal years 2007 to 2016, average age of unique applicants, awardee’s degrees, awardee’s age at first R01, and award rates. Results: About two-thirds of RPG applicants and awardees were men. Although there were significantly more male applicants and awardees, there was no significant difference in award rate by gender, and there was no significant award rate variation through time or by degrees. The average ages of RPG applicants were similar for genders for all degrees, except that male dentists and PhD-dentists applying to the National Institute of Dental and Craniofacial Research were older and male MDs and PhD-dentists from dental schools applying to the NIH were older. Conclusions: This study demonstrated that men in the dental/oral health workforce submit more applications and receive more NIH awards than do women; however, there was no difference in award rates between women and men and no difference in ages by gender at which the first R01 awards are received. Knowledge Transfer Statement: Analyses of the implications of this study by the academic dentistry and oral health community could lead to establishing opportunities to expand the representation of women in dental and oral health research. Increasing the number of applications submitted by women may help achieve an equitable balance of grantees in the workforce.

Published
2019

38. SMAD3 Negatively Regulates Serum Irisin and Skeletal Muscle FNDC5 and Peroxisome Proliferator-activated Receptor γ Coactivator 1-α (PGC-1α) during Exercise

Author

Danielle A. Springer, Joseph P. Tiano, and Sushil G. Rane

Subjects
Male, medicine.medical_specialty, Blotting, Western, Peroxisome proliferator-activated receptor, Adipose tissue, White adipose tissue, Real-Time Polymerase Chain Reaction, Biochemistry, Cell Line, Mice, Transforming Growth Factor beta, Physical Conditioning, Animal, Internal medicine, Coactivator, medicine, Animals, Smad3 Protein, Muscle, Skeletal, Promoter Regions, Genetic, Molecular Biology, chemistry.chemical_classification, integumentary system, biology, Myogenesis, Skeletal muscle, Cell Biology, Transforming growth factor beta, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, FNDC5, Fibronectins, Mice, Inbred C57BL, Endocrinology, medicine.anatomical_structure, chemistry, biology.protein, Electrophoresis, Polyacrylamide Gel, Additions and Corrections, Transcription Factors
Abstract

Beige adipose cells are a distinct and inducible type of thermogenic fat cell that express the mitochondrial uncoupling protein-1 and thus represent a powerful target for treating obesity. Mice lacking the TGF-β effector protein SMAD3 are protected against diet-induced obesity because of browning of their white adipose tissue (WAT), leading to increased whole body energy expenditure. However, the role SMAD3 plays in WAT browning is not clearly understood. Irisin is an exercise-induced skeletal muscle hormone that induces WAT browning similar to that observed in SMAD3-deficient mice. Together, these observations suggested that SMAD3 may negatively regulate irisin production and/or secretion from skeletal muscle. To address this question, we used wild-type and SMAD3 knock-out (Smad3(-/-)) mice subjected to an exercise regime and C2C12 myotubes treated with TGF-β, a TGF-β receptor 1 pharmacological inhibitor, adenovirus expressing constitutively active SMAD3, or siRNA against SMAD3. We find that in Smad3(-/-) mice, exercise increases serum irisin and skeletal muscle FNDC5 (irisin precursor) and its upstream activator peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α) to a greater extent than in wild-type mice. In C2C12 myotubes, TGF-β suppresses FNDC5 and PGC-1α mRNA and protein levels via SMAD3 and promotes SMAD3 binding to the FNDC5 and PGC-1α promoters. These data establish that SMAD3 suppresses FNDC5 and PGC-1α in skeletal muscle cells. These findings shed light on the poorly understood regulation of irisin/FNDC5 by demonstrating a novel association between irisin and SMAD3 signaling in skeletal muscle.

Published
2015
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39. A prototype car converted to solar hybrid: project advances and road tests

Author

Gianfranco, Rizzo, Antonio, Tiano Francesco, Maria, D'Alessio Pietro, Matteo, Marino, Luca, Bonci, Antonio, Di Natale, Claudia, Bonaccorso, and Enrico, Bianconi

Abstract

A project for upgrading conventional cars to hybrid electric vehicles is presented. The project is carried out by four Italian partners within a EU project financed by the LIFE programme. Hybridisation to a through the road parallel hybrid structure is obtained by integration of wheel motors in rear wheels, the addition of an additional battery, of flexible photovoltaic panels and a Vehicle Management Unit. The technical aspects related to vehicle conversion and the results of test bench and road tests on first prototypes are presented and discussed, as well as the perspectives related to the industrialization of such system.

Published
2022
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40. Estrogen receptor α protects pancreatic β-cells from apoptosis by preserving mitochondrial function and suppressing endoplasmic reticulum stress

Author

Sushil K. Mahata, Senta Georgia, Prashant Rajbhandari, Marc Liesa, Vicent Ribas, Kenneth S. Korach, Karen Reue, Britany R. Reddish, Sylvia C. Hewitt, Timothy M. Moore, Peter Tontonoz, Franck Mauvais-Jarvis, Orian S. Shirihai, Nai-Wen Chi, Brian G. Drew, Kate Whitney, Joseph P. Tiano, Andrea L. Hevener, Amy H. Fluitt, Alexander M. van der Bliek, Laurent Vergnes, and Zhenqi Zhou

Subjects
0301 basic medicine, Cell Survival, Estrogen receptor, Apoptosis, CHOP, Biochemistry, Mitochondrial Proteins, 03 medical and health sciences, Mice, 0302 clinical medicine, Insulin-Secreting Cells, Mitophagy, Animals, Insulin, Molecular Biology, Mice, Knockout, Gene knockdown, Chemistry, Endoplasmic reticulum, Estrogen Receptor alpha, Molecular Bases of Disease, Cell Biology, Endoplasmic Reticulum Stress, Cell biology, Mitochondria, 030104 developmental biology, Metalloproteases, Mitochondrial fission, Female, Reactive Oxygen Species, Estrogen receptor alpha, 030217 neurology & neurosurgery, Transcription Factor CHOP
Abstract

Estrogen receptor α (ERα) action plays an important role in pancreatic β-cell function and survival; thus, it is considered a potential therapeutic target for the treatment of type 2 diabetes in women. However, the mechanisms underlying the protective effects of ERα remain unclear. Because ERα regulates mitochondrial metabolism in other cell types, we hypothesized that ERα may act to preserve insulin secretion and promote β-cell survival by regulating mitochondrial-endoplasmic reticulum (EndoRetic) function. We tested this hypothesis using pancreatic islet-specific ERα knockout (PERαKO) mice and Min6 β-cells in culture with Esr1 knockdown (KD). We found that Esr1-KD promoted reactive oxygen species production that associated with reduced fission/fusion dynamics and impaired mitophagy. Electron microscopy showed mitochondrial enlargement and a pro-fusion phenotype. Mitochondrial cristae and endoplasmic reticulum were dilated in Esr1-KD compared with ERα replete Min6 β-cells. Increased expression of Oma1 and Chop was paralleled by increased oxygen consumption and apoptosis susceptibility in ERα-KD cells. In contrast, ERα overexpression and ligand activation reduced both Chop and Oma1 expression, likely by ERα binding to consensus estrogen-response element sites in the Oma1 and Chop promoters. Together, our findings suggest that ERα promotes β-cell survival and insulin secretion through maintenance of mitochondrial fission/fusion-mitophagy dynamics and EndoRetic function, in part by Oma1 and Chop repression.

Published
2018

41. STATE OF ARTS OF MONUMENTAL STONES DIAGNOSIS AND MONITORING

Author

C. Riminesi and P. Tiano

Subjects
Moisture content, lcsh:Applied optics. Photonics, Schedule, Engineering, Salt content, Context (language use), Imaging techniques, 01 natural sciences, Civil engineering, lcsh:Technology, 010309 optics, Hardness, Spectroscopy techniques, 0103 physical sciences, Scheduled maintenance, Protocol (science), Planned maintenance, business.industry, lcsh:T, 010401 analytical chemistry, Portable diagnostic tools, lcsh:TA1501-1820, 0104 chemical sciences, Biodeterioration, lcsh:TA1-2040, State (computer science), business, lcsh:Engineering (General). Civil engineering (General)
Abstract

The conservation and maintenance of a monumental stone building is a complex aim where different disciplines are involved. First step is concerning the determination of the state of conservation of stone material present, than determine its modification on time, as such and after conservation treatments applied on: cleaning, protecting, strengthening. In order to fulfill such objectives suitable parameters must be selected and the most appropriate diagnostic techniques for their quantitative evaluation operated. In this context, the determination of the surface water absorption, moisture content, colour variation and mechanical properties are important parameters for the control, and the monitoring over time, of the state of conservation of the monumental stone surfaces. These parameters are strongly related not only to the stone characteristics but also to the evaluation of products’s performance: efficiency and durability. Their rate of variation, determined in monitoring campaigns, is fundamental for elaborate by properly predictive model a schedule maintenance protocol.

Published
2018

42. Molecular Mechanisms of Estrogen Receptors' Suppression of Lipogenesis in Pancreatic β-Cells

Author

Joseph P. Tiano and Franck Mauvais-Jarvis

Subjects
STAT3 Transcription Factor, medicine.medical_specialty, Time Factors, Estrogen receptor, AMP-Activated Protein Kinases, Models, Biological, Cell Line, Islets of Langerhans, Mice, Endocrinology, AMP-activated protein kinase, Insulin-Secreting Cells, Internal medicine, medicine, Animals, RNA, Messenger, Protein kinase A, STAT3, Carbohydrate-responsive element-binding protein, biology, Lipogenesis, Diabetes-Insulin-Glucagon-Gastrointestinal, Fatty acid synthase, Diabetes Mellitus, Type 2, Receptors, Estrogen, biology.protein, Sterol Regulatory Element Binding Protein 1, Fatty Acid Synthases
Abstract

The gonadal steroid, 17β-estradiol (E2), suppresses pancreatic islet fatty acid and glycerolipid synthesis and prevents β-cell failure in rodent models of type 2 diabetes. β-Cell estrogen receptors (ER) mediate these actions by suppressing the expression and enzymatic activity of fatty acid synthase (FAS). Here, we explored the mechanism of FAS suppression. We show that E2, and pharmacological agonists for ERα, ERβ, and the G protein-coupled ER, suppress mRNA and protein expression of the transcriptional regulators of FAS, namely, sterol regulatory element-binding protein 1c (SREBP1c) and carbohydrate response element binding protein (ChREBP) in insulin-secreting INS-1 cells. ER suppress SREBP1c and ChREBP mRNA and protein expression via an extranuclear localization. Using two mouse lines with pancreas-specific null deletion of either ERα or the signal transducer and activator of transcription 3 (STAT3), we show that ERα activation in vivo reduces SREBP1c and ChREBP mRNA expression via a direct islet action involving STAT3 activation. The master regulators of lipogenesis, liver X receptor (LXR) α and β, transcriptionally up-regulate SREBP1c and ChREBP. We find that activation of ERα, ERβ, and G protein-coupled ER suppresses LXR's mRNA expression in INS-1 cells. We also observe that activation of ERα in mouse islets in vivo suppresses LXR mRNA in a STAT3-dependent manner. Finally, we show that E2 also activates and uses AMP-activated protein kinase in INS-1 cells to suppress SREBP1c protein expression. This study identifies extranuclear ER pathways involving STAT3 and AMP-activated protein kinase in the genetic control of lipogenesis with therapeutic implications to protect β-cells in type 2 diabetes.

Published
2012
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43. Selective estrogen receptor modulation in pancreatic β-cells and the prevention of type 2 diabetes

Author

Franck Mauvais-Jarvis and Joseph P. Tiano

Subjects
STAT3 Transcription Factor, Selective Estrogen Receptor Modulators, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Estrogen receptor, Cell Line, Mice, Endocrinology, Insulin-Secreting Cells, Internal medicine, medicine, Animals, Raloxifene, Triglycerides, Hormone response element, biology, Raloxifene Hydrochloride, Article Addendum, Fatty acid synthase, Diabetes Mellitus, Type 2, Receptors, Estrogen, Selective estrogen receptor modulator, Lipogenesis, biology.protein, Female, GPER, hormones, hormone substitutes, and hormone antagonists, medicine.drug
Abstract

We recently showed that the female hormone 17β-estradiol (E2) protects against β-cell failure in rodent models of type 2 diabetes (T2D) by suppressing islet fatty acids and glycerolipids synthesis, thus preventing lipotoxic β-cell failure. E2 anti-lipogenic actions were recapitulated by pharmacological activation of the estrogen receptor (ER)α, ERβ and the G-protein coupled ER (GPER) in cultured rodent and human β-cells. In vivo, in mouse islets, ERα activation inhibited β-cell lipogenesis by suppressing fatty acid synthase expression (and activity) via an extranuclear, estrogen response element (ERE)-independent pathway requiring the signal transducer and activator of transcription 3. Here, we show that in INS-1 insulin-secreting cells, the selective ER modulator (SERM), Raloxifene, behaves both as ER antagonist with regard to nuclear ERE-dependent actions and as an ER agonist with regard to suppressing triglyceride accumulation. This additional finding opens the perspective that SERMs harboring ER agonistic activity in β-cells could have application in postmenopausal prevention of T2D. Additional studies using novel generation SERMs are needed to address this issue.

Published
2012
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44. Estrogen receptor activation reduces lipid synthesis in pancreatic islets and prevents β cell failure in rodent models of type 2 diabetes

Author

Franck Mauvais-Jarvis, Meenakshi Kaw, Cédric Le May, Saja S. Khuder, Sonia M. Najjar, Kenneth S. Korach, Martin G. Latour, Viviane Delghingaro-Augusto, Marc Prentki, Suhuan Liu, Surabhi A. Bhatt, Joseph P. Tiano, unité de recherche de l'institut du thorax UMR1087 UMR6291 (ITX), Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), and Université de Nantes (UN)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Male, STAT3 Transcription Factor, medicine.medical_specialty, medicine.medical_treatment, Cell, Estrogen receptor, 030209 endocrinology & metabolism, Islets of Langerhans, Mice, 03 medical and health sciences, 0302 clinical medicine, Insulin resistance, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Insulin-Secreting Cells, Internal medicine, [SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], medicine, Animals, Humans, Receptor, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, 0303 health sciences, biology, Insulin, Pancreatic islets, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, Lipid metabolism, General Medicine, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, medicine.disease, Lipids, Rats, Rats, Zucker, Disease Models, Animal, Fatty acid synthase, medicine.anatomical_structure, Endocrinology, Diabetes Mellitus, Type 2, Receptors, Estrogen, biology.protein, Fatty Acid Synthases, Gene Deletion, Research Article
Abstract

The failure of pancreatic β cells to adapt to an increasing demand for insulin is the major mechanism by which patients progress from insulin resistance to type 2 diabetes (T2D) and is thought to be related to dysfunctional lipid homeostasis within those cells. In multiple animal models of diabetes, females demonstrate relative protection from β cell failure. We previously found that the hormone 17β-estradiol (E2) in part mediates this benefit. Here, we show that treating male Zucker diabetic fatty (ZDF) rats with E2 suppressed synthesis and accumulation of fatty acids and glycerolipids in islets and protected against β cell failure. The antilipogenic actions of E2 were recapitulated by pharmacological activation of estrogen receptor α (ERα) or ERβ in a rat β cell line and in cultured ZDF rat, mouse, and human islets. Pancreas-specific null deletion of ERα in mice (PERα–/–) prevented reduction of lipid synthesis by E2 via a direct action in islets, and PERα–/– mice were predisposed to islet lipid accumulation and β cell dysfunction in response to feeding with a high-fat diet. ER activation inhibited β cell lipid synthesis by suppressing the expression (and activity) of fatty acid synthase via a nonclassical pathway dependent on activated Stat3. Accordingly, pancreas-specific deletion of Stat3 in mice curtailed ER-mediated suppression of lipid synthesis. These data suggest that extranuclear ERs may be promising therapeutic targets to prevent β cell failure in T2D.

Published
2011
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45. Efficiency and quality raising in preventive archaeology: work in progress of the project ARCHEO 3.0

Author

Andrea Azelio Mencaglia, Salvatore Siano, I. Cacciari, Silvia Rescic, G F Pocobelli, G Andreini, G Grosso, Fabio Fratini, R. Manganelli del Fà, Cristiano Riminesi, and P Tiano

Subjects
Engineering, business.industry, media_common.quotation_subject, Archeo 3.0, archaeological excavation, POR-CReO 2014-2020, multidisciplinary integration, Quality (business), Engineering ethics, Work in process, business, Raising (linguistics), media_common
Published
2018
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46. Extranuclear estrogen receptor-α stimulates NeuroD1 binding to the insulin promoter and favors insulin synthesis

Author

Benita S. Katzenellenbogen, Cédric Le May, Sylvia C. Hewitt, Franck Mauvais-Jarvis, Winifred P.S. Wong, Kenneth S. Korach, John A. Katzenellenbogen, Suhuan Liu, Stéphane Dalle, Joseph P. Tiano, unité de recherche de l'institut du thorax UMR1087 UMR6291 (ITX), Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), and Université de Nantes (UN)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
medicine.medical_specialty, Transcription, Genetic, medicine.medical_treatment, Estrogen receptor, Nerve Tissue Proteins, 030209 endocrinology & metabolism, Response Elements, Islets of Langerhans, Mice, 03 medical and health sciences, 0302 clinical medicine, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Internal medicine, Insulin receptor substrate, Basic Helix-Loop-Helix Transcription Factors, [SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO], medicine, Animals, Insulin, Promoter Regions, Genetic, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, Cell Nucleus, Mice, Knockout, 0303 health sciences, Multidisciplinary, Estradiol, biology, Estrogen Receptor alpha, [SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology, Biological Sciences, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, Protein Transport, Insulin receptor, Glucose, src-Family Kinases, Endocrinology, Organ Specificity, biology.protein, Mitogen-Activated Protein Kinases, Signal transduction, Estrogen receptor alpha, Tyrosine kinase, Protein Binding, Signal Transduction, Proto-oncogene tyrosine-protein kinase Src
Abstract

Estrogen receptors (ERs) protect pancreatic islet survival in mice through rapid extranuclear actions. ERα also enhances insulin synthesis in cultured islets. Whether ERα stimulates insulin synthesis in vivo and, if so, through which mechanism(s) remain largely unknown. To address these issues, we generated a pancreas-specific ERα knockout mouse (PERαKO −/− ) using the Cre-loxP strategy and used a combination of genetic and pharmacologic tools in cultured islets and β cells. Whereas 17β-estradiol (E2) treatment up-regulates pancreatic insulin gene and protein content in control ERαlox/lox mice, these E2 effects are abolished in PERαKO −/− mice. We find that E2-activated ERα increases insulin synthesis by enhancing glucose stimulation of the insulin promoter activity. Using a knock-in mouse with a mutated ERα eliminating binding to the estrogen response elements (EREs), we show that E2 stimulation of insulin synthesis is independent of the ERE. We find that the extranuclear ERα interacts with the tyrosine kinase Src, which activates extracellular signal-regulated kinases 1/2 , to increase nuclear localization and binding to the insulin promoter of the transcription factor NeuroD1. This study supports the importance of ERα in β cells as a regulator of insulin synthesis in vivo.

Published
2010
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47. Effect of targeted estrogen delivery using glucagon-like peptide-1 on insulin secretion, insulin sensitivity and glucose homeostasis

Author

Joseph P. Tiano, Richard D. DiMarchi, Bin S. Yang, Chandra R. Tate, and Franck Mauvais-Jarvis

Subjects
Male, endocrine system, medicine.medical_specialty, medicine.drug_class, medicine.medical_treatment, Cell Culture Techniques, Estrogen receptor, Biology, Article, Islets of Langerhans, Mice, Drug Delivery Systems, Insulin resistance, Glucagon-Like Peptide 1, Insulin-Secreting Cells, Diabetes mellitus, Internal medicine, medicine, Animals, Homeostasis, Humans, Insulin, Glucose homeostasis, Drug Carriers, Multidisciplinary, Insulin tolerance test, Estrogens, Middle Aged, medicine.disease, Glucagon-like peptide-1, 3. Good health, Glucose, Endocrinology, Estrogen, Body Composition, Insulin Resistance, hormones, hormone substitutes, and hormone antagonists
Abstract

The female estrogen 17β-estradiol (E2) enhances pancreatic β-cell function via estrogen receptors (ERs). However, the risk of hormone dependent cancer precludes the use of general estrogen therapy as a chronic treatment for diabetes. To target E2 to β-cells without the undesirable effects of general estrogen therapy, we created fusion peptides combining active or inactive glucagon-like peptide-1 (GLP-1) and E2 in a single molecule (aGLP1-E2 and iGLP1-E2 respectively). By combining the activities of GLP-1 and E2, we envisioned synergistic insulinotropic activities of these molecules on β-cells. In cultured human islets and in C57BL/6 mice, both aGLP1 and aGLP1-E2 enhanced glucose-stimulated insulin secretion (GSIS) compared to vehicle and iGLP1-E2 without superior efficacy of aGLP1-E2 compared to GLP-1 alone. However, aGLP1-E2 decreased fasting and fed blood glucose to a greater extent than aGLP1 and iGLP1-E2 alone. Further, aGLP1-E2 exhibited improved insulin sensitivity compared to aGLP1 and iGLP1-E2 alone (HOMA-IR and insulin tolerance test). In conclusion, targeted estrogen delivery to non-diabetic islets in the presence of GLP-1 does not enhance GSIS. However, combining GLP-1 to estrogen delivers additional efficacy relative to GLP-1 alone on insulin sensitivity and glucose homeostasis in non-diabetic mice.

Published
2015
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48. SO YOU WANNA FLY SCALE?

Author

TIANO, FRANK

Abstract

Some radial-engine airplanes can use opposed twin-cylinder engines to great advantage. Some can even use one of the new 4-cylinder engines, while other designs will have room for streamlined in-line twin-cylinder engines. Exclusive to radial-engine subjects, you might have a chance to substitute a large single-cylinder powerhouse for a more compact twin or 4-cylinder engine of more displacement. In most cases, switching over to multi cylinders ensures that all of the engine stays inside the cowl. [Extracted from the article]

Published
2020

50. VQ Warbirds Tiger Moth.

Author

TIANO, FRANK

Abstract

The article offers information on the Tiger Moth DH.82 model airplane from VQ Warbirds.

Published
2019

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